health

Ringworm

A Breeder’s Experience with Ringworm (Part 1)

Diagnosis Ringworm: The Summer of my OCD  I first saw innocent-looking scabs on one of the barn cats (Tiger) in late winter.  It looked like a line of tiny dots, about 1/3 of an inch long.  He got a second one some time later and I was not alarmed.  I thought he might be allergic to something.  I took Tiger to the vet and she surmised that he probably had an allergy and sent me home with some kind of allergy medication.  About a week later a second cat, Golden Boy, showed a similar scab.  At that point I realized that there was something contagious going on and took him back to the vet.  She ran a culture for fungus and looked at some tissue under the microscope and thought she might be looking at some kind of mite.  Well I wasn’t happy, but still thought things could be worse.  I dosed all of the barn cats with Revolution.  By then I had put one of the house cats in the barn for breeding.  A cat in the house, Happy, that had been isolated because she was new to the house and because the other queens couldn’t tolerate her, came down with a now-familiar scab.  I got the call a few days later and the nightmare began.  The culture showed ringworm and there was no doubt: a little colony of spores was growing in a bright red sea.  I am writing this to tell what worked and the mistakes I made that prolonged treatment  There are three parts of treatment for ringworm: treating from the inside out (medication), treating from the outside in (the dreaded sulfur dip baths), and treating the environment.  Here is a list of things I used to that end that I consider absolutely necessary: Itraconazole: sources below.   Lyme-Dyp (Lyme sulfur dip available at Revival) A Hurricane Mister ($170.00 at Revival) A-33 and Trifectant.  You should have this on hand anyway.  You use it in the mister. Gallons of Clorox and little 1-quart spray bottles, but keep in mind that Clorox is not     very effective on organic (wood) surfaces. An old fashioned dust mop, where you can remove the cloth part and launder it. A vacuum cleaner that you use only for the infected area.  Mine was about $80.00.   Lots of vacuum bags because you need to discard a bag every time you vacuum.   HealthGuard laundry additive from Revival  Here is what I think is very nice to have:  Your own cultures (revival charges about $50.00 + $30.00 for overnight shipping, which is necessary because it has to be kept cold.)   Sterile toothbrushes from Wal-Mart for doing toothbrush cultures Pinot Grigio, for obvious reasons  The medical treatment The first thing I did was order Sporanox from a local pharmacy.  The cost for 20 capsules was just over $200.00.  The dose was ½ capsule a day for 3 (10 lb) cats and 1/3 capsule a day for a fourth, (7 lb.) cat.  I divided each capsule in half, putting the little beads in another empty capsule.  It’s important that you put both halves in the same baggie because if day one is short for cat 1, it gets compensated for on day 2.  One cat got 1/3 of a capsule so she had a baggie with 3 capsules.  When dosing, I sprinkled the beads on Gerber’s baby turkey or chicken.  This was a huge treat for the cats: I’d scoop out a tablespoon of baby food and sprinkle the beads on it.  They’d gobble it up.  I did not plan to dose the one queen because I expected she was in the early stages of  pregnancy.    The original protocol was to give each cat Sporanox daily for 2 weeks and then “pulse” with Sporanox for 2 days a week for 6 weeks.   This was a mistake.  The cats should have been dosed with Sporanox daily for 4 weeks and then pulsed for 6 weeks: I ended up doing that eventually.    Rule # 1: Medicate all cats that have contact with the affected cat or its environment. Mistake #1: Don’t try to shorten the treatment to save money.  The external treatment: The next thing I did was order LymeDyp from Revival.  I bathed each cat, including the pregnant one, twice weekly for about 4 weeks.  Here is how I did it.  I brought each cat into the small part of a tile-floored bathroom and shut the door so it couldn’t escape.  I poured the lyme-dip over the cat, saturating with a washcloth while holding the cat on the floor.  Bengals are short-haired so it could have been worse.  I let the solution dry on the cat.  The snows did not turn too green.  Poor Golden Boy did feel the need to mark sections of the bathroom where he waited until the solution dried.  I used Urine-Off on those areas.  You can spot treat with Lyme-Dip too.  Mistake #2: I tried all kinds of preparations for spot treatments: This included Betadine, Clorox, and walnut hull extract and various antifungal creams.  I think it was all a waste of money except for the creams:  when I broke out, they were helpful for my own lesion.  Mistake #3: Program doesn’t work by itself and it doesn’t work combined with Lyme Dip.  As Matilda’s pregnancy developed, her baths became so traumatic that I stopped bathing her.  I treated her, unsuccessfully, with Program.  I had kept her in the barn because I didn’t want to expose the indoor cats, all of whom were breeding queens.  After awhile I moved her back into isolation in the house because, not having the Sporanox, she could re-contaminate the barn cats and the environment.  By that time, her skin had turned grey and she had lost hair on about 1/3 of her body and had lost weight.  At the 4th week of pregnancy, I began treating her with Sporanox, ¼ capsule a day.  She responded within days.  I treated her room the same way I treated the barn, vacuuming and disinfecting but not daily, more like every other day.  Sometimes I swept with a Clorox-solution-sprayed broom and followed up with a Clorox-solution-sprayed dust mop.  I put Matilda in a cage outside while the disinfectant dried, then disinfected the cage.  When I left her room in the house, I sprayed the soles of my shoes with Desenex.  By the time she delivered her kittens she was totally non-symptomatic.   I did the opposite with Happy.  When Matilda moved into the house, Happy was moved into the barn because she was on the same protocol as the barn cats.  When Happy went into the barn, I disinfected the room she’d been in, including the underside of the bed she liked to sleep under, and I sent the rug out for professional cleaning.  That’s when I found my diamond bracelet, lost some 9 months before: the cats had thrown in on the floor and scooted it to the inside center of the rug, between the rug and rug pad.   Here’s the environmental protocol:  Take all bedding and wash it daily and rinse with HealthGuard Throw away all carpeted cat furniture.  It will only reinfect.  This hurt, as I’d invested at Least $500.00 in cutsie little towers and stuff.   Throw out all plastic dishes.  They contribute to acne anyway. Soak all food dishes in Clorox 1:10 overnight (Use a plastic bucket—metal gets kind of      funny.) Vacuum daily.  Then remove the bag, spray the vacuum inside with Clorox and water 1:10, including the little filter thing.  Soak the wand and attachments that you use in the same dilution of Clorox.  Buy stock in Clorox. Mist with your Hurricane Mister daily, using A-33. You do this until you get negative     cultures, about 6 weeks.  My cats were in the runs while I did this.  After the A-33     dried, they’d go back in the barn, and I’d disinfect the runs. Don’t forget to disinfect the little cat doors or flaps—especially if they’re “double,”  installed in walls. Throw out all litter daily, mist the litter boxes with A-33 and put them in the sun.  Fill the ones you cleaned yesterday with clean litter.   After being in the environment with the ringworm, remove your clothing, wash and rinse in Healthguard.  Don’t track the spores through your house, they are airborne.  Install an air conditioner.  In summer, my barn would have been a Petri dish without it.  Don’t forget to disinfect it, though. Varnish or paint all wood surfaces: ringworm loves wood.  Rule #2: decontaminate everything, every day.  Send your own carpets out for cleaning if your cats have been in the same room with them.  Mistake #4: scrubbing your carpeted cat furniture can’t kill all the spores even if you leave them out in the sun.  Matilda was miserable in isolation and paced and whined constantly.  At 4:00 a.m on the  morning she delivered, I put her back in the barn because she was keeping me awake with her crying (she’d been on Sporanox for 5 weeks at that point).  I went out at 6:00 a.m. to feed the cats, and she had just delivered her first kitten, placenta as yet undelivered.  I scooped her and the attached kitten up and carried them back into her room, where she delivered another 5 kittens.  No kitten broke with ringworm, ever.  However, one kitten had pectus excavatum, apparently unrelated to the Sporanox.  Rule #3: use the list members as resources.  Breeders hide ringworm, as if it were a social disease.  We probably need to stop that.  This is the place where I want to thank people who offered me advice: I am not mentioning names because a few of you asked that your experiences be kept private and I can’t remember which ones wanted that.  But I do remember who told me about the Hurricane Mister, who helped me work with the cultures, who advised me that only 2 weeks of Sporanox was not enough and who supported me in giving Sporanox to my pregnant queen.   And on and on.  Sources of Itraconazole: Sporanox 100mg at your local pharmacy: $200.00 for 20 capsules Sporanox at Universal Drugstore in Canada: About $125.00 for 30 capsules (at least 3 weeks for delivery) Sporal 100 mg at 1meds.com: $75.00 for 52 caps (from Southeast Asia but delivery  within a week, no prescription necessary. Sporal 100 mg at 1Drugstore-Online.com: $152.00 for 40 caps You can also get a generic Itraconazole from Mexico that some people swear by but my vet warned me against.  There is powder in the capsules making it harder to  divide, but it’s the cheapest yet, $30.00 for something like 40 capsules.  Here’s how you run a culture Take a sterile toothbrush and run it over your cat’s fur, with special attention to the neck area..  with sterile tweezers, place the hairs you get on the culture medium.  Press them into the medium.  Cap it, label it, then loosen the cap.  Keep it in a dark place and look at it daily.  The mold for ringworm has to grow at the same time the medium turns red.  If your cat is taking Sporanox, do not consider the test negative before 3 weeks time.  If it is not medicated, and there is ringworm, you should see growth within a week but keep it for 3 weeks.  Timeline The first 4 weeks: Sporanox daily, vacuum & disinfect daily, 2 dips weekly  The next 6 weeks: “pulse” with 2 days on, 5 days off, reduce cleaning to every other day At 5 weeks, run 1st culture At 7 weeks, run 2nd culture.  Decontaminate weekly after 2nd negative culture.  Rule #4: Symptomatic cure is not mycologic cure.  You can’t tell if the cat is cured by looking.  Cure is 2 negative cultures, 2 weeks apart.

A Breeder’s Experience with Ringworm (Part 2)

Ringworm Treatment

Several years ago I had a ringworm outbreak and 2 cats had dark grey pigmentation in the area where they lost their hair.  Oddly the other cats simply had scabs, but they all had ringworm.  I wrote this in reply to someone’s post on one of the lists and immediately had several people e-mail for more information so I’m downloading.

First you put every cat on Sporanox once a day for 4 weeks.  I’d culture at 3 weeks and if it’s negative “pulse” with 2 days on 5 days off until you get a second negative culture at 6 weeks.  That’s the easy (but expensive) part.  you can get Sporanox cheapest from 1meds online–they import if from Thailand.  You can also get if from your local pharmacy at $10.00 a capsule and I’d be inclined to do that to get treatment started right away.  Each 8-10 lb cat gets 1/2 capsule a day.  Smaller cats get 1/4 -1/3 capsule.  You can sprinkle the little beads on Gerbers turkey or chicken and the cats think they’re getting a treat.  When you divide the capsules, put the unused part in a baggie with that cat’s name so if you’re short one day you make up for it the next.  My vet does not trust the sporanox from Mexico so I never used it.  The Thai  brand is called “Sporal”  and it’s made by Jannsen.
 
The huge thing is the environmental cleanup. You need a Hurricane sprayer (Revival) which will set you back $175.00 but is absolutely essential.  You need also A-33 (Revival) and Healthguard (also Revival).  I also bought a cheap vacuum specifically for the use of the cat barn where I had the ringworm.  Lay in a supply of bags because you’ll change it every day.
 
Throw out any cat furniture that has carpet covering.  you simply can’t guarantee that you’ll kill the fungus in them.
 
Here is what you do every day for one month: Put the cats in a cage.  Vacuum the area where the cats live,  Wash all flat surfaces with Clorox and water 1:10 and then spray everything with A-33.  Be sure you get the walls and cat flaps.  Let the cats back in when it dries and then do the same for the cages that they were just in.  Then  discard the vacuum bag and spray the inside of the vacuum with 1:10 clorox and water & rinse out the little filter.  Soak the vacuum hose and attachments in clorox and water.  Sun is good–everything should dry in the sun.
 
Empty every litter box and hose down every toy and litter box and spray with A-33.  Every day.  Leave in the sun to dry.  Every day collect your feed dishes and soak them in clorox and wather over night.  throw out any soft toys that you can’t soak in clorox.
 
You bathe each cat twice a week in Lyme Dyp for about 4-6 weeks.  Let the solution dry on them.  I did mine in a tiled bathroom and stood them on the floor and poured the solution over them.  It smells awful and discolors metal.
 
Wash any cat bedding and the clothes you wear for cleaning in clorox and water every day and rinse with Health Guard.
 
Be careful of your clothing.  When you finish cleaning put your clothing directly in the wash–don’t walk around it it.  I also sprayed the soles of my shoes with desenex spray whenever I left a contaminated room.
 
Don’t skimp on any of this (especially the 4-weeks of Sporanox) because you’ll just prolong the treatment.  You can get your own culture medium from (again) Revival and save a lot of money on vet fees.  What I did was bring my cat to the vet for a final culture 3 weeks after I had 2 negative cultures.  You give the culture 3 weeks to grow after they’re on the Sporanox because that inhibits the growth but there could still be live fungus.
 
The disappearance of the symptoms does not mean cure–you need the full four weeks of Sporanox.  After that, I cleaned about every 3 days for several months.  Now I do once a week.
 
For this to work you need to confine the cats to a small living area–I don’t know your circumstances.  My affected cats were in my cat barn and I brought one pregnant queen into a spare bedroom because she couldn’t ahve the sporanox until her pregnancy was advanced and I was afraid she’d continue the contamination,
 
After it was all over I sent my inside rugs out for cleaning and sprayed my whole house with A-33.  This was nearly 3 years ago and I’ve not had ringworm since.  (When I rolled up one rug to send it out I found a diamond bracelet that had been missing for months–the cats had pushed it under the rug)

Ringworm and Lufenuron (Program) – by Carol Johnson DVM

Science and the Breeder: Ringworm and Lufenuron

Carol W. Johnson, DVM PhD

Microsporum canis, the most common cause of ringworm, is a parasitic fungus that is highly adapted to cats. Once introduced into a cattery, ringworm can rapidly spread and can infect most or all of the cats in a cattery before the breeder is aware that there even is a problem. In an infected cattery, the lesions often appear to resolve in adult cats after several months and kittens often will no longer show lesions as they approach maturity. In most cases, however, these cats still harbor low levels of fungus and serve to infect the kittens that are born into a cattery. Ringworm can also infect humans. While ringworm infections tend to be self-limiting in most adults, children and immunosuppressed individuals may develop severe infections that may take weeks or months to eradicate. One elderly woman told me of suffering for months after her children surprised her with a purebred kitten to provide companionship during her post-kidney transplant convalescence. The kitten carried ringworm and the poor woman developed huge skin sores and lost her hair. She became quite ill from the antifungal treatment, then almost lost her transplanted kidney during the effort to get rid of the fungal infection. Children, also, can get very severe lesions and ringworm infections of the head are considered to be fairly serious by pediatricians.

Some of the biggest impediments to all catteries becoming ringworm-free has been the expense of treatment and the limited safety of the less expensive drugs. Griseofulvin (Fulvicin) is inexpensive and moderately effective against ringworm, but causes severe neutropenia and immunosuppression that can be fatal in up to 10% of the treated cats. Itraconazole (Sporonox) is much more effective and safer, but can cost up to $200 to treat a cat. Those of us who claim a ringworm-free cattery have often had to spend thousands of dollars to maintain that status and treatment of a large cattery is often beyond the economic ability of some breeders. However, an exciting recent article [Ben-Ziony Y, Arzi B. Use of lufenuron for treating fungal infections of dogs and cats: 297 cases (1997-1999) JAVMA 217(10) (Nov 15) 2000] describes what may prove to be an economically viable treatment and prevention for ringworm.

A veterinarian in Israel noted that dogs and cats treated with lufenuron for flea prevention did not appear to develop ringworm, even though they were not being treated for ringworm. Lufenuron (sold in the US by Novartis under the brand name PROGRAM) is a chitin synthetase inhibitor used for flea control. Chitin is a structural molecule in the exoskeleton of insects and their eggs. After administration, lufenuron sequesters in the fat and is slowly released into blood where it is ingested by a female flea. The drug then interferes with the production of chitin in the eggs, which leads to the eggs drying out after they are laid. Chitin is not found in mammalian tissues, but is a structural component of the fungal cell wall. Thus, this drug does not appear to affect mammalian enzymes and as a result has had an excellent safety record when used according to its product insert.

The Israeli clinic systematically tested lufenuron in ringworm-infected cats and dogs. Over the 2-year period, they treated 201 cats and followed 23 on a daily basis. Most cats treated with lufenuron doses ranging from 51.2 to 266 mg/kg (23.1 to 120.9 mg/lb) cultured negative for ringworm in 8.3 days and began growing hair in 12 days. Four cats either cultured positive for ringworm or developed lesions again but responded well after a second treatment. None of the cats showed signs of toxicity.

I had some concerns regarding the safety of this treatment because the article used between 5 and 20 times the recommended dose used to treat fleas, so I called Novartis’ Customer Service line and spoke with a veterinarian. He reported that Novartis had no information on the use of lufenuron for ringworm and the article took the company by surprise. Because this is off-label use, he can not recommend the drug for this indication. However, Novartis is very excited about the article and its potential. We extensively discussed the safety data Novartis had performed for registration, and then I reviewed the safety data on the FDA website made possible through the Freedom of Information Act. Safety studies in both dogs and cats showed the drug had a wide margin of safety. Reproduction studies were performed in dogs and cats and lufenuron did not to cause toxicity or congenital defects at the doses tested. Because this is off-label use and one article does not prove efficacy or safety, I can not recommend lufenuron for the treatment of ringworm in cats. However, for those breeders determined to try it, I have some suggestions.

Lufenuron is sold under the brand name PROGRAM. SENTINEL also contains lufenuron, but in addition contains milbemycin, which may be toxic when given at the overdoses suggested by the article. So do NOT use SENTINEL for ringworm. Lufenuron comes as a tablet, a suspension, or as an injectable. The injectable lasts 6 months, but can leave a lump (granuloma) at the injection site, and this may be a consideration for show cats. Novartis found that the tablet appears to have better efficacy than the suspension. I have not used PROGRAM, but understand that some cats do not like the taste of the suspension, so this may be a consideration when treating some cats.

If you are going to try it to see if it works on a few cats, try to keep them separate from other ringworm-infected cats. Ringworm, like many parasitic organisms, can become drug resistant and it will do neither the breeder nor the rest of the cat fancy any good to develop Lufenuron resistant ringworm. Similarly, once the decision to treat a cattery is made, break down, bite the bullet, and treat the whole cattery and not just a few cats. Couple treatment of cats with physically cleaning the cattery to get rid of the spores so the cats are not reinfected. Getting rid of the problem will be cheaper in the long run than living with it and will be much less likely to generate resistant forms.

Plan to treat once monthly for 2 to 3 months to make sure it is really gone. Yes, the article had good success after one treatment, but a cattery situation is very different than the average pet household. If it works please let other breeders know! Me? I currently have a ringworm-free cattery. But I sometimes show adjacent to cats that have ringworm lesions (yes, I notice those things) and have, on occasion, brought ringworm home from the shows. So I will probably treat my show cats with the lufenuron dose recommended for fleas. At those doses it is unlikely to hurt the cats and may help keep them from bringing ringworm home.

Treating Ringworm – by Donna Stewart DVM

Treating Ringworm

by DR. Donna Stewart

For ringworm, I highly recommend the protocol outlined by Lorraine Shelton with a little modification. I have found fluconazole to be superior to other anti-fungals and recommend 5mg/lb once a day unless a cat is under 2#.

Don’t forget the Program. You will see a jump start in recovery when you give it, but it will not be sustained. Keep using it every 2 weeks. I give a 400 mg tab to a grown cat, 200 mg to a cat 4-6#, and 100mg to a nursing kitten.

The azoles and griseofulvin cannot be used on pregnant cats and the azoles affect male fertility. Pregnant cats are the greatest challenge. I have tried Lamosil and in one case it appeared to blister the ears. These cats require more bathing and religious use of Program until giving birth. The azoles do reach the milk, however, it does not seem to have adverse effects on the kittens that dosing them individually does. I do not recommend the azoles to kittens under 1#. It adversely affects the liver. These kittens will sit around hunched up as if they have abdominal pain and they will not eat. Discontinuing the medication and supportive care will allow them to recover, however, I would just recommend more vigorous bathing and program. I personally cannot stand the odor of lime sulfur and do not use it, but if you use it in nursing queens, be sure to rinse well.

I also recommend isolation in quarters where all surfaces can be cleaned daily with 10% bleach. That means that you not use any fabrics except a blanket for bedding that can be washed. There should be no carpeted cat furniture. Consider any horizontal surface and any litter dust to be contaminated with spores. Sweep up all dust and loose litter daily and throw away. Wipe down all horizontal surfaces with 10% bleach daily.

Bathe the cat 3x weekly with miconazole shampoo for the first couple of weeks and then when he is not getting any new spots, bathe 2X weekly. Change his bedding with every bath. If he gets lesions on his feet, throw out the litter and start fresh. If he is getting lesions on his head, dismantle the cage and clean vigorously with 10% bleach.

Think about isolation and cleaning. The vacuum cleaner, whisk broom and any other objects using for cleaning are contaminated with spores, so set aside the items to only be used around the contaminated area. Clean them with 10% bleach after using them. Use gloves around the infected cat(s), care for them last, and wash well after caring for infected cats to prevent spreading it throughout the cattery.

Good luck. I know it seems too hard, but persistence pays off. Donna

Treatment Protocol for Ringworm – by Lorraine Shelton

From the archives of the Fanciershealth group on Yahoogroups (updated 4/28/06)

Treating feline ringworm (microsporum canis infection) can be one of the biggest health challenges that can face a cat breeder. Ringworm can be a self-limiting disease that will often “cure itself” in 4-6 months in adult, shorthaired cats with strong immune systems. However, longhaired cats, kittens, and cats with weaker immune systems usually need an aggressive approach to completely clear them of “the grungy fungi.” This is a zoonotic disease (transmittable to humans), so it should not be taken lightly by cat fanciers. Ringworm can not be successfully treated by applying topical creams or solutions to a cat. The only effective and efficient way of curing a cat or a whole cattery of ringworm is to combine the use of an oral antifungal drug with a topical treatment and to thoroughly clean the environment to prevent reinfection.

Griseofulvin (Fulvicin) is the most commonly used antifungal drug. Treatment must continue for at least 12-16 weeks. Some cats, in particular Persians, can experience a deadly form of bone marrow suppression or liver damage when treated with Fulvicin. This reaction is independent of the dose received. The dose for Fulvicin is 7 mg per pound of the microsized formulation twice a day, or 3.5 mg per pound of the ultra-microsized formulation twice a day. Fulvicin must also be given with a fatty meal to be absorbed. Fulvicin should not be used in breeding males, pregnant queens, or within less than two months of breeding a queen.

Safer and more effective antifungal drugs include itraconazole (Sporonox) at 5 mg per pound once a day, fluconazole (Diflucan) at 5 mg per pound once a day or every other day, and terbinafine (Lamisil) at 20mg per pound once a day. Mycological clearance with these drugs usually takes about half to 2/3 the time of treatment with Fulvicin. These drugs should not be used in pregnant queens, but do not affect males like Fulvicin does. No comparative, controlled studies have been performed to find out which of these three newer drugs is more effective. Ketoconazole (Nizoral) is far more toxic than any of the other drugs mentioned and should not be used in cats.

I personally recommend as an adjunct treatment, because of its extremely low toxicity and expense, the use of Program (lufenuron) at 40-50 mg per pound every two weeks. It is better to “overdose” than to underdose. All adult cats should receive one of the largest dog tablets (450 mg).  Kittens can be treated anytime over the age of eight weeks and should receive half of a large dog tablet or one complete liquid dose of the large cat size oral suspension. Treatment of kittens under eight weeks of age is off-label, but there is no reason to believe it would not be harmless. Program is safe in pregnant and nursing queens. Program is only absorbed if given with a LARGE meal, the fattier, the better. Mix the crushed tablet up with a treat your cat will gobble up and then follow it immediately with your cat’s favorite meal. For high risk catteries (and I consider ALL Persian catteries “high risk”), owners may wish to continue to dose once a month indefinitely. Although the ability of Program to prevent ringworm has been disproven in controlled studies, this drug does appear to have a slight inhibitory effect on ringworm growth. However, Program should never be used alone to try to treat a ringworm infected cat. IMPORTANT: The injectible form of Program can not be substituted for the oral form.

The only topical treatment proven to be efficacious in controlled laboratory studies is lime sulfur dips (1:32 or 1:16 dilution). Do not shave short or medium coated cats, as the skin irritation caused by the clipper blades can cause the ringworm infection to become worse. Persians, however, should be shaved with a #10 blade (not a surgical blade) because of the large volume of hair that can cause reinfection of the cat and its environment. Clipping also opens up the hairs and releases spores, but for Persian cats the advantages of clipping outweigh the disadvantages. Cats should be shaved off the premises, if possible, to prevent contaminating the environment with spores from the broken hairs. Throw away the clipper blade and immediately dip the cat in lime-sulfur afterwards. Lime-sulfur is safe in kittens, pregnant, and nursing queens. Do not allow the cat to lick itself until the dip has dried (collar if necessary). After the lime sulfur has dried, wash the nipples of nursing queens before reintroducing kittens. Dip at least once a week, twice a week is preferred.

Other shampoos have claimed to be fungicidal, but none have demonstrated efficacy by independent laboratory testing as yet. Stated efficacy against the microsporum canis fungus itself is insufficient, it is the SPORES that cause reinfection. Shampooing cats can make them worse, as the hairs break off from scrubbing and infect the surrounding skin. Dipping is better.

Once a week eniconazole dips (0.2%) have also been demonstrated to be effective to treat cats topically for ringworm, but there have been scattered reports of toxicity. Care should be taken and a Elizabethian collar used until the cat is completely dry to prevent the cat from ingesting the dip.

TREAT EVERY CAT IN THE HOUSE. Not doing so will only create a cattery with chronic carriers of ringworm and recurrent infections.

 Cleaning up the environment is the hardest part. The spores are almost unkillable, only concentrated bleach, highly carcinogenic chemicals that you don’t want in your home, and enilconazole are effective in fighting the spores. Some folks have reported success fogging with solutions such as Virkon, but the efficacy of this agent has not been confirmed by controlled laboratory studies. Bleach only works on a CLEAN surface, it does not work in the presence of organic material, so dipping cats in bleach is worthless. Treating the environment with enilconazole (Clinifarm fogger) is effective, but there may be toxicity issues with cats, so this should be used with care.

Keep in mind that the spores are carried inside of hairs, so removing all cat hair from the environment is the most important cleaning step. Discard all carpeted/fabric surfaces if possible. Bleach all surfaces (A freshly prepared solution of 1:10 bleach is recommended and should be applied multiple times). High temperature steam may also be effective. This is not the normal steam cleaning offered by your local furniture and carpet cleaner… you need HIGH TEMPERATURE steam. And vacuum, vacuum, vacuum, discarding the bag each time and spraying down the vacuum with 1:10 bleach after each use. Buy a true HEPA filtered vacuum. Blow torching metal cages is an excellent apporoach if you have the resources to do so.

The ringworm vaccine is worthless as a preventative, but may help individual cats clear their lesions faster. It is no longer marketed in the United States. Not all ringworm can be visualized with a Wood’s Lamp (“black light”). Do not rely on this as a diagnostic tool.

Other diseases CAN mimic ringworm, most notably body mites. If treatment with antifungal drugs is not working, treat with ivermectin twice, two weeks apart, and see if there is improvement. Not all ringworm looks the same. Ringworm can be completely asymptomatic or exhibit itself as a mild case of “dandruff”, skin discoloration, subcutaneous “tumors”, or large weeping lesions. Some cats are more susceptible to ringworm than others and this susceptibility can be inherited. Ringworm outbreaks can be a symptom that a cat has a weakened immune system.

How long do you treat? This is the question I get asked most often. There is only one answer: AS LONG AS IT TAKES TO ACHIEVE MYCOLOGICAL CLEARANCE. There is no “magic time” after which your cats will be cured. You can only determine whether your cats are cleared of the infection through CULTURING. The Mackensie brush technique is used to screen for ringworm. A new, sterile toothbrush is combed through the entire coat of the cat and then pressed into culture medium. Multiple cats can be cultured on one culture “slant” to help keep costs down when screening an entire cattery. Isolate cats that still culture positive from cats that culture negative. Keep treating and culturing until two cultures of the entire cattery come back negative, done at least a week or two apart. DO NOT assume a cat is “cured” simply because the lesions are gone. Cats with no lesions whatsoever can be your most potent carriers and sources of reinfection. Isolate cats as they culture negative for ringworm.

To prevent infection in the first place, culture all incoming cats before and after their quarantine period. Isolate all show cats and bath them upon returning from a cat show. But despite your best efforts, reinfection *is* common.

Ringworm has been described as “an extremely well evolved parasite of feline keratin”. It isn’t easy to avoid. The most successful warriors in this battle are the most aggressive and the most determined. DO NOT GIVE UP. Good luck!

–Lorraine Shelton

Feline Leukemia Virus

Although my cat has tested positive, it is healthy in all other respects. How can I prevent an FeLV-related disease from becoming active in its system?

There is no sure way to keep your cat healthy. Eventually, an FeLV-related disease will probably develop no matter what you do. However, one way in which a disease is likely to develop is if you stress your cat’s system. If a cat’s system is stressed, its body can’t put as much energy into fighting off illnesses (just like you always seem to get sick during exams or when you have to make a presentation to your boss). “When all my cat does is eat and sleep 20 hours a day, how can it possibly be stressed?” you may ask. Anything which is upsetting or unpleasant for your cat may stress it, such as going for very long periods without food or water, overcrowding, movement to new territory, territorial conflicts, sending your cat to be boarded for long periods of time, or pregnancy and lactation. (Of course one should NEVER breed a FeLV+ queen as it will expose not only the tom, but all the kittens will be FeLV+. There is also an indication, although no proof, that FeLV causes abortions in queens. For the same reasons, neither should FeLV+ toms be bred.) Basically, keep in mind things which you have noticed in the past that seriously upset your cat. These are things which are more likely to lower your cat’s natural immune system and give a disease the chance to attack.

Do I have to get my cats vaccinated?

No one can force you to vaccinate your pets, though there are laws in some areas regarding certain diseases like rabies. Check with your vet to see what vaccines are required in your area.

Feline Leukemia References?

References

  • CancerNet Factsheet is available via gopher to gopher.nih.gov following the menu path Health and Clinical Information/CancerNet Information/Fact Sheets from the NCI/Risk Factors and Possible Causes. Or you can call the Cancer Information Service toll free at 1-800-422-6237 (1-800-4-CANCER).
  • Hardy, William D., Essex, Myron, and McClelland, Alexander J. (eds). Feline Leukemia Virus. Elsevier/North-Holland, Inc. New York, 1980.
  • Loar, Andrew S. “Feline Leukemia Virus: immunization and prevention” in Veterinary Clinics of North America: Small Animal Practice. 23(1):193-211, 1993.
  • Barlough, J.E. “Seriodiagnostic aids and management practice for retrovirus and coronavirus infections” in Veterinary Clinics of North America: Small Animal Practice 14(5):955-969, 1984.
  • Olsen, R.G. et al “Oncogenic viruses of domestic animals: in Veterinary Clinics of North America: Small Animal Practice 16(6):1129-1144, 1986.

 

Additional Readings

  • Hardy, W.D. Jr, et al. “Biology for Feline Leukemia Virus in the natural environment” in Cancer Res. 36:582, 1976.
  • McClleland, A.J. et al. “Prognosis of healthy Feline Leukemia Virus infected cats” in Rev. Cancer Res. 4:121, 1980.
  • Rojko, J.L., and Hardy, W.D. Jr. “Feline Leukemia Virus and other retroviruses” in The Cat: Diseases and Clinical Management, NY: Churchill Livingston, 1989.
  • Rojko J.L. et al. “Reactiviation of latent Feline Leukemia Virus infection” in Nature (Lond.) 198:385, 1982.
  • Also, the Journal of the Am. Vet. Med. Association, 199(10), Nov. 15, 1991 is devoted entirely to feline viral diseases.

How is FeLV detected?

Your vet will do a blood test; there are two types of blood tests which can be performed. Some vets will automatically do one of the tests before vaccinating your cat to make sure it is not already positive for the virus. The first (ELISA test) is where the vet takes some of your cat’s blood, mixes it with a chemical and watches for a color change. If the blood changes color then your cat has tested positive for the virus. False positives are not uncommon in this form of test, so if your cat tests positive it may be a good idea to have it retested. “Light positives” are where the treated blood only changes color slightly. This means your cat is infected with the virus, but the virus is not very active in its system. The second type (IFA test) involves sending the blood sample to a special lab. This lab tests to see if the virus is being produced in the bone marrow. If this second test is positive, it is unlikely that your cat will ever test negative. Below is a flow chart (from a lecture by Dr. William Hardy, U of Penn. Vet School) which depicts what you should do if your cat tests positive on the ELISA test:

  • If positive:

    • whether healthy or sick, confirm by Indirect Fluorescent Antibody test (IFA)

     

  • If negative:

    • if healthy and not exposed to a positive cat then no need to retest
    • if healthy but exposed to a positive cat then retest in 3 months because the healthy cat may be incubating the virus.
    • if sick then confirm the ELISA test with an IFA test

How is it transmitted?

FeLV is transmitted via saliva, mucus, urine, feces and blood. This means mutual grooming and biting/fighting are the most likely methods of transmission, although sneezing, hissing, sharing food/water bowls and sharing litter boxes are also possible means of transmission.

How long does a cat who tests positive have to live?

There is no set time period for how long an FeLV+ cat will live. One person on the internet said they had a cat which lived for 20 years with the virus, while others have given dates as long as 10 or 12 years, although these are probably extremes. I have not found any truly long-term studies to document, but it seems that of the studies done, 83% of FeLV+ cats do not live beyond 4 years. (Hardy, et al 1980). All cats which do not later test negative, but in all other ways are healthy, are carriers for the virus. Even though they do not have acute symptoms, they can still spread the virus to cats which are not infected. Often people do not have their cat tested for the presence of FeLV until the cat is noticeably sick, and by this time the FeLV-related disease may have progressed too far for the cat to recover.

I already have a cat(s) and I found another which I want to bring home. What precautions should I take regarding FeLV (and other diseases)?

This depends on the environment the new cat comes from. If it is a stray, or from a shelter which does not routinely test for the viruses (make sure you ask this of any shelter you visit), or from a household where you have reason to doubt the person has had the cat tested/vaccinated, then keep the new cat separated from yours until you can have a vet examine it for many things. Keep it in a separate room and provide its own food dish, water bowl and litter. DO NOT let your cats share any of these things, or share the same space, until your vet checks out the new one. If it is a stray cat, it may never have been vaccinated against FeLV and Rabies, or if it was a housecat it may be past its time for an update and have been exposed. Cats which have been on the street may also have fleas, tapeworm, ringworm or other parasites which are transmittable to you and your pets.

One of the most unfortunate situations that occurs far too often is when someone, out of the kindness of their heart, takes in a stray or unwanted cat — either permanently or in the hopes of finding it another home. This is often done spur-of-the-moment, and unfortunately sometimes has dire consequences. If you find a cat in a bad situation and you want to help it, keep it isolated or ask your vet to board it until all the test results have returned. It is never worth the lives of your current pets in an attempt to save another.

I have an FeLV+ cat and I want to find it a playmate. What should I do?

There a few options. The only thing which you really ought NOT to do is get a healthy cat as a playmate or let your cat outside for excitement. Dogs cannot become infected with the Feline Leukemia Virus, and some dogs and cats, especially those raised together can be very close. One word of warning: getting a dog (or any pet) for the sole reason of keeping a cat company is not a good idea. If you consider getting a dog, make sure you understand the amount of time and responsibility that goes into caring for a dog (which is much more than that of a cat); otherwise you will regret the decision and both you and the dog will suffer. (There are excellent dog FAQs which will give you as much information on the matter as you can handle).

Another option is getting a second FeLV+ cat. The obvious down side is that you not only have twice the vet bills, but you also put yourself at risk for twice the heart-ache when one or both become ill. However, if you are willing to take the risk you can search for FeLV+ cats by putting an ad in the newspaper and calling all your local vets and animal shelters and explaining your situation. They may put you on a list and should they receive any cats which test positive, they may give you a call. Make sure you give your current vet as a reference as most shelters and other vets will want to make sure you understand the responsibility of owning an FeLV+ cat or to make sure that you are not some psychopath looking for sick kitty-cats to do nasty things to (of course most people, especially your relatives, will think you are a psychopath anyway, for keeping and seeking out more FeLV+ cats).

I have an FeLV+ cat that is otherwise healthy, I do not want to put it to sleep, but I can’t keep it. What can I do?

Similar to the above answer, place ads in the newspaper and contact your local shelters and vets and tell them you have an FeLV+ cat which you are willing to give to a good home. A good home is someone with another FeLV+ cat, or someone who does not have any other cats and will keep the cat indoors. Also, there are animal shelters which specifically take in FeLV+ cats. Again, contact your local vets and shelters to see if they are aware of any such haven to which you could send your cat. Almost all regular shelters will put to sleep any cat they receive which tests positive because the virus is so contagious. If you are going to do this, however, you should understand that is it unlikely that you will get instant results. If you expect to find a new home for an FeLV+ cat within a few days of making inquiries, you can pretty much forget it. Be prepared to hold on to the cat for a few weeks at least, while searching for a new home.

If you choose to put an ad in the paper you MUST take the responsibility of making sure the people who express interest in your cat are doing so for legitimate reasons. You should interview them in person and check references if possible. There are people who will lie to get cats to feed to other pets, to sell to labs or to abuse. Think about this as you interview each potential candidate.

I have an FeLV+ kitten that I have decided to keep. Should I have it neutered/spayed?

I’ve only encountered one case of a vet recommending not to spay a kitten because it was FeLV+. Unfortunately, going into repeated heat cycles was very stressful on her, and that owner believes it caused her to suffer ill effects of the disease sooner than she may have otherwise (of course there is no proof to this). It is true that there is a small added risk to anesthetizing an FeLV+ cat, but that risk will well worth the alternatives. Especially since a whole cat will have a very strong desire to roam, thus further spreading the disease. In my personal experience, my vet did a very careful screening to make sure my FeLV+ cat could handle the anesthesia before operating. It really should not be much of a problem, but always make sure if your cat needs surgery that you remind the vet and staff that your cat is FeLV+.

I have had several cats for a long time. One of them recently tested positive, but the others have not. Do I need to get rid of the FeLV+ one?

This is a tough situation, for which there is no pat answer. You should discuss the matter with your vet. One vet I spoke with felt that chances are the other cats have already been exposed and it is probably best to just keep them up on their vaccinations and not change the household drastically. One study (Barlough, 1984) says that in a survey of 45 households from which FeLV+ cats were removed, 99.5% of the FeLV- cats remained negative. However households in which the FeLV+ cats were not removed had infection rates 40 times greater. It is probably best to remove the infected cat if it can be sent to a good home without causing too much disruption in your household, and your mental psyche.

I’ve heard FELV is like AIDS. Can I catch AIDS or anything else from it?

People often use the “it’s like AIDS” phrase to describe a number of illnesses in the animal (and human) community with the idea that most people know so much about AIDS that this analogy is useful. Unfortunately most people don’t know much about AIDS and the resulting effect is to scare people out of their wits and have them dump their cats or dogs at the nearest pound because they are so deathly afraid of AIDS. They are similar to AIDS in that they affect and weaken the body’s immune system. The ONLY similarity between FeLV, FIV (Feline Immunodeficiency Virus) and FIP (Feline Infectious Peritonitis) is in their genetic makeup. All are RNA (as opposed to DNA) viruses, and FeLV and FIV are what are known as “retroviruses.” FIP is a “coronavirus.” (See the FIP FAQ for more information on this disease).

If I don’t get my cat vaccinated, what are its natural defenses against the virus?

According to the literature, neonatal kittens are 100% susceptible to catching the virus from one exposure. 8-week-old weanlings are 85% susceptible from one exposure. There is serious debate over the likelihood of non-vaccinated, healthy adult cats becoming infected with the virus but it seems that ~40% of cats exposed become immune, ~30 percent become persistently infected (show acute signs of a related-disease) and ~30 percent become infected, but the virus is latent in their system. (Hardy, et al, 1980).

If I get my cat vaccinated, isn’t there a chance that it will catch the virus from the vaccine?

No. As of July 1992, all of the vaccines which are approved for sale in the United States are incapable of causing a positive FeLV test result. (Sorry, but I don’t have figures for vaccines in other countries. If anyone does, feel free to append them onto this FAQ.)

Is it possible for a cat to test negative when it really is positive?

Unfortunately, yes. Although false negatives are not very common, they do occur, especially if you are dealing with a young kitten. Sometimes the cat has been recently exposed to FeLV, so the antibodies have not yet had enough time to build up enough of a response to appear on the test. To be absolutely sure a cat is not FeLV+ you should test it twice, a few weeks apart (the cat should remain isolated from other cats during this period, too, otherwise there is little point in doing a second test). The likelihood of getting a false negative is increased depending on the nature of the test. The ELISA test will show more false negatives than the IFA test. Some mail-order catalogues now offer FeLV testing kits using saliva or tears as the medium. These are more likely to trigger a false response than the ELISA test which uses blood. Fortunately, the false negative rate on the ELISA test (which is what most vet offices use for standard FeLV tests) is low enough that most people don’t bother with the second test.

Is the vaccine expensive and how often do my cats need to be vaccinated?

After your cat has gone through its more elaborate set of kitten-shots, the FeLV vaccine should be given once a year. If you adopt an adult cat and don’t know if it has been vaccinated for FeLV, start it immediately on its annual shots. If you are unsure if your adult cat needs be vaccinated, talk to your vet. Prices vary between vets, locally and nationally. I surveyed readers of rec.pets.cats and contacted vets around the country and found that prices for the vaccination alone cost between $9 and $30 dollars. The average was $18 (not including the vet-visit charge). It seems that the FeLV test costs about the same, but I didn’t do a full-scale survey.

Is there a vaccine?

Yes, there are several commercial vaccines available. Unfortunately the USDA does not have standard requirements for FeLV vaccines, so different manufacturers can publish ‘Effectiveness Ratings’ which cannot be compared with each other due to a lack of uniformity in testing terms and requirements. Estimating the effectiveness of the vaccines is difficult and most vets I’ve spoken with estimate them to have ~75-85% effectiveness (this means cats challenged with the virus will fight off infection 7-8 times out of ten). Published studies show that there are irreconcilable differences and bias in Effectiveness Ratings put out by the manufacturers so currently it is impossible to estimate the actual effectiveness of and between vaccines. Suffice it to say that your cat is MUCH better off trying to fight the virus having received the vaccine, but the vaccine is not 100% effective so you should not expose your cat to undue risks. (Note: NO vaccine, whether it be for cats, dogs or people, is 100% effective. Some are about close to being as fully effective as possible, however the FeLV vaccine is not one of them).

Since writing the first version of this FAQ, I’ve had a number of people tell me that a cat has only a 30% likelihood of catching the disease, and even then if only in persistent close contact. I have found nothing in the recent literature to support this claim, and every veterinarian I have spoken with states that the likelihood of becoming infected depends on the level of exposure, which vary in different locales and situations. Since most tests are done in controlled situations, it would be impossible to come up with true “real world” statistics. In one vet’s words “But what if it is only 30%? Would you stop wearing seat belts if there was only a 30% chance of serious accidents if you commuted in a car every day? I hope the odds are far less than that … and yet I still hope you are taking the appropriate safety cautions. Unless the vaccine has been proven to cause serious harm, it is a good precaution to take, regardless of the percent chance of disease transmission.”

Is there any risk in getting my cats vaccinated?

There is always a risk that your cat may have a bad reaction to a vaccine, ANY vaccine. It is a good idea to wait in your vet’s waiting room for 30 minutes after receiving a vaccination, ANY vaccination, to make sure your cat does not have an adverse reaction, and if it does the vets will be on hand to deal with the situation.

There is also some evidence that vaccinations in general may be the cause of tumors (known as postvaccinal sarcomas or fibrosarcomas). The chance of this happening is estimated to be approximately 1-2 in 10,000, but you should be aware of it nonetheless. This has not been limited to FeLV vaccines, in fact it was originally thought to pertain solely to rabies vaccines, but this is not thought to be the case any more. Since this form of cancer seems to have a high recurrence rate, and little is known about it, if you have *strictly* indoor-only cats, you may want to discuss with your vet if the risk of fibrosarcoma is greater than the risk of being exposed to FeLV if the cat gets out. This is an individual decision that will be different for each household. You should contact your vet immediately if you notice any lumps in the vaccine injection area.

My cat gets sick after it gets vaccinations. Why should I put my cat through that?

Some cats do have bad reactions to vaccines. However, it is better to have a cat sick for one day per year from being vaccinated than to have it die a miserable death from an FeLV-related disease. If your cat has a bad reaction to a shot, ANY shot, and the reaction lasts more than 12-24 hours, you should immediately bring your cat to the vet. Even if your cat has a mild reaction, you should at least discuss the matter to see what are the best options for next year’s vaccinations. It may be best to spread your cat’s annual vaccinations out over a few months, or have them all administered at once. If your cat has had a *very* bad reaction, it very well may be best to discontinue vaccinating for FeLV. Definitely discuss this with your vet.

My cat has tested positive. Should it be put to sleep?

The mere fact of testing positive is not enough to merit putting a cat to sleep, although there may be other significant factors involved which do make putting the cat to sleep the best option. There are vets who recommend putting all FeLV+ cats to sleep. If your vet recommends this and you feel comfortable with that decision, then that is the best solution. Sometimes putting an FeLV+ cat to sleep is the best option for the cat, especially if it has acute symptoms and is in pain. This is never an easy decision and one which should not be taken lightly. If you do not feel you are capable of emotionally dealing with having an FeLV+ cat (or cannot keep the cat indoors), but do not want to put the cat to sleep, there are other alternatives which are discussed below. The one thing you should not do is ignore the virus. If your cat has tested positive, then you have a responsibility to take some action. FELINE LEUKEMIA VIRUS WILL NOT GO AWAY IF YOU JUST IGNORE IT!

My cat recently passed away from FeLV. How long should I wait before getting another cat and are there any special precautions I should take?

Well, your own grief issues aside, from a medical point of view you do not need to wait very long. The virus is fragile outside the host, and I know of one vet who has even stated that it would be safe the next day. Personally, I would wait a week at least. You should definitely discard the litter box and food/water bowls, or else clean both well with household detergents or a 1:32 bleach solution.

My cats are indoors-only. Why should I bother getting them vaccinated?

    The answer to this question all boils down to a risk/benefit assessment.

    If you live in a high-rise, do not plan on moving in the next year, and do not plan on exposing your cat to other cats (such as getting a new kitten, or temporarily housing a stray), then there is really no need to get the cat vaccinated. If it is somehow possible for your cat to make it to the outside world, whether it be because of a break-in, or a landlord who forgets to close the window they just fixed, or a visitor doesn’t realize the cat is not allowed outside (all of which are real-life cases of people I know whose indoor-only cats have gotten outside) then your cat is at SOME risk. Many people who lived through Hurricane Andrew or the LA Earthquake can tell you that some of their indoors-only cats ended up on the street for days. Fortunately disasters like these are infrequent, but the point is accidents can happen. In the few hours or days that your cat is outside it could come in contact with an infected cat, and it is better to give your cat that 75-85% boost to its natural resistance.

    But, some people feel the risk of adverse reaction and possible fibrosarcomas from vaccinating are not worth the risk if the cat is not likely to go be exposed to FeLV+ cats, even if it did get outside for a short period. What YOU as the cat’s owner (not your vet, not your cat’s breeder, not your friend of a friend who knows a lot about cats, and not someone who wrote something you read on the internet) must decide is how much risk is there for your cat getting out and being exposed, and is that risk worth the other risks associated with the vaccine?

My cat is a purebred, and I’ve heard the vaccine should not be given to purebreds. The breeder I bought the cat from discourages getting the vaccine.

    This is a touchy subject because there is often the general feeling among vets that many breeders don’t know what they are doing, and the feeling among breeders that vets don’t know much about purebreds. There is probably a little bit of truth to both sides. It is true that some breeders may think they understand veterinary medicine better than they really do, and unfortunately rely on word-of-mouth advice of other breeders rather than vets (eg: “Jane Smith has been breeding for 15 years and she knows a lot so if she doesn’t like this vaccine, it must be bad”). But it is also true that most vets do not deal specifically with purebred issues. There is no course in vet school called “Purebreds 101” and vets are often just as guilty as anyone in misidentifying mixed breeds as purebreds, of being too quick to diagnose a “breed specific” illness with less data than if they would if the cat were not a purebred, or of not being aware of conditions which may affect one breed more than another.

    Keep in mind that some veterinarians are also breeders, or work within the CFA, TICA, ACFA (AKC for dogs) or other purebred registries, and these vets are most likely going to be more knowledgeable about conditions which are more common to certain breeds. Also remember that not all purebreds are the same, each breed is different and has its own characteristics. Just like you can’t say “don’t vaccinate Europeans for smallpox,” because there are *many* different cultural and ethnic groups in Europe.

    The immune system of purebred cats has NEVER been tested to determine if it is different than that of mixed breed cats. It is impossible to state one way or another if the purebred immune system, because of inbreeding, has any reason to adversely react to vaccines that are tested on a largely mixed-breed cat population. Some people feel there is a significant difference between the two based on antecdotal evidence and won’t vaccinate for that reason, and some people feel this is nonsense.

    But that doesn’t answer the question because this one is going to have to be answered by you and your own gut feeling. Who do you trust more with the combined necessary knowledge of vaccines, as well as about your purebred? Talk to your breeder and see if s/he is aware of the vet literature, or is repeating word-of-mouth arguments. Many of them are well aware, many read the literature more than vets do, so don’t be afraid to ask them why they hold the opinions they do. Talk to your vet and ask how familiar they are with your partiuclar breed of cat as well as purebreds in general. Get a feel for both. Keep in mind that many breeders do not vaccinate their own breeding cats because FeLV vaccines can cause miscarriages and stillbirths, or it may just be cheaper for the breeder to test their cattery every year and every cat that comes into the cattery rather than to vaccinate, especially as cats from a cattery are less likely to escape to the outside world (remember the risk/benefit assessment above). Make sure you find out exactly why the breeder does not recommend the vaccine as it may very well be that the breeder has had numerous negative experiences with the vaccine in his/her particular line of cats, and that your cat may be genetically predisposed to have a bad reaction. If this is the case, you should still discuss the matter with your vet, and it may be best not to get the vaccine.

Should I continue to vaccinate my cat if it is FeLV+?

The literature recommends against continued FeLV vaccinations. Other feline vaccinations (panleukopenia, rabies, etc.) should be continued.

So some cats who test positive can later test negative?

Yes. If you have a cat which tests positive on the ELISA test, you should immediately have an IFA test done. If it tests negative on the IFA test, you should have your cat retested with the ELISA test in 3 months. If a cat does not test negative again in roughly three months, chances are it will always test positive. Vets and virologists have devised an entire classification scheme of the different types of infected cats (transiently infected, persistently infected, etc.) based on the ELISA and IFA tests. It can be very confusing and if you are interested in learning the details you should consult with your vet regarding your particular cat’s status.

What are symptoms for which I should be on the lookout?

Unfortunately, since FeLV is a retrovirus that attacks your cat’s immune system, your cat can become ill from many things as a result. This makes looking for a ‘sure sign’ very difficult. Often the immune system is weak so your cat will become chronically infected with certain conditions such as stomatitis, gingivitis, oral ulcers, abscesses and non-healing wounds of the skin, upper respiratory infections or FIP. Some cats whose digestive tracts are affected have been described as staring at their food bowl seemingly unable to remember how to eat, or their breathing will be very difficult and loud. Basically, whenever your cat shows chronic, peculiar and/or unhealthy behavior, take it to a vet to be examined.

What does the virus do to a cat?

In sum, once the virus gains entry (usually via saliva or mucus membranes) it will reproduce in the lymph tissue which is your cat’s first system of immune defense. Some cats are able to mount a successful immune response against it and defeat the virus at this stage. In cats who don’t successfully destroy the virus here, the virus will then move into the bone marrow where red and white blood cells are produced. It may stay latent in the marrow for many years. After that it will attack other tissues, including possibly causing a breakdown in several stages of the immune response system.

What is a retrovirus?

Retroviruses carry with them an enzyme that causes a process to occur in the DNA known as “reverse transcription.” RNA normally pairs up with DNA, copies itself, and thus increases/replicates itself. When an RNA retrovirus does this, it fools the DNA to copy *it*, instead of the normal RNA, thus causing even more of the retrovirus to be created. So as long as a particular cell is affected with the retrovirus, that cell will be affected for its whole life. One would have to kill the cell before it reproduces to eliminate any chance of that cell making any more FeLV or FIV RNA. This is one of the reasons why it is so difficult to get rid of, because you must kill all the cells which contain the virus, and attempting to do this may either kill the animal itself, or it is simply impossible to tell which cells have the virus in the first place. Basically, a retrovirus is a parasite at the genetic level, a DNA-tapeworm, if you will.

What is Feline Leukemia Virus and can I catch it?

Feline Leukemia Virus is a virus that is specific to cats    only.  It is considered to be the most common cause of serious    illness and death in domestic cats. It causes a breakdown in your    cat’s immune system causing your cat to become susceptible to many    diseases which it might otherwise be able to fight off. It CANNOT    be transmitted to humans (including children) nor can it be    transmitted to other species such as dogs. The National Cancer Institute and the National Institutes of Health have written a CancerNet Factsheet which is available via gopher. See the References section for more information on this.

What will happen to my cat now that it has tested positive?

Because there are so many different ways to respond to the presence of the virus, it is impossible to predict exactly what will happen (and when it will happen) to your cat. I’ve noticed that any 5 vets you ask will give you 5 different answers to this question. The scientists who experiment and publish on the disease are also in disagreement. I have presented two different (published) viewpoints below. According to Hardy, et al (1980), (and these people seem to be the authorities on the disease) roughly half of all cats who test positive (and do not test negative again within a three month period) are persistently infected and show acute signs of FeLV-related diseases. The other half are latently infected and are in all other aspects ‘healthy’ although they are still carriers. 17% of all cats which test positive (and do not later test negative) will live past 4 years. The next point of view is taken from a much more recent article and has radically different statistics. According to Loar (1993), of cats which test positive for the disease only 5% will immediately become infected with an FeLV-related disease. The other 95% will enter the latent phase which will last for months to years. These 95% are still carriers for the disease and can infect other cats.

Will I infect my healthy cat if I pet an FeLV+ cat, then pet my cat?

No. Not unless you were to go immediately from one cat to another, and have wet saliva, urine or blood on your hand. Even then the chances would be slim. FeLV needs to be transferred through the media above, and will not live long outside the host (the infected cat). Warm, dry environments will deactivate the virus and common household detergents and disinfectants will eliminate it from any contacted surfaces. If you wash your hands with soap after touching an infected cat, you will not infect an FeLV negative cat.

Drugs and Therapies

Azithromycin Use and Dosages – by Lorraine Shelton

Dosing Your Cat with Azithromycin Pediatric Suspension

By Lorraine Shelton

To join a community of cat fanciers and health professionals interested in cattery related health issues, visit http://groups.yahoo.com/group/fanciershealth

Azithromycin, produced by Pfizer under the brand name Zithromax or Azitrocin, has emerged as a very valuable antibiotic for the treatment of various infections in the cat. It is well tolerated, even by young kittens, and its efficacy in the treatment of upper respiratory infections (including bordetella and chlamydia), in particular, is unequalled by other anitbiotics. It is cleared very slowly from feline tissue, resulting in dosage schedules that are very convenient for the cat owner. A single dose maintains effective drug levels in the cat’s tissues for as long as a week. The correct dose for the use of azithromycin in cats is 5 mg/kg (5 mg of drug for every 2.2 pounds of cat or 2.3 mg per pound of cat).

Because of the persistance of this drug in feline tissues, DO NOT try to translate any protocol given for the use of this drug in humans and try to apply it to your cat. This mistake has been made by numerous veterinarians and pharmacists. DO NOT double the amount of the drug given with the first dose, as is done with humans. This drug should be given as a single dose treatment for minor URI, or once a day for three days in more serious cases. Five days after the first series of three doses, another series of three doses may be given if necessary. For chronic conditions, dosing the cat once or twice a week for extended periods of time may be appropriate.

Elizabeth Hodgkins, DVM feels that the above dosage schedule may be too low for many cats and recommends a dosages schedule of 5-10 mg/kg for six days, with a double dose the first day. Her recommendation: “I generally use 10-20 mg of the suspension per cat (.25-.5 cc of the oral suspension) twice daily for the first day of treatment for cats 3-8 lbs in weight. I then use the same dose once daily for another 6 days straight. In heavier cats, I will use 30-40 mg twice daily for the first day and then once daily for an additional 6 days. I have tried the alternating days dosing as well as the abbreviated (3 day) dosing and have found that these regimes invariably predispose to relapse and prolongation of treatment and clinical signs. I am convinced that, at least in my hands, the protocol described above gives the most consistently positive results in cats with no side effects whatsoever (sound of wood knocking). Also, response is best when the drug is given on an empty stomach and food is withheld for at least an hour after administration.”

Another treatment regimen used to prevent early chlamydial infections was developed by an Australian veterinarian. It is comprised on a single dose at 20 mg/kg. More information about this protocol.

This drug, like any other, must be given carefully and dosed correctly. The instructions below are to be used as a guideline only and should be confirmed by your veterinarian.

The amount of drug (the weight of which is measured in milligrams or “mg”) that you administer to a cat is based on the weight of the animal (measured in pounds “lb” or the metric unit kilograms “kg”). Drug doses are, for the most part, given in the units “mg/kg” (the standard unit for drug doses) and may also be translated into “mg/lb” (1kg = 2.2 lb). If a dose is given as “2.3 mg/lb”, for example, it means that the cat must receive 2.3 mg of the drug for every pound of the cat’s body weight. In order to determine how much of any particular drug in solution, paste, powder, or other form you must give a cat, you must know how much drug is delivered in a certain volume of product (i.e. the concentration of the solution, amount of drug in each tablet, etc.).

Commercial drug solutions are labeled with the concentration (for instance, 200mg/5mL means that each 5 mL of solution contains 200 mg of drug. A powder, paste, tablet or liquid version of drug is usually comprised of mainly “carrier” (inert substance) with very small amounts of the drug distributed in it. Keep in mind that the drug is not always distributed evenly throughout the product. DO NOT stuff oral suspension powders into little capsules, for example… you have no clue how much of the real drug is getting into those capsules!!

The calculation of how much liquid preparation of a drug to administer to a cat is calculated as given below. The weight of the cat is multiplied by the dose. This figure is then divided by the concentration of the solution in order to give the volume of solution to be administered. WATCH UNITS CAREFULLY, remembering that a solution with a labeled concentration of 200mg/5mL (200 mg in five mLs) must be translated to the equivalent (reduced) term 40mg/mL (40 mg in one mL) to use this formula.

FORMULA: Volume of liquid solution to administer (mL) = Weight of cat (lbs) X Dose of drug (mg/lb) divided by Concentration of solution (mg/mL)

EXAMPLE: Let’s say we are going to dose a cat with the pediatric suspension form of the antibiotic azithromycin. The dose for this drug is 2.3mg/lb (5mg/kg). Our cat weighs nine pounds (4 kg). Our solution container is labeled 200mg/5mL. First, translate the concentration into the units “mg/mL”: 200mg in 5mL = 40mg/mL (divide 200 by 5). Now use our formula: Weight of cat (lbs) X dose (mg/lb) is 9 lbs X 2.3 mg/lb. The concentration (mg/mL) is 40mg/mL.

Thus: [9lbs X 2.3 mg/lb] / 40mg/mL = 0.52 mL

Therefore, for each dose, your nine pound cat needs to receive about 0.5 mL of a solution containing 200mg/5mL azithromycin.

CAUTION:

Reconstitute your oral suspension according to package directions. Now examine the syringe you will use to administer the solution to your cat. It is best to use a new and sterile syringe, even when administering drugs by mouth. Use a new syringe for each cat and for each dose. Use a syringe of the appropriate size. If you are administering amounts of 1 mL or less, use a tuberculin or insulin syringe (with the needle removed, of course). Make sure you are comfortable with the markings on your syringes and the volumes they indicate before drawing up the dose of drug. For our purposes, the abbreviations mL and cc are interchangeable.

CAUTION: Sometimes a drug will only be available in a form that is difficult to administer to a cat, for instance a large tablet or foul tasting solution. Crushing a tablet and diluting it in a palatable solution or mixing a bitter solution with something more attractive to your cat is an option, but this will affect the stability of the drug. When you dilute a tablet in water or otherwise change the form of the drug, you must administer the appropriate dose immediately and discard the rest. Many drugs become inactive quickly if dissolved into an aqueous solution, unless that solution is carefully formulated with drug stabilizing ingredients. Keep this in mind when purchasing your drugs and deciding between different forms. An inexpensive one gram packet of drug is no bargain if it must be discarded after giving only one dose, compared to a more expensive pediatric solution that is stable in liquid form for the duration of treatment in accordance with the storage conditions listed on the label.

A NOTE ABOUT AZITHROMYCIN STORAGE

The only appropriate reconstitution instructions and expiration date backed up with DATA for any particular compound is that stated on the label. The expiration date for the powder is printed on the bottle and, once reconstituted, the solution is good for ten days at room temperature. Follow this and you’ll always have an azithromycin solution with a potency of at least 95% of what it left the manufacturer at. This is amazingly effective drug, and although it seems wasteful to throw the excess out, curing a cat is certainly worth the $30-40 one bottle of azithromycin costs. End of story.

HOWEVER. For those of us in the field that generate data for the FDA of this nature, we know what tests the FDA demands and what that translates to in “real life”. There is also a mathematic equation that factors in called the Arrhenius equation (this work won the Nobel prize in 1903).

With some basic (and debatable) assumptions, if a solution is stable at room temperature for a week, it is also stable in the refrigerator (approx. 5°C) for 3 months. Because the Arrhenius equation is also lovingly called by stability scientists “the Erroneous equation” (!) combined with the fact that your home refrigerator does not have a temperature and humidity monitoring device on it, I compromise and have been frequently quoted as giving the refrigerated solution of pediatric azithromycin a refrigerated shelf life of one month. An even easier way of handling this drug is to draw up the reconstituted solution into 1 ml syringes and store the syringes in the freezer for up to three months. I think that this is MORE than reasonable based solely on my personal experience with pharmaceutical stability testing and FDA protocols. However, I have NOT done complete stability testing of azithromycin in solution personally.

DO NOT take a “teaspoon of azithromycin and dissolve in X ml of water”. The powder in the container does NOT have drug distributed evenly throughout it. Reconstitute the WHOLE THING and draw up into syringes to ensure that your cat gets an ACCURATE dose of medication. Packing powder into capsules is also not an accurate way to dose your cat with azithromycin.

This is a very viscous solution and should be brought to room temperature and MIXED WELL before dosing if you are refrigerating the whole bottle. Mark the reconstituted bottle with the date so you can keep track of the actual time it has been “on the clock”. Enter the bottle ONLY with a new sterile syringe, not just a washed one.

The stability of the dry powder is a even “fuzzier” area. For the most part, powdered drugs are VERY stable if labelled for room temperature storage for periods of one year or greater. Often the final expiration date is based more on marketing goals and how long a company chose to wait to release their first three batches of product than on real science.

The thing to remember is that with few exceptions (BUT THERE ARE EXCEPTIONS!!), a drug doesn’t suddenly become worthless the day after the date on the bottle. It degrades slowly and that degradation is a function of the temperature the solution is stored at and the degree of sterility maintained. Keep all your “room temperature” drugs at COOL room temperature and return refrigerated drugs to the refrigerator immediately after using them. Maintain sterility in the container to the greatest degree possible.

Some drugs degrade into toxic substances if kept *long* after their expiration dates or stored incorrectly. The safest route is to simply follow the package directions. But “fudging a little” is often an economic reality, especially with expensive drugs like azithromycin. Each person must determine the risks of outdated or improperly reconstituted solutions vs. the costs/availability of these drugs for themselves.

If you have any questions, contact Lorraine Shelton at featherland@earthlink.net

If you are at all uncomfortable with the math, DO NOT calculate drug dosages yourself. Mistakes can result in overdosing, underdosing, or even killing your cat. Consult your veterinarian or pharmacist before administering any drug to any cat.

Baycox for Treatment of Coccidia

Use of Baycox liquid or Marquis paste to control coccidiosis in
catteries

by Lorraine Shelton and Della Hengel

Baycox (toltrazuril) is a new treatment that may actually cure
coccidiosis, instead of just suppressing it. The drug is available
in  Canada and Australia, but not the US. Albon and Tribrissen are used for years
to control coccidia infection, but these drugs don’t cure it and the animal
may continue to shed spores (remain infectious to other animals). Marquis paste is made from a similar
drug, ponazuril, which is a metabolite of toltrazuril.

Baycox may be obtained from Interpet: http://www.interpet.biz/Baycox.html or from Pet Supplies International: http://www.psol.com.au/int/index.html
Since the Baycox is a special order item, it’s not shown on
the PSI website. You need to email the owner (who incidentally is a vet):
questions@psol.com.au (Geoff Turnbull). No prescription is needed. If
you’re in the US, the cost for 200 ml (the only size it comes in, original
Bayer packaging — he does NOT repackage) at today’s exchange rate is
under $90. DO NOT use the 2.5% solution sold as a pigeon remedy, as it can be caustic to the mucus membranes of cats.

Do not use this drug in pregnant cats as the terratogenic effects of
this drug has not been adequately researched as yet.

The dose of Baycox is 20 mg/kg (10 mg per pound). This is 0.2 ml per pound
of cat when using the 5% suspension. In a published study, a single
dose of Baycox cured coccidiosis in puppies, as long as adequate
environmental clean-up is performed. However, I’d recommend repeating
it weekly for a couple of weeks. Clean up of the environment is
critical to get rid of coccidia. This drug works best when it is used
at the age of 4-6 weeks to PREVENT coccidia infection in kittens.

An alternative to Baycox is the similar drug ponazuril, marketed as
Marquis paste for horses. The dose is 20mg/kg once a day for 1-3 days.
The paste contains 150mg ponazuril per gram of paste. The plunger is
marked for horses weighing 600 – 1200 pounds. You want to take the
amount for a 600# horse and dilute it to a total volume of 14 ml in
something tasty. Dose at 0.1 ml per pound of cat. Discard the unused
volume.
         
Here is the journal abstract I posted to the Fanciershealth Yahoogroups list in 2001:
Toltrazuril treatment of cystoisosporosis in dogs under experimental
and field conditions. A Daugschies, HC Mundt, V Letkova
Parasitology Research, 2000, Vol 86, Iss 10, pp 797-799

Coccidia of the genus Cystoisospora cause mild to severe diarrhoea in
dogs. The effects of toltrazuril treatment on cystoisosporosis were
studied under experimental and field conditions. Twenty-four puppies
were experimentally infected each with 4 x 10(4) oocysts of the
Cystoisospora ohioensis group. Three groups of six puppies were
treated 3 dpi with 10, 20 or 30 mg/kg body weight of toltrazuril
suspension (5%); the remaining six puppies served as non-treated
controls. Toltrazuril suspension or microgranulate were given once
in a dose of 10 or 20 mg/kg body weight, respectively, to naturally
infected puppies in conventional dog breeding facilities, depending
on the coproscopical evidence of infection. Oocyst excretion and
clinical data were recorded.

Under experimental conditions, the non-treated puppies excreted
oocysts beginning at 6 dpi and suffered from catarrhalic to
haemorrhagic diarrhoea. On 12 dpi, four of six non-treated puppies
died. Irrespective of the dose, toltrazuril treatment totally
suppressed oocyst excretion and no diarrhoea or other signs of
disease were observed in the treated groups. Natural Cystoisospora
infections were regularly found during the 3rd or 4th week of age
in dog breeding facilities although not always associated with
diarrhoea. A single oral application of toltrazuril abrogated oocyst
shedding and the treated puppies remained generally coproscopically
negative during the following 2-4 weeks.

Cystoisospora is pathogenic for puppies and can induce severe
disease. Natural infections are common in conventional dog breeding
facilities. Toltrazuril treatment is suitable for controlling
cystoisosporosis under experimental and field conditions. A single
oral treatment for puppies in the 3rd/4th week of age is recommended.

Here is some information directly from Dr. Bruce Kilmer at Bayer
Canada:

Thank you for your interest in Baycox. Unfortunately, Baycox
isn’t registered for cats and therefore I can’t provide a package
insert. On a second point, Baycox is not available in the US, except
black market goods coming in by whomever. Bayer In Canada can not
sell product into the US. Baycox is a triazine derivative. The drug
active is toltrazuril, which has a cidal mode of action on protozoan.
The toltrazuril will kill all single cell stages of coccidiosis. Once
an animal has diarrhea and you can find oocysts on fecals, the drug
can not penetrate the oocysts so technically it is too late to treat.
In the actual clinical cases, treatment is still worthwhile to shorten
the length and severity of the diarrhea as there is still development
of the life cycle in the small intestine that will be controlled.

The idea is to dose the cat before there are clinical signs. For
example, the normal situation would be a cattery having regular
problems with coccidiosis in young kittens. The kittens normally would
break with diarrhea at about 5 weeks of age. The treatment would be
given around day 28, killing the early stages of the protozoa and
preventing clinical disease. You will not have the history on a
rescue cat so treatment would be best at the earliest hint of an
outbreak and then repeat treatment in 7 days.

Baycox treatment will not cause sloughing of the intestinal
epithelial cells. The coccidiosis does a fine job of that on its own.
We have electron micrograph studies of sections of intestine 24 hours
post treatment with Baycox. The intestinal cells remain intact and
functional while the single cell stages of the cocci are dead, as
evidenced by staining techniques. because Baycox is cidal, the kitten
does not have to depend on its immune system to eliminate the cocci as
what would occur with a static drug like sulfadimethoxine.

Remember that Baycox should be given during the preclinical stage.
This is very difficult to judge as the kitten will be at a stage when
it is infected but the cocci are only in the first stages of their life
cycle. The intent is to kill the protozoa before there is damage to the
villi to clear the infection. In this way, the kittens will not develop
the normal clinical signs of diarrhea. If you can identify oocysts on
fecal exam, the damage has already been done and the protozoa has
completed its reproductive cycle. Drug can not penetrate the oocyst wall
to kill this stage. Treatment at the first signs of a clinical case will
still help to limit the severity and duration of the infection as the
Baycox will kill the single cell stages that have not reproduced
sexually yet.

Try to determine the usual age that you see outbreaks. For example, many
catteries will see diarrhea sometime around day 35. The time to treat is
therefore at day 28. Likely the kittens had an infective dose of oocysts
by this stage but minimal damage has occurred. Treatment will eliminate
the coccidiosis before there is damage and the kittens will not break
with diarrhea. Studies in other species indicate that the animal will
have developed immunity to subsequent exposure.

The dose is 20 mg/kg by oral dosing.

Toltrazuril is quite lipid soluble so absorption and distribution into
tissue is very good. Baycox has a unique mode of action and there is no
reason to be concerned with an adverse reaction or a drug-drug reaction.
We have never had an adverse reaction reported after millions of
treatments, often concurrent with other medications.

I have never heard of any adverse reactions to treatment at this dose
in puppies or kittens or on the repeat seven days later.As Baycox only
has activity against protozoa, there is no effect on upset of intestinal
flora and the formulation is very well tolerated. The only time I have
heard of any reaction occurred when someone used the Baycox 2.5% Poultry
Concentrate by direct oral dosing in 3 day old piglets. This formulation
is designed to be diluted in the drinking water for poultry. To be
soluble in water, the product undiluted is very alkaline, pH 11.4.
Direct oral dosing of the undiluted product is very irritating to
mucous membranes and will cause immediate vomiting. Make sure you are
using the correct formulation.

Regards,
Bruce Kilmer DVM
Manager, Veterinary Affairs/Product Development Bayer Inc.

Commonly used feline drugs and their dosages

Dosages for drugs commonly used in treating cats. Dosages are given per pound (0.4536 kg) of body weight, except as noted. WARNING: Not be used as a substitute for your veterinarian. Many drugs have adverse side effects, some of which can be LETHAL!

 

Albendazole

 

Valbazen Giardia 12 mg/lb Twice a day for two days

Amoxicillin

 

Amoxi-Drops, Biomox, Polymox Bacterial infections 5-10 mg/lb Once to twice a day

Amoxicillin-potassium clavulanate

 

Augmentin, Clavamox, Synulox Bacterial infections 2.5-5 mg/lb Twice a day

Ampicillin

 

Polycillin, Polyflex Bacterial infections 10-15 mg/lb Three times a day

Azithromycin

 

Zithromax, Azitrocin Bacterial/mycoplasmal infections 2.5 – 10 mg/lb Once a day to every other day

Cefaclor

 

Ceclor Bacterial infections 5-15 mg/lb Twice to three times a day

Cefadroxil

 

Cefa-Drops, Cefa-Tabs, DuriCef Bacterial infections 5-15 mg/lb Twice to three times a day

Cefazolin

 

Ancef, Kefzol Bacterial infections 5-15 mg/lb Twice to three times a day

Cefpodoxime proxetil

 

Simplicef, Vantin Bacterial infections 2 to 5 mg/lb once a day

Cephalexin

 

Keflex Bacterial infections 5-15 mg/lb Twice to three times a day

Chloramphenicol

 

Chloromycetin bacterial infections 6-12 mg/lb twice a day

Ciprofloxacin

 

Cipro Bacterial infections 5 mg/lb twice a day

Clarithromycin

 

Biaxin Bacterial/mycoplasmal infections 2.5 mg/lb Twice a day

Clindamycin

 

Antirobe Bacterial infections, especially in the mouth 5-10 mg/lb Once a day

Clomipramine

 

Anafranil Urine spraying 0.1-0.25 mg/lb Once a day

Domperidone

 

Motilium Lactation stimulation 0.025-0.05 mg/lb Once or twice a day

Doxycycline

 

Vibramycin Bacterial and mycoplasma infections, chlamydia 3 mg/lb Twice a day. MUST be given with water or as a suspension.

Enrofloxacin

 

Baytril Bacterial infections 2 mg/lb Once a day. DO NOT exceed 2.3 mg/pound per day

Erythromycin

 

Bacterial infections 2 -10 mg/lb Three times a day

Febental

 

Drontal Plus Giardiasis 56.5 mg per cat Once a day for five days

 

 

Fenbendazole

 

Panacur Roundworms, giardia 23 mg/lb Once a day for three days

Fipronil

 

 

 

 

Frontline Fleas, mites 4 mg/lb Once a month. If using dog formulation, one drop (0.05ml) per pound.

Fluconazole

 

Diflucan Fungal infections/ringworm 5 mg/lb Every other day

Griseofulvin

 

Fulvicin Ringworm 7 mg/lb microsized, 3.5 mg/lb ultramicrosized Twice a day

Imidacloprid

 

Advantage Fleas 5 mg/lb Once a month. If using dog formulation, one drop (0.05ml) per pound.

Itraconazole

 

Sporonox Fungal infections/ringworm 5 mg/lb Once a day

Ivermectin

 

Ivomec Roundworms, mites 0.2-0.4 mg/lb Treat once. Repeat in 2-3 weeks. 0.05 ml of 0.27% solution per pound or 0.1 ml of 1% solution PER ADULT CAT

L-Lysine

 

Herpesvirus infections 250 mg per cat Twice a day

Medroxyprogesterone acetate

 

Depo-Provera, Ovaban Contraception 2.5 to 5 mg PER CAT once every 7-14 days

Methylprednisolone acetate

 

Depo-Medrol Anti-inflammatory 2.3 mg/lb SC every 3-8 weeks, depending on condition

Metoclopramide

 

Reglan Anti-emetic, milk production 0.1-0.2 mg/lb every eight hours

Metronidazole

 

Flagyl Giardia, IBD 5-20 mg/lb Once to twice a day, given with food

Moxidectin

 

Advantage Multi/Advocate External/internal parasites 0.5 mg/lb Topically, once a month

Orbifloxacin

 

Orbax Bacterial infections 1-3.5 mg/lb Once a day

Oxytocin

 

Pitocin Dystocia 1-2 IU per cat Given once

Penicillin

 

Penicillin G Procaine, Pen BP-48, Crystiben, Dual-Pen Bacterial infections 10,000-20,000 IU Every 4-48 hours, check label. Newborns: 0.05 ml at birth of 150,000 IU/ml Pen BP

Ponazuril

 

Bayer Marquis Paste Coccidiosis 10 mg/lb Given once, repeat in one week

Praziquantel

 

Droncit Tapeworms 0.05 ml/lb inj., 2.5 mg/lb oral Treat once

Propulsid

 

Cisapride megacolon, constipation 0.5 mg/lb twice a day, give 15 mins. before feeding

Pyrantel Pamoate

 

Nemex-2, Strongid T, Pyratabs, D-Worm, Evict Roundworms 2.5 mg/lb Treat once. Repeat in two weeks

 

 

 

 

 

Ronidazole

 

Tricho Plus tritrichomonas intestinal parasites 15-25 mg/lb once a day for two weeks

Selamectin

 

Revolution Fleas, mites, roundworms 3 mg/lb Once a month. If using a dog formulation, one drop (0.05ml) per two pounds. CAUTION: this practice may increase the incidence of adverse reactions!

Sulfadimethoxine

 

Albon Coccidiosis 12.5 mg/lb, double first dose Once a day

Terbinafine

 

Lamisil Fungal infections/ringworm 15-20 mg/lb Once a day

Tetracycline

 

Albaplex, Panamycin Bacterial infections 10 mg/lb Two to three times a day. MUST be given with water or as a suspension.

Tinidazole

 

Tindamax anti-protozoal 7 mg/lb Once a day

Toltrazuril

 

Baycox Coccidiosis 0.2 ml of 5% solution/lb Dose once, repeat in one week

Triamcinolone acetonide

 

Vetalog Inflammation 0.01-0.1 mg/lb Once a day, use lowest effective dose

Trimethoprim/Sulfadiazine and Trimethoprim/Sulfamethoxazole

 

Tribrissen, Septra, Bactrim Bacterial infections 15 mg/lb Once a day

Tylosin

 

Tylan 50 Bacterial infection 10-20 mg/lb Twice a day

 

 

 

 

Commonly used feline drugs and their dosages

Albendazole Valbazen Giardia 12 mg/lb Twice a day for two days
Amoxicillin Amoxi-Drops, Biomox, Polymox Bacterial infections 5-10 mg/lb Once to twice a day
Amoxicillin-potassium clavulanate Augmentin, Clavamox, Synulox Bacterial infections 2.5-5 mg/lb Twice a day
Ampicillin Polycillin, Polyflex Bacterial infections 10-15 mg/lb Three times a day
Azithromycin Zithromax, Azitrocin Bacterial/mycoplasmal infections 2.5 – 10 mg/lb Once a day to every other day
Cefaclor Ceclor Bacterial infections 5-15 mg/lb Twice to three times a day
Cefadroxil Cefa-Drops, Cefa-Tabs, DuriCef Bacterial infections 5-15 mg/lb Twice to three times a day
Cefazolin Ancef, Kefzol Bacterial infections 5-15 mg/lb Twice to three times a day
Cefpodoxime proxetil Simplicef, Vantin Bacterial infections 2 to 5 mg/lb once a day
Cephalexin Keflex Bacterial infections 5-15 mg/lb Twice to three times a day
Chloramphenicol Chloromycetin bacterial infections 6-12 mg/lb twice a day
Ciprofloxacin Cipro Bacterial infections 5 mg/lb twice a day
Clarithromycin Biaxin Bacterial/mycoplasmal infections 2.5 mg/lb Twice a day
Clindamycin Antirobe Bacterial infections, especially in the mouth 5-10 mg/lb Once a day
Clomipramine Anafranil Urine spraying 0.1-0.25 mg/lb Once a day
Domperidone Motilium Lactation stimulation 0.025-0.05 mg/lb Once or twice a day
Doxycycline Vibramycin Bacterial and mycoplasma infections, chlamydia 3 mg/lb Twice a day. MUST be given with water or as a suspension.
Enrofloxacin Baytril Bacterial infections 2 mg/lb Once a day. DO NOT exceed 2.3 mg/pound per day
Erythromycin Bacterial infections 2 -10 mg/lb Three times a day
Febental Drontal Plus Giardiasis 56.5 mg per cat Once a day for five days

Fenbendazole Panacur Roundworms, giardia 23 mg/lb Once a day for three days
Fipronil Frontline Fleas, mites 4 mg/lb Once a month. If using dog formulation, one drop (0.05ml) per pound.
Fluconazole Diflucan Fungal infections/ringworm 5 mg/lb Every other day
Griseofulvin Fulvicin Ringworm 7 mg/lb microsized, 3.5 mg/lb ultramicrosized Twice a day
Imidacloprid Advantage Fleas 5 mg/lb Once a month. If using dog formulation, one drop (0.05ml) per pound.
Itraconazole Sporonox Fungal infections/ringworm 5 mg/lb Once a day
Ivermectin Ivomec Roundworms, mites 0.2-0.4 mg/lb Treat once. Repeat in 2-3 weeks. 0.05 ml of 0.27% solution per pound or 0.1 ml of 1% solution PER ADULT CAT
L-Lysine Herpesvirus infections 250 mg per cat Twice a day
Medroxyprogesterone acetate Depo-Provera, Ovaban Contraception 2.5 to 5 mg PER CAT once every 7-14 days
Methylprednisolone acetate Depo-Medrol Anti-inflammatory 2.3 mg/lb SC every 3-8 weeks, depending on condition
Metoclopramide Reglan Anti-emetic, milk production 0.1-0.2 mg/lb every eight hours
Metronidazole Flagyl Giardia, IBD 5-20 mg/lb Once to twice a day, given with food
Moxidectin Advantage Multi/Advocate External/internal parasites 0.5 mg/lb Topically, once a month
Orbifloxacin Orbax Bacterial infections 1-3.5 mg/lb Once a day
Oxytocin Pitocin Dystocia 1-2 IU per cat Given once
Penicillin Penicillin G Procaine, Pen BP-48, Crystiben, Dual-Pen Bacterial infections 10,000-20,000 IU Every 4-48 hours, check label. Newborns: 0.05 ml at birth of 150,000 IU/ml Pen BP
Ponazuril Bayer Marquis Paste Coccidiosis 10 mg/lb Given once, repeat in one week
Praziquantel Droncit Tapeworms 0.05 ml/lb inj., 2.5 mg/lb oral Treat once
Propulsid Cisapride megacolon, constipation 0.5 mg/lb twice a day, give 15 mins. before feeding
Pyrantel Pamoate Nemex-2, Strongid T, Pyratabs, D-Worm, Evict Roundworms 2.5 mg/lb Treat once. Repeat in two weeks

Ronidazole Tricho Plus tritrichomonas intestinal parasites 15-25 mg/lb once a day for two weeks
Selamectin Revolution Fleas, mites, roundworms 3 mg/lb Once a month. If using a dog formulation, one drop (0.05ml) per two pounds. CAUTION: this practice may increase the incidence of adverse reactions!
Sulfadimethoxine Albon Coccidiosis 12.5 mg/lb, double first dose Once a day
Terbinafine Lamisil Fungal infections/ringworm 15-20 mg/lb Once a day
Tetracycline Albaplex, Panamycin Bacterial infections 10 mg/lb Two to three times a day. MUST be given with water or as a suspension.
Tinidazole Tindamax anti-protozoal 7 mg/lb Once a day
Toltrazuril Baycox Coccidiosis 0.2 ml of 5% solution/lb Dose once, repeat in one week
Triamcinolone acetonide Vetalog Inflammation 0.01-0.1 mg/lb Once a day, use lowest effective dose
Trimethoprim/Sulfadiazine and Trimethoprim/Sulfamethoxazole Tribrissen, Septra, Bactrim Bacterial infections 15 mg/lb Once a day
Tylosin Tylan 50 Bacterial infection 10-20 mg/lb Twice a day

Diarrhea Medications – by Fitz Usmany

Diarrhea Medications – by Fitz Usmany

Other than Flagyl, these medications only help with diarrhea or loose stools when it is caused by parasites or protozoa sensitive to the medicine. Metronidazole does help with most diarrhea because it soothes the bowel, but that is only treating the symptom and not the cause. It’s also not recommended for kittens. Another med to treat symptoms is Endosorb, but I don’t always find that helps. If the diarrhea is bacterial, I find Biosol does a good job at curing that, usually almost immediately.

Metronidazole (Flagyl) is an antibiotic, antiprotozoal, and has anti-inflammatory effects in the bowel. It is used for protozoal infections such as giardia or entamoeba, and for bacterial infections. It is also used for inflammatory bowel disease, colitis caused by other antibiotics, and diarrhea of undetermined cause. It is tolerated better when given with food. The dosage for treatment of giardia is 5-11 mg/lb (10-20 mg/kg) orally twice a day for 10 days. Because giardia can be persistent I would give it for 10 days, stop for 5-7 days, then give it again for another 10 days. Metronidazole causes birth defects and should not be given to pregnant animals. It is also excreted in breast milk so should not be given to lactating females. It should also not be given to kittens. This is not the most effective medication for giardia.

Dosage for Strongid: 9 mg/lb (20 mg/kg) once, then repeat in 7 days. I always give a third dose in 7 more days, as recommended by my vet. Using the Strongid from Revival (Pyrantel Pamoate 250mg/5ml): Give 0.2 ml per pound (0.4 mL/kg).

Panacur: Efficacy is increased when given with food. Dosage is 23mg/lb (50 mg/kg). If treating roundworms, give this dose for three days in a row. If treating for giardia, give this dose daily for 14 days, stop for one week, and repeat for 14 more days. Using the Panacur granules from Revival: Mix one packet with 10ml water. Give 0.2 mL/lb (0.4 mL/kg).

Diarrhea Medications – by Fitz Usmany

Diarrhea Medications – by Fitz Usmany

Other than Flagyl, these medications only help with diarrhea or loose stools when it is caused by parasites or protozoa sensitive to the medicine. Metronidazole does help with most diarrhea because it soothes the bowel, but that is only treating the symptom and not the cause. It’s also not recommended for kittens. Another med to treat symptoms is Endosorb, but I don’t always find that helps. If the diarrhea is bacterial, I find Biosol does a good job at curing that, usually almost immediately.



Metronidazole (Flagyl) is an antibiotic, antiprotozoal, and has anti-inflammatory effects in the bowel. It is used for protozoal infections such as giardia or entamoeba, and for bacterial infections. It is also used for inflammatory bowel disease, colitis caused by other antibiotics, and diarrhea of undetermined cause. It is tolerated better when given with food. The dosage for treatment of giardia is 5-11 mg/lb (10-20 mg/kg) orally twice a day for 10 days. Because giardia can be persistent I would give it for 10 days, stop for 5-7 days, then give it again for another 10 days. Metronidazole causes birth defects and should not be given to pregnant animals. It is also excreted in breast milk so should not be given to lactating females. It should also not be given to kittens. This is not the most effective medication for giardia.



Dosage for Strongid: 9 mg/lb (20 mg/kg) once, then repeat in 7 days. I always give a third dose in 7 more days, as recommended by my vet. Using the Strongid from Revival (Pyrantel Pamoate 250mg/5ml): Give 0.2 ml per pound (0.4 mL/kg).



Panacur: Efficacy is increased when given with food. Dosage is 23mg/lb (50 mg/kg). If treating roundworms, give this dose for three days in a row. If treating for giardia, give this dose daily for 14 days, stop for one week, and repeat for 14 more days. Using the Panacur granules from Revival: Mix one packet with 10ml water. Give 0.2 mL/lb (0.4 mL/kg).

Bordetella Bronchiseptica: Is YOUR Cattery at Risk...

Bordetella? Isn’t that a DOG disease? Why would I worry about THAT?

Yes, Bordetella Bronchiseptica is more commonly known as Kennel Cough, affecting dogs who spend time in crowded conditions (like a kennel). It causes a whooping like cough, with little or no additional signs. Occasionally, an untreated dog will suddenly develop acute pneumonia, and will die unless treated quickly.

More significantly, Bordetella has been isolated in numerous other mammalian species, such as pigs, horses, sheep, goats, monkeys and humans. It has not, however, been previously recognized in cats, and an otherwise unenlightened veterinarian will look at you oddly if you request a Bordetella culture.

Bordetella has been affecting numerous catteries from coast to coast (I have seen reports from Washington, California, Texas, and various east coast states). It has been a serious problem, with high mortality, and surprising tenacity. A breeder I spoke to here in the San Francisco Bay Area lost 28 kittens in 18 months before it was finally identified at UC Davis and properly treated. She has begun vaccinating, and has had healthy kittens since.

One good thing, however–Bordetella is a bacteria, NOT a virus, and can be eliminated with good husbandry and appropriate antibiotics!

Can I vaccinate for it?

Yes! The canine vaccines, both the killed injectable and the intra-nasal modified live have been successfully used.

For unaffected catteries: Killed injectable to all cats (every 6 months), and queens 3 weeks before breeding. Intra-nasal MLV to kittens at 6 and 9 weeks.

For affected catteries: Killed injectable to all cats, queens 3 weeks before breeding, at 21 days of pregnancy, and 24 hours post birthing. Intra-nasal MLV to kittens at 10 days (or when eyes open), 3, 6, and 9 weeks. Queens should follow the same regimen as the kittens.

In addition, since the Herpes virus is so opportunistic in conjunction with this infection, vaccination of all cats with a MLV (modified live) 3 or 4-way Flu vaccine is highly recommended for all those catteries that previously only used killed. The killed vaccine is simply not effective enough when challenged with both diseases. Affected catteries should also vaccinate kittens with a MLV intra-nasal 2 or 3-way Flu vaccine at 8, 10, and 12 weeks.

Bordetella vaccines successfully used: Killed-Coughgard-B, Bio-Cor. MLV–Ft. Dodge vaccine (don’t know name), IntraTrac II ADT or Bronchi-shield II (the last two contain vaccine for canine parainfluenza. This has not reported to give any problems), and the SmithKlineBeecham vaccine.

There has been some indication on the Internet regarding an unnamed company exploring the possibility of marketing a feline Bordetella vaccine. There is no solid evidence at this time, and it will, at minimum, be awhile before one is made available to the public. We hope this will be more successful than the FIP “vaccine”!

How do I treat this?

Bordetella is resistant to Amoxicillin, but seems to be sensitive to just about every other antibiotic. The most commonly used are Clavamox and Baytril, either in conjunction, or alternating weeks. The most important thing–treatment must be continued for at least 14 days! Some veterinarians recommend a 21 day treatment period.

Other drugs used: Chloromycetin, Kanamycin, Gentamicin (2mg/lb up to 4 weeks old, 4mg/lb after), Tetracycline, Cephalasporine (at 4x the normal dose), Doxycycline (50mg daily per adult cat), Antirobe, Cephalothin, Trimeth-sulfa, Primaxin (the most effective, but also the most expensive. Dose is given 3x/day by IM injection). A caution–Gentamicin should be used judiciously in kittens, because it can cause permanent kidney damage in some cats.

Another point–if one cat in the household has been diagnosed, all cats have been exposed and must be treated for the full 14-21 days, or you will experience repeated outbreaks of more and more resistant strains.

Even after a full scale treatment, breeders have reported re-breaks that required isolation and additional treatment.

How do know I have it?

Symptoms in healthy adult cats can range from none to moderate, usually manifesting as a dry, “hairball like” cough, which may or may not be preceded by vomiting. In the more severely affected kittens, the cough can become progressively more “wet” sounding, exhibiting a “barking” or “whooping” type cough, with the cat struggling to catch it’s breath.

Pneumonia can develop rapidly, with the cat seeming fine one minute, and near death 12 hours later.

Young kittens are the hardest hit. They can seem fine when you go to bed, and be dead from pneumonia the next morning. A small sniffle, cough, or runny eye can progress rapidly in 12 hours to a dead kitten. Mortality is nearly 100% in young (under 6 week old) kittens. Older kittens can have copious nasal discharge, be unable to smell or eat, but seem fine otherwise. Mortality among older kittens is closer to 50%.

The most dangerous thing about this disease is the asymptomatic cat! Cats that show no symptoms, and appear healthy even after veterinary examination, have been known to have walking pneumonia!

Diagnosis is made by your veterinarian via a tracheal wash and a culture and sensitivity. Your vet must submit the sample as “canine”–labs have different charts for different species, and Bordetella does not appear on the feline chart!

Bordetella can appear by itself or in conjunction with other respiratory viruses, so individual catteries may experience varying symptoms. It seems to be found most often in conjunction with feline Herpes virus (Rhinotracheitus), with an infection by one weakening the immune system in invitation for the other.

Feline Skin Conditions

Chin Acne

Treatment of Chin Acne in Cats To join a community of cat fanciers interested in cattery related health issues, visit http://groups.yahoo.com/group/fanciershealth We’ve had quite a few discussions on the treatment of chin acne on the fanciershealth list. I’ve compiled a list of suggestions from our members of things to try: 1) switch to glass or metal bowls… no plastic. Disposable paper plates for food. 2) hydrogen peroxide 3) shaving the chin area to facilitate cleaning 3) topical ointment with antibiotic and anesthetic (Band-Aid brand) 4) medicated powders, like ear powder or Ammens. 5) fullers earth powder to keep the area dry 6) polysporin ointment 7) antifungal cream (such as miconozole or ketoconazole) 8) Hibiclens or Nolvasan (Chlorhexidine gluconate) 9) Panalog cream 10) Gentocin Topical 11) try switching food 12) hot wash cloths on the chin to stimulate draining 13) Micro-tek shampoo 14) Pyoben Shampoo 15) Pink Solution http://www.pinksolution.ca/ If topical treatments fail: 1. Combo antibiotics – enrofloxacin (Baytril) and amoxicillin/clavulanate (Clavamox, Augmentin). 1st course for 10 days. 10 days off. Then another 10 days on. 2. Systemic antifungal treatment, itraconazole (Sporonox) or fluconazole (Diflucan) –Lorraine Shelton, List Administrator

Nasopharyngeal Polyps

Ear Polyps – by Cat Moody

Ear Polyps – Frequently asked questions (by Cat Moody)

Disclaimer: I am not a veterinarian, just a breeder who experienced the problem of polyps many, many times. Please consult your veterinarian for proper diagnosis and treatment of the problem. This is just intended to give some practical background information on what polyps are, what my experience has been, and treatment options. 

My background: My name is Cat Moody, and I was a breeder/exhibitor of Maine Coon cats for about twelve years, under the cattery name of Stormwatch. In the first seven years of breeding, I twice had cats who were affected by polyps, both after a bout of upper respiratory illness, one adult and one kitten. That’s a pretty statistically normal experience. However, in the last five years, I had at least 25 kittens affected, with no signs of upper respiratory illness. The incidence increased over the years until in the last year I bred, routinely 50-75% of my kittens were affected, and I stopped breeding as we were unable to determine the cause. 

What causes them?: There are several theories as to what causes polyps, but no answers. Commonly, vets think it may have to do with herpes or calici viruses, but since most cattery cats are positive for both viruses, it makes no sense that polyps typically affect only some breeders and not others. Typically, the vets most experienced with polyps have worked at animal shelters, where ill kittens are brought in with untreated ear infections. 

Genetics:  While there may be a genetic component, that was conclusively ruled out in my case. My stud males were unrelated to each other, and most of the queens were as well. I got equal percentages of polyps from either male, or even from using outside males for stud. Every female in my house produced at least one affected kitten at some point,unless she was sent to live elsewhere for her entire pregnancy and while she raised the kittens. No females sold from my house (with one exception) ever produced an affected kitten, even if both the parents had been affected themselves, or even if the female herself had had a polyp when young. All of my affected kittens were diagnosed before they reached l4 weeks of age – if no polyp was evident at that point, the kitten would never have one. I know, this makes no sense, but we tested my cats for everything under the sun, and it remains a mystery – it had to be something environmental, but we couldn’t figure it out. We have had veterinarians all over the world take a look at this case, and all kinds of biopsies and tests done, with no result.  It did drive me out of breeding, due to the expense and emotional torment. I have never heard of another cattery being affected by this, so consistently and over so many years. 

So the only silver lining in this cloud is that I’ve been through a lot of polyps, and am routinely referred to in some circles as “The Polyp Queen”.  I get a lot of requests from folks looking for help, so thought it would be easier to just post a FAQ sheet. 

How it forms: A polyp is a fleshy stalk that grows out of the inner ear, or the “bulla”. This innermost part of the ear is a ball-shaped boney structure. Normally, any debris that accumulates in the bulla is flushed out from one of the two exits – out to the outer ear canal, or down the back of the throat through the eustachean tube. If for some reason the debris builds up, it forms a fertile base for the formation of a polyp. The polyp forms its roots in the bulla, and begins to grow. It can exit either way – through the ear (referred to as an “aural” polyp), or through the eustachean tube and down the back of the throat (the “nasopharyngeal” polyp). Veterinary literature suggests that the nasopharyngeal polyp is more common, but approximately 75% of mine were aural. As the polyp grows, it can either start to come right through the eardrum, or obstruct the breathing of a cat. In either event, its important to remove it as soon as it is diagnosed. Our only fatality from a polyp was in a kitten that had to delay surgery (he also had a heart defect, so we wanted to wait until he was older), and the polyp grew so large that it adhered to a major blood vessel, which was nicked during surgery and the kitten bled to death. Left untreated, a large polyp in the throat can completely obstruct breathing and the kitten/cat can choke to death. 

Bilateral: I think I have the only current case in veterinary literature of a cat who had bilateral polyps, which were discovered several months apart. Generally, it will only form on one side or the other. There doesn’t seem to be any more susceptibility for a cat who has had one polyp to ever develop another. 

Symptoms: They can manifest in many ways. I’m sure the most common things that vets see are kittens who present with nasty ear infections or coughing, but the signs can be far more subtle than that. Over the years, I got so used to them that I found them long before they would be visible with an ear scope. What I usually noticed for a nasopharyngeal polyp was an odd clicking or snorting, or sometimes the kitten would seem to be gulping or gagging oddly. You might notice a problem in breathing or swallowing.  For an aural polyp, the first indication was usually a very sticky whitish discharge from the ear. You might not even notice except that the fur under the ear would get clumpy and stiff. There may be a reddish irritation in the base of the ear. Those are very early warning signs, and do not necessarily indicate a polyp (unless the kitten was born at Stormwatch LOL). 

However, in an older kitten or cat, or one in which the polyp has progressed unnoticed, the symptoms can be sudden and severe. Vestibular syndrome can come on abruptly and dramatically – I’ve literally seen it appear in under a minute. A kitten who appears completely normal suddenly starts staggering in circles, with a severe head tilt. The head will tilt down on the side of the affected bulla, and the kitten will  continuously turn in that direction. Another aspect of this is Horner’s Syndrome, where the third eyelid (again, on the affected side) comes up and completely obscures the eye. Nystagmus is also seen sometimes, where the pupil on the affected side shakes rapidly from left to right. To be honest, it looks awful, as if your cat has had a stroke – but its completely normal, because the polyp (or resulting swelling) is pressing on a cranial nerve.

 And take note – I’ve run across a few emergency room vets who have confidently told me that “cats don’t get vestibular syndrome” on the phone, implying that I must have looked up a fancy word somewhere….and then recanted an hour later when I put a circling, drunken kitten on the floor in front of them. Too many times I’ve heard of this behavior being immediately diagnosed as neurological – and while that may be the case, its also a very common manifestation of a polyp. These symptoms typically resolve completely several weeks after surgery, but in my experience, the longer we’ve waited after symptoms appear to have the surgery, the more likely the cat may retain a head tilt. Its sort of endearing and doesn’t seem to bother the cat much. 

In one case, we had a kitten we were POSTIVE had a polyp, but one never showed up despite all her symptoms. We finally had the surgery done months later, and they found no polyp, but the bulla was so infected it was causing all the same symptoms. She has a permanent head tilt…and  is, of course, still called “Tilt” by her new owners. 

Surgical Corrections: Polyps must be treated surgically, not medically. No amount or combination of antibiotics is going to make it disappear. There are two basic methods. 

One is generally referred to as “plucking”, and is less invasive and less expensive than the alternative. Unfortunately, it has a dismal success rate. The kitten/cat is sedated, and the vet goes in through the mouth or the ear and grabs the exposed part of the polyp with a puller and extracts it. The problem is, just like pulling a dandelion, the roots are likely to remain in the bulla, and the polyp grows back – 70% of the time. The only time I made use of this method was in a very young kitten who was too small a candidate for successful surgery, who was literally choking to death on the polyp (which made sedating her even more risky). We plucked it and bought her some time to grow up and put on weight. It grew back within four weeks, but by then she was big enough to sail right through her surgery with no problem. 

By far the preferred method is the ventral bulla osteotomy, or VBO. It is expensive (in this area, its about $l200-$l500), you need a skilled surgeon, and there is a recovery period – but we’ve never had one grow back. The only complication we ever had, which is extremely rare, is a bone infection at the surgery site that manifested several months later (and was successfully resolved). The vet surgically opens up the bulla through the side of the neck, scrapes it clean and dislodges the root of the polyp. The polyp is then pulled out, and a drain inserted. The kitten is usually at the vet from 2-4 days, and about ten days of after-care are involved – generally, just giving an antibiotic, making sure the incision and drain are clean, and hot-compressing the area to reduce the swelling. The kitten usually seems to feel much better in a couple of days. Even if the kitten did not have symptoms prior to the surgery, they will post-surgically – typically, a head tilt and Horner’s syndrome. In most cases, those symptoms will take 2-4 weeks to completely resolve. 

The good news, again, is that having the VBO done is 99% effective, and no polyp should ever recur. Its one of the few diagnoses a cat can have that there is a reliable and long-term solution for. It does, however, bring up some difficult considerations for a breeder – you have to be able to justify spending $l500 to “fix” a kitten and then sell the kitten for $500 or whatever. On the plus side, its 90% or better cure-able, the kitten will never be affected again, and the new parents and the kitten can anticipate a completely normal life. I never once chose to put a kitten to sleep if just money could cure the problem – but you can see how it drove me out of breeding financially. I don’t know too many breeders who have unlimited funds, and cost might be a factor for most in making the decision. The success rate is high, the risk is low…..but the price to be paid is very expensive. 

Our only complications were one fatality due to bleeding (and I think that was unavoidable in retrospect), one permanent head tilt, and complete deafness in the one cat who was bilateral. I can’t say for sure if all the aural polyps do result in deafness, because you wouldn’t notice a cat who was deaf in one ear. 

 I’m often asked if I would breed a cat who had a polyp, or had an affected littermate, or had a parent with a polyp – that is an individual breeder’s decision. In my case, we knew it was not a matter of genetics, and that was not a factor in our breeding decisions. We also knew that in this cattery, although all of our cats were probably herpes and calici positive, we didn’t have a single incidence of manifested illness or typical ear infections  in either cats or kittens during those five years (I know, its odd). Our kittens were always fully isolated from adults, so if it was viral in nature, it must have been something that the mother cats were shedding at a certain point in gestation or in nursing. We won’t ever know – and I hope none of you go through that! Most of the cases I’ve heard of were in a single, older kitten or cat, or a particular litter that had several affected kittens. I don’t know if it is because I bred Maine Coons and that’s the people who refer to me, but most of the cases I have heard of were in Maine Coons. 

If you have other questions that I can try to answer, you can email me at mailto: Catmoody@aol.com - but please remember that I am NOT a vet, only a breeder, and you should be consulting with a vet if you suspect or confirm a polyp. This is just intended to share what I’ve gone through, to make the process a little more familiar to others who have the problem.

By Cat Moody (Stormwatch Maine Coons)

Litter Box Issues

Evaluation of Litterbox Problems – by Donna Stewart DVM


Evaluation of Litterbox Problems

by Donna Stewart, DVM
Originally posted to the FanciersHealth Yahoogroup

These cases can be complicated and frustrating, and frankly I cringe when they come through the door. I start with a thorough history looking for such clues as changes or disruptions in the normal routine and lifestyle of the cat and of other people and cats in the household. I focus on where the cat is urinating: is the feces outside the litter pan? is it on horizontal or vertical surfaces? is it near doors and windows? I inquire as to the appearance of the urine and the behavior of the cat: is he straining a lot? is there blood in the urine? does he have a prior history of urinary problems?

I also ask about his current diet and whether there has been a change in diet. I look for primary health reasons (other than urinary) why it might be happening, such as arthritis that makes it hard to get into a tall litter pan, increased thirst, change in appetite, change in weight, restlessness and crying. Quite often, it is a behavior problem, but I always give the cat the benefit of the doubt. If it is a geriatric cat with no history of urinary problems, I likely will do a full blood panel with a urinalysis (UA). If there are indications of cystitis or even if I still suspect a behavior problem, then I start with a UA by cystocentesis. If there is a history of bladder problems, I might add a urine culture to the UA. If there is a chronic pattern, I may immediately add radiographs.

I will focus on your cat with the information you have given me and without ever examining him. When you say that he urinates on everything, you need to be more specific. In this case (referring to a fanciershealth message thread) what you have given me is a list of your personal items and those of a new baby only. BINGO! This is important information. Secondly you have told me that this cat was once allowed free access to the out of doors and is now confined to the house. BINGO! You have said that his former pattern was to urinate just outside the litter pan. BINGO! You have said that he is geriatric. BINGO! Now I have a list of potential causes.

I am ruminating over multiple causes, but I am focusing on this cat’s potential anger at you over the drastic change in his life. You have not only clipped his wings, but you have given him competition for the attention that he craves from you, especially during those long boring days with no other activity. A cat has few ways of showing displeasure just as your newborn infant. When things are wrong in an infant’s life, she cries, and you do something to put her world back in order. This cat appears to me to be trying to get your attention by urinating on your things. You noticed, didn’t you? Next he is urinating on the new baby’s things. I think he might be telling you why he is mad at you. Sometimes a cat has additional issues and it just makes it easier to urinate outside the litter pan when the cat is already angry. Litter aversion often is corrected with simple, cheap, non-clumping litter. Perhaps the litter pan is in a noisy part of the apartment where the other children are bustling around. Maybe this fellow is in kidney failure also and produces more urine than he used to. He might have increased urgency to urinate.

So you need to rule out medical reasons for not using the litter pan and if they don’t yield anything, focus on making his life more enjoyable. Start by putting yourself in his position. Imagine that you have moved from a large home with a view of the ocean into a studio apartment. Then one day your husband brings home another woman and announces that you are all going to live together. How would you feel and react? What would you need? Well, I think you would need some additional attention from your husband. You would need some activity that would keep you from feeling confined and stifled. You would need some mental and physical stimulation. If you expressed unhappiness, you would not need punishment. You would need reassurance.

Start by never, never yelling at the cat when he does this. The war will escalate and he will win. Treat him as “poor unhappy baby.” Try to find some time in your impossibly busy day to spend with him alone focusing entirely on him. Try to talk to him and stroke him lovingly everytime during the day that you walk past him. Close the baby’s door and get a monitor. As absurd as this sounds, many behaviorists recommend calling the addition “(Kitty’s) new baby” when you deal with them at the same time. Maybe it just creates a shift in human thinking instead of the cat’s thinking. Then introduce the baby to the cat in a manner similar to introducing a new kitten – slowly and reassuring the old resident. Can you breast feed and allow the cat to sit next to you for petting at the same time? Then he might actually look forward to the time you spend with the baby, because there is a payoff for him.

Finally do what you can to create what I call “cat space.” Think vertical like a cat does. Construct someway for the cat to climb above the furniture and create high places for the cat to stay. This has the effect of increasing the size of the available space for the cat. Some people mount shelves around the room close to the ceiling. Think about creating hiding spaces for the cat such as plastic storage containers with openings cut in them. Think about creating activity situations for him like a tall post to climb to get to the shelf or a series of shelves requiring jumping, or putting the tall shelves at different heights. Create mental stimulation for him. Put out bird feeders or hummingbird feeders to attract active animals to the window. If there are squirrels or other such animals around, you might consider feeding them. You children will enjoy it too. If your situation permits, consider building an outdoor cage where he can enjoy the out of doors without threat. I have made these using modified dog run panels and allowed access through an open window. Once I saw a cage like structure that could be built out from a window and it did not touch the ground.

The bottom line for this cat is that if it is behavioral, then he may need to be rehomed. It is better for him to live happily with someone else than unhappily with you. It may be that the children are also feeling confined and their increased activity level in the apartment is an additional stress to the cat. That would make the outside cage, indoor hiding places, and high perches especially important. It removes him from the children’s activity. Perhaps in the past he just went outside when they were rowdy.

Donna Stewart, DVM

Other hints from Fanciershealth List members

First and foremost, a vet needs to check the cat out to make sure there is no infection or anything medically going on. If this is a urination problem, there could be an infection, UTI. If this is a defecaton problem, the cat could have worms, giardia, or an allergy to a new food. If this has already been done, then just follow the next steps.

Second and also very important, do not allow the cat to have the run of your house. The cat needs to be confined to one small room like a bathroom or laundry room. The room should not have carpet.

Has there been Any changes in the cat’s life style: new pet, new baby, new house, new/change of litter brand or type, additive such as deodorizer to litter, different type of litter box, person leaving home, or any other change? Cats do not like change.

The cat should have two litter boxes, one covered and one uncovered put in it’s room. Make one of the litter boxes a larger box than the cat usually uses, sometimes they need additional space. Some cats do not like covered boxes because they can be cornered with no escape route. Some cats like to use one box for urination and one for defecation. You will quickly find the answers to these questions when you clean the boxes. You will know which type of box the cat prefers.

The room should have a bed, food and water as well as favorite toys. The food should not be close to the litter box. Use only bottled or filtered water. Sometimes a change in water will cause a problem.

The boxes need to be scooped or dumped twice a day, morning and night, so that the cat does not have an issue with whether the boxes are clean. If you find that scooping does not work, use only a small amount of litter and dump it daily. You can use the cheapest clay litter if this happens.

After a week if the cat is using the litter box, let the cat out while you are home. Let the cat out for only a few short hours a day as long as the cat continues to use the litter box. The cat should spend the night or any alone time in it’s room.

After a week of this, let the cat out permanently as long as the cat uses the litter box.

If the cat should have an accident, it needs to be cleaned up immediately and thoroughly. If the accident is on carpet, an enzyme cleaner needs to be used so that the smell is totally destroyed. Simple Solution by Brampton or Nature’s Miracle are good cleaners and deodorizers. Carpet pad may need to be pulled out.

There is also a product called Feliway that is guaranteed to work. It is used on the area where the accident occurred. Feliway also has a plug in for electric outlets.

Thoroughly clean the litter boxes at least once a week. Do not use bleach unless you rinse all the bleach out and let the box dry in the sun. Bleach and urine make gas and also create ammonia. Bleach will cause a cat to stop using the litter box.

Please save this information should you need it or to pass along to anyone who’s at their “wits end” with litterbox problems. Soiling “outside the box” is the #1 reasons cats are abandoned or put down so this information could save a cat’s life!

Last week I attended a lecture by Dr. Andrea Tasi of Kingstowne Cat Clinic on “Litterbox Blues” and learned some very useful information. You can print out more information about preventing Litterbox Blues at: http://www.preciouscat.com/WebPages/litterBoxSolutions.html

RULE OUT MEDICAL CAUSES FIRST: Dr. Tasi said that over the course of her practice she has found that medical problems are the #1 reason cats stop using the box. So she encourages cat people to always rule that out first. (I had urine withdrawn externally with a needle from my 14-year-old cat last month. It really wasn’t that bad and was over in about 3 seconds; the cost was under $30 and was well-worth doing.) Cats are “associative beings.” That means that if they associate the cat box, or type of litter, with painful urination or defecation, even after curing the infection, they will “still associate” pain with the litterbox. Therefore, in order to break the “associative disorder” its advised to buy a NEW box and perhaps a new litter type, and go from there. REMEMBER: Cats aren’t trying to get back at you by soiling, they are doing it for perfectly logical reasons — you need to think like a cat in order to change your cat’s behavior. Never, ever punish your cat as you will not change the behavior, but only make your cat fear you.

USE SANDY TEXTURES: As we all know, cats originated as desert animals and, as such, they truly prefer SOFT, sandy textures. Dr. Tasi said AVOID the new crystal products, and coarse litters, as they are painful to the tender pads of many cats, and “just don’t feel right.” Dr. Tasi generally recommends clumping litters, except for kittens under 4 weeks, who can inhale or ingest the clumping substance and develop health problems, sometimes fatal. She especially likes a product called “Dr. Elsey’s (unscented) Precious Cat Litter.” Dr. Elsey also makes another product called “Cat Attract” that attracts them to the box. You can take a look at his products at: www.preciouscats.com, or call toll free at: 877-311 CATS (2287). If you want a clay free litter product, try “World’s Best” which is made with corn. Dr. Tasia recommends filling the box 2-3″ with litter.

TAKE THE HOOD OFF & DUMP THE SCENTED LITTERS: She said that cats NEVER go into dark, enclosed spaces to eliminate because that puts them in a very vulnerable position. So if a cat is avoiding a hooded box, take the hood off or don’t use one in the first place! It is another “turn off” to cats and will often make them go elsewhere. Dr. Tasi said that our cats’ noses are 1000% more sensitive than ours and hoods trap the odors and dust. Also, “out of sight, out of mind,” may make us forget to scoop the box as often as we should (at least twice a day). Would you want to go to the bathroom in a dirty toilet? Your cat doesn’t either! Cats also find the smells of roses and cheap perfumes in the litter repulsive, so always choose unscented litter. Try mixing about 1/2 cup baking soda into the box if odor is a problem to your nostrils.

TRY A DIFFERENT SIZED BOX: Especially for those overweight cats, or cats whose urine sprays outside the box; go to Home Depot, Walmart, etc and buy a BIG Rubbermaid or plastic storage box. If s/he’s a sprayer, get one that’s very high and cut out an oval entrance in front. If s/he has arthritis, put a little ramp up to the entrance. If they kick litter all over the place, buy one of those large plastic washing machine liners and put your box(es) into it. It’s much cheaper to buy these items at a department store than from a pet store. BEST, CHEAPEST SCOOPER: Best scoopers are flat metal utensils with little holes or slits — I’ve found the best ones at the dollar store!

LOCATION OF BOX: Please put a box on EACH LEVEL of your house in a quiet, out of the way location, that’s not next to a heater, washing machine or applicance that could suddenly start up and frighten your cat. Be mindful of older cats who may suffer from arthritis and bladder problems and might find a long trip to the basement painful and difficult (put a ramp or phone book in front of the box entrance to help them step up). Though cats see better than us in low light, CATS CAN’T SEE IN THE DARK, so please don’t put their box in a pitch dark basement. Also, the general rule of thumb is to have one box for each cat and put each box in a different location so they aren’t competing for the box. And don’t place them next to their food or water. Would you want to eat next to your toilet?

CLEANING THE BOX DOESN’T JUST MEAN SCOOPING OUT THE POOP!: Again, back to that 1000% nose, look at the box itself next time you clean it. After scrubbing it with soap and water and perhaps a bit of bleach, rinse it out thoroughly. You may want to place it in the sun to dry as sunshine is a natural disinfectent. Then put your nose into the box and take a deep sniff. If there’s a lingering odor or it’s covered in scratches and discoloration, throw it out and buy a nice new one at Walmart or Home Depot.

CLEANING STAINS & ODORS OUTSIDE THE BOX: You’ve got to use an enzymatic cleaner to get rid of those stains and odors. Remember your cat’s 1000% nose will bring him back to previous elimination spots and s/he will pee/poop there again. There’s some great products available, including “Simple Solution” Stain & Odor Remover. Dr. Tasi’s favorite product is “Anti-Icky-Poo” in Veterinary Practice Strength (she doesn’t like it in “regular” strength) . Check your vet’s office for it or order online at: http://www.mistermax.com/products.html Dr. Tasi said you must first SATURATE the spot with solution and KEEP IT WET for 24 hours, covering it with pastic & spraying it several times. Remember that the urine soaked in deeply and then spread horizontally throughout the fibers, so you must get the product deeply into whatever is stained or smells. DO NOT USE ANYTHING THAT IS AMMONIA-BASED, because of its “urine-like” scent to a cat.

OTHER TIPS: Dr. Tasi also recommends another product called “Feliway.” This smells like friendly pheromones to a cat and when sprayed in a cat’s environment, it creates a comforting, reassuring feeling that reduces the impulse to urine mark or scratch. (A cat’s pheromones are between his eye and ear; when s/he rubs his head against you, s/he’s putting friendly pheromones on you.)

PLAY WITH YOUR CAT – STRESS CAN CAUSE ELIMINATION PROBLEMS: Dr. Tasi says that many elimination problems stem from boredom. Cats are designed to be hunters and become incredibly bored and frustrated when they are denied the opportunity. She says to spend at least 15 minutes each day playing with your cat. Toys like “da bird” are excellent (ask for it at your local pet store); anything interactive that makes your cat run and chase. Dr. Tasi says laser toys are OK — NEVER shine in your cat’s eyes — but can frustrate the cat as they are never able to catch anything. Be sure your cat has plenty of toys to stalk and chase. Here’s a great site for toys. You might also want to consider acquiring another cat or two so your pet has somebody to play with. CAUTION: Do not leave string toys lying around as your cat can choke to death on string or it can end up wrapped around his internal organs and intestines.

WONDERFUL FINAL TIP FOR ACQUIRING A NEW CAT: Apart from “Introducing a Cat to a New Home” instructions which are another topic in itself, I learned this simple new tip: While keeping the cats separated in different rooms, try wiping each cat’s fur with a separate towel daily. Then place each cat’s food dish on top of the other cat’s towel. They will associate each other’s scent with the positive experience of being fed, and grow tolerant of each other quickl!

The Poop Patrol – by Terri Jorgensen

THE POOP PATROL

Compiled by Terri Jorgensen

Describing characteristics of Feline Fecal Matter as it relates to Parasitic, Bacterial and Digestive maladies and infestations.

Special thanks to Tom Ward, D.V.M. of Kansas City, Marie Hollingsworth and to professional breeders and fanciers the world over for their contributions to this endeavor.

Profits to benefit the Devon Rex Rescue League.

One of the major issues clouding the development of specific guidelines for descriptive characteristics relates directly to the color and consistency of foods eaten by our furred feline friends. Type of food can change both color and consistency of feces. This handy reference guide does not attempt to discern what the cat was fed. Thus there may be differing and seemingly conflicting data contained herein. Please take this into account and know that this is the primary reason that this information has eluded us until now. The tables, charts and compilations below are drawn from the most common results seen in Veterinary literature, combined with the vast wealth of knowledge of professional breeders and fanciers everywhere who responded with their input from personal knowledge and experience.

Thank You.

Poop Patrol – Table 1:

General Guidelines of Feline Fecal Characteristics

COLOR

Yellow or Greenish Stool = Rapid transit

Black Tarry Stool = Bleeding in upper digestive tract

Red Bloody Stool = Bleeding in the lower bowel (colon)

Pasty, Light-colored Stool = Lack of Bile (liver disease)

Large Gray, Rancid-smelling Stool = Inadequate digestion, Malabsorption Syndrome (often with oil on hair around anus)

CONSISTENCY

Soft Bulky Stool = Overfeeding or poor quality food high in fiber

Watery Stool = Bowel wall irritation with rapid transit and decreased absorption

Foamy Stool = Suggestive of bacterial infection

ODOR

The more watery the stool, the greater the odor!

Foodlike smell or sour milk smell = both incomplete digestion and inadequate absorption

Putrid smell = infection or blood

FREQUENCY

Several small stools per hour with straining = colitis

3-4 large stools per day = malabsorption or inflammatory bowel

(Note: any pathogen or parasite that would trigger rapid transit of food through the bowel would also result in malabsorption)

(Adapted in part from: Cat Owner’s Home Veterinary Handbook by Delbert Carlson, D.V.M. and James Griffin, M.D.)


Poop Patrol – Table 2: Enteric Parasites

Compiled by Terri Jorgensen

Giardia

Coccidia (Isospora)

Characteristics

soft, mucous, foamy to frothy, fatty, occasional blood, “lumpy, pudding”, “chocolate pudding”

watery, mucous, occasional blood,“instant oatmeal”, “chocolate mousse”, “soft frozen yogurt”, grainy,

Color

yellow, green, gingerbread, brown

white, yellow, deep tan, camelhair, normal, dark brown.

Odor

rancid, stinky normal, “green”

sweet decay, “sweet broken, green twig”, “pseudomonas smell”, heavy, hangs in the air, capable of clearing 3 rooms with a single poop

Other symptoms

weight loss, lethargy, flatulence, abdominal distention, poor hair coat

anorexia, lethargy, weight loss, dehydration, lots of flatulence

Incubation time

ingestion to shedding 5-16 days, can be shed for 27-35 days or years if carrier

ingestion to shedding 5-10 days (ingest oocytes 12-48hrs) can be shed for 1-5 weeks

Treatment

Fenbendazole (Panacur) 50mg/kg, Daily, 5 days

Albendazole (Valbazen) 25mg/kg, BID, 5 days

Metronidazole (Flagyll) 15mg/kg, BID, 7-10 days

Sulfadimethoxine (Albon) 25mg/kg, BID, 10-14 days

Nitrofurazone 15mg/kg daily, 5-7 days

Disinfectants

cysts are very resistant, boiling water, 10% ammonia, bathe cat in regular shampoo to remove cysts in the coat, wash rectum of cat with same ammonia solution and rinse area after 5 minutes

10% ammonia for several minutes, steam, wash cages and litter boxes with boiling water, freezing raw meats prior to feeding decreases oocyte counts


Metronidazole (Flagyll) is a very useful drug in that it has the added advantage of having antibacterial as well as anti-inflammatory properties. In situations in which it is unclear whether diarrhea is due to giardiasis, bacterial overgrowth, or mild inflammatory bowel disease, Metronidazole is an excellent choice. It is however only 70% effective in eliminating giardia even though it is widely prescribed. If a positive diagnosis is made, Albendazole or Fenbendazole are the better choices.

Metronidazole (Flagyll) and Albendazole (Valbazen) are both suspected to have teratogenic effects. Therefore, Fenbendazole (Panacur) is the drug of choice for pregnant or lactating females.

Interestingly, Coccidia are obligate intracellular parasites found in the intestinal tract. Coccidia is a large blanket term defining the family. Coccidian genera that infect cats are Isospora, Toxoplasma and Cryptosporidium. Interesting, in that before this research, I was unaware that Toxoplasma and Cryptosporidium were Coccidian. The above report deals with Isospora, which is what the majority of us call “Coccidia”.

Drugs for treatment of Coccidia are Coccidiostatic rather than curative. This means that they do not kill the organism but instead keep it from reproducing until it is out of the system. Severe diarrhea from Coccidia is usually linked to an immunosuppressed animal. The parasite can burrow into tissue and remain dormant and not shed only to manifest during stress and resulting immunosuppression such as weaning, shipping or change in ownership thus infecting or reinfecting the host long after the initial exposure. Sporulated oocytes can survive in the soil for 18 months or longer.



Enteric Viral Pathogens

Compiled by Terri Jorgensen

Enteric Coronavirus

Rotavirus

Astrovirus

Infectious agent

Feline Coronavirus

Feline Rotavirus

Feline Astrovirus

Incubation time

2- 10 days

1 day

2-5 days

Source

shedding cats

+ cats shed10-14 days

+cats shed 14days

Mode of transmission

Fecal/oral route-inhalation

probably ingestion

Oral

Fever

low grade

—–

biphasic>39.5oC

Vomiting

common initial sign

——

Rare

Frequency

Increase

can be intermittent

Volume

Characteristics

soft pasty mucoid becoming fluid, may contain blood

Loose

Watery

Color

Yellow

varies-white, yellow, brown

Green

Smell

Fetid

Other symtoms

depressed, anorexic

Anorexic

Treatment

withold food 24hrs. fluid repalcement

non specific

fluid if needed

Prognosis

good unless it mutates to FIP

Good

Good

Disinfectants

hypochlorite(bleach)

Hypochlorite

Means of Diagnosis

EM(electron microscopy)

EM, viral culture

EM, IFA

Site of infection

small intestine

Differential diagnosis

other enteric pathogens,nutritional

other enteric pathogens

Feline Behavior

Evaluation of Litterbox Problems – by Donna Stewart, DVM

Evaluation of Litterbox Problems

by Donna Stewart, DVM
Originally posted to the FanciersHealth Yahoogroup

These cases can be complicated and frustrating, and frankly I cringe when they come through the door. I start with a thorough history looking for such clues as changes or disruptions in the normal routine and lifestyle of the cat and of other people and cats in the household. I focus on where the cat is urinating: is the feces outside the litter pan? is it on horizontal or vertical surfaces? is it near doors and windows? I inquire as to the appearance of the urine and the behavior of the cat: is he straining a lot? is there blood in the urine? does he have a prior history of urinary problems?

I also ask about his current diet and whether there has been a change in diet. I look for primary health reasons (other than urinary) why it might be happening, such as arthritis that makes it hard to get into a tall litter pan, increased thirst, change in appetite, change in weight, restlessness and crying. Quite often, it is a behavior problem, but I always give the cat the benefit of the doubt. If it is a geriatric cat with no history of urinary problems, I likely will do a full blood panel with a urinalysis (UA). If there are indications of cystitis or even if I still suspect a behavior problem, then I start with a UA by cystocentesis. If there is a history of bladder problems, I might add a urine culture to the UA. If there is a chronic pattern, I may immediately add radiographs.

I will focus on your cat with the information you have given me and without ever examining him. When you say that he urinates on everything, you need to be more specific. In this case (referring to a fanciershealth message thread) what you have given me is a list of your personal items and those of a new baby only. BINGO! This is important information. Secondly you have told me that this cat was once allowed free access to the out of doors and is now confined to the house. BINGO! You have said that his former pattern was to urinate just outside the litter pan. BINGO! You have said that he is geriatric. BINGO! Now I have a list of potential causes.

I am ruminating over multiple causes, but I am focusing on this cat’s potential anger at you over the drastic change in his life. You have not only clipped his wings, but you have given him competition for the attention that he craves from you, especially during those long boring days with no other activity. A cat has few ways of showing displeasure just as your newborn infant. When things are wrong in an infant’s life, she cries, and you do something to put her world back in order. This cat appears to me to be trying to get your attention by urinating on your things. You noticed, didn’t you? Next he is urinating on the new baby’s things. I think he might be telling you why he is mad at you. Sometimes a cat has additional issues and it just makes it easier to urinate outside the litter pan when the cat is already angry. Litter aversion often is corrected with simple, cheap, non-clumping litter. Perhaps the litter pan is in a noisy part of the apartment where the other children are bustling around. Maybe this fellow is in kidney failure also and produces more urine than he used to. He might have increased urgency to urinate.

So you need to rule out medical reasons for not using the litter pan and if they don’t yield anything, focus on making his life more enjoyable. Start by putting yourself in his position. Imagine that you have moved from a large home with a view of the ocean into a studio apartment. Then one day your husband brings home another woman and announces that you are all going to live together. How would you feel and react? What would you need? Well, I think you would need some additional attention from your husband. You would need some activity that would keep you from feeling confined and stifled. You would need some mental and physical stimulation. If you expressed unhappiness, you would not need punishment. You would need reassurance.

Start by never, never yelling at the cat when he does this. The war will escalate and he will win. Treat him as “poor unhappy baby.” Try to find some time in your impossibly busy day to spend with him alone focusing entirely on him. Try to talk to him and stroke him lovingly everytime during the day that you walk past him. Close the baby’s door and get a monitor. As absurd as this sounds, many behaviorists recommend calling the addition “(Kitty’s) new baby” when you deal with them at the same time. Maybe it just creates a shift in human thinking instead of the cat’s thinking. Then introduce the baby to the cat in a manner similar to introducing a new kitten – slowly and reassuring the old resident. Can you breast feed and allow the cat to sit next to you for petting at the same time? Then he might actually look forward to the time you spend with the baby, because there is a payoff for him.

Finally do what you can to create what I call “cat space.” Think vertical like a cat does. Construct someway for the cat to climb above the furniture and create high places for the cat to stay. This has the effect of increasing the size of the available space for the cat. Some people mount shelves around the room close to the ceiling. Think about creating hiding spaces for the cat such as plastic storage containers with openings cut in them. Think about creating activity situations for him like a tall post to climb to get to the shelf or a series of shelves requiring jumping, or putting the tall shelves at different heights. Create mental stimulation for him. Put out bird feeders or hummingbird feeders to attract active animals to the window. If there are squirrels or other such animals around, you might consider feeding them. You children will enjoy it too. If your situation permits, consider building an outdoor cage where he can enjoy the out of doors without threat. I have made these using modified dog run panels and allowed access through an open window. Once I saw a cage like structure that could be built out from a window and it did not touch the ground.

The bottom line for this cat is that if it is behavioral, then he may need to be rehomed. It is better for him to live happily with someone else than unhappily with you. It may be that the children are also feeling confined and their increased activity level in the apartment is an additional stress to the cat. That would make the outside cage, indoor hiding places, and high perches especially important. It removes him from the children’s activity. Perhaps in the past he just went outside when they were rowdy.

Donna Stewart, DVM

Other hints from Fanciershealth List members

First and foremost, a vet needs to check the cat out to make sure there is no infection or anything medically going on. If this is a urination problem, there could be an infection, UTI. If this is a defecaton problem, the cat could have worms, giardia, or an allergy to a new food. If this has already been done, then just follow the next steps.

Second and also very important, do not allow the cat to have the run of your house. The cat needs to be confined to one small room like a bathroom or laundry room. The room should not have carpet.

Has there been Any changes in the cat’s life style: new pet, new baby, new house, new/change of litter brand or type, additive such as deodorizer to litter, different type of litter box, person leaving home, or any other change? Cats do not like change.

The cat should have two litter boxes, one covered and one uncovered put in it’s room. Make one of the litter boxes a larger box than the cat usually uses, sometimes they need additional space. Some cats do not like covered boxes because they can be cornered with no escape route. Some cats like to use one box for urination and one for defecation. You will quickly find the answers to these questions when you clean the boxes. You will know which type of box the cat prefers.

The room should have a bed, food and water as well as favorite toys. The food should not be close to the litter box. Use only bottled or filtered water. Sometimes a change in water will cause a problem.

The boxes need to be scooped or dumped twice a day, morning and night, so that the cat does not have an issue with whether the boxes are clean. If you find that scooping does not work, use only a small amount of litter and dump it daily. You can use the cheapest clay litter if this happens.

After a week if the cat is using the litter box, let the cat out while you are home. Let the cat out for only a few short hours a day as long as the cat continues to use the litter box. The cat should spend the night or any alone time in it’s room.

After a week of this, let the cat out permanently as long as the cat uses the litter box.

If the cat should have an accident, it needs to be cleaned up immediately and thoroughly. If the accident is on carpet, an enzyme cleaner needs to be used so that the smell is totally destroyed. Simple Solution by Brampton or Nature’s Miracle are good cleaners and deodorizers. Carpet pad may need to be pulled out.

There is also a product called Feliway that is guaranteed to work. It is used on the area where the accident occurred. Feliway also has a plug in for electric outlets.

Thoroughly clean the litter boxes at least once a week. Do not use bleach unless you rinse all the bleach out and let the box dry in the sun. Bleach and urine make gas and also create ammonia. Bleach will cause a cat to stop using the litter box.

Please save this information should you need it or to pass along to anyone who’s at their “wits end” with litterbox problems. Soiling “outside the box” is the #1 reasons cats are abandoned or put down so this information could save a cat’s life!

Last week I attended a lecture by Dr. Andrea Tasi of Kingstowne Cat Clinic on “Litterbox Blues” and learned some very useful information. You can print out more information about preventing Litterbox Blues at: http://www.preciouscat.com/WebPages/litterBoxSolutions.html

RULE OUT MEDICAL CAUSES FIRST: Dr. Tasi said that over the course of her practice she has found that medical problems are the #1 reason cats stop using the box. So she encourages cat people to always rule that out first. (I had urine withdrawn externally with a needle from my 14-year-old cat last month. It really wasn’t that bad and was over in about 3 seconds; the cost was under $30 and was well-worth doing.) Cats are “associative beings.” That means that if they associate the cat box, or type of litter, with painful urination or defecation, even after curing the infection, they will “still associate” pain with the litterbox. Therefore, in order to break the “associative disorder” its advised to buy a NEW box and perhaps a new litter type, and go from there. REMEMBER: Cats aren’t trying to get back at you by soiling, they are doing it for perfectly logical reasons — you need to think like a cat in order to change your cat’s behavior. Never, ever punish your cat as you will not change the behavior, but only make your cat fear you.

USE SANDY TEXTURES: As we all know, cats originated as desert animals and, as such, they truly prefer SOFT, sandy textures. Dr. Tasi said AVOID the new crystal products, and coarse litters, as they are painful to the tender pads of many cats, and “just don’t feel right.” Dr. Tasi generally recommends clumping litters, except for kittens under 4 weeks, who can inhale or ingest the clumping substance and develop health problems, sometimes fatal. She especially likes a product called “Dr. Elsey’s (unscented) Precious Cat Litter.” Dr. Elsey also makes another product called “Cat Attract” that attracts them to the box. You can take a look at his products at: www.preciouscats.com, or call toll free at: 877-311 CATS (2287). If you want a clay free litter product, try “World’s Best” which is made with corn. Dr. Tasia recommends filling the box 2-3″ with litter.

TAKE THE HOOD OFF & DUMP THE SCENTED LITTERS: She said that cats NEVER go into dark, enclosed spaces to eliminate because that puts them in a very vulnerable position. So if a cat is avoiding a hooded box, take the hood off or don’t use one in the first place! It is another “turn off” to cats and will often make them go elsewhere. Dr. Tasi said that our cats’ noses are 1000% more sensitive than ours and hoods trap the odors and dust. Also, “out of sight, out of mind,” may make us forget to scoop the box as often as we should (at least twice a day). Would you want to go to the bathroom in a dirty toilet? Your cat doesn’t either! Cats also find the smells of roses and cheap perfumes in the litter repulsive, so always choose unscented litter. Try mixing about 1/2 cup baking soda into the box if odor is a problem to your nostrils.

TRY A DIFFERENT SIZED BOX: Especially for those overweight cats, or cats whose urine sprays outside the box; go to Home Depot, Walmart, etc and buy a BIG Rubbermaid or plastic storage box. If s/he’s a sprayer, get one that’s very high and cut out an oval entrance in front. If s/he has arthritis, put a little ramp up to the entrance. If they kick litter all over the place, buy one of those large plastic washing machine liners and put your box(es) into it. It’s much cheaper to buy these items at a department store than from a pet store. BEST, CHEAPEST SCOOPER: Best scoopers are flat metal utensils with little holes or slits — I’ve found the best ones at the dollar store!

LOCATION OF BOX: Please put a box on EACH LEVEL of your house in a quiet, out of the way location, that’s not next to a heater, washing machine or applicance that could suddenly start up and frighten your cat. Be mindful of older cats who may suffer from arthritis and bladder problems and might find a long trip to the basement painful and difficult (put a ramp or phone book in front of the box entrance to help them step up). Though cats see better than us in low light, CATS CAN’T SEE IN THE DARK, so please don’t put their box in a pitch dark basement. Also, the general rule of thumb is to have one box for each cat and put each box in a different location so they aren’t competing for the box. And don’t place them next to their food or water. Would you want to eat next to your toilet?

CLEANING THE BOX DOESN’T JUST MEAN SCOOPING OUT THE POOP!: Again, back to that 1000% nose, look at the box itself next time you clean it. After scrubbing it with soap and water and perhaps a bit of bleach, rinse it out thoroughly. You may want to place it in the sun to dry as sunshine is a natural disinfectent. Then put your nose into the box and take a deep sniff. If there’s a lingering odor or it’s covered in scratches and discoloration, throw it out and buy a nice new one at Walmart or Home Depot.

CLEANING STAINS & ODORS OUTSIDE THE BOX: You’ve got to use an enzymatic cleaner to get rid of those stains and odors. Remember your cat’s 1000% nose will bring him back to previous elimination spots and s/he will pee/poop there again. There’s some great products available, including “Simple Solution” Stain & Odor Remover. Dr. Tasi’s favorite product is “Anti-Icky-Poo” in Veterinary Practice Strength (she doesn’t like it in “regular” strength) . Check your vet’s office for it or order online at: http://www.mistermax.com/products.html Dr. Tasi said you must first SATURATE the spot with solution and KEEP IT WET for 24 hours, covering it with pastic & spraying it several times. Remember that the urine soaked in deeply and then spread horizontally throughout the fibers, so you must get the product deeply into whatever is stained or smells. DO NOT USE ANYTHING THAT IS AMMONIA-BASED, because of its “urine-like” scent to a cat.

OTHER TIPS: Dr. Tasi also recommends another product called “Feliway.” This smells like friendly pheromones to a cat and when sprayed in a cat’s environment, it creates a comforting, reassuring feeling that reduces the impulse to urine mark or scratch. (A cat’s pheromones are between his eye and ear; when s/he rubs his head against you, s/he’s putting friendly pheromones on you.)

PLAY WITH YOUR CAT – STRESS CAN CAUSE ELIMINATION PROBLEMS: Dr. Tasi says that many elimination problems stem from boredom. Cats are designed to be hunters and become incredibly bored and frustrated when they are denied the opportunity. She says to spend at least 15 minutes each day playing with your cat. Toys like “da bird” are excellent (ask for it at your local pet store); anything interactive that makes your cat run and chase. Dr. Tasi says laser toys are OK — NEVER shine in your cat’s eyes — but can frustrate the cat as they are never able to catch anything. Be sure your cat has plenty of toys to stalk and chase. Here’s a great site for toys. You might also want to consider acquiring another cat or two so your pet has somebody to play with. CAUTION: Do not leave string toys lying around as your cat can choke to death on string or it can end up wrapped around his internal organs and intestines.

WONDERFUL FINAL TIP FOR ACQUIRING A NEW CAT: Apart from “Introducing a Cat to a New Home” instructions which are another topic in itself, I learned this simple new tip: While keeping the cats separated in different rooms, try wiping each cat’s fur with a separate towel daily. Then place each cat’s food dish on top of the other cat’s towel. They will associate each other’s scent with the positive experience of being fed, and grow tolerant of each other quickl!:

Cattery Management

Eye Envy formula

Daily eye cleaner  (marketed as Eye Envy, originally published in Persian News)

Recipe #1:

  • Take a Gallon of distilled water and pour 4 cups out into a pitcher.
  • Add the contents of one bottle of Tylan 50 (100ml) (available from Revival)
  • Add one 16 oz bottle of Witch Hazel (buy at the grocery store pharmacy)
  • Add 4 Tablespoons of boric acid powder (buy at the grocery store pharmacy)
  • Mix well
  • Pour enough of the reserved 4 cups of distilled water back into the gal jug to fill it up.
  • Store the solution in the refrigerator.

Recipe #2:

  • Combine the following into a clean container:
  • 10 cc Tylan 50 injectable (available from Revival)
  • 8 ounces of witch hazel (buy at the grocery store pharmacy)
  • 4 ounces of boric acid solution (buy at the grocery store pharmacy)
  • 1 gallon minus two cups of pure *distilled* water
  • Shake well and store the solution in the refrigerator.

Recipe #3:

  • Combine the following into a clean container:
  • One cup boiling water
  • One teaspoon Boric Acid Powder (buy at the grocery store pharmacy)
  • 1 teaspoon witch hazel (buy at the grocery store pharmacy)
  • 500 Mg amoxicillin powder (buy as Fish-Mox capsules from any pet supply company)

Pour any of the above solutions over round cotton cosmetic pads and store in a container in the refrigerator. Use to clean around the eyes daily.

For Severe Staining

Stain removal and eye packing powder:

Combine two tablespoons calcium carbonate,powder with two and half tablespoons boric acid powder.

When ready to use, take a small amount of powder and add 3% peroxide to make a paste.

Carefully apply to stained fur. 

When the proportions are correct, the paste coats the hair but does not flow to the skin.

Let dry, then brush off with a small eyebrow brush.

CAUTION

Use the stain removal paste *ONLY* rarely and only for extremely stubborn stains after initially cleansing the area.

The cause of staining must be identified first and controlled. Brown tears can be cleared up with oral antibiotics.

Do not apply close to the eye or anus, only on cheeks and chin or fur on the back of the legs if those are stained.

Do *not* apply to dark or tipped fur – it does bleach!

Inherited Diseases

Flat Chested Kittens – by Aurora Burmese Cattery

Flat Chested Kittens – from Aurora Burmese Cattery
Updated 2004
“Working together for the benefit of our cats”

NB: I am not a veterinarian or a geneticist – just passionate about Burmese and all pedigreed breeding cats. The following data contains some of the results and my conclusions of 12 years voluntary research into birth defects and nutritional needs of pregnant and lactating queens.
I started this research before I bred my first litter and found it so interesting that I am still doing this voluntary work with the helpful input of dedicated breeders.  
Because of the fact that there are many breeders who do not understand the complexities of the science of animal husbandry and others who know a hell of a lot more than I do, I have tried to simplify my findings to a level that the majority will comprehend without being derogatory to anyone. There is always something new to learn, even for the professionals!
Always discuss your problems with your vet! Don’t be afraid to ask for a second opinion.
_________________________________________________________________

Worldwide, birth defects are occurring in all breeds of pedigreed cats and also in domestic cats. Some behaving erratically which makes the mode of inheritance (or if inherited at all) difficult to establish. Most Universities and research teams are of the opinion that birth defects are under-reported. I know for a fact that this is very true. Many breeders do not discuss their problems for obvious reasons. Don’t blame each other when things go wrong; just be diligent in selecting and caring for your breeding animals. Somebody recently said to me “wherever you have livestock you will also have dead stock”. This is sad but so true –  as all farmers will tell you.

 Just some of the problems reported in cats are:

1.    Flat chests.
2.    Funnel chests.
3.    SpinaBifida
4.    Cranial deformities.
5.    Hypokalaemia
6.    Cutaneous Asthenia (stretchy skin disease)
7.    Renal diseases including PKD.
8.    Heart defects.
9.    Eye diseases.
10.    Tail defects – common (Congenital and Recessive and accidental- also may be linked to Copper deficiency – see Winn Foundation update)
11.    Hernias – often an accident of birthing.
12.    Cleft palates.
13.    Diabetes.
14.    Testicular anomalies.
15.    Paw and limb defects.
16.    Allergies.
17.    Bowel disease.
18.    Spasticity
19.    Hind limb paralysis.
20.    Loss of colour pigmentation.
21.    Polymyopathy.
23.    HD
24.    Blood group incompatibility.

Definition of Teratogenicity
<pharmacology> The ability to cause defects in a developing foetus. This is distinct from mutagenicity, which causes genetic mutations in sperms, eggs or other cells. Teratogenicity is a potential side effect of many drugs, such as thalidomide.

The main topic here is Flat Chested Kittens Syndrome.

Breeds that are presently documented to be afflicted with flat chests. There may be more now. Some go back decades.
1)    Abyssinians
2)    Bengals
3)    Birmans
4)    Bobtails
5)    Bombays
6)    British    
7)    Burmese
8)    Burmillas    
9)    Domestics.
10)    Exotcs
11)    Maine Coons
12)    Norwegian Forest Cats
13)    Ocicats
14)    Orientals
15)    Persians
16)    Ragdolls
17)    Russians
18)    Siamese
19)    Singapuras
20)    Spotted Mists    
21)    Tonkinese
(Prof.Niels Pedersen told me he has seen it in domestics and others in UC Davis’ 1000 cat breeding colony many years ago now.) It might be connected to the Siamese albino gene. The beginning of the Burmese had far too small a genepool.

Other species with the same or very similar problems:
    Dogs – very common Flat chests in puppies treated with Vit E by some breeders.
    Humans – (We don’t marry relatives and our gene pool is trillions- in humans it is a dominant gene)
There are probably many more, but I don’t have sufficient time to check everything out.

Some Dog Breeders are treating Flat Chests successfully with Vit.E….DIETARY MANAGEMENT and reverting the diet back to the “old fashion” bones and raw meat. This BARF diet is promoted by Dr Ian Billinghurst of Bathurst NSW and he has written 2-3 books on this subject.

Many cat breeders have “gut feelings” about some dietary imbalance being a large part of their problems, and have had improved results by dietary changes. A lot more research still needs to be done and accurate records kept by as many breeders as possible. Most recent data suggests bacterial infections in the dam might be a big part of the problem.

Some experienced and successful Burmese breeders are equally adamant that the problem is- Congenital. (Not genetic – but environmental – like German Measles in humans) and it is known that flu affects foetus, as will any virus in early pregnancy. Recent 2004 data suggests that bacterial infections in the dam and poor diet leads to FCK kittens being born. 5 breeders in Qld recently had a gut/bowel infection in their dams and all had FCKs in those litters where Mum was infected. All these aspects need to be considered as the way in which it turns up is very erratic.

Researchers believe it is most likely to be in the DNA. Some have suggested a mutant gene is assorting in the cat population as a whole. I have been told that it is in wild cats too. When white tigers are mated to white tigers they get birth defects, but no specific information was volunteered. Whites have to go to goldens. Tigers will not mate close relatives! Their gene pool is also too small and food supplies insufficient as their habitats are being destroyed. Cheetahs, in particular, suffer when kept in captivity with many succumbing to F.I.P. The diets for wild cats in captivity do not meet the normal requirements of these animals. Many wild animals, of several species, fail to breed successfully in captivity. Their fertility suffers and their babies often die. There is a documented colony of Lions living in a valley in SA and they never leave this valley surrounded by steep rocky cliffs. They have bred amongst themselves for a very long time (complete details elude me for the moment) and they are the healthiest colony ever studied. (Just trying to open up the big picture and make the topic more interesting.) I have found via research that outcrossing doesn’t necessarily fix the problem for the queen, which could indicate that it has a dominant mode of transmission that is also incomplete and erratic. It also suggests that it could simply be a developmental problem with some kittens. If one breeds from an affected kitten, this could also explain total disasters in some litters.

An American breeder of Singapuras believes that only deep-sea fish, not estuary fish, should be fed as she thinks Potassium Iodine deficiency is the cause of FCKs. She conversed with a university research team and was very thorough in her studies. This breeder got FCKs in her first litters and altered the diets, and learned how to detect carriers. (You can feel a slight ridge or angle anywhere in the ribcage… these kittens carry the defect. It can be very minimal, easily missed and transient – lasting only a day or so.)

Well, I can see how all of these opinions can be justified and so I will try to explain what I have found to date.

I do not believe that this is caused by a recessive gene. (For those who don’t understand this point I will try to simplify what this means. Recessive faults are passed to offspring when BOTH PARENTS carry the fault, or for that matter it could be a good thing, which you wish to breed into your line, such as a preferred coat colour (for want of a better example.) You get approximately 25% of progeny affected in this manner. But beware, you also get another 50% carriers!

There are breeders in the program that have had FCKs 50-100% of the litter affected regardless of which stud they have used.(I know one who used 5 different studs). Many breeders have seen whole litters affected and that is not what a recessive gene normally does. UK research teams say that 66% of Burmese worldwide are suspected carriers of FCKs, and about 4-5 years ago a new cattery per week was being added to their data bank of FCKs in England.

(Prof.Pedersen, not a geneticist – but extremely highly qualified teaching and research veterinarian of USA and a person whom I hold in high regard, states that when he has seen FCKs, even in domestics, and it does not fit any genetic pattern that he is aware of and believes the environment is involved. This was a long time ago now and professional opinions might be different today.)

One genetic researcher dismissed the 50-100% of affected kittens in any one litter, saying that the breeder has bred from a flat chested kitten to be getting these results. I do not think that this is always true because some bloodlines are more affected than others. (ie: Familial) But I do know breeders who choose to breed from kittens that were “only a little bit flat” and their problems are still ongoing. Some mildly affected kittens might sneak through when breeders are trying to assess litters, as these mild cases can be difficult to pick up if you are not taught how to identify them.

Any type of Dominant Gene needs only to be carried by one parent to show up in the kittens. An Incomplete Dominant Gene will occur erratically causing confusion to the breeder when trying to assess their breeding programs, especially if they have been told that a recessive gene is the cause of their woes. Some breeders have desexed stock on this theory only to find that the problem is still there sometimes in worse numbers that before. Dominant genes cause higher numbers of progeny to be affected than recessive genes. Many of you have had or know of someone who has had whole litters severely flat chested. This should not occur if a recessive gene is involved. The other thing to be considered is that if all FCK producers were desexed, would we just breed in other, perhaps worse, problems ie Hypokalaemia and stretchy skin disease. I consider these to be worse because they affect the health of your kittens for the rest of their lives. Don’t forget that desexing reduces the size of the gene pool. I guess it depends on how serious you perceive your problem to be? And, what if, the defect is dietary/environmental, like extreme heat during pregnancy?

POLYGENES are to be suspected when the incidence occurs a great deal more in one family of cats than in the general population. This also fits the bill more accurately than the recessive theory. THRESHOLD CHARACTERS   “set the point at which development goes past a certain threshold and mutation occurs” Perhaps you can imagine line breeding to set the length of fur in a long-haired cat and when you achieve results then continue to breed and in-breed with these animals until all your progeny appears with the desired coat length. These animals have reached a desired threshold regarding your goal of coat length and you have “locked” it in so you always get what you want. This is a simplified way of describing what “threshold” means. Once it is there it can take many years to reverse the process. Picture a little graph with short coats being at one end and long coats being at the other end. Somewhere between is the point (threshold) at which the coat changes from short-medium to long. This is your threshold character and any cats above or beyond this point will always produce long coats when mated to any cat with average length of hair. It can also be the point at which mutation occurs and when a gene mutates it remembers how it did it and will do it over and over again. The late Roy Robinson was writing a paper for me on how to breed out threshold characters when he died. He was extremely interested in data from my research and felt that breeders in the past had not given him accurate data and had, in fact, under-reported their FCKs. When breeders do this, it makes it impossible for geneticists to come to a correct decision as maths play an important part in their calculations. Roy and I were corresponding after his 3rd edition of Genetics for Cat Breeders went to press.

The CONGENITAL THEORY … I can see why some breeders are convinced that this is the case and it makes a lot of sense. If I hadn’t been told by several experienced breeders about when and how FCKs got into our Australian stock, then this theory would make the most sense of all, especially since other breeds and species have the defect. Congenital means that something happens in the environment during pregnancy causing birth defects. A good example is human babies being born deaf as a result of their mothers coming into contact with German Measles during their pregnancy, and also what happened to babies whose Mothers had taken Thalidomide. It can also be a problem relating to diet. Don’t forget the problem in dogs. They are also fed largely commercial diets and, these days, a lot of dried food.

The gene causing rib cage deformities in man is a dominant gene, which affects mainly males.

So, what do I think is happening? I believe what is being inherited is a possible metabolic hiccup of a familial nature  causing a developmental anomaly that is manageable by good husbandry and that all kittens can be at risk. Kittens are not born completely developed (can’t see, don’t immediately get up and run like a foal for example, need some stimulation to pee etc. and various little “triggers” in their brain start to “switch on” after birth.) I think that some of the problems breeders have told me about points to a dietary imbalance and possible infections in the dam during pregnancy and that a good balanced supplement several times a week after the first trimester of pregnancy along with vitamin A (5000 iu) once a week only in the last three weeks of pregnancy and twice in the first week of lactation at the same time using a vitamin E (200mg) supplement can be helpful in decreasing the risk factors for most queens. Vitamin A doesn’t work well by itself, but is better given with Vit E. Plus give all newborn kittens from queens who have produced FCKs 2 drops of calcium syrup 3 times a day in the first week of their lives or give them 2 drops of Nutridrops vitamin syrup several times a day until they are mobile. (usually around 10 days).

Cats have a high requirement for Vitamin A normally…1500iu daily, and if they don’t eat raw meat, liver etc then they may not be getting all they need. Also, the pregnant queen needs even more attention to her diet because she is trying to support life. If she is “at risk” then it is foolhardy to ignore her diet.  Of course there are “tough” little girls who do well throughout their pregnancies and lactation without needing any intervention from you, but I believe there are significant numbers of queens (especially Burmese) that do not fit into that bracket. Australia’s leading cat specialist has told me that if any cat is going to be adversely affected by drugs, anaesthetic or chemicals applied to the skin you can bet your bottom dollar that it will be a Burmese every time! Vitamin E is a good antioxidant and one can get all the information on these Vitamins and their benefits from any health food shop. We must not forget that our pets are not living a normal life, are subjected to high stress levels and certainly are not eating what God intended them to eat. ie: what cat can go out hunting and come home with “bikkies” and a tin opener? They are not vegetarians but would naturally get their plant matter from the digested contents of their prey’s stomachs. We do our very best for them and some commercial foods are as good as one could expect them to be, but not what the cat would first choose. Older textbooks connected FCKs to a deficiency of Vitamin A and nutritionists believe that quality commercial foods adequately cover all needs. But don’t forget that nobody knows what is normal for Burmese because nobody is doing the amount of research that is required to build data banks of what NORMAL is! Also I have been informed that the standards to which the pet food industry conforms allow a large range to qualify as satisfactory. The differences in the range are so wide that it is possible that they are erring on the low side of acceptable. One fully qualified professional person working in the pet food industry said it may be an enzyme problem – we were talking about dried food at the time because most of the queens reported to me were big bikkie eaters.

Another interesting point is one breeder who has been around for a long time said that she got FCKs in the first two litters of a mother and her daughter about 28 years ago or more now – but never had it again until she worked with new outcrossed stock. I asked her what she did about it at the time and she said “nothing – same girls, same stud and no changes in the environment (including food). These cats bred on for years without another hiccup. On thinking about this – it was about 25-30 or so years ago that significant changes were made to the food industry standards – and that change was an addition of Taurine which scientists had proved to be causing birth defects and which was not in the diet in sufficient quantities at the time. (Ref; Feline Husbandry – Diseases and Management in the Multiple Cat Environment. N.Pedersen. USA)

Prof.C.J.Wilkinson has been quoted as saying cats store Vit A in their liver and every time they are stressed they deplete the stores. It is quickly used by calling, mating, showing, birthing, lactating, illness and so on. It does not take long to be all gone if the diet does not contain enough to keep topping up supplies ahead of demand. Calling induces stress especially if not being mated. So it does not necessarily mean that one litter a year is the answer. It depends on the cat involved.

Cats cannot properly process Vit A that comes from plant material. It is better in the natural diet. Raw meat supplies a lot of Vit A and Taurine, but not enough calcium. Older breeders used to give one Cod Liver Oil capsule once a week to their breeding cats.

TAURINE may also be involved,( or at least the way a cat’s metabolism processes it) and a team in England was investigating this quite a long time ago now.

Taurine: Many breeds are troubled by defects connected to Taurine deficiencies. Recorded Taurine blood levels in Burmese FCKs and their littermates are extremely high but still nobody knows if these levels are “normal” or not. Burmese FCKs and their littermates have the highest ever-recorded blood taurine levels. Apparently it should be in tissue not blood, which I believe is pointing once again to metabolic errors in the breed or a deficiency of something else that is needed to “balance” the diet and process it more efficiently.

You might find it interesting that it appears to be known that the same cat that brought FCKs into Australian bloodlines is thought to have introduced Hypokalaemia (Potassium deficiency). Many breeders were asking for help with Potassium deficiencies and I declined at this stage because of an already heavy workload, but my curiosity was wetted and I started to look into this problem whilst working on the diet and found that Potassium is needed in certain levels for cats to make the best use of their available Taurine and Calcium. An English Nutritionist, who phoned me re my research, was interested in a possible connection between Potassium and FCKs as it is possible that stress during birthing might be causing a drop in Potassium which, in turn, is affecting the metabolism creating a much higher than normal demand for other significant vitamins, ie Vit A, E etc.  

It is often noted by breeders that queens with the problem are not always good “doers”, picky eaters, often not prolific callers, more often than not, do not eat placentas or give much attention to the newborns during labour, also don’t seem to like liver in their diet, often prefer dried food and crave for the attention & contact with their owners as a desexed pet would do. Some experienced breeders think it is basically a problem in the dam, but can’t figure out what is wrong. A reasonable amount of data suggests that either parent can pass on the fault. It does not seem to be sex linked (like haemophilia in people) but more often than not the typiest kittens are the ones affected and also the biggest kittens. (Threshold character effect?) For a long time in England they thought that Lilacs were clear of the defect, but my research proved exactly the opposite in Australia. Hundreds of lilacs and chocolates a year appearing as FCKs. The hotter the weather, the more frequent this and multiple other gross abnormalities presented. About 4-5 Summers ago when bush fires raged across NSW, Vic, and SA, birth defects of kittens born as blobs sent a message of concern from many catteries. Other observant breeders have noticed kittens on heat pads in Winter suddenly “start going flat” only to recover quickly when the heat pad is removed. Post mortems performed at Qld Uni. found nothing wrong with bones but something definitely not right about rib cartilage. One kitten had a “floating rib cage”. Other breeders who have not participated in the program have said that when they get the problem they just increase the vitamin supplements to the queen. A few breeders have told me that they have had a couple of FCKs in a litter and at some later stage admitted that the problem was not just FCKs but some kittens had SpinaBifida, tail defects and a “monster” as well. Sometimes, well-meaning friends will say that there wasn’t 1 FCK but 50% of the kittens were deformed. This is why we know that defects are under-reported and incomplete data is just a nuisance to researchers. Nobody can help you if you fail to report accurately. Also, with medical teams working on spina bifida in humans and treating with folates, then when litters arrive with Fcks and spina bifida in the same litter, if diet is causing one problem, then it may be causing the other also.

Vets involved in canine research express some concern that processed food may be “too good” and promote growth faster than the bones can support body weight. One Labrador breeder I know has returned her breeding animals to an all-fresh and natural diet, heavily supplemented with a wide range of vitamins and minerals with excellent results and no more skeletal problems since. This diet is explained in Dr Ian Billinghurst’s books and it is referred to as The BARF diet (Bones and fresh raw food) Be aware that dog food is not just what cats should eat as their metabolism is different but the basics are the same, except that dogs will eat things that are “off” where cats are fussier.

Another point I wish to bring up is that many of the meat industry are using more and more growth promoting hormones and special supplements to chooks and cattle to get better meat. So you can see that nutrition is an extremely complex subject and common sense should prevail. Experiment by all means, but make sure that the diet is overall good for cats. One dog breeder is raising two of my pet kittens on BARF and they are thriving, healthy, sturdy and good muscular development. They devour the food with great excitement, have no bowel or gut problems, or mouth problems either. And the litter tray smells better. NB: Keep the calcium/phosphorous ratio about 1:1.

Some truth may be in all of the above and that is why I choose to give good balanced supplements to all my pregnant queens as often as I remember and Vit A & E twice after birthing. Every one of my queens consume large amounts of Nutrigel (or Nutripet/Energel) during labour and it helps restore energy and combats sudden drops in nutrients whilst under stress. Yet other breeders say that by giving supplements you are simply masking the problem. Well, my reply is, what about the breeders who have always, as part of their normal husbandry routine, done exactly this or fed differently, and never had the defect. They don’t know or think that they are masking any problem. How many untroubled breeders doing this might be out there? Would you say, change your habits to see if you get faults in your lines? I can imagine their reactions. They simple say that breeders with defects don’t know what they are doing, don’t know how to handle kittens, and don’t have the background knowledge of pedigrees. They might be right, but most breeders are really trying to do their best with a fairly small gene pool.(PS: a large number of cats doesn’t necessarily mean a huge genepool if they all came from the same “pack of cards”.) I have noticed that for a while (about 20 years ago) breeders would cross FCK and Hypokalaemic lines and get some very good results, but that doesn’t seem to always work these days and the defect of potassium deficiency is on the increase now. Most of the books I have read suggest that a 3-5% defect rate is acceptable when practising any animal husbandry. Each person must decide for themselves what they are prepared to work with. There are far worst things than FCKs. If you have many cats and only have problems with one or two, then desex those and rebuild with the “safer” ones. This includes males as well as females. But if you have had all queens and studs produce the occasional FCK, then work harder on the diet and the environment, especially stress levels. Any queen which has several FCKs in multiple litters is not worth continuing with as she was most likely affected at birth and it has been missed during the selection process. Because most bloodlines are fairly closely related, sometimes outcrossing makes no difference at all. Better results with father/daughter matings than with someone else’s stud have been recorded. I do not advise new breeders to inbreed, because they often do not have the background knowledge of bloodlines and it is usually safer to outcross than inbreed.

Probably, one of the important things about all of the above is the occurrence in other breeds and species. At first it seemed to occur in all cats with any connection to Siamese. I know of one breeder who had it in his Burmese litters, desexed his stock and then got it in his Siamese queen. What did they have in common? Diet and environment. She was on lease and the previous owner claimed to not have had problems with her. She had been mated to the same stud as before. More recently I have been told of other breeders who have had FCK kittens in different breeds of cats in the same time frame. Definitely suggests that something other than genetics is going on.

I would like as much feedback from as many breeders as possible about diet and environment. Give Vitamins A & E as above and carefully monitor your results. Vit A = 5000 iu a week (and even up to 10000 iu a week has been used successfully by Persian breeders) in the last trimester of pregnancy if some but not a complete improvement is shown. For those brave enough, then repeat troubled matings try the above and document the results for me, please. .NB TOO MUCH VIT A IS TOXIC AND WILL CAUSE BIRTH DEFECTS – IT WAS TO BE WITHDRAWN FROM SHELVES BECAUSE OF THE RISK FOR PREGNANT WOMEN. LIKE SOME ALTERNATE REMEDIES THE AMOUNT AND TIMING IS CRITICAL. Always give Vit E at the same time as Vit A. Older breeders used to feed more fresh foods, cod liver oil, bones, cheese, eggs and some tin food. Their diets were similar to Dr. Ian Billinghurst books. (one being Grow Your Pups With Bones). Canine Control Bodies appear to be far more helpful to dog breeders than Feline Control Bodies are to cat breeders. Also I have found dog breeders to be far more open and helpful to each other than cat breeders in general. Most cat breeders blame the stud if they own the dam and vice versa. Also, many supplements designed for cats and kittens do not contain Taurine. Mavlab (Qld) used to manufacture a taurine supplement but it was taken off the market due to low demand. Taurine is a very necessary and very important dietary need of cats.

Flat chested kittens can be saved, especially if detected early enough, and the vast majority of the “recoveries” go on to lead normal, healthy and active lives. I am currently trying to ascertain a safe level of potassium supplement for breeding cats. Potassium gluconate is safer than other forms of Potassium, but at this stage I would suggest that minimal dose be supplemented in the latter stage of pregnancy. In UK, a scientist who has written to me, has used:

Treatment of FCK, as suggested by Bristol:

Dissolve 1 ‘Sandos K’ tablet in 100 ml warm water
Give 0.025 ml to affected kitten (about 2 drops) x 2 daily
(no rapid improvement until the kitten is 2 weeks old, then gradual improvement)

FCK seems to be affected by the environmental condition of the queen: any adverse situation during pregnancy seems to render the queen liable to produce FCKs.

Since Sandos K is unavailable in Australia, I am waiting on a reply regarding a suitable alternative.

The next paragraph is well worth noting because I have seen it give great results, not only by using Calcium syrup but breeders have had great success with Nutridrops (good balanced supplement for cats and kittens).
A vet in WA reported that he has successfully treated FCK Persians with 0.25 mil of Calcium syrup every 6 hours (night too) until the condition corrects. These Persian kittens have been taken home by the nurse for treatment, so that means that they have also been fed a milk formula. Good formulas like Troy Animalac don’t cause scouring and contain all the vital ingredients. I always use this one for any routine feeding of kittens born into very large litters. It is normal for my females to have 7-9 kittens in a litter (have had 12) and I choose to help the Mum feed them. It gives me great pleasure and the Mums like me being with them.

When a kitten is badly affected some vets will do a surgical correction, but this, so I am told, is very traumatic for the kitten. Also they are reluctant to do this because they believe it will lead to FCKs being kept or sold for breeding.  A very clever new breeder saved a kitten by making a cast out of the cardboard centre of a toilet roll. You cut it about 1”– 1.5” long, slit it down the length, place a thin layer of wadding under the front legs and sticky tape the cardboard around the chest. Put a small thick elastic band on the kitten as a collar and then tape the front and back of the cast to it to stop the cardboard from slipping down over the back legs. This helps the kitten to take the weight off its chest. It can then lay on its back and sides, is less stressed, breathes easier, then gains strength and suckles better. Feed the kitten yourself but leave it with Mum for comfort and warmth and soon the kitten will be back on Mum and suckling off her again. I saw her kitten, almost dead, laboured breathing, going cold, make a miraculous recovery and almost back to normal within a week. Of course you need to have the kitten’s heart and lungs checked by a vet before placing it in a pet home. Never be tempted to breed from a FCK. All cats can produce this but if you breed from one you will get more FCKs in higher numbers in subsequent generations.

Some information via Internet about Vit E:

 Vitamin E and selenium are closely related in their nutritional biochemistry, and we see a similar close relationship in the diseases associated with their deficiency.  

Deficiency states of vitamin E and/or selenium place young growing animals at risk of acute severe diseases, which in Australasia are commonest and best recognized in sheep, cattle, pigs and horses, and less commonly in chickens. In this situation, the most vulnerable organs are the skeletal muscles and the heart, with the liver also a recognized target in the pig. In chickens the vascular endothelium is the prime target site, with secondary complications developing in the nervous tissue of the hindbrain.
 In the young, rapidly-growing, post-natal mammal, the enlarging cells of type1 (oxidative) fibers of skeletal muscle are at highest risk of this kind of injury. Similarly in the neonate, the growing fibers of cardiac muscle are in the same category.

Go to the WINN FELINE FOUNDATION WEB PAGE FOR THE LATEST REPORT REGARDING COPPER AND PREGNANT QUEENS, ALSO THE FELINE ADVISORY BUREAU.

Read as much as you can about genetics and nutrition and consult your vet when in doubt.

Recommended basics;

1    Feed fresh raw meats every day. Some cooked meat for variety. Cooking does destroy nutrients.
2    Cooked deep-sea fish is rich in nutrients including potassium iodine and copper as is shellfish.
3    Cheese or a calcium supplement. Bal Cal is good as the calcium/phosphorous ratio is maintained. Bones are good too, and chicken necks but be careful of bacteria in chicken and hormones. This bacteria can cause bowel bacteria in cats to flourish out of control. I like to feed lamb spare ribs in preference to chicken necks or wings.
4    Yoghurt to maintain good gut and bowel flora balance. Acidophilous capsules can be sprinkled on food. Always give these capsules after illness or medications.
5    Brewers Supa Yeast Supplement (contains Potassium and minerals including copper) sprinkled like salt on meals 2-3 times a week. Most of the B group vitamins here.
6    General vitamin supplement for queens considered at risk.
7    Quality dried food in minimal quantity. Preferrable those without chemical preservatives and no chicken by-products. My queens who don’t eat dried food and those who only have a little dried food have not had FCK kittens. On the other hand I once had a queen who would not eat anything else but dried food and she had an ongoing problem. Her daughter was the same and even an outcrossed stud did not solve the problem. Both were desexed.
8    Feed queens in labour large quantities of Nutrigel paste which boosts energy and supplies heaps of vitamins. Give a calcium supplement after birthing.
    Give newborn kittens calcium/vitamins as above.
9    Sprinkle Iodised Table Salt on main meal sometimes (source of potassium iodine.)
10    Offer a good feed of raw calf or lamb liver about every 10 days to those that love it. Sauté some for those who won’t eat it raw. Nutrient rich Liver is very important part of the diet and a good source of copper, taurine, Vit A etc.
11    Cooked lamb/beef hearts occasionally.
12    A little tinned food for those who are picky. Tinned food may be causing renal potassium loss and over activity of the bowel. You don’t want the nutrients in the litter tray. Snappy tom tinned fish doesn’t contain chicken by-products, cereals, vegetables or chemical preservatives either.
13    Give Vit A and E together as soon as birthing is over and again 2-3 days later.
14    Last trimester Vit A & E for girls that don’t eat liver or very much raw meat. Not before mating or in the first trimester.
15    Don’t use heat pads very much at all. Prefer covered hot water bottles placed in a corner of the kitten box where mum and babies can move away if they wish. All of room heating set low is better than direct heat.
16    Provide fans for cooling but be aware that newborn kittens cannot adjust their body temperature like we do and die quickly of hypothermia.
17    Handle newborns a lot and stop them from lying on their stomachs all the time.
18    Have a “rough and lumpy” bed for mum and babies. Slippery surfaces in kittening pens or boxes do not give kittens the traction they need to get up and off their chests.
19    Supplement all kittens if they are hungry and always those that are not gaining much weight.
20    Keep stress levels in all breeding animals as low as possible. Simply providing cattery cats with their own accommodation and grassed and sunny exercise runs often helps in this area. Cats do get Vit K from grass and D3 from the sun. Try to keep their lives as natural as possible with safety of course. Fresh air and exercise is very important.
21    I prefer not to worm or apply flea treatment to pregnant girls.
22    I also do not vaccinate pregnant females.
23    Flu kills in utero.
24    Treatment for ringworm causes birth defects if given to pregnant queens and currently working studs.
25    Many drugs cause birth defects.
26    Burmese are allergic to many things.
27    Keep catteries clean and scrubbed. Don’t use chemicals like round-up in the area.
28    Cuddle every cat each day.
29    Make an effort to be with queens in labour.
30    Fresh clean water daily.
31    Litter trays done at least once a day, more if needed.
32    Disinfect with AviSafe, (or similar), pool chlorine, and ammonia – but not at the same time of course. Hot water and detergent kills most bugs on utensils. Different cleaning products work for different things.
33    Protect your stud by not allowing queens to use his litter tray, food or water bowls. Keep contact to a minimum. This reduces the risk of infection with virus or bacteria. Studs need fresh air, sun and grass too.
34    Wash your cats after a show before they have contact with other cats in the house.
35    Bacterial infections cause bowel disease in kittens and it is not genetic, and is triggered by feeding weanlings tinned food or food too rich for them.
36    Inbreeding can set problems in lines. Health & vigour & temperament should not be sacrificed for Best in Show awards.
37    If your pregnant girl has diarrhoea or vomiting she may suffer some potassium loss as well as other vital nutrients, which can lead to problems with the kittens.

If any breeder wants more help they may contact me.
Contact your vet if you are not sure of anything in this letter.

VETS AND BREEDERS SHOULD WORK TOGETHER FOR THE HEALTH OF OUR CATS.

Hoping you found this document interesting and helpful.

Pyruvate Kinase Deficiency – by Kendall Smith

PK Deficiency from a Breeder’s Perspective
Kendall Smith, Kenipurr Cattery

     Let me tell you about Brandy, which is why I am here tonight.  Brandy was 20 months old, and I was showing her toward a Regional win.  In the fall of 1998, she began cycling heavily.  By December, she was losing weight so I planned to breed her after Christmas.  While I was away, my American Shorthair male got loose and bred two of my Aby girls, Brandy included.  In January, she was still losing weight and began vomiting.  A vet exam turned up the pregnancy and severe anemia.  My vet was convinced she was bleeding out somewhere.  As there was no apparent injury, he suggested a bone marrow biopsy.  That result came back as “normal, regenerative cells.”  Her FeLV test was negative.  Next he suggested a special fecal test which was negative for blood in the intestines.   I had her spayed, hoping that hormones were playing a role in her anemia, but still she went downhill.  At that point, my vet held a phone conference with two veterinary clinical pathologists.  They told him Brandy had “some aspect of AIHA, but not AIHA.”  We didn’t know what else we could do, and she continued her cycle of vomiting and losing weight, then no vomiting and gaining back weight.  Soon after, both Kim Ghobrial and Erin with SABRE posted the information about PK anemia testing to the Aby list.  The words, “cyclical anemia” jumped out at me.  I tested Brandy, and her results showed her to be affected.  She has two mutant genes.  Privately, from some of you wonderful  people, I learned about the experimental splenectomy surgery.  My vet was willing, and on Aug. 24, weighing 4.9 pounds, Brandy had her surgery.  On Sept. 29, just 36 days later, she weighed 7 pounds.  She has returned to the show ring that she loves, and is just 2 points shy of granding as an alter

     Through a friend, I discovered that Dr. Lothrop, one of the leading experts in erythrocyte metabolism involved in PK deficiency, was at the Scott-Ritchey Research Center where his focus is on dogs.  He said that Dr. Giger discovered the normal sequence and mutation for PK in cats and was the best source of information.   Since Dr. Giger has not yet published his findings (although I do have his rough draft if anyone wishes to read it), for the time being, he is the only one able to provide this DNA test.   Molecular diagnosis is THE way to do carrier screening.   In response to my question of what do I say to the unconvinced, Dr. Giger said, “As we have experienced with other hereditary diseases, the breeders and pet owners are somewhat hesitant to accept a new hereditary disease in their breed.  DNA testing is one of the most accurate tests available as it looks specifically for the mutated gene in an animal.  Most certainly, we have no plans to provide a test that is not useful.  Developing this test and running this test is considerably more expensive than what we are presently charging.”  I actually told him that I REALLY want to believe in a faraway lab with unknown people performing a test I’ve never seen.  The cost of the test itself is $75.  Add to that a blood draw fee and shipping.  I use overnight FedEx so that I can track the package.  It costs me about $20 for shipping and amounts to about $100 per cat.

    Have any of you lost an Aby with a diagnosis of  “anemia of some sort,” “a fluke anemia,” “probably Hemobartenella,” or “some aspect of Autoimmune Hemolytic Anemia”?  Have you heard others talk about the anemia that “follows dilute lines”?  Think about this; PK is a recessive gene.  When you breed for dilutes, you are breeding for a recessive gene.  Of course if the PK mutation is there, you’re going to see it quicker!  If my line-chasing is accurate, it’s out there almost everywhere, but because it’s a recessive, many breeders seldom see it.  Or it was a pet with an owner who never notified the breeder.  Or it was a breeding cat with an owner who didn’t want to notify the breeder.  Or it was a cat misdiagnosed with hemolytic anemia.  Or it was a breeder/owner who doesn’t want to admit it.  

     This is a simple recessive, easily removed from the gene pool through DNA testing.  A cat who has PK deficiency has 2 mutant genes, one from each parent.  This means that both parents are at the least, carriers.  Some males have lived long, healthy, productive lives only to test as affected at 8-12 years of age.  Think about the numbers of carrier or affected kittens that male produced before being tested.  Females don’t seem to be so lucky.  Affected females appear to have trouble with their first litters:  aborting, premature delivery, or death of the female.

     In order to not lose cats and bloodlines, you breed a known carrier to a known clear cat.  Then test any kitten you consider keeping.  Keep the clear kitten.  You have the genetic components in  a non-carrier package.  With RA so rampant in our Abys, it is imperative that we use some of  the carriers, but only keep clear kittens.  Carriers will not become ill with the disease, and when bred to clear cats, no offspring will become ill.  If a cat is affected, you alter it.  I personally wouldn’t breed a known affected female since everything I’ve heard indicates that she will die soon after the first litter.  If it is VERY important to use a male, breed the affected male to a known clear female and keep one of the kittens.  Without testing, that kitten will be a carrier.  Breed that kitten to known clear cats, and test any of those that you keep.

     When  I told Dr. Giger about this meeting and asked for information to pass on, he wrote a short “speech” for me to read to you.

Feline Infectious Peritonitis

Have there been any more recent studies?

In a recent study cats were tested in the same manner as in the vaccine manufacturer’s tests. At the end of an 8-week period, 30% of cats vaccinated, and 60% of the controls demonstrated FIP-positive conditions from tissue examinations. This demonstrates a 50% “preventable percentage.”

Another recent field trial ran for 16 months using 500 cats in a no-kill shelter with endemic FIP. The fact that this is a shelter makes it a different makeup than a cattery (and some multi-cat households) because the average age of a cat was approximately 2 years old, and there were no kittens under 16 weeks old. However ALL cats tested were seronegative prior to exposure in the shelter. During the time of the study, 0.8% of the vaccinated cats died and 3.25% of controls died of FIP. [This is statistically significant at p=.048, which means that there is a 95.2% probability that this result is not random] So, for seronegative cats over the age of 16 weeks, this study shows a 75% efficacy rate. Vaccination after exposure (after a cat is already seropositive) is not helpful in preventing the disease.

How is it transmitted?

Wouldn’t we all like to know! Seriously, there seems to be two schools
of thought. One group (from Cornell-based publications and seminars)
states that the spread is not known with certainty, but is believed to
be by ingestion or inhalation of the virus. The other school of thought
(from Dr. Pedersen and the UC, Davis based publications) believes that
transmission is most prevalent when cats have close contact with other
infected cats or their feces/urine. Both schools seem to feel that feces
may play a large role in the method of transmission.

Some studies suggest that viruses that can cause FIP can survive
on dry surfaces (food/water bowls, litter boxes, human clothing, etc.) and
can survive at room temperature probably up to 2 or 3 weeks. If this is
the case, then the two schools of thought on methods of transmission may
not be so far apart, especially given that litter can contain dust to
which small particles of feces can adhere. Thus the virus can possibly be
spread via litter dust on shoes or clothing or etc. making it behave as if
it were an airborne virus!

I have a lot of cats, what can I do to keep the risk of FIP down?

Limit the number of new cats and isolate each for at least one month,
preferably two. I know it sounds like a long period of time, but
consider the alternatives! You could lose every cat in your household.
During the one month’s time period, make sure you watch carefully for
signs of illness. You should give the coronavirus titer test at the
beginning and the end of the quarantine period, and the titer should
decrease over that time period.

Scoop the litter box daily, discard the rest of the litter weekly and
disinfect the boxes with a 1:32 solution of bleach. The area around the
boxes should be swept and disinfected, there should be at least one box
for every two cats in the household. Again, weekly discarding of the
scoopable litter may seem like a waste, but so far the ONLY thing the
sources agree upon with regard to transmission is that it is definitely
transmitted through the feces, if nothing else. In the words of one
breeder: “It cost me approximately $3,000 in veterinary and laboratory
services to diagnose the incidence of FIP in my cattery, test and
retest (and retest) all of my cats. Believe me it is FAR less expensive
to discard the litter” (Polli, p. 81). If your cats have long hair and
fecal matter tends to stick to the britches, this hair should be kept
clipped short.

Change food and water daily, disinfect the bowls weekly. Do not mix the
bowls all around the house, keep the same set of bowls with the same
cats, and keep the same set of litter boxes with the same cats.

I’ve heard FIP is like AIDS. Can I catch AIDS or anything else from it?

People often use the “it’s like AIDS” phrase to describe a number of
illnesses in the animal (and human) community with the idea that most
people know so much about AIDS that this analogy is useful.
Unfortunately most people don’t know much about AIDS and the resulting
effect is to scare people out of their wits and have them dump their
cats or dogs at the nearest pound because they are so deathly afraid of
catching AIDS from them. The ONLY similarity between FIP, FIV (Feline
Immunodeficiency Virus) and FeLV (Feline Leukemia Virus) to HIV (which is
believed to cause AIDS) is in their genetic makeup. All are RNA (as
opposed to DNA) viruses, and FeLV and FIV (and HIV) are what are known as
“retroviruses.” FIP is a type of “coronavirus” which makes it even less
similar to HIV. To make it clear: THERE IS
ABSOLUTELY NO WAY TO CATCH AIDS FROM A CAT, NO MATTER WHAT FELINE
DISEASE THAT ANIMAL MAY HAVE
. See the FeLV FAQ for more
information on retroviruses.

If the virus can last so long on dry surfaces, what happens if I unknowingly come in contact with a cat with FIP? Can I give it to my cats?

Most household soaps, detergents and disinfecting agents will
kill the virus. Make sure you wash any part thoroughly that has come in
contact with the cat (don’t forget your pants if the cat rubbed up against
you). Bleach in a 1:32 solution is suggested for decontamination
purposes.

Interview with Dr. Pedersen 2008 – by Nancy L. Reeves

Understanding Feline Infectious Peritonitis
Niels C. Pedersen, DVM, PhD

Dr. Niels C. Pedersen is Director of the Veterinary Genetics Laboratory and Director of the Center for Companion Animal Health at the University of California at Davis. Dr. Pedersen is an international authority on infectious diseases and immunological disorders in small animals and in comparative genetics. His current areas of research focus on infectious diseases of cats and dogs in shelter and multi-animal environments, and on applied feline and canine genetics.

What is Feline Infectious Peritonitis – FIP?
FIP is caused by a feline coronavirus; coronaviruses of various species exist in most types of animals and humans and usually cause acute respiratory or enteric disease. FIP is the cause of death of 1 in 100 cats seen at veterinary teaching hospitals throughout the U.S. The incidence can be 5 to 10 times greater among young cats coming from catteries and shelters and is the major cause of abdominal fluid (ascites) and intraocular and neurologic inflammatory disease in cats under 3-5 years of age. FIP is virtually 100% fatal and there is no good prevention. The emotional toll of FIP is especially great, because it strikes suddenly weeks, months and even years after initial infection. Therefore, cat lovers usually experience this disease long after they have developed strong emotional bonds with their new pet.

Does FIP only affect pedigreed cats?
FIP affects both pure- and random-bred cats. However, the disease usually starts in young kittens, so it is closely linked with cat breeding. The disease is also enhanced by improper husbandry, especially resulting from overcrowding (shelters, large multiple cat households). We also know that genetic susceptibility may account for 50% or more of the risk of developing FIP. Although FIP occurs in all breeds, there is no doubt that certain bloodlines, and therefore certain matings, are more apt to produce kittens that eventually die from FIP. These genetic factors are most likely a result of the inbreeding that goes into breed development. Therefore, catteries are at the highest risk because they are subject to all three risk factors (kitten production, dense housing, genetic susceptibility). The likelihood that any given cattery will suffer at least one outbreak of FIP over a five year period is very high, and mortality in catteries can be 5-10 times higher than it is in the general population. Shelters have the second highest risk, and the greatest incidence is among kittens adopted during periods of overcrowding and prolonged stays. Most shelter kittens are random bred, with many coming from the feral cat pool. Random bred kittens are more genetically diverse in general, so husbandry factors are more important in causing FIP in this population than genetic factors. Husbandry factors are greatly influenced by the seasonal influx of kittens.

Why are you particularly interested in cats and FIP?
I was raised on a poultry farm in southern California. My dad fed many feral cats so they would stay around and keep the rodents down. As a result, I experienced and loved cats for as long as I can remember. When people came to the farm to buy eggs, I would sit with a box of kittens to give away, and sometimes I would get 25 cents for a kitten, which at the time I thought was a fortune. At first I wanted to be a cattle doctor, because I also grew up around beef and dairy cows and had show steers in high school. But when I went to veterinary school, I discovered that nobody knew much about cats and cat diseases. In those days there were lots of deaths associated with feline leukemia virus, but of course we did not know this virus existed until several years later. But from the beginning I had the most fascination for FIP. The first reported clinical cases of FIP were in 1963. My first publication on FIP was in 1965. I’ve been a member of the faculty at Davis since 1972.

What is the History of FIP?
FIP was first recognized as a specific clinical entity in the late 1950’s. This timeline was based on decades of meticulous necropsy records kept by pathologists at the Angell Memorial Animal Hospital. There was a steady increase in the incidence of the disease in the 1960’s onward, and it is currently one of the leading infectious causes of death among young cats from shelters and catteries. The reason for the sudden emergence of FIP is not known, but there are at least two possible explanations. First, it is noteworthy that FIP appeared within a decade
of the initial descriptions of transmissible gastroenteritis (TGE) of pigs in North America. The causative virus of FIP is closely related to TGEV of pigs and canine coronavirus (CCV), although they are still genetically distinguishable. However, mixtures between these three viruses are known to occur. At least one strain of canine coronavirus can induce mild enteritis in cats and enhance a subsequent infection with FIPV, indicating a special closeness to feline coronaviruses. Therefore, CCV may be a more likely parent of FECV in this scenario. Another related possibility is that the FIP mutation occurs only in a relatively new strain of FECV, and that this new strain only evolved in the 1950’s. Coronaviruses such as FECV are continuously mutating as a result of the manner in which their genetic material (RNA) is replicated. Therefore, genetic change, either among themselves or through genetic mixing with closely related coronaviruses from other species, could have either allowed a coronavirus of another species to take up host in cats or to alter a strain that existed prior to the 1950s.
An alternative non-genetic explanation may involve changes in how cats were viewed as pets and their husbandry. There was a dramatic shift in the status, keeping, and breeding of cats as pets after WWII. The numbers of pet cats greatly increased, purebreeding and cattery rearing became increasingly popular, and more cats, and in particular kittens, found themselves in shelters. These large multiple cat indoor environments are known to favor feline enteric coronavirus (FECV) infection and FIP. Interestingly, feline leukemia virus (FeLV) infection also became rampant among indoor multiple cat households during this period, and FeLV infection was a significant enhancing factor for FIP until it was pushed back into nature as a result of testing, elimination/isolation, and eventual vaccination in the 1970s and 1980s.

How is the coronavirus spread between cats?
Coronviruses are ubiquitous among all cat populations and the principle one of cats is correctly referred to as feline enteric coronavirus (FECV). FECV is present in virtually all catteries with 6-8 or more cats and in 40% or so of the kittens relinquished to shelters. The enteric virus in the cat population lives in the digestive tract and is shed in feces. Cats can shed the virus for 4-6 months, or for a year or more in a continuous or intermittent fashion. Recurrent infections are also common. FECV is easily spread through litter and litter dust, and can be carried from place to place on people’s bodies and clothing. Virus contaminated material is easily transferred to the paws and fur of susceptible cats and then ingested during grooming. Kittens are infected by other cats at about 9-10 weeks of age, although one report places it as early as 3 weeks.

How does the coronavirus turn into FIP?
FIP is caused by a mutation of FECV, which is ubiquitous among cats. Although the mutation of FECV to FIPV is common, it is fortunate that only a small percentage of cats exposed to this mutant virus will get FIP.
FECV is undergoing continuous mutation and several genetic forms of the virus may co-exist in the same animal at the same time. Most of these mutations have very little effect on the behavior of the virus and merely serve to genetically reflect the region from which the virus originated. However, mutations that inhibit or knock out the function of a certain small gene (called 3c) have a pronounced effect on the biologic behavior of the virus. All known isolates of FIP virus that we have studied, and that have been reported by others, have various types of mutations in the 3c gene. Mutations within the 3c gene with the potential of causing FIP are common. One study indicated that 20% of the kittens infected with FECV will produce an FIP mutant. Of course, only a fraction of the mutants will go on to produce FIP, depending on host resistance factors (genetic or non-genetic). This FECV to FIPV genetic change is referred to as the internal mutation theory. The internal mutation theory has two corollaries: 1) that each cat that develops FIP, even if it is a littermate, closely related or commonly housed, has a different mutation in the 3c gene, and 2) that horizontal (cat-to-cat) transmission of the FIPV mutant is uncommon. We have reconfirmed corollary 1, and have confirmed corollary 2 in concept but not in fact. Reconfirmation for the internal mutation theory came from a recent outbreak in three kittens in a litter of Scottish Folds and in a half-sibling from a second litter. All four FIPVs had significant, but different, mutations in their 3c genes, but were closely related in all of their other genes to one of two different FECVs detected in the feces of one of the kittens. We have found that many cats with FIP are in fact shedding the same FIPV in their feces that is in their diseased tissues. However, for some reason, it does not appear to be highly contagious.

What are the signs of FIP?
Signs of FIP arise weeks, months, and in rare cases years after initial infection. During this quiescent stage, the cat may be asymptomatic or suffer from vague signs such as stunted growth or increased susceptibility to other common infections. Many breeders and even clinicians believe that FIP can cause upper respiratory disease signs during its early stages; this is not technically correct, because upper respiratory disease is usually caused by herpesvirus, chlamydophilla, mycoplasma, etc., and not directly by FIPV. With time, many cats win their battle with this infection, while others lose. However, “losing the battle” may occur over a very long period of time; only terminally, when the cat’s defenses collapse, do the more characteristic signs of FIP develop. This capitulation to the virus explains why cats with FIP seldom recover, because a loss of immunity is extremely difficult to reverse. Cats who develop clinical cases of FIP may initially show nonspecific symptoms such as loss of appetite, depression, rough coat, weight loss, a fluctuating antibiotic resistant fever, and increased susceptibility to secondary infections (such as respiratory disease). More specific signs of FIP vary depending on the form of the disease (wet vs. dry) and the organs that are involved.
The most common form of the disease is referred to as “wet FIP.” Wet FIP is caused by inflammation of the linings of the abdominal viscera, and less commonly of the thoracic organs. This inflammation exudes large volumes of a characteristic mucinous, yellow-tinged fluid (exudate). Therefore, the major clinical sign in the wet form of FIP is ascites and abdominal distension (abdominal involvement) or dypnea (thoracic involvement).
FIP can also take a more chronic form referred to as “dry FIP.” Dry FIP, as the name implies, is not associated with fluid accumulations in the abdomen or chest, but rather with more localized masses in the kidneys, spleen, liver and terminal bowel, eyes, and the linings of the lungs and heart, and central nervous system. Uveitis (intraocular inflammation) can affect the eyes, making them look cloudy and changing the color of the iris. Inflammation can enter the brain and spinal chord and cause a spectrum of progressive neurologic abnormalities. FIP accounts for over one-half the cases of inflammatory intraocular and nervous system disease in cats under 3-5 years of age. Although unappreciated in the past, we now know that cats in the terminal stages of FIP are often severely immunocompromised. This explains why common bacterial infections may complicate the disease picture in cats with FIP.

Is FIP contagious?
Cats with FIP do not appear to be very contagious to cats that they come in contact with. Although this has been based mainly on clinical observations, it has also been confirmed by laboratory studies. We have not observed contact transmission in experimental settings. Furthermore, cat-to-cat transmission implies that every FIPV isolated from a group outbreak of FIP will be genetically identical in its 3c gene mutation. As I mentioned earlier, we have yet to observe this. However, we now know that FIPV is present in the feces of most cats with FIP, so horizontal transmission is theoretically possible, although very uncommon.

How do genetics, stress, and other infections play a role in FIP?
FIP is not a breed specific disease, but does follow certain bloodlines within breeds. Heritability accounts for about 50% of the incidence. Environmental factors influence the other half.
The age of the cat at the time of initial FECV exposure plays an extremely important role in whether a cat dies from FIP. Kittens usually began shedding FECV at around 9-10 weeks of age, which places their actual exposure a few days to a week earlier. The immune system of the kitten is rapidly maturing during the period between 6-16 weeks of age. Therefore, the first exposure of most cats to FIP causing mutants occurs during a time period when their immune systems are still developing. This lack of development enhances the likelihood of a FIPV mutant to gain a strong foothold into the body. Just as there is an age susceptibility, there also appears to be an age resistance. FIP is seldom seen in cats over 3-5 years of age, and most cases occur before 16 months of age.
In the 1970s, when tests for FeLV became available, we discovered that one third to one half of all cats with FIP were also FeLV positive. In later experiments, we showed that cats that had resisted infection with FIP virus would develop FIP shortly after being infected with FeLV. This meant that FeLV infection somehow interfered with the ongoing immunity to FIPV. With the elimination of FeLV as a major infection of cats, we no longer see such a strong relationship, especially among catteries and shelters where FeLV control programs are in effect. Most cats with FIP in the present age, with the exception of a few household pet cats, are not FeLV infected.
Anything that stresses cats can depress immunity and also increase the likelihood that FIPV will establish itself in the body. Stress may also allow an FIPV that is being successfully contained to become active. The effect is even more powerful if the stress occurs at or shortly after the time the cat is exposed to the virus. Stressors can include overcrowding, weaning, spaying or neutering, other infections, being placed in a new and strange household, adding new cats to a household, shipping cats to new owners or other catteries, or stresses of pregnancy, parturition and lactation. Disease caused by feline herpes virus and other common upper respiratory pathogens are good indicators of cattery or shelter stresses. If a cattery or shelter is having a lot of problems with these upper respiratory infections, it is likely that they will also have problems with FIP (especially if the genetics are unfavorable as well). For instance, an area SPCA had a huge FIP problem in the kittens they were adopting out. It was kitten season and the facility was overcrowded with cats and they had to stay for longer periods awaiting adoption. There was also a lot of upper respiratory disease. After limiting their intake of cats, overcrowding was eliminated and cats were adopted after shorter stays. The FIP problem decreased to negligible levels, as did the respiratory infections.

Is there a definitive test for diagnosing FIP?
The diagnosis of FIP should be relatively simple, given its affinity for younger cats, its strong tendency to involve catteries and shelters, the typical physical and historical findings, and numerous characteristic laboratory abnormalities. Nonetheless, it somehow remains one of the most difficult of diagnoses for many veterinarians. The truth is that veterinarians have little trouble in placing FIP high, or at the top, of their diagnostic list, but have great difficulty, and even reluctance, in confirming their diagnosis. This is probably because FIP is viewed as a death sentence, and we are reluctant to confer such a sentence without certain proof.
Although a definitive test result would assist decision making, a certain diagnosis can be based on cumulative odds rather than a single, simple, definitive test result. A young cat from a cattery or shelter with chronic uveitis and/or neurologic signs, high serum proteins, hyperglobulinemia and hypoalbuminemia, fluctuating antibiotic unresponsive fever, leukocytosis with a lymphopenia, and an anemia of chronic disease can have no other disease than dry FIP based on odds alone. Likewise, the same cat with similar history and laboratory findings, but with yellow-tinged, mucinous, inflammatory ascites is highly unlikely to have any other disease than wet FIP. It is interesting that a cattery owner or cattery worker is often the one to cue in on the correct diagnosis based on the simplest of observations and intuition.
In an attempt to reach the elusive definitive diagnosis, veterinarians rely on dozens of tests that claim to highly correlate with the disease or to be diagnostic. I do not have time to go into the dozens of tests that fall into this category, or the good tests that are improperly done, or improperly interpreted, that lead to misleading positive or negative results. In truth, the only good definitive way to diagnose FIP is to identify the virus in macrophages within lesions or ascetic/pleural fluid by a procedure called immunohistochemistry. PCR would work equally well on diseased tissues or fluids, but many of the current tests are improperly designed and conducted and frequently yield misleading results. In some cases, the proper fluid or tissues cannot be obtained pre-mortem. However, there is no excuse for not doing such definitive tests post-mortem.
This brings me to a final point, a necropsy should be done by a qualified veterinary pathologist on any cat that requires a proper diagnosis. However, even veterinary pathologists will hem and haw about a definitive diagnosis, even when faced with incontrovertible historical, clinical and histological evidence. Make them make a definitive diagnosis, either based on proper reading of the odds or by doing immunohistochemistry on lesions.

What is the best way to care for a cat that has FIP?
There is currently no cure for FIP; therefore, the primary concern needs to be making the cat comfortable and deciding when to quit. Cortisone can help reduce inflammation and encourage appetite. Good nutrition, hydration and non-stressful environments are also important, but in almost all cases they serve only to prolong the inevitable. Therefore, we will encourage some owners to go with symptomatic treatment, but only if the animals are not suffering. There have been reports that the feline interferon omega is effective in combating FIP. We actually tested it against FIP years ago and it did not work. Fortunately, a double blind, placebo controlled study was recently reported from Europe on the use of interferon omega in treating FIP. Cats receiving this very expensive treatment fared no differently than placebo treated cats. This will hopefully stop the use of this treatment in the US and other countries, although some people still believe more in anecdotes than scientific trials. Unfortunately, veterinary medicine is filled with anecdotal treatments.

How do you know when to euthanize a cat that has FIP?
This is a decision only you can make, and it is a difficult one. I would never suggest euthanizing a cat, even with FIP, as long as it looks and acts fairly normal. Miracles do happen, but they can’t happen unless they are provided time to happen. However, I also cannot argue with those owners that decide to end suffering at an earlier stage, given the grave prognosis.
I always tell owners to decide to put an animal down when it no longer takes pleasure in life. But cats can feign health to the last moment and you often regret in retrospect not making the decision earlier. I did the same thing with one of my cats that was dying of cancer. He actually was dead one morning, even though I still thought he had time to live and seemed reasonably content. There is also a myth that if a cat is still purring that it is still enjoying life. But research has shown that cats purr even when in extreme pain, it is another way that they mask illness.

After you have had FIP in an environment, how long should you wait before a new cat or kitten is brought in, and what other steps should you take?
Remove any cat related items that you cannot wash or disinfect, such as a scratching post or soft toys. Clean and disinfect everything else in the environment that you can. Time will take care of the rest, because viruses of this type are not long-lived in the environment. We generally recommend a couple of months. These steps are undoubtedly an overkill when it comes to FIP, but these recommendations are standard for most infectious diseases and we try to keep everything simple and consistent.

If FIP occurs in a cattery, how do you decide whether and which cat to spay/neuter?
We know that genetics play a strong part in FIP – at least 50% of the incidence or more has a heritable component. We know that susceptibility is carried both in paternal and maternal lines, but we have suggested, at a minimum, that paternal lines that throw kittens that die from FIP not be used for breeding. This is because toms breed multiple queens and sire dozens or hundreds of kittens, and have the greatest influence on how bloodlines are developed. This is true of a lot of diseases – the “Founder effect.” If females are genetically weak, and bred to weak toms, that is when you get into problems. If toms are genetically strong, and queens are genetically weak, the male’s resistance genes seem to mask this weakness. The best scenario is to not breed either susceptible toms or queens, but not using problem toms is the best possible alternative in the interest of doing the most with the least disruption of breeding practices and bloodlines. However, if there are multiple losses from FIP in a litter, remember that susceptibility comes both from the paternal and maternal lines. It’s also important to consider the cat – if you believe the cat may be at risk for FIP, avoiding the stress of being a breeding cat may help prevent the disease for that individual.

If one kitten in a litter has FIP, how likely is it that other littermates will be affected as well?
We know that if one kitten in a litter gets it, that the others are several times more likely, but this is not absolute. If the overall incidence is 5% across the spectrum of young cats produced in a cattery, it could be 10-50% or higher among the remaining littermates. I have seen one kitten in a litter of 6 killed by FIP and I have also seen 5 out of 6 develop the disease. Time is the only thing that will determine the fate of healthy siblings.

Sometimes both bacterial and viral infections exist in a cat with FIP – which came first?
It is really impossible to say which came first, because it is like chickens and eggs. A given cat could have had some underlying immunosuppression that made it susceptible to a number of common feline pathogens as well as FIP. It is also possible that the cat suffered from FIP for a long time and that this was the cause of immunosuppression and the other infections were secondary.

What is the best way for breeders to prevent FIP?
Resistance is the ability of the immune system to cope with a disease. We know that 50% of the incidence is heritable, and we know that resistance (or susceptibility) factors exist in both toms and queens. However, culling problem toms is the simplest genetic procedure to reduce incidence. Toms produce far more litters and kittens than queens, and therefore have a much bigger effect on the disease. Good judgment and husbandry will influence the other 50% of the equation. Pick the largest and strongest in a litter to keep for breeding and avoid kittens that are slow growing and prone to other infections. Spay and neuter cats that throw FIP and adopt them into good homes. Avoid stress and overcrowding; maintain only those cats deemed necessary for your breeding program and chose mating wisely to limit kitten numbers. Keep cats in small, separate groups. Consider isolating the kittens from the mother at weaning to avoid exposure to the virus. Don’t mix very young kittens with older kittens. If you can limit coronavirus exposure until 12-16 weeks of age, when the immune system is better developed, the likelihood of developing FIP will be less. Follow accepted protocols for vaccinations and practice good husbandry to limit other infections. Clean and disinfect cages and litter boxes regularly. The corona virus is easily killed by bleach and other disinfectants.

Is it possible to have a corona virus free cattery?
This is extremely difficult, because the virus is ubiquitous in the environment and easily spread by cats and on people. Isolation of queens and early weaning has been touted in the UK and is used in the US. However, UK catteries are small and such a program can only succeed in smaller catteries and with exceptional isolation facilities and quarantine procedures. Moreover, even if you could produce a virus free cattery environment, the moment a kitten or cat goes to new environments such as a pet home it will most likely be exposed to FECVs. Therefore, we do not recommend this procedure unless simpler husbandry practices totally fail to reduce the problem.

Isn’t there an FIP Vaccine?
A vaccine was developed and is available. However, it has to be used in kittens at least 16 weeks of age (most cats are already exposed to coronavirus at this age), it is not effective in cats already exposed to coronavirus (which is most cats), it is not effective against the common serotype of FIPV, and even when all factors are optimal, it has low efficacy. In short, it does not work in the environments where it is needed most (catteries and shelters) and is not justified in older pet cats where FIP is hardly seen. We do not recommend its use.

Why is there hope now for progress on finding ways to prevent and treat FIP?
It is true that there is still no cure, or totally effective prevention. But we understand the virus and the infection much better now. We have new tools that allow us to look at viruses at the molecular level. Any knowledge about the virus and how the host cat responds to it will have influence down the road. The Feline Genome has been sequenced and in 2 years it will be complete. We will be able to identify viral genes responsible for causing disease (which will facilitate antiviral drug development) and host genes that confer resistance/susceptibility (which will facilitate genetic control).
There are only two ways to affect the corona virus at the current time – through husbandry and careful matings. Husbandry techniques can help prevent the spread of the virus – a great deal of research has been done and continues in this area at the Shelter Medicine program at Davis.
Understanding how the immune system affects both resistance and the form of the disease (wet vs. dry) will be important. Immunity studies focus on how to modify the immune system’s reaction to the virus. Understanding how to block inflammation and the development of anti-viral drugs would be ways we could fight it. There is no reason why these can’t be developed. In fact this was happening following the appearance of the severe acute respiratory syndrome (SARS) – another coronavirus disease, but of humans. However, this research was curtailed when SARS failed to spread to the general population and was easily contained. But it made human researchers interested in the corona virus. Drugs could be developed and used in FIP with some effect – like HIV/AIDS it could become a manageable disease
If we can discover the genetic basis for susceptibility, we will be able to offer genetic testing and breeders can breed out the trait over several generations, while preserving valuable bloodlines. This is exactly what breeders are doing with many other genetic diseases, such as polycystic kidney disease in Persians and breeds with Persian blood.

How can Burmese and Birman breeders help with FIP research?
Genetic research has great potential, but it takes time and money. Because FIP is a purely animal disease, there will be limited funding from sources such as the NIH. It’s important to start banking DNA and assembling pedigrees showing relationships between affected and healthy cats. Breeders should not be ashamed of FIP. If you breed enough cats, long enough, you will experience FIP. The reluctance of breeders to talk about it has been a huge detriment to FIP research. For instance, if every one would cooperate, we could determine whether or not there is a genetic basis for FIP resistance or susceptibility in rapid time. If there is a genetic basis, we could then determine the gene or genes involved and develop tests to predict which cats to breed or not to breed. Fortunately, some breeders are now coming forward and cooperating in raising funds for FIP research and providing information and materials (such as DNA and FIP virus isolates) from the field. Such people have come out in the past, but they usually get frustrated and give up after a while. So if we want to succeed in understanding this disease we must all work on together to collect the DNA, case and pedigree information that will help us advance our research.
FIP affects all breeds, but we cannot spread our genetic studies across all breeds. We only need two breeds, which are inbred to a degree and have relatively small to moderate numbers in their registries. We have seen a number of FIP cases in Burmese and Birmans this year, especially in certain bloodlines. Burmese and Birman breeders seem to know a great deal about bloodlines and certain matings that result in FIP. Because Burmese breeders have cooperated so well on the head defect project, they know what is needed for another genetic study. Birmans do not have head defects, but Birman breeders appear equally involved and knowledgeable about the genetics of their breed. We are trying to get as many breeders of these cats as possible to come together and provide at least three generational pedigrees, with DNA samples (cheek swabs with Q-tips), of families known to produce affected kittens. These families are essential for determining the genetic basis for FIP susceptibility
We need FULL cooperation from breeders of these two breeds. We can code the information we receive – so confidentiality will be maintained. It’s my hope this will reassure breeders to provide us with full data and pedigrees on FIP cases and related cats they have experienced in their catteries.
There are two types of studies we want to do. Whole genome linkage mapping requires at least three generations of cats with 30 or more members and with accurate identification of FIP affected and non-affected individuals. Similar information can be obtained by combining information from a number of smaller families, providing breed pedigrees are made available to determine degrees of relatedness among these families.
Whole genome association mapping involves two large groups of cats of the same breed – one group of cats that have had FIP, the second that have not had the disease. This can be two different catteries, one with problems and one without (but please be honest about your status, as false classification will doom this type of study). These two groups can also come from different bloodlines in the same cattery – breeders have strong intuition on which cats are problems and which are not. We need a total of 100 or more cats in each group (affected and non-affected) for association mapping.
Breeders, besides information from your cattery, talk to clients. We want information on siblings and parents and grandparents of FIP cats. Get DNA on everybody in your cattery and from relatives whenever possible. Now is the time to start to collect and bank DNA for when the feline genome is complete. It is also important for future research on other feline diseases.
We will also need fecal samples to collect viral RNA for studies on the origins of FECVs and FIPVs. We need to know if certain strains of FECV are more apt to mutate to FIPV, and if catteries having these strains are therefore more likely to suffer high FIP loses. It is extremely important that FIP is accurately diagnosed. We can help to review veterinary records to see if there is enough evidence to confirm the diagnosis. We can accept proper tissue samples taken at necropsy or biopsy from your veterinarians and test them for FIP. We can also do necropsies at Davis when possible and necessary.

How much money is needed for this research at Davis?
All money given to Davis will go right into FIP research. Some of this research will be clinical in nature, and some bench top. We need $50,000 – 75,000 a year just for a single technician or graduate student, and the more such people we can engage in research the faster we will reach our goals. The genetic testing will be expensive – the DNA chip arrays will cost $400 or more each just to purchase (once they are developed by commercial companies), read, and analyze. These are certainly daunting figures, but doable if everyone admits to their problems and work together. As demonstrated by our predecessor, SOCK it to leukemia, a lot of money can be raised by ordinary people (cat breeders, cat owners, cat lovers), and a lot can be accomplished with that money if it is concentrated in the hands of knowledgeable and capable researchers.

What about other universities and institutes that are studying FIP?
Though we are trying to focus on U.C. Davis for greater impact, the scientific community is very collaborative and pedigree/disease information and DNA samples will be useful for meaningful collaborations. We are aware that others are interested in this same approach. Our goal is to solve FIP and in the end it really does not matter how it is accomplished or who does it. Scientific competition is always good. We are also aware that other groups may be raising money to study FIP, and this is also respected and accepted. A world full of researchers have studied this disease for over 40 years, and although we know a lot more about it, we still do not have effective ways to totally prevent or cure this disease. Hopefully, this worldwide research effort will finally bear the needed fruit. We can only do the best as our part.

My heartfelt gratitude to Dr. Pedersen for answering my many questions about the disease – questions I know are shared by others. I believe the comprehensive information he has provided will help breeders, rescue and shelter workers, veterinarians, and cat lovers in general to gain a better understanding of FIP and ways to prevent it in our cats. I also hope it will encourage Burmese and Birman breeders and fanciers to participate in this important research.
Nancy L. Reeves, United Burmese Cat Fanciers

Is my cat at risk?

If your cat comes in regular contact with other cats (i.e.: a multi-cat household), the answer is YES! The lowest risk groups are indoor only, single-cat households. The higher the number of cats, the more risk of FIP. The higher the number of cats, the higher the titer test results (more on titers below). Single-cat households are generally free of all coronaviruses. FIP occurs in greatest incidence in cats between six months and two years old, although infections are high up to five years old. Of course the most susceptible group to catching FIPV are kittens because under the age of 16 weeks their immune system is very bad in general. Studies also show that poor nutrition, high stress levels or poor husbandry increase the likelihood of getting FIP. Outside exposure, exchanging of animals, especially kittens and young cats, highly inbred cats, and cats in actively breeding households increase the risk. Males and females are equally affected. There also appears to be a genetic component to FIP that may put some family groups at a particularly high risk.

Is there a test?

There is a test which will look for the presence of coronavirus
antibodies in your cat’s blood. If your cat has been exposed to a
coronavirus, ANY coronavirus, its immune system will build up
antibodies to it, and the titer tests for the level of those antibodies
in the blood. But it does not distinguish between antibodies made
specifically against FIP, or FECV, or any other coronavirus. A
positive titer means only that your cat has created antibodies
(therefore been exposed to) SOME form of coronavirus. The higher the
titer, the more antibodies the cat has created.

As if there were not enough problems with the
coronavirus test, there
is no uniformity between different labs. One cannot compare results
from one lab to another. Some labs just specify positive or negative if
the results are above or below a given titer (often these labs do not
even specify the titer). There are no standards for setting up a lab,
there is no regulatory body that oversees them, and no requirement for
validation of test results. It is also possible for a cat which has
received the vaccine (more below) to have enough antibodies to appear
on the titer test. To top it all off, false positives occur in up to
30% of the tests. In sum: DO NOT PLACE MUCH CREDENCE IN THE TITER TEST,
AND UNDER NO CIRCUMSTANCES SHOULD A CAT BE EUTHANIZED BASED SOLELY ON
THE RESULTS OF THE TITER TEST.

There are some clinical indicators which your vet may discuss with you
if s/he suspects that a cat has FIP, particularly if it is showing
likely symptoms. Some blood tests can help your vet pinpoint FIP as a
cause for your cat’s condition, this includes looking for a high amount
of gamma globulin proteins and a low amount of albumin proteins in the
blood.

There has also been talk of a polymerase chain reaction (PCR) test, in
the hopes that it can tell the difference between FIP and other
coronaviruses. Significant scientific studies have yet to be concluded
on this method. However, given that the most common way of a cat
coming down with FIP is via the mutation of FECV, this test may have
little or no value in the great majority of cases.

Is there any evidence for this?

A 1992 study found the following: 400 kittens were divided into 41
household with various FIP histories. In one group the kittens were
allowed to freely associate with all the cats. In a second group the
kittens were isolated only with their mother. In the third group, the
kittens were isolated by themselves starting at age 2-6 weeks. Only in
this last group did all of the kittens remain seronegative for any/all
coronaviruses.

My vet believes that my cat has FIP, what is the best thing to do?

Usually by the time the vet is able to pinpoint FIP as the cause of
your cat’s condition, the cat is pretty far along. So long as your cat
is in pretty good shape, not in any pain or discomfort, there is no
reason to euthanize it. Even if your cat is happy and healthy, however,
you MUST make sure you keep it indoors and away from other cats. If you
feel that this will be too great a compromise on its quality of life, it
is better to euthanize it. Since the cause of transmission
is not known, by allowing your FIP+ cat outside, you could cause
numerous other cats to become ill, and even further spread the disease.
But please keep your cat’s welfare foremost in your mind. When its
systems begin to fail, when it is in obvious discomfort, you are only
making things worse by delaying the inevitable. Keep him or her as
happy and as comfortable for as long as possible, that is unfortunately
the only solution at this point.

Second International FIP Symposium 2002 – by Jen Lacey

Second International Feline Coronavirus & Infectious Peritonitis
Symposium - a report by Jen Lacey

Intro
-----
The Second International Feline Coronavirus / Feline Infectious
Peritonitis Symposium was held in Glasgow, Scotland, UK 4-7 August
2002. Like the hugely successful first FECV/FIP Workshop hosted by
Prof. Niels Pedersen in UC Davis, the second welcomed scientists,
Veterinary surgeons, cat breeders, cat rescue charities and industry.
Prof. Niels Pedersen began the meeting by giving an overview of Feline
Coronavirus and Feline Infectious Peritonitis. The conference co-
ordinator was Dr Diane D. Addie. The proceedings will be published in
the Journal of Feline Medicine and Surgery.
Scientific committee: Prof. Niels Pedersen, Prof. Hans Lutz, Prof.
Marian Horzinek, Prof. Oswald Jarrett, Dr Diane D. Addie. Local
organising committee, Dr Diane D. Addie, Prof. Oswald Jarrett, Dr
Margaret Hosie.

The Beginning
-------------
The Scottish welcome was very warm, with a ceilidh, haggis, kilts and
pipers, plus the wee dram, of course, all contributing. Whilst most
other parts of the UK seemed to be having torrential downpours or heavy
mist, we were bathed in warm sunshine . There was the little matter of
cryptospiridium in the water supply, but nothing to panic veterinary
scientists! These had come from all parts of the world. Australia,
Japan, Australia and South Africa were represented, as well as North
America, many European countries and the UK. It was satisfying to put
faces to some well known names, Dr Neils Pedersen, Dr Janet Wolf, and
Dr Susan Little were there; and it was good to meet in person, Dr Diane
Addie of Glasgow University who had co-ordinated the event, but mostly
because she was taking a special interest in the FIP outbreak amongst
my own cats and kittens. Over the 3 days the Symposium had 4 main
sessions presenting papers on: Diagnosis & treatment of FIP,
Epidemiology of FCoV Infection, Pathogenesis & Immunopathogenesis of
FIP and Prevention of FcoV Infection/FIP. They were preceded by two
speakers who gave a history of the study of the disease (Pedersen) and
what it's like to actually live with an FCoV household (Sue Perry from
Sleaford, whose tribe were all rescues of the sort nobody else would
take on). On the final afternoon we broke for workshops, on
'Diagnosis', 'Minimising Disease Spread', or 'Recommendations for
Future Research'. One of my reasons for being there was to learn all I
could from the second and it was a stimulating afternoon. Taking the
event as a whole though, I can't say there was much cause for celebration. That had absolutely nothing to do with the quality of the
speakers or the presentations. I suppose the tone was set by Dr
Pedersen in his introduction when he told us that the disease had been
named in 1963 and fully described by scientists from Cornell in 1966.
We also saw a slide of a photo taken in 1912 that showed a little cat
with the typical swollen abdomen of the effusive form of FIP, so it's
something that's known to have been around for a long time. He defined
FIP as an important cause of death for young cat from catteries and
shelters, but said that the years of study had not yet brought any easy
way to prevent the disease and no way at all to cure it. He also
admitted some blind alleys. The worst of which was the publication of a
paper in the 70s which indicated FIP could be detected from an antibody
titre test. Unfortunately, there was a weakness in the study as no
comparison had been made with cats in multicat households (MCH). Within
quite a short the data was available and corrections made, but still
today probably more cats are euthanised because of a positive FcoV
antibody titre than die of FIP. So prevention difficult, with the only
available vaccine in no way helpful to those who most need it, kittens
of 8+ weeks who have already been exposed to the virus in their MCH or
shelter, and no cure. All the years had brought was a lot greater
understanding. The research presented at the Symposium would add to
that, and there were a couple of gleams of light from beyond the
boundaries of feline medicine as both mouse hepatitis and dengue fever
(human) developed and progressed as FIP did in cats, so studies of
these could contribute. He had hoped FIP would reduce as FeLV was
effectively beaten, but it had made no significant difference. As yet
then only a hard road ahead. I'll try tomorrow to give more detail of
those studies I found most interesting, and then I'll describe the
conclusions of the workshop on what we as breeders could do. I've pages
of notes, but big lashings of info without the pictures and diagrams
that went in to illustrate aren't that digestible.

Breeder Study
-------------
Kinetics of FCoV Infection in Kittens Born in Catteries of High Risk
for FIP Under Different Rearing Conditions - Lutz H. et al, University
of Zurich. This was a significant paper for me as on the day it was
given my litter born to a queen with a high titre (she was newly
pregnant as FIP was diagnosed in my cattery) were three weeks old. Dr
Addie's recommendation was that I should separate the kittens from
their mother at five weeks (early weaning) in an attempt to prevent
them becoming infected with FCoV. I had reservations, not because the
actual weaning process would be difficult, but because the maternal
bond in Korats is strong and queens continue to be protective and
caring for their kittens at least twice as long as this, thus playing a
significant role in their socialisation. However, I wanted to do all I
could to protect them from FIP so I went to the Symposium really torn
and hoped to get information to help me reach a decision. The purpose
of the study was to determine the course and viral load of natural FcoV
infection in conventionally and early weaned kittens and to consider
the role of vaccination in those who were seronegative. 18 breeders
took part. All were highly motivated as they had a history of FIP in
the past and wanted to do all they could to prevent it. Their selection
was on these 2 criteria. 226 kittens in 63 litters were studied, with
half early weaning and the other raised with their mother and (later)
other cats of the household in conventional fashion as a control group.
FCoV shedding in the faeces of the kittens started as early as 2 weeks
whether the queens were quarantined with their kittens or not. By week
4 20%, and by week 6 50% of kittens tested positive. At this point the
conventionally raised kittens were shedding significantly more FcoV
than the early weaned, but at the age of 9 weeks, and 12 weeks, the
levels were the same for both groups. The two groups were followed for
a total of 21 months. At this point 9 of the kittens had died from FIP.
5 were from the conventionally raised group and 4 from the early
weaned. It was concluded that although the early weaning prevented a
high viral load at a young age it was not found able to keep kittens
free of FCoV infection under field conditions. The vaccination part of
the trial was not followed through as no kittens in the study were FcoV
negative. Of course Dr Lutz was asked if he could produce any reason
for the different results in his trial to Dr Addie's. The size of the
catteries in terms of numbers and space was considered. Dr Lutz
wondered if we all had bigger homes in UK and were more able to
separate cats effectively to prevent contamination of the isolation
necessary for early weaning. Dr Janet Wolf said that in the trials she
had conducted with breeders in USA none had been able to produce FcoV
negative kittens by this method, and Dr Pedersen said that even under
the strictest lab conditions it was difficult not to introduce FCoV to
a clean area, he'd had it happen.Dr Gunn-Moore(Edinburgh) and one of
the Europeans (who also added that she came from a small country
confirmed success for the method. Considering again, Dr Lutz believed
that the answer could well lie with the queens. They were all
significant virus shedders, which correlated strongly with high antibody titres. Dr Addie' groups hadn't been selected on this basis,
and it was agreed she had reported lack of success with some litters
from high titre dams. This report made my own choice harder than ever.
Dr Addie hoped very much that it hadn't put me off trying to early
wean, and I had to admit concern that I could be putting mother and
kittens through a stressful situation for little gain. By the end of
the conference I'd decided on a compromise. Yesterday I sent faeces and
a blood sample from Shula (dam) and faecal swabs from the kittens off
to Glasgow. I should then know whether Shula's titre has decreased
significantly in her 11 week isolation period, and discover whether or
not she's shedding virus at this point in time. I shall also know whether or not the kittens have already been infected from whether
there is evidence of the virus in their samples. If it happens that
their mother is positive and they are clear then I shall separate them
in an effort to protect them.. However, I do it with the knowledge of
the virulence of the virus that infected my cats, I'm not saying that
it's a must for all, and indeed this particular paper shows that it's
just about impossible to achieve the desired result when starting with
cats at high risk of producing kittens, some of whom will go on to
develop FIP (about 4%).

Diagnostics
-----------
I think these papers deserve a report, but I must admit it was rather
tough going. The most breeder relevant bit is in the final paragraph so
skip to that if you're not wrestling with the is it/isn't it stage of
FIP. I can't give those of you with specialist knowledge much detailed
information on this subject as I'm not a scientist. I picked up on the
fact that when effusion exists and fluid can be extracted it's not too
difficult to come to a diagnosis of FIP, taking the other clinical
signs into account. What would be useful for clinicians is a diagnostic
to rule out FIP in its dry form so that further investigation could
then go on to decide what the actual problem was. It was encouraging to
find when chatting to other delegates socially that several of them
were there from firms who had not yet worked on this to see if it was
worth putting money into the development of diagnostic tests. I hope
they returned home keen and eager. The first paper was AGP Measurement
as an Aid to the Diagnosis of FIP given by S Duthie of Glasgow
University. AGP is an acute phase protein produced by the liver in
response to inflammation. It was monitored in cats with FIP and
diseases with a similar clinical presentation. It was found that
specific levels were of value in distinguishing field cases of FIP from
look alike conditions. Indeed it was concluded that it was more
efficient than the albumin:globulin measure used at present. It is able
to give results within 36 hours. Further research to be done as this
looked promising. The second study (K Hartmann) compared different
diagnostic tests. In all cases FIP had been confirmed or not by
necropsy and histology. The conclusion was that for cats with effusions
diagnostic tools based on the analysis of the fluid have good
predictive values, but this was impossible in many cases where there
was no effusion. Therefore it was recommended that diagnosis should be
made by the more invasive methods of laparotomy, laparoscopy and organ
biopsy. Several of the vets there confirmed that these were now a
preferred option to get a confirmed diagnosis to rule FIP in or out of
the picture in cases with no effusion. To reinforce the last study
research in Poland (P Kita) on RT-PCR to detect FCoV in blood was
evaluated. The test was found to give false positives, with the
inevitable conclusion that the detection of FcoV sequences in blood by
RT-PCR has a limited value as a method of FIP diagnosis. However,
research done in Utrecht was more upbeat on detection in blood. The RT-
PCR was designed to detect mRNA a genetic element of most, if not all,
field CV strains. The most significant result was that of a group of 49
cats, cats with pathologically proven FIP 94% were positive in the mRNA
PCR, whereas the 12 proven to be non-FIP remained negative (100%).
Finally, and perhaps of most interest to breeders, Dr Addie gave an
evaluation of the Feline Coronavirus Antibody immunocomb. This could be
used as an in-house test for vets. It scored well against the
immunoflorescent antibody tests (84% & 85% for two different readers).
From 110 samples 2 with a 0 titre and 3 with a titre of 1:10 scored
higher indicating that it could give false positives, and cats with a
low positive score would need to be screened in the usual way. However,
no false negatives were recorded, so it was concluded that it could be
used with confidence in for entry into a FcoV stud or cattery.

Treating cats sick with FIP
---------------------------
The outlook is very poor for cats diagnosed to have FIP (by effusion
sample in the wet form, by biopsy in the dry). It's believed that any
said to have recovered probably didn't have FIP in the first place,
particularly as nothing claimed as effective has ever been able to be
repeated in lab conditions. However, recently, since the advent of
veterinary interferon, hopes have been raised that this could at least
put the disease into remission so that cat and owner could enjoy extra
months, if not years, together. The one paper on FIP treatment was from
T Ishida of the Akasaka Animal Hospital, Japan. He reported on an
evaluation of the therapeutic effects of a feline interferon currently
commercially available in Japan, UK and EC. The cases considered were 6
males and 6 females, all FIP diagnosed on 5 counts (they didn't want to
use any animals whose symptoms were vague). A treatment regime was
initiated in which alpha interferon was used in conjunction with
glococortoid treatment (dexamethasone & prednisalone). More detail of
exactly what was given, with the specific amounts is detailed in the
abstract, but I think that anyone wanting their vet to follow the same
path would need to consult with the Japanese institute involved, rather
than anything I copied out. The results were interesting. There was an
age split. 4 of the cats responded to the therapy and have survived
without illness for more than 2 years (though it must be said that full
health and strength did not return). 2 showed a partial response and
survived for 4 months and 5 months. All 6 had effusion initially and
were over 5 years old. The other 6 were 3m-5y.o. or they had no
effusion. On death these were shown to have had FIP by necropsy. So it
was interesting that both age and form of FIP had significance for
recovery. One criticism of this study that came from the floor after
the paper was presented, was that there had been no control group
receiving the glutocortoids only. Other scientists were interested to
know whether prednisalone alone, plus the general treatment, would have
had the same effect. How vital was the interferon? Work for the future
there.

Epidemiology
This is the study of the prevalence of a disease, or put another way
Corona Virus, where it's at. None of the papers presented in this
section gave the slightest bit of comfort to me as a breeder. Without
exception it was shown that there are two 'exposure factories' for
FCoV: rescue shelters and pedigree breeders, with other MCHs also
featuring. For instance, 'Operation Catnip' Gainesville, Florida was a
typical, catch, neuter and release of ferals. (Ear tops were clipped to
ensure the same cat didn't get 'done' twice over). Blood sample were
taken from 250 of these to test for the prevalence of a variety of
diseases. A measure of FIP antibodies was just one of a range. Those
involved were surprised to find that only 18% of this group tested
positive for FCoV, and of these 29 cats that did, only 6 had a titre
greater than 1:320. Dr Addie had conducted a much wider study in
Britain of 2,207 cats relinquished to cat rescue shelters. Where
possible she had obtained information of the cat's background. Its sex
didn't make any difference to whether it was sero-positive, the sick
and the young had a slightly greater chance than the healthy and and
the adult. But with a 17% chance overall of being positive, and only an
11% chance for an adult feral, if the cat was designated as a pedigree
or a pedigree x on reception it had a whopping 74% chance of being FcoV
positive. The number of pedigrees taken at the shelters in her survey
even skewed the statistics for the spread of FCoV after arrival and the
subsequent FIP cases, with those taking the greatest numbers having the
worst record, despite husbandry practices being very much the same. Not
feeling too bad yet? Then contrast the findings of Dr Pedersen in
California, where he found of 50 kittens under age weeks of age of
feral/outdoor owned origin coming into a shelter none was FcoV
positive, against Dr Lutz's Swiss study, I detailed earlier, where 226
kittens from 18 catteries were 100% were positive by 8 weeks. OK, these
were breeders who had asked for help because of FIP problems, but in a
second study by Dr Lutz on 132 cats & kittens in 8 catteries 90% were
positive and shedding virus for at least a portion of 24 week period.
Of course we all breathe a sigh of relief as FeCV does not mutate to
become FIP in the overwhelming majority of cases. We are not talking
about an epidemic with cats dropping like flies After all it was only
4% of those in Dr Lutz's study. and in each case the cattery had had
previous FIP cases. Still can't say I'm easy though with conclusions
such as: These data are consistent with the belief that feline corona
infection is primarily a disease of cats that live together in large
groups. Feral cats are an unlikely to be a significant reservoir for
infection with feline corona virus of owned outdoor cats." AM Legendre
(University of Florida) "Since FCoV is transmitted faecal-orally, it
was expected that life-styles which engender more contact of cat s with
the faeces of other cats would predispose to a higher prevalence of
FcoV seropositivity. Feral cats were less likely to be SP than pets or
strays. Pedigree cats were significantly more likely to be SP than
domestic cats, associated with originating from an MCH." D Addie
(University of Glasgow) "FCoV shedding in faeces is widespread in
catteries and represents an important source of FCoV spreading." Lutz H
(University of Zurich). Personally, I don't like being thought of as
one of a group responsible for spreading infection, possible deaths and
the ensuing misery each life lost brings. I shall do my best over the
coming months to put into practice suggestions made at the workshop for
prevention on the last afternoon (I've yet to write up the details,
saving it as a conclusion) and aim to lose no more lives to this. 4 in
every hundred is still too higher price by my reckoning.

Prevention
----------
I think I've just about reached the last chapter of my reports. I
suppose those I've bombarded with just too much information have
probably switched off by now, but the conference was just about the
steepest learning curve I've been on for a good few years, and I felt I
had to share as much as possible. If there's been a certain sour note
to what I've had to say at times, please remember that my losses to FIP
happened this year and are very fresh in my memory. Just by being there
I rubbed a very sore spot, and some of what I heard had the same effect
as adding vinegar to the wound. This was a self inflicted injury only.
No one I spoke to directly had anything but sympathy for my situation,
and the speakers referring to the high incidence of FCoV in breeding
catteries were doing so to define situations where the MOST HELP was
needed, rather than dishing out condemnation. Those following this most
closely will have realised I've skipped the immunopatholgy and
pathology papers. I was too way out my depth here to be able to
summarise the reports, but I do know the papers gave important new
research detailing how the disease progressed within the cats, which
could help with early diagnosis, and prevention perhaps in the future.
The cell mediated immune response (which is what prevents cats getting
FIP, antibodies don't) is an exciting new area of study. In Utrecht
University they are currently comparing the CMI in cats that either
survived or succumbed to FIP, and when the difference has been under-
stood that should be be a major step forward. Dr Radford is pursuing an
understanding of CMI at Liverpool too, to gain knowledge of specific
genetic predisposition to cope with disease. I mention his study
because DNA from a family of my cats (given when Korats were being
screened for GM) has been used in the study. I took comfort from the
fact that in a very small way I'd contributed something positive.
Before breaking for the workshops on Wednesday there were four papers
on new vaccine approaches, 2 from Utrecht, one from Bristol and the
other from Virbac (France). There were some promising leads that would
be further explored, but Dr Pedersen's view given at the beginning of
the Prevention' session was that we can't just sit around and wait for
a vaccine, because anything new that will be effective for all is most
probably years away. The efficacy, or not, of Primucell wasn't a
discussion topic, so I won't comment either, as I know absolutely
nothing about it (not licensed for use in UK). The only point of note
is that to be of any great use a vaccine should be able to protect
those already exposed to FCoV at an early age, as it's been frequently
demonstrated that it's this group who are at most risk. Primucell makes
no claim to do that. The workshop brief was, "Recommendations for
Minimising Disease Spread in Breeding, Rescue and Boarding Catteries,
In Veterinary Practices and at Cat Shows". The last three we dropped
After a very brief discussion. That's not to say that FCoV cannot be
transmitted from one cat to another at any of these places. Dr Addie's
household study demonstrated that a new virus strain can be introduced
without a known source, but situations where litter boxes are not
shared, and some disinfection procedures are being used, can be
considered low risk. (Incidentally, when Dr Pedersen learnt that our
boarding catteries are inspected and licensed he was most impressed.)
For shelters and rescue centres the key word was HOUSING. No two or
more litters of kittens should share the same accommodation unit at any
time during their stay. The same should also go for foster homes used
by any rescue organisation. Unless separate facilities are available,
one litter at each should be the rule for fostering, and any well
meaning person letting kittens mix should only get one warning (CP
vet). Any available money for expansion, updates etc, then improving
the husbandry facilities of the young should be a priority. As an aside
Dr Pedersen believed that well-meaning people think they're doing
abandoned kittens a favour by taking them to a shelter. If they could
only do, as used to be the case, and find homes for them themselves,
the kittens would have a greater chance of remaining healthy. For
breeding catteries LITTER BOX HYGIENE and NUMBERS were prime
considerations. Keeping litter faeces free, not sharing boxes between
different groups of cats, keeping any scoops, brushes etc specific for
each place; these measures have been discussed several times. As far as
the number of cats for a household was concerned it was considered that
FIVE was enough for any home that did not have facilities to house
separate groups. Two or three in any one group would be ideal to
prevent disease spread. Never had FIP in your cattery? Then you are are
either FCoV negative, by design or good luck, or your cattery strain of
FCoV is a non-FIP causing FECV. There's enough evidence to indicate
that there are differing strains, the goodies and baddies, and Dr
Addie's household data showed that variation in a strain, as it was
replicated and transmitted within a household, was little. It's just
that as yet there's no way of knowing whether any strain will mutate
and cause FIP until it actually does. Should you do anything other than
practice good husbandry and not let numbers spiral?
a) Don't visit studs or have queens to visit without antibody testing
both parties. Obviously this is essential if you are maintaining a
negative cattery, but otherwise consider 1:400 or below as the guide.
Dr Lutz's study demonstrated that the higher the antibody titre, the
greater the viral load and viral shedding, and you certainly can't tell
a goodie from a baddie. (I'm 99.9% sure this is how I introduced my
virulent virus, though no cat belonging to either owner, or their
breeders, had cats with FIP as far as was known.) Even where there has
been no FIP, you don't want to swap viruses if you can prevent it, so
don't let the stud and queen share litter boxes. House them separately
if you possibly can.
b) Before introducing new cats into your cattery, titre test, and again
use the 1:400 as a guide. Isolate a newcomer for 3 weeks on arrival,
and certainly don't let let him/her mix with any kittens you have.
Sporadic Incidence of FIP, or wanting to reduce/eradicate FCoV? As
above. Also: a) Titre test all and isolate those with a high titre.
Test and re-test these at 6 weekly intervals. Consider most strongly
adoption to single cat homes for those that maintain a consistently
high titre over 3 testings. There are 2 reasons for this. These are
cats shedding great amounts of virus who are infecting and reinfecting
other cats in your household. In spite of care to separate out mothers
and kittens it is very difficult not to take virus from one part of a
cattery to another when there is a high viral load (difficult to
downright impossible according to the recent studies). Also these cats
that do carry and shed greater amounts of virus are probably the least
resistant to it. The aim should be to breed from cats that can cope
with it effectively. Those whose antibody levels drop to 0, or at least
below 1:400 are those who are dealing with it, and have the healthy
immune system you want to pass on to the next generation. b)Use early
weaning if you are happy to do this. It has been shown to be effective
in eliminating FCoV from kittens and they go to new homes seronegative.
If you're not comfortable with this because of stress to mother and
kittens, or have difficulty weaning them at an early age, then at least
keep each litter isolated with their mother away from all other cats in
the household. Keep separate litter boxes for queen and kittens, and
part them for periods so that mother uses her own, and ensure the
kittens have no access to it. c) Studies (Pedersen at Davis, J Norris,
who reported this year a disproportionately high incidence of FIP in
the Australian Mist population) have shown there is a genetic link.
Don't breed together cats that both have had kittens die of FIP.
Consider removing from the breeding programme a male that sires kittens
who succumb to FIP, with 2 or more females. (It's not that males carry
genetic predisposition any more than females. It's that by the number
of kittens they may produce they have a much greater genetic input to
future generations than females). d) As stress is a factor in FIP
developing, it's probably also useful to take into account the
temperament of breeding cats. e) Don't have a constant throughput of
cats in your cattery, buying in show and/or breeding stock frequently.
It causes stress and adds to chances of importing fresh viral strains.
Work with what you have. (That goes for all breeders not just those
With a FIP problem). I think that's just about covers it. I don't think
there's a lot that 's actually new, other than testing for, and
removing the high viral shedders, and recommendations of a titre score
to go below. I should just add that testing should be done by the
recommended Universities and Institutes rather than commercial labs.

Jen Lacey
Jenanca Korats at the Cottage Cattery

Second International FIP Symposium 2002 – by Jen Lacey

Second International Feline Coronavirus & Infectious Peritonitis
Symposium - a report by Jen Lacey

Intro
-----
The Second International Feline Coronavirus / Feline Infectious
Peritonitis Symposium was held in Glasgow, Scotland, UK 4-7 August
2002. Like the hugely successful first FECV/FIP Workshop hosted by
Prof. Niels Pedersen in UC Davis, the second welcomed scientists,
Veterinary surgeons, cat breeders, cat rescue charities and industry.
Prof. Niels Pedersen began the meeting by giving an overview of Feline
Coronavirus and Feline Infectious Peritonitis. The conference co-
ordinator was Dr Diane D. Addie. The proceedings will be published in
the Journal of Feline Medicine and Surgery.
Scientific committee: Prof. Niels Pedersen, Prof. Hans Lutz, Prof.
Marian Horzinek, Prof. Oswald Jarrett, Dr Diane D. Addie. Local
organising committee, Dr Diane D. Addie, Prof. Oswald Jarrett, Dr
Margaret Hosie.

The Beginning
-------------
The Scottish welcome was very warm, with a ceilidh, haggis, kilts and
pipers, plus the wee dram, of course, all contributing. Whilst most
other parts of the UK seemed to be having torrential downpours or heavy
mist, we were bathed in warm sunshine . There was the little matter of
cryptospiridium in the water supply, but nothing to panic veterinary
scientists! These had come from all parts of the world. Australia,
Japan, Australia and South Africa were represented, as well as North
America, many European countries and the UK. It was satisfying to put
faces to some well known names, Dr Neils Pedersen, Dr Janet Wolf, and
Dr Susan Little were there; and it was good to meet in person, Dr Diane
Addie of Glasgow University who had co-ordinated the event, but mostly
because she was taking a special interest in the FIP outbreak amongst
my own cats and kittens. Over the 3 days the Symposium had 4 main
sessions presenting papers on: Diagnosis & treatment of FIP,
Epidemiology of FCoV Infection, Pathogenesis & Immunopathogenesis of
FIP and Prevention of FcoV Infection/FIP. They were preceded by two
speakers who gave a history of the study of the disease (Pedersen) and
what it's like to actually live with an FCoV household (Sue Perry from
Sleaford, whose tribe were all rescues of the sort nobody else would
take on). On the final afternoon we broke for workshops, on
'Diagnosis', 'Minimising Disease Spread', or 'Recommendations for
Future Research'. One of my reasons for being there was to learn all I
could from the second and it was a stimulating afternoon. Taking the
event as a whole though, I can't say there was much cause for celebration. That had absolutely nothing to do with the quality of the
speakers or the presentations. I suppose the tone was set by Dr
Pedersen in his introduction when he told us that the disease had been
named in 1963 and fully described by scientists from Cornell in 1966.
We also saw a slide of a photo taken in 1912 that showed a little cat
with the typical swollen abdomen of the effusive form of FIP, so it's
something that's known to have been around for a long time. He defined
FIP as an important cause of death for young cat from catteries and
shelters, but said that the years of study had not yet brought any easy
way to prevent the disease and no way at all to cure it. He also
admitted some blind alleys. The worst of which was the publication of a
paper in the 70s which indicated FIP could be detected from an antibody
titre test. Unfortunately, there was a weakness in the study as no
comparison had been made with cats in multicat households (MCH). Within
quite a short the data was available and corrections made, but still
today probably more cats are euthanised because of a positive FcoV
antibody titre than die of FIP. So prevention difficult, with the only
available vaccine in no way helpful to those who most need it, kittens
of 8+ weeks who have already been exposed to the virus in their MCH or
shelter, and no cure. All the years had brought was a lot greater
understanding. The research presented at the Symposium would add to
that, and there were a couple of gleams of light from beyond the
boundaries of feline medicine as both mouse hepatitis and dengue fever
(human) developed and progressed as FIP did in cats, so studies of
these could contribute. He had hoped FIP would reduce as FeLV was
effectively beaten, but it had made no significant difference. As yet
then only a hard road ahead. I'll try tomorrow to give more detail of
those studies I found most interesting, and then I'll describe the
conclusions of the workshop on what we as breeders could do. I've pages
of notes, but big lashings of info without the pictures and diagrams
that went in to illustrate aren't that digestible.

Breeder Study
-------------
Kinetics of FCoV Infection in Kittens Born in Catteries of High Risk
for FIP Under Different Rearing Conditions - Lutz H. et al, University
of Zurich. This was a significant paper for me as on the day it was
given my litter born to a queen with a high titre (she was newly
pregnant as FIP was diagnosed in my cattery) were three weeks old. Dr
Addie's recommendation was that I should separate the kittens from
their mother at five weeks (early weaning) in an attempt to prevent
them becoming infected with FCoV. I had reservations, not because the
actual weaning process would be difficult, but because the maternal
bond in Korats is strong and queens continue to be protective and
caring for their kittens at least twice as long as this, thus playing a
significant role in their socialisation. However, I wanted to do all I
could to protect them from FIP so I went to the Symposium really torn
and hoped to get information to help me reach a decision. The purpose
of the study was to determine the course and viral load of natural FcoV
infection in conventionally and early weaned kittens and to consider
the role of vaccination in those who were seronegative. 18 breeders
took part. All were highly motivated as they had a history of FIP in
the past and wanted to do all they could to prevent it. Their selection
was on these 2 criteria. 226 kittens in 63 litters were studied, with
half early weaning and the other raised with their mother and (later)
other cats of the household in conventional fashion as a control group.
FCoV shedding in the faeces of the kittens started as early as 2 weeks
whether the queens were quarantined with their kittens or not. By week
4 20%, and by week 6 50% of kittens tested positive. At this point the
conventionally raised kittens were shedding significantly more FcoV
than the early weaned, but at the age of 9 weeks, and 12 weeks, the
levels were the same for both groups. The two groups were followed for
a total of 21 months. At this point 9 of the kittens had died from FIP.
5 were from the conventionally raised group and 4 from the early
weaned. It was concluded that although the early weaning prevented a
high viral load at a young age it was not found able to keep kittens
free of FCoV infection under field conditions. The vaccination part of
the trial was not followed through as no kittens in the study were FcoV
negative. Of course Dr Lutz was asked if he could produce any reason
for the different results in his trial to Dr Addie's. The size of the
catteries in terms of numbers and space was considered. Dr Lutz
wondered if we all had bigger homes in UK and were more able to
separate cats effectively to prevent contamination of the isolation
necessary for early weaning. Dr Janet Wolf said that in the trials she
had conducted with breeders in USA none had been able to produce FcoV
negative kittens by this method, and Dr Pedersen said that even under
the strictest lab conditions it was difficult not to introduce FCoV to
a clean area, he'd had it happen.Dr Gunn-Moore(Edinburgh) and one of
the Europeans (who also added that she came from a small country
confirmed success for the method. Considering again, Dr Lutz believed
that the answer could well lie with the queens. They were all
significant virus shedders, which correlated strongly with high antibody titres. Dr Addie' groups hadn't been selected on this basis,
and it was agreed she had reported lack of success with some litters
from high titre dams. This report made my own choice harder than ever.
Dr Addie hoped very much that it hadn't put me off trying to early
wean, and I had to admit concern that I could be putting mother and
kittens through a stressful situation for little gain. By the end of
the conference I'd decided on a compromise. Yesterday I sent faeces and
a blood sample from Shula (dam) and faecal swabs from the kittens off
to Glasgow. I should then know whether Shula's titre has decreased
significantly in her 11 week isolation period, and discover whether or
not she's shedding virus at this point in time. I shall also know whether or not the kittens have already been infected from whether
there is evidence of the virus in their samples. If it happens that
their mother is positive and they are clear then I shall separate them
in an effort to protect them.. However, I do it with the knowledge of
the virulence of the virus that infected my cats, I'm not saying that
it's a must for all, and indeed this particular paper shows that it's
just about impossible to achieve the desired result when starting with
cats at high risk of producing kittens, some of whom will go on to
develop FIP (about 4%).

Diagnostics
-----------
I think these papers deserve a report, but I must admit it was rather
tough going. The most breeder relevant bit is in the final paragraph so
skip to that if you're not wrestling with the is it/isn't it stage of
FIP. I can't give those of you with specialist knowledge much detailed
information on this subject as I'm not a scientist. I picked up on the
fact that when effusion exists and fluid can be extracted it's not too
difficult to come to a diagnosis of FIP, taking the other clinical
signs into account. What would be useful for clinicians is a diagnostic
to rule out FIP in its dry form so that further investigation could
then go on to decide what the actual problem was. It was encouraging to
find when chatting to other delegates socially that several of them
were there from firms who had not yet worked on this to see if it was
worth putting money into the development of diagnostic tests. I hope
they returned home keen and eager. The first paper was AGP Measurement
as an Aid to the Diagnosis of FIP given by S Duthie of Glasgow
University. AGP is an acute phase protein produced by the liver in
response to inflammation. It was monitored in cats with FIP and
diseases with a similar clinical presentation. It was found that
specific levels were of value in distinguishing field cases of FIP from
look alike conditions. Indeed it was concluded that it was more
efficient than the albumin:globulin measure used at present. It is able
to give results within 36 hours. Further research to be done as this
looked promising. The second study (K Hartmann) compared different
diagnostic tests. In all cases FIP had been confirmed or not by
necropsy and histology. The conclusion was that for cats with effusions
diagnostic tools based on the analysis of the fluid have good
predictive values, but this was impossible in many cases where there
was no effusion. Therefore it was recommended that diagnosis should be
made by the more invasive methods of laparotomy, laparoscopy and organ
biopsy. Several of the vets there confirmed that these were now a
preferred option to get a confirmed diagnosis to rule FIP in or out of
the picture in cases with no effusion. To reinforce the last study
research in Poland (P Kita) on RT-PCR to detect FCoV in blood was
evaluated. The test was found to give false positives, with the
inevitable conclusion that the detection of FcoV sequences in blood by
RT-PCR has a limited value as a method of FIP diagnosis. However,
research done in Utrecht was more upbeat on detection in blood. The RT-
PCR was designed to detect mRNA a genetic element of most, if not all,
field CV strains. The most significant result was that of a group of 49
cats, cats with pathologically proven FIP 94% were positive in the mRNA
PCR, whereas the 12 proven to be non-FIP remained negative (100%).
Finally, and perhaps of most interest to breeders, Dr Addie gave an
evaluation of the Feline Coronavirus Antibody immunocomb. This could be
used as an in-house test for vets. It scored well against the
immunoflorescent antibody tests (84% & 85% for two different readers).
From 110 samples 2 with a 0 titre and 3 with a titre of 1:10 scored
higher indicating that it could give false positives, and cats with a
low positive score would need to be screened in the usual way. However,
no false negatives were recorded, so it was concluded that it could be
used with confidence in for entry into a FcoV stud or cattery.

Treating cats sick with FIP
---------------------------
The outlook is very poor for cats diagnosed to have FIP (by effusion
sample in the wet form, by biopsy in the dry). It's believed that any
said to have recovered probably didn't have FIP in the first place,
particularly as nothing claimed as effective has ever been able to be
repeated in lab conditions. However, recently, since the advent of
veterinary interferon, hopes have been raised that this could at least
put the disease into remission so that cat and owner could enjoy extra
months, if not years, together. The one paper on FIP treatment was from
T Ishida of the Akasaka Animal Hospital, Japan. He reported on an
evaluation of the therapeutic effects of a feline interferon currently
commercially available in Japan, UK and EC. The cases considered were 6
males and 6 females, all FIP diagnosed on 5 counts (they didn't want to
use any animals whose symptoms were vague). A treatment regime was
initiated in which alpha interferon was used in conjunction with
glococortoid treatment (dexamethasone & prednisalone). More detail of
exactly what was given, with the specific amounts is detailed in the
abstract, but I think that anyone wanting their vet to follow the same
path would need to consult with the Japanese institute involved, rather
than anything I copied out. The results were interesting. There was an
age split. 4 of the cats responded to the therapy and have survived
without illness for more than 2 years (though it must be said that full
health and strength did not return). 2 showed a partial response and
survived for 4 months and 5 months. All 6 had effusion initially and
were over 5 years old. The other 6 were 3m-5y.o. or they had no
effusion. On death these were shown to have had FIP by necropsy. So it
was interesting that both age and form of FIP had significance for
recovery. One criticism of this study that came from the floor after
the paper was presented, was that there had been no control group
receiving the glutocortoids only. Other scientists were interested to
know whether prednisalone alone, plus the general treatment, would have
had the same effect. How vital was the interferon? Work for the future
there.

Epidemiology
This is the study of the prevalence of a disease, or put another way
Corona Virus, where it's at. None of the papers presented in this
section gave the slightest bit of comfort to me as a breeder. Without
exception it was shown that there are two 'exposure factories' for
FCoV: rescue shelters and pedigree breeders, with other MCHs also
featuring. For instance, 'Operation Catnip' Gainesville, Florida was a
typical, catch, neuter and release of ferals. (Ear tops were clipped to
ensure the same cat didn't get 'done' twice over). Blood sample were
taken from 250 of these to test for the prevalence of a variety of
diseases. A measure of FIP antibodies was just one of a range. Those
involved were surprised to find that only 18% of this group tested
positive for FCoV, and of these 29 cats that did, only 6 had a titre
greater than 1:320. Dr Addie had conducted a much wider study in
Britain of 2,207 cats relinquished to cat rescue shelters. Where
possible she had obtained information of the cat's background. Its sex
didn't make any difference to whether it was sero-positive, the sick
and the young had a slightly greater chance than the healthy and and
the adult. But with a 17% chance overall of being positive, and only an
11% chance for an adult feral, if the cat was designated as a pedigree
or a pedigree x on reception it had a whopping 74% chance of being FcoV
positive. The number of pedigrees taken at the shelters in her survey
even skewed the statistics for the spread of FCoV after arrival and the
subsequent FIP cases, with those taking the greatest numbers having the
worst record, despite husbandry practices being very much the same. Not
feeling too bad yet? Then contrast the findings of Dr Pedersen in
California, where he found of 50 kittens under age weeks of age of
feral/outdoor owned origin coming into a shelter none was FcoV
positive, against Dr Lutz's Swiss study, I detailed earlier, where 226
kittens from 18 catteries were 100% were positive by 8 weeks. OK, these
were breeders who had asked for help because of FIP problems, but in a
second study by Dr Lutz on 132 cats & kittens in 8 catteries 90% were
positive and shedding virus for at least a portion of 24 week period.
Of course we all breathe a sigh of relief as FeCV does not mutate to
become FIP in the overwhelming majority of cases. We are not talking
about an epidemic with cats dropping like flies After all it was only
4% of those in Dr Lutz's study. and in each case the cattery had had
previous FIP cases. Still can't say I'm easy though with conclusions
such as: These data are consistent with the belief that feline corona
infection is primarily a disease of cats that live together in large
groups. Feral cats are an unlikely to be a significant reservoir for
infection with feline corona virus of owned outdoor cats." AM Legendre
(University of Florida) "Since FCoV is transmitted faecal-orally, it
was expected that life-styles which engender more contact of cat s with
the faeces of other cats would predispose to a higher prevalence of
FcoV seropositivity. Feral cats were less likely to be SP than pets or
strays. Pedigree cats were significantly more likely to be SP than
domestic cats, associated with originating from an MCH." D Addie
(University of Glasgow) "FCoV shedding in faeces is widespread in
catteries and represents an important source of FCoV spreading." Lutz H
(University of Zurich). Personally, I don't like being thought of as
one of a group responsible for spreading infection, possible deaths and
the ensuing misery each life lost brings. I shall do my best over the
coming months to put into practice suggestions made at the workshop for
prevention on the last afternoon (I've yet to write up the details,
saving it as a conclusion) and aim to lose no more lives to this. 4 in
every hundred is still too higher price by my reckoning.

Prevention
----------
I think I've just about reached the last chapter of my reports. I
suppose those I've bombarded with just too much information have
probably switched off by now, but the conference was just about the
steepest learning curve I've been on for a good few years, and I felt I
had to share as much as possible. If there's been a certain sour note
to what I've had to say at times, please remember that my losses to FIP
happened this year and are very fresh in my memory. Just by being there
I rubbed a very sore spot, and some of what I heard had the same effect
as adding vinegar to the wound. This was a self inflicted injury only.
No one I spoke to directly had anything but sympathy for my situation,
and the speakers referring to the high incidence of FCoV in breeding
catteries were doing so to define situations where the MOST HELP was
needed, rather than dishing out condemnation. Those following this most
closely will have realised I've skipped the immunopatholgy and
pathology papers. I was too way out my depth here to be able to
summarise the reports, but I do know the papers gave important new
research detailing how the disease progressed within the cats, which
could help with early diagnosis, and prevention perhaps in the future.
The cell mediated immune response (which is what prevents cats getting
FIP, antibodies don't) is an exciting new area of study. In Utrecht
University they are currently comparing the CMI in cats that either
survived or succumbed to FIP, and when the difference has been under-
stood that should be be a major step forward. Dr Radford is pursuing an
understanding of CMI at Liverpool too, to gain knowledge of specific
genetic predisposition to cope with disease. I mention his study
because DNA from a family of my cats (given when Korats were being
screened for GM) has been used in the study. I took comfort from the
fact that in a very small way I'd contributed something positive.
Before breaking for the workshops on Wednesday there were four papers
on new vaccine approaches, 2 from Utrecht, one from Bristol and the
other from Virbac (France). There were some promising leads that would
be further explored, but Dr Pedersen's view given at the beginning of
the Prevention' session was that we can't just sit around and wait for
a vaccine, because anything new that will be effective for all is most
probably years away. The efficacy, or not, of Primucell wasn't a
discussion topic, so I won't comment either, as I know absolutely
nothing about it (not licensed for use in UK). The only point of note
is that to be of any great use a vaccine should be able to protect
those already exposed to FCoV at an early age, as it's been frequently
demonstrated that it's this group who are at most risk. Primucell makes
no claim to do that. The workshop brief was, "Recommendations for
Minimising Disease Spread in Breeding, Rescue and Boarding Catteries,
In Veterinary Practices and at Cat Shows". The last three we dropped
After a very brief discussion. That's not to say that FCoV cannot be
transmitted from one cat to another at any of these places. Dr Addie's
household study demonstrated that a new virus strain can be introduced
without a known source, but situations where litter boxes are not
shared, and some disinfection procedures are being used, can be
considered low risk. (Incidentally, when Dr Pedersen learnt that our
boarding catteries are inspected and licensed he was most impressed.)
For shelters and rescue centres the key word was HOUSING. No two or
more litters of kittens should share the same accommodation unit at any
time during their stay. The same should also go for foster homes used
by any rescue organisation. Unless separate facilities are available,
one litter at each should be the rule for fostering, and any well
meaning person letting kittens mix should only get one warning (CP
vet). Any available money for expansion, updates etc, then improving
the husbandry facilities of the young should be a priority. As an aside
Dr Pedersen believed that well-meaning people think they're doing
abandoned kittens a favour by taking them to a shelter. If they could
only do, as used to be the case, and find homes for them themselves,
the kittens would have a greater chance of remaining healthy. For
breeding catteries LITTER BOX HYGIENE and NUMBERS were prime
considerations. Keeping litter faeces free, not sharing boxes between
different groups of cats, keeping any scoops, brushes etc specific for
each place; these measures have been discussed several times. As far as
the number of cats for a household was concerned it was considered that
FIVE was enough for any home that did not have facilities to house
separate groups. Two or three in any one group would be ideal to
prevent disease spread. Never had FIP in your cattery? Then you are are
either FCoV negative, by design or good luck, or your cattery strain of
FCoV is a non-FIP causing FECV. There's enough evidence to indicate
that there are differing strains, the goodies and baddies, and Dr
Addie's household data showed that variation in a strain, as it was
replicated and transmitted within a household, was little. It's just
that as yet there's no way of knowing whether any strain will mutate
and cause FIP until it actually does. Should you do anything other than
practice good husbandry and not let numbers spiral?
a) Don't visit studs or have queens to visit without antibody testing
both parties. Obviously this is essential if you are maintaining a
negative cattery, but otherwise consider 1:400 or below as the guide.
Dr Lutz's study demonstrated that the higher the antibody titre, the
greater the viral load and viral shedding, and you certainly can't tell
a goodie from a baddie. (I'm 99.9% sure this is how I introduced my
virulent virus, though no cat belonging to either owner, or their
breeders, had cats with FIP as far as was known.) Even where there has
been no FIP, you don't want to swap viruses if you can prevent it, so
don't let the stud and queen share litter boxes. House them separately
if you possibly can.
b) Before introducing new cats into your cattery, titre test, and again
use the 1:400 as a guide. Isolate a newcomer for 3 weeks on arrival,
and certainly don't let let him/her mix with any kittens you have.
Sporadic Incidence of FIP, or wanting to reduce/eradicate FCoV? As
above. Also: a) Titre test all and isolate those with a high titre.
Test and re-test these at 6 weekly intervals. Consider most strongly
adoption to single cat homes for those that maintain a consistently
high titre over 3 testings. There are 2 reasons for this. These are
cats shedding great amounts of virus who are infecting and reinfecting
other cats in your household. In spite of care to separate out mothers
and kittens it is very difficult not to take virus from one part of a
cattery to another when there is a high viral load (difficult to
downright impossible according to the recent studies). Also these cats
that do carry and shed greater amounts of virus are probably the least
resistant to it. The aim should be to breed from cats that can cope
with it effectively. Those whose antibody levels drop to 0, or at least
below 1:400 are those who are dealing with it, and have the healthy
immune system you want to pass on to the next generation. b)Use early
weaning if you are happy to do this. It has been shown to be effective
in eliminating FCoV from kittens and they go to new homes seronegative.
If you're not comfortable with this because of stress to mother and
kittens, or have difficulty weaning them at an early age, then at least
keep each litter isolated with their mother away from all other cats in
the household. Keep separate litter boxes for queen and kittens, and
part them for periods so that mother uses her own, and ensure the
kittens have no access to it. c) Studies (Pedersen at Davis, J Norris,
who reported this year a disproportionately high incidence of FIP in
the Australian Mist population) have shown there is a genetic link.
Don't breed together cats that both have had kittens die of FIP.
Consider removing from the breeding programme a male that sires kittens
who succumb to FIP, with 2 or more females. (It's not that males carry
genetic predisposition any more than females. It's that by the number
of kittens they may produce they have a much greater genetic input to
future generations than females). d) As stress is a factor in FIP
developing, it's probably also useful to take into account the
temperament of breeding cats. e) Don't have a constant throughput of
cats in your cattery, buying in show and/or breeding stock frequently.
It causes stress and adds to chances of importing fresh viral strains.
Work with what you have. (That goes for all breeders not just those
With a FIP problem). I think that's just about covers it. I don't think
there's a lot that 's actually new, other than testing for, and
removing the high viral shedders, and recommendations of a titre score
to go below. I should just add that testing should be done by the
recommended Universities and Institutes rather than commercial labs.

Jen Lacey
Jenanca Korats at the Cottage Cattery

So are these the only test results?

Well, Cornell concluded from the above that vaccine efficacy in a
laboratory setting is highly dependent on the challenge. It offers
protection at low challenge doses, none at higher doses. The problem is,
no one
knows what the “real world” dose level is.

Another problem is that there are actually two strains of FIPV. Just as
there are many different flu strains or cold strains which cause you to
get sick several different times with the flu or a cold, because each
time you catch a different strain for which you aren’t already immune.
Type I strain of FIP is believed to be the most prevalent in the “real
world” but it is the most difficult to reproduce in a laboratory. Type
II is easier to reproduce, but not as prevalent outside. It is not
known how effective a vaccine against one type will be against the
other type.

So, while some of the studies have found the current vaccine effective
against the Type II strain of FIP, there is no evidence either way as
to if it will work against the Type I strain.

So that is Cornell’s opinion, are there any other points of view?

The consensus arrived at the seminar sponsored by the Winn
Foundation on FIP/FECV is that the enhanced disease effect is a laboratory
phenomenon, especially since that study by Cornell only used seropositive
cats in the first place.

So what *is* FIP?

FIP is not caused by a retrovirus but by a type of coronavirus.
One of the reasons FIP is such a problem for vets is because there may be
no way to differentiate an FIP virus from certain other viruses. Current
thinking is that FIP is caused by a mutation of the Feline Enteric
Coronavirus (FECV). FECV is very common, and an FECV infection can have
symptoms ranging from none, to flu-like with or without diarrhea. These
are most common in kittens, but can occur in cats of any age. If the
immune system is not functioning properly, a mutant FECV can become a more
systemic infection that we call FIP. All FIP tests appear to react the
same way to every type of coronavirus. So, if your cat had FECV as a
kitten, it may cause the same reaction in the current test as true FIP
(more on the tests below).

For the purpose of this FAQ, however, I am going to continue referring
to an “FIP Virus” or “FIPV.” Just keep in mind that in fact, there may
not be a difference between FIPV and FECV per se, just a difference in
the way a cat’s immune system responds.

So what does this all mean?

In sum, if you know your cats are seronegative, and they are
older than 16
weeks, the vaccine is recommended by both the Cornell Feline Health
Center and the consensus reached at the Winn Foundation sponsored
FIP/FECV seminar. If your cat is already seropositive, there is not
much evidence that the vaccine will help.

The vaccine will be more of
a help when

  • the manufacturers demonstrate its effectiveness
    against the Type I strain of FIP
  • it is shown to be effective in
    seropositive cats, and
  • it could be shown to be safe and effective for
    kittens under the age of 16 weeks.

However, it appears that there is work being done to develop a
FECV vaccine. Preventing FECV infections in the first place, and
thus preventing FECV from mutating into FIP, might turn out to be
another technique in trying to protect against FIP.

That sounds absolutely ridiculous! Who would go through all that?

Nobody says a breeder HAS to do any of this. These are merely the
precautions currently recommended by the Cornell Feline Health
Center and the recommendations which came out of the Winn
Foundation sponsored Seminar on FIP/FECV. It is an option kitten
buyers can use in determining which breeder to select if they so
choose, but it is by no mean mandatory.

What about the vaccine?

There is a vaccine available, but it is controversial and some vets
do not recommend it, although others highly encourage it. The
manufacturer’s tests state that it has an efficacy rate (protection
rate in this case) of 69%. Cornell Feline Health Center then did a
study which said the vaccine failed to show any protection, and that it
accelerated the disease in 52.5% of exposed cats. However, this study
used a different challenge virus strain and the route of administration
was different than the manufacturer’s tests. The ‘real-life’
significance of this has not yet been determined, neither Cornell nor
the manufacture has received reports from the field of abnormally high
numbers of cats which get the disease as a result of the vaccine.
However, this study has caused a lot of people to swear-off the
vaccine.

It really is between an individual cat owner and their vet to determine
the whether or not to vaccinate based on the best information available
at the time.

What are the differences between FIP and FECV?

FIP is a disease. Normally the disease/virus relationship is
simple, but this is not the case with FIP. FIP may be caused by many
things, perhaps an isolated FIP virus (FIPV), perhaps a mutation of FECV,
or perhaps there are multiples viruses which can all lead the the same
disease complex known as FIP. There is little question, however, that the
most common cause of FIP is via FECV.

For the most part, FECV is limited largely to the intestines and is
dealt with quite well by the
cat’s immune system. However, as recent studies seem to indicate, FECV
can mutate into FIP and, if the cat’s immune system is not operating
properly, this mutant FECV stops being just an infection of the
intestine and becomes the more systemic infection we call FIP.

Thus, wherever you have FECV you could have FIP! Some cats never
get FIP, but can continue to shed the FECV virus (now thought to be
spread via the feces). The good news, however, is that since it
seems that the dry form is becoming more prevalent, that cats are
gradually becoming more able to resist FIP infection in general.

What are the symptoms of FIP?

FIP usually appears in one of two forms: Effusive (wet) and
Non-Effusive (dry). It should not be thought, however, that there are
two different FIP diseases. The results of the infection are a
continuum on a scale, with the ‘wet version’ being one end, the ‘dry
version’ being in the middle, and a ‘carrier’ being the other end (a
carrier is where the cat has successfully fought off the disease but
may still be able to expose other cats to the virus). The way this
happens is when a cat is exposed to FIPV, if its immune system gives a
poor response, the wet form will develop. If it gives a better
response, the dry form will develop. In the best responses, the cat
will not develop either form of FIP, although it may be a carrier of
the FIP virus.

Wet

The wet form is more common, and more rapid in progression than the dry
form. It is characterized by the abdomen and/or chest progressively but
painlessly distending with fluid. If this occurs in the chest,
respiratory distress can occur due to compression of the lungs and
release of fluid into the airways. The lining of the affected cavity
will be covered with white, fibrin-containing areas (fibrin is a
protein that is the center of a blood clot), often on the liver and
spleen. Certain types of lymph nodes may be enlarged. Other signs
include jaundice; mild anemia; and gastrointestinal, ocular (e.g. eye
ulcers or severe conjunctivitis), and neurological signs may also occur.

Dry

The dry form is more rare (but appears to be becoming more common), and
more slow in progression, often making diagnosis difficult. There is
minimal fluid build-up, although weight loss, depression, anemia, and
fever are almost always present. Signs of kidney failure, liver
failure, pancreatic disease, neurologic disease or ocular disease may
be seen in various combinations. Often the organs in question
develop a characteristic pyogranulomatous inflammation (this is a chronic
inflammation resulting in a thickening of the tissue and local
accumulation of white blood cells). Unfortunately biopsy of these lesions
is the only definitive way to diagnose this form of FIP and is usually
done in the form of a post-mortem diagnosis.

What if one of my cats if pregnant?

It is suggested that queens be completely isolated from other cats
(isolated in its own room, not its own cage within a room). This room
should be empty for one week prior to placing the queen there, and
should be disinfected with a 1:32 solution of bleach. The queen should
be placed in the isolation room 10-14 days prior to delivery. All bowls
and litter boxes should be used exclusively for that room, and not
interchanged with any others. You should disinfect your hands when
entering and leaving the isolation room. If possible, you should even
try to have separate clothing, such as a smock and slippers which are
restricted to the isolation room to decrease risk.

If the queen is not seronegative, you may want to consider an early
weaning program. The queen should be removed from the kittens at age
4-6 weeks and never returned. During the first 4-6 weeks of a kitten’s
life, it gets its antibodies from their mother, therefore they are
immune to anything she may be shedding. After that time period, they
start making their own antibodies. If the queen is a carrier of
coronaviruses, she can shed FECV to the kittens, and they are most
likely to become infected during that time period. Regardless of
whether the kittens are weaned early and isolated from the mother, they
should be kept isolated from all other cats in the household. In
addition to minimizing the risk of the kittens developing FIP, the risk
of exposure to other viruses and diseases will be reduced.

Kittens should be raised in complete isolation from the queen and all
other cats/kittens in the household until they leave the cattery. If
the kitten is to be kept in the cattery, it should be isolated for 16
weeks, and then the FIP vaccination series should be completed before
allowing the kittens to interact with the other cats.

What is a seropositive cat?

Some cats test positive on the coronavirus titer test, some do not.
Those which have never been exposed to ANY form of coronavirus are
called “seronegative.” Those which have been exposed to some form of
coronavirus are called “seropositive.” The Winn Foundation-sponsored
research felt the
Cornell study was flawed because it used cats which had already been
exposed to some form of coronavirus (were “seropositive”) and then
attempted to test the vaccine.

This is not to be confused with the terms “FIP negative” and “FIP
positive” which are used by many labs to indicate that the
coronavirus titer is less than (negative) or more than (positive)
some predefined threshold level.

What is the purpose of this FAQ?

The purpose of this FAQ is to answer frequently asked questions about Feline
Infectious Peritonitis (FIP), which is one of the most difficult diseases in
the feline community today. This FAQ is divided into two parts, the first is
general information about the disease, and the second is about management of
FIP in a multi-cat and cattery environment. The sources for this FAQ are
listed at the end, as well as some additional recommended readings.
Recently an excellent source of information on FIP has become available on
the WWW as well. This article is much more technical and many cat owners
may find it much more dense than this FAQ.

Disclaimer:

I want to point out first and foremost that I am not a veterinarian,
nor even a person who has training in animal science such as a veterinary
technician. I am a graduate student of physical anthropology, and an
ailurophile. My goal with these FAQs is to take information from the
medical literature and convey the parts that are most useful to the
average cat owner and translate them into general terms that are easy to
understand. I attempted to keep the FAQ as untechnical as possible, but
unfortunately with such a complex disease that becomes very difficult. I
hope this prooves to be of some usefulness. Also keep in mind that this
disease is one of the most controversial subjects in feline health care.
This is not a definitive guide to FIP, but only an attempt to compile
the most current information
. Ideally the reader of this FAQ should
use this as a starting point when discussing FIP with their veterinarian.
Vets and breeders will hold a wide variety of opinions on this disease,
some of which may be based on current information, some of which may be
based on hearsay and anecdotal evidence. You can only do your best to
become as educated as possible and make your decisions on the course of
treatment or preventive care. Always remember, your cats is YOUR
responsibility, and no one, not your vet, not a breeder, not a
friend-who-knows-everything-there-is-to-know-about-cats, nor the writer of
an internet FAQ can force you do take an action that you don’t feel
comfortable with. Do what you think is best for your cat. Period.


Summary

To begin and unfortunately in sum: There is NO effective treatment, there is
NO diagnostic test, there is NO way to positively identify asymptomatic
carriers (cats which shed the virus, but do not themselves show outward
signs of illness), the incubation time is UNKNOWN, NO one is 100% sure of
how it is spread between cats, and there is NO proven effective way to
control its spread in a multi-cat household or cattery. So what is known?
Read on.

Internal Parasites

Ivermectin for Internal and External Parasites – by Lorraine Shelton

Use of Ivermectin to Control Ear Mites, Body Mites, and Roundworms in Catteries and Multiple Cat Environments

by Lorraine Shelton
Originally posted to the FanciersHealth Yahoogroup

I’ve been getting lots of private requests for information on dosing ivermectin to treat ear mites, body mites and roundworms.

Can you tell me what the dose is? What strengh of Ivermectin?

I recommend using the 0.27% swine formulation only. The dose is “one drop per pound” (0.05 ml per pound, 0.5 ml for an adult cat). If using the 1% solution, the dose is 0.1 ml for an adult cat, but must be carefully diluted to be accurately dosed in kittens. Diluting one part 1% ivermectin to three parts mineral oil will create a solution that can be dosed topically in the same amounts as the 0.27% solution. Here is a link to where you can buy Ivomec 0.27%

Is it injected? Oral? Ivermectin can be injected or given orally, but it is also well aborbed through the skin. Personally, I apply the dose directly into the ear canal. This causes the cat less pain than the injection and eliminates the risk of injection site problems, such as hair loss or abcess.

How old does a kitten have to be to get it? I like to wait until the kitten is 8 weeks old, although ivermectin has been proven to be safe in random-bred kittens 4 weeks old and up. It is also safe to use in pregnant queens, although I prefer to wait until the last trimester of pregnancy.

What is the dose of the 1% ivermectin used for kittens if it is injected? The dose for 1% ivermectin is 0.05 ml for a kitten weighing at least four pounds. This is a VERY tiny amount (one drop), so make sure your syringe has a total volume of only 0.5 ml (insulin syringe). Getting ivermectin to draw into an insulin syringe is an ordeal in itself (it is a very viscous solution) If kittens under that weight are to be dosed via injection, the solution must be diluted in propylene glycol. I recommend diluting one part ivermectin with three parts propylene glycol and then injecting at a rate of 0.05 ml per pound.

Personally, I prefer to dose ivermectin topically rather than by injection. This drug does sting when injected. When used topically, the drug can be diluted in mineral oil instead of propylene glycol.

Would one treat body mites (Cheyletiella) by applying the Ivermectin topically in the ear canal too? Yes, ivermectin is absorbed very efficiently through the skin into the bloodstream.

How often would one repeat the treatment? Ivermectin treatment should be repeated in 2-3 weeks to catch life stages that were not killed by the first treatment. Prevention of reinfection is important and can be accomplished by cleaning the environment thoroughly and treating all cats in the cattery at the same time. Mites do not live for significant amounts of time in the environment, so treatment of the carpet, scratching posts, etc. with an insecticide is not necessary.

Ivermectin use is NOT without risks. Side effects are primarily neurological in nature and can be serious, especially if the drug is accidentally overdosed. There are safer drugs to use for roundworm infection (pyrantel pamoate, also known as “Nemex” or “Strongid”, for example). But in a cattery or multiple cat situation, the convenience, spectrum of efficacy, and low cost of ivermectin is worth consideration in my opinion. –Lorraine Shelton, copyright 2004

Ivermectin for Internal and External Parasites – by Lorraine Shelton

Use of Ivermectin to Control Ear Mites, Body Mites, and Roundworms in Catteries and Multiple Cat Environments

by Lorraine Shelton
Originally posted to the FanciersHealth Yahoogroup

I’ve been getting lots of private requests for information on dosing ivermectin to treat ear mites, body mites and roundworms.

Can you tell me what the dose is? What strengh of Ivermectin?

I recommend using the 0.27% swine formulation only. The dose is “one drop per pound” (0.05 ml per pound, 0.5 ml for an adult cat). If using the 1% solution, the dose is 0.1 ml for an adult cat, but must be carefully diluted to be accurately dosed in kittens. Diluting one part 1% ivermectin to three parts mineral oil will create a solution that can be dosed topically in the same amounts as the 0.27% solution. Here is a link to where you can buy Ivomec 0.27%

Is it injected? Oral? Ivermectin can be injected or given orally, but it is also well aborbed through the skin. Personally, I apply the dose directly into the ear canal. This causes the cat less pain than the injection and eliminates the risk of injection site problems, such as hair loss or abcess.

How old does a kitten have to be to get it? I like to wait until the kitten is 8 weeks old, although ivermectin has been proven to be safe in random-bred kittens 4 weeks old and up. It is also safe to use in pregnant queens, although I prefer to wait until the last trimester of pregnancy.

What is the dose of the 1% ivermectin used for kittens if it is injected? The dose for 1% ivermectin is 0.05 ml for a kitten weighing at least four pounds. This is a VERY tiny amount (one drop), so make sure your syringe has a total volume of only 0.5 ml (insulin syringe). Getting ivermectin to draw into an insulin syringe is an ordeal in itself (it is a very viscous solution) If kittens under that weight are to be dosed via injection, the solution must be diluted in propylene glycol. I recommend diluting one part ivermectin with three parts propylene glycol and then injecting at a rate of 0.05 ml per pound.

Personally, I prefer to dose ivermectin topically rather than by injection. This drug does sting when injected. When used topically, the drug can be diluted in mineral oil instead of propylene glycol.

Would one treat body mites (Cheyletiella) by applying the Ivermectin topically in the ear canal too? Yes, ivermectin is absorbed very efficiently through the skin into the bloodstream.

How often would one repeat the treatment? Ivermectin treatment should be repeated in 2-3 weeks to catch life stages that were not killed by the first treatment. Prevention of reinfection is important and can be accomplished by cleaning the environment thoroughly and treating all cats in the cattery at the same time. Mites do not live for significant amounts of time in the environment, so treatment of the carpet, scratching posts, etc. with an insecticide is not necessary.

Ivermectin use is NOT without risks. Side effects are primarily neurological in nature and can be serious, especially if the drug is accidentally overdosed. There are safer drugs to use for roundworm infection (pyrantel pamoate, also known as “Nemex” or “Strongid”, for example). But in a cattery or multiple cat situation, the convenience, spectrum of efficacy, and low cost of ivermectin is worth consideration in my opinion. –Lorraine Shelton, copyright 2004

Treating Coccidia

Use of Baycox liquid or Marquis paste to control coccidiosis in
catteries


by Lorraine Shelton and Della Hengel

Baycox (toltrazuril) is a new treatment that may actually cure
coccidiosis, instead of just suppressing it. The drug is available
in Canada, but not the US. Albon and Tribrissen are used for years
to control coccidia infection, but they don’t cure it and the animal
may continue to shed spores. Marquis paste is made from a similar
drug, ponazuril, which is a metabolite of toltrazuril.

Baycox may be obtained from Interpet: http://www.interpet.biz/Baycox.html or from Pet Supplies International: http://www.psol.com.au/int/index.html
Since the Baycox is a special order item, it’s not shown on
the PSI website. You need to email the owner (who incidentally is a vet):
questions@psol.com.au (Geoff Turnbull). No prescription is needed. If
you’re in the US, the cost for 200 ml (the only size it comes in, original
Bayer packaging — he does NOT repackage) at today’s exchange rate is
under $90. DO NOT use the 2.5% solution sold as a pigeon remedy, as it can be caustic to the mucus membranes of cats.

Do not use this drug in pregnant cats as the terratogenic effects of
this drug has not been adequately researched as yet.

The dose of Baycox is 20 mg/kg (10 mg per pound). This is 0.2 ml per pound
of cat when using the 5% suspension. In a published study, a single
dose of Baycox cured coccidiosis in puppies, as long as adequate
environmental clean-up is performed. However, I’d recommend repeating
it weekly for a couple of weeks. Clean up of the environment is
critical to get rid of coccidia. This drug works best when it is used
at the age of 4-6 weeks to PREVENT coccidia infection in kittens.

An alternative to Baycox is the similar drug ponazuril, marketed as
Marquis paste for horses. The dose is 20mg/kg once a day for 1-3 days.
The paste contains 150mg ponazuril per gram of paste. The plunger is
marked for horses weighing 600 – 1200 pounds. You want to take the
amount for a 600# horse and dilute it to a total volume of 14 ml in
something tasty. Dose at 0.1 ml per pound of cat. Discard the unused
volume.

Here is the journal abstract I posted to the list in 2001:
Toltrazuril treatment of cystoisosporosis in dogs under experimental
and field conditions. A Daugschies, HC Mundt, V Letkova
Parasitology Research, 2000, Vol 86, Iss 10, pp 797-799

Coccidia of the genus Cystoisospora cause mild to severe diarrhoea in
dogs. The effects of toltrazuril treatment on cystoisosporosis were
studied under experimental and field conditions. Twenty-four puppies
were experimentally infected each with 4 x 10(4) oocysts of the
Cystoisospora ohioensis group. Three groups of six puppies were
treated 3 dpi with 10, 20 or 30 mg/kg body weight of toltrazuril
suspension (5%); the remaining six puppies served as non-treated
controls. Toltrazuril suspension or microgranulate were given once
in a dose of 10 or 20 mg/kg body weight, respectively, to naturally
infected puppies in conventional dog breeding facilities, depending
on the coproscopical evidence of infection. Oocyst excretion and
clinical data were recorded.

Under experimental conditions, the non-treated puppies excreted
oocysts beginning at 6 dpi and suffered from catarrhalic to
haemorrhagic diarrhoea. On 12 dpi, four of six non-treated puppies
died. Irrespective of the dose, toltrazuril treatment totally
suppressed oocyst excretion and no diarrhoea or other signs of
disease were observed in the treated groups. Natural Cystoisospora
infections were regularly found during the 3rd or 4th week of age
in dog breeding facilities although not always associated with
diarrhoea. A single oral application of toltrazuril abrogated oocyst
shedding and the treated puppies remained generally coproscopically
negative during the following 2-4 weeks.

Cystoisospora is pathogenic for puppies and can induce severe
disease. Natural infections are common in conventional dog breeding
facilities. Toltrazuril treatment is suitable for controlling
cystoisosporosis under experimental and field conditions. A single
oral treatment for puppies in the 3rd/4th week of age is recommended.

Here is some information directly from Dr. Bruce Kilmer at Bayer
Canada:

Thank you for your interest in Baycox. Unfortunately, Baycox
isn’t registered for cats and therefore I can’t provide a package
insert. On a second point, Baycox is not available in the US, except
black market goods coming in by whomever. Bayer In Canada can not
sell product into the US. Baycox is a triazine derivative. The drug
active is toltrazuril, which has a cidal mode of action on protozoan.
The toltrazuril will kill all single cell stages of coccidiosis. Once
an animal has diarrhea and you can find oocysts on fecals, the drug
can not penetrate the oocysts so technically it is too late to treat.
In the actual clinical cases, treatment is still worthwhile to shorten
the length and severity of the diarrhea as there is still development
of the life cycle in the small intestine that will be controlled.

The idea is to dose the cat before there are clinical signs. For
example, the normal situation would be a cattery having regular
problems with coccidiosis in young kittens. The kittens normally would
break with diarrhea at about 5 weeks of age. The treatment would be
given around day 28, killing the early stages of the protozoa and
preventing clinical disease. You will not have the history on a
rescue cat so treatment would be best at the earliest hint of an
outbreak and then repeat treatment in 7 days.

Baycox treatment will not cause sloughing of the intestinal
epithelial cells. The coccidiosis does a fine job of that on its own.
We have electron micrograph studies of sections of intestine 24 hours
post treatment with Baycox. The intestinal cells remain intact and
functional while the single cell stages of the cocci are dead, as
evidenced by staining techniques. because Baycox is cidal, the kitten
does not have to depend on its immune system to eliminate the cocci as
what would occur with a static drug like sulfadimethoxine.

Remember that Baycox should be given during the preclinical stage.
This is very difficult to judge as the kitten will be at a stage when
it is infected but the cocci are only in the first stages of their life
cycle. The intent is to kill the protozoa before there is damage to the
villi to clear the infection. In this way, the kittens will not develop
the normal clinical signs of diarrhea. If you can identify oocysts on
fecal exam, the damage has already been done and the protozoa has
completed its reproductive cycle. Drug can not penetrate the oocyst wall
to kill this stage. Treatment at the first signs of a clinical case will
still help to limit the severity and duration of the infection as the
Baycox will kill the single cell stages that have not reproduced
sexually yet.

Try to determine the usual age that you see outbreaks. For example, many
catteries will see diarrhea sometime around day 35. The time to treat is
therefore at day 28. Likely the kittens had an infective dose of oocysts
by this stage but minimal damage has occurred. Treatment will eliminate
the coccidiosis before there is damage and the kittens will not break
with diarrhea. Studies in other species indicate that the animal will
have developed immunity to subsequent exposure.

The dose is 20 mg/kg by oral dosing.

Toltrazuril is quite lipid soluble so absorption and distribution into
tissue is very good. Baycox has a unique mode of action and there is no
reason to be concerned with an adverse reaction or a drug-drug reaction.
We have never had an adverse reaction reported after millions of
treatments, often concurrent with other medications.

I have never heard of any adverse reactions to treatment at this dose
in puppies or kittens or on the repeat seven days later. As Baycox only
has activity against protozoa, there is no effect on upset of intestinal
flora and the formulation is very well tolerated. The only time I have
heard of any reaction occurred when someone used the Baycox 2.5% Poultry
Concentrate by direct oral dosing in 3 day old piglets. This formulation
is designed to be diluted in the drinking water for poultry. To be
soluble in water, the product undiluted is very alkaline, pH 11.4.
Direct oral dosing of the undiluted product is very irritating to
mucous membranes and will cause immediate vomiting. Make sure you are
using the correct formulation.

Regards,
Bruce Kilmer DVM
Manager, Veterinary Affairs/Product Development Bayer Inc.

Tritrichomonas Foetus – by Dave Condon

All I Know About Tritrichomonas Foetus – by Dave Condon, Highgait Cattery

Since many of you may not be inclined to read all of this let me state
here that the information I am giving is from material published by Dr
Jody Gookin (http://www.cvm.ncsu.edu/mbs/gookin_jody.htm) and email
correspondences with her. Additionally the folks at BioMed and Westlab
contributed.

TF is an emerging parasite in the feline world. Surveys have suggested
that approximately one third of all purebred cats are infected. It is
rarely tested for and may be responsible for many of the cases of
chronic diarrhea (e.g. IBD) in cats. If you are a cat owner please take
some time to read this page and acquaint yourself with this ‘new’ parasite.

Where did TF come from?:Tritrichomonas foetus (TF) is a protozoan that
infects bovines (cattle). It is considered a venereal disease in that
industry. It was first discovered in felines in 1996 but was not
associated with diarrhea in felines at that time. As best as I can learn
it appears that Dr Jody Gookin made (or suspected?) this association in
1999. The other researcher investigating TF is Dr Stan Marks at UC
Davis. Why TF was not considered more widely as a cause of diarrhea in
cats until very recently is a mystery to us.

A TF organism looks very similar to Giardia so if viewed by in a fecal
smear a misdiagnoses of Giardia is common. Fecal floats and Giardia snap
tests are insensitive to TF. TF is a fragile organism whose life span
out of the body is normally less than an hour. This lack of hardiness is
due to the fact that TF cannot form a cyst. ). If TF drys out, if it is
refrigerated or if it experiences temperatures above 105°F it will die.
Obviously bleach will kill it too but it will probably be dead by the time you
clean the surface. The primary infection path is probably the litter box
where a well timed use by two cats can transfer the parasite fecal/orally. Dr.
Gookin has commented that TF can live for 3-4 days in a wet stool (wet
is the key word).

TF lives in the intestinal lining of the large bowel. It causes “cow pie”
like stool that is often gassy and malodorous. The health of the cat is
not usually adversely affected. Several breeders have commented that in
symptomatic cats that the smell of the stool is a significant clue of an
infection. It is important to note that an infected cat may or may not have
clinical signs of TF. I have a positive female that has good stools. Infected
cats can treated with Ronidazole. Cats not treated usually cure themselves of
the parasite within 2 years (9 months is the median).

Our TF History: We first learned about TF in January 2006. The symptoms
of this parasite matched some of the symptoms we were seeing in some of
our Abys. We purchased the equipment and tests required to detect TF and
began testing in February. We found TF in 10 of our Abys (8 adults and 2
kittens). Working with our vet we have treated our Abys and are now
regularly testing to insure our Abys are TF free.

Current TF Status: Since our initial TF test we have performed 110 TF
tests. All of our adult female have now repeatedly tested negative. None
of our kittens in our current litters have tested positive. We do have
one new problem. Two of our young intact male studs have failed
treatment. A theory has been proposed by Dr Gookin (TF researcher) that
intact males may be able to harbor TF in their sex organs which may be
beyond the reach of the drug used to treat TF. We are now treating these
males with a different drug. It will take about three weeks before we
know how effective this treatment has been. These males have been
isolated so they do not pose a threat of infection to our other Abys.

There are three testing methods I know of. 1) The least sensitive method is
a microscopic examination of a fecal smear. The probability of detecting
TF in an infected cat has been estimated to be less than 20%.
Additionally two other organisms, Giardia and Pentatrichomonas hominis
may confuse the diagnosis. 2) The gold standard of TF testing is a
Polymerase Chain Reaction (PCR) test. A stool sample can be sent to
Dr Gookin’s vet college (http://www.cvm.ncsu.edu/docs/documents/tritrichomonas_PCR_submission.pdf)
for this test. This is a very sensitive but unfortunately very
expensive ($100/ test) test. 3) Alternatively, you or your vet can use the
BioMed Diagnostics InPouchTF test (http://www.biomed1.com/) 1-800-964-6466.
This test is about $5/test and when you consider the number of tests that most
of us will have to perform this is the only sensible economic approach.

I decided to do my own tests and then have my findings confirmed by my
vet (she did not offer TF testing at the time). I purchased InPouchTF
tests and to be sure I knew what to look for, I also purchased a positive
live TF culture. Initially I sampled our Abys by inserting a Q-tip
(cotton bud for our Aussie friends) wetted with fluid from the pouch
into their rectum. Later I began using stool samples but I only used
those that we just deposited. You need use only a tiny amount of fecal
matter (wet just 1/4 of the tip of the Q-tip) or the bacteria in the
stool will overwhelm the antibiotics in the pouch and turn the culture
very cloudy. Fecals don’t have to be incubated but I prefer to speed the
process among by incubating. Normally, positives are seen in 3-4 days
but the range can be broad. My earliest positive result was “immediately” and
the latest was 10 days. You must keep the pouches for 12 days before you can
declare a negative. Another note, Giardia may exist in the pouch for
the first 24 hours, so always monitor positives for a few days.

A low cost microscope is all you need to examine these pouches for TF.
Once the pouches are inoculated, you never need to open them again. You
examine through the pouch. I bought a microscope off of Ebay for $45. You
need 40X and 100X magnification. Your scope should also have an iris to
control the illumination of the sample. TF doubles in the pouch every 8
hours. A positive culture is not subtle, you will hundreds of thousands
of organisms. So if you can focus a microscope, you can perform this test.

Prognosis: Until Dr Gookin published her findings last year there was no
effective drug treatment. Dr Gookin has stated that “Most cats have
spontaneous resolution of diarrhea in two years. More than half the cats
remained positive for presence of the organisms however, up to 4-years
after diagnosis and possibly many can carry the infection for life.” In
a multiple cat environment this could mean an endless cycle of reinfection.

Working with my vet, we confirmed my positives and she phoned in
prescriptions to the pharmacy Dr Gookin’s recommended: Westlab Pharmacy
(352) 373-8111. With the scripts in place I deal directly with Westlab.
They are extremely helpful. Give them the weight of the cat and they
will make up capsules of Ronidazole. Cost is approximately $12 per pound of cat
for a two week supply (given twice a day). Another note: the dosage
range is very narrow, typically 35-45 mg/Kg. If you have a kitten
rapidly gaining weight, the dose my go sub-therapeutic in the second
week. Westlab can make you extra capsules to compensate. Keep weighing
your cat(s). Kittens as young as 6 weeks have been successfully treated. My kitten was 13 weeks.

The Ronidazole used by Westlab is imported from Belgium, it is 100%, not the
10% concentration used for pigeons. Doses, even for cats, are in small
#4 capsules. I’m told it is a very bitter drug and cannot be compounded
to be made palatable for cats. This drug is a potential carcinogen in humans.
The toxicity in felines is probably not known. Temporary neurological side
effects may occur, especially at doses of 45 mg/Kg and above. So far, we have
seen no negative side-effects. We are dosing at 35-40 mg/Kg with very positive
results. Stools returned to normal in less than a week.

As for other side effects, I have received one email reporting that their cat
experienced liver failure while on RDZ. Fortunately it was reversible and the
cat returned to normal. It is not known if this cat was treated within the
recommended dosage range. There are some, not necessary the one who had the
liver problem, who in an effort to save costs who are using RDZ formulated for
pigeons which at a 10% concentration. Accurate measuring and dosing with
this form of RDZ may be difficult. We have experienced no adverse
side-effects nor has any others been reported to us. Westlab have said
that they have had reported to them some temporary neurological symptoms
in a few cases but in large side-effects are few.

Post treatment testing can begin 3 days after the last dose. Westlab
told me there have been some failures, but most these were at the 30 mg/Kg
dose. They assumed that a second course of treatment was successful
since they have not received any call backs. According to Dr Gookin a
relapse can occur up to 20 weeks after Ronidazole is discontinued.

We begin testing 10-14 days after RDZ treatment. We wait this time period to
make sure that no residual RDZ is present to bias the test. We are repeating
the test approximately every 14 days afterward. We expect to lengthen this
period slowly until 20 weeks is reached. Since cats have sensitive guts,
diarrhea (and vomiting) are not unusual occurrences in cats. If we observe any
loose stool we test it. So far these events have been transient and these
tests have all been negative.

**UPDATE JUNE 2006**
As previously posted I reported a problem treating TF two intact male
Abys with ronidazole (RDZ). I have sent Dr Gookin TF cultures from these
males and in time she will test them for RDZ resistance. A resistance is
probably unlikely unless it is gender specific (possible?). Dr G also
suggested that the TF may be able to hide in the male sex organs. This
is just a educated guess not fact and the main reason why I want to hear
from anyone who has or had problems treating male cats for TF.

We also had an additional male relapse. This male was infected when he
was intact but neutered before treatment. He remained TF negative for
six weeks but relapsed when placed in a new ‘only cat’ home. Our seven
females are still negative and so far none of the kittens in three
litters have tested positive. In our cattey we test for TF alot, since
mid-Feb we have performed 124 InPouch TF tests.

The two intact males have just completed a 10 day course of tinidazole
(TDZ). We are now in the wait period before testing. Preliminary results
are about a week away. Neither have any symptoms of TF. Keep in mind
that many adult cats are asymptomatic. This is why TF testing is so
important if your trying to clear TF from your cattery. Assuming you can
clear TF by just medicating is like assuming you can clear RW without
fungal cultures. It is possible but not probable.

A common thread among most breeders I correspond with is the lack of
testing. Most will test symptomatic cats, some will test asymptomatic
cats and a very few will perform post treatment TF testing . Most will
rely on the observation of symptoms. If we did this we would have
declared our two infected but asymptomatic males clear of TF. Then it
wouldn’t be difficult to see how another round of TF infection could occur.

I realize unless you have a vet who is testing for the cost of a test
pouch because he/she wants to learn (has happened) that testing can be
expensive. The only alternative that is cost effective is to DIY. To get
started you need to invest $200-250 for a microscope, electronic
thermometer and 20 test pouches. Payback is quick and since you sample
and inoculate the pouches yourself the likelihood of the TF in the
sample dying on the way to the vet clinic is greatly reduced. Also
interpretation of the results is very easy, no vet or biology skill needed.

The information sources: Material published by Dr Jody Gookin
(http://www.cvm.ncsu.edu/mbs/gookin_jody.htm) and email correspondences with
her. Addition information was obtained from the folks at BioMed
(http://www.biomed1.com) and Westlab Pharmacy (http://www.westlabpharmacy.com/). Also
experiences and the experiences of other breeders who are corresponding
with us were included. Neither I nor any breeder I know would suggest
that anyone, in matters of feline health, treat their cats independently
of their vet.

Additional TF information

Dr Gookin’s TF paper:
http://www.cvm.ncsu.edu/docs/documents/ownersguide_tfoetus_revised042808.pdf

Dr Gookin’s (May 2006): Efficacy of Ronidazole for Treatment of Feline
Tritrichomonas Foetus Infection (abstract is free, the rest will cost
$30, worth it if you have an infected cat):
http://tinyurl.com/r8c99

— Dave Condon, Highgait’s Paws Cattery

Reproduction and Neo-natal Care

Pyometra and CEH – by Susan Little DVM

Cystic Endometrial Hyperplasia/Pyometra

Susan Little DVM
Diplomate ABVP (Feline)
Bytown Cat Hospital
Ottawa, Canada

a) Etiology:
It has typically been believed that because cats are induced ovulators, the incidence of cystic endometrial hyperplasia (CEH)/pyometra is lower than in dogs. However, recent studies have shown a great many cats are also spontaneous ovulators, and therefore may experience prolonged diestral periods without pregnancy. Repeated pseudopregnancies may predispose the uterus to CEH, which is a disorder of proliferative and degenerative changes in the endometrium associated with aging. Most queens with pyometra were in estrus some time in the preceding 60 days. Potter et al (1991) reported that 40% (16/40) of queens with pyometra or endometritis had CLs. Lawler et al (1991) reported that 67% (20/30) queens with pyometra had luteal phase ovaries.

Progesterone causes hyperplasia of the endometrium and endometrial glands. Other effects of progesterone include inhibition of local leukocyte responses to infection in the uterus and decreased myometrial contractility. Estradiol causes an increase in the number of estrogen and progesterone receptors in the endometrium. It also causes cervical dilation during estrus and therefore allows bacteria that are part of the normal flora of the vagina (especially E. coli and Streptococcus spp) to ascend into the uterus. It is normal for cats to have both aerobic and anaerobic bacteria in the vagina. Younger cats have more vaginal bacteria than older cats, and cats in heat or pregnant have more bacteria than anestrus cats. Vaginal cultures are therefore hard to interpret since the queen has normal bacterial flora. This combination of ascending bacteria and an abnormal endometrium predispose queens to pyometra.

b) Clinical symptoms and diagnosis:
Cats with CEH may or may not have endometritis. CEH tends to be a chronic subclinical condition and may be hard to diagnose definitively without biopsy of the uterus. A presumptive diagnosis of endometritis may be made from response to antibiotic treatment, which should last for 2-4 months. Uterine pathology, mostly secondary to CEH and endometritis, is common in queens over 5 years of age. CEH is very common in unbred queens over 3 years of age. Perez et al (1999) found that 88.2% of queens older than 5 years in a breeding colony had CEH, versus a 30% incidence in queens 2-4 years old. A group of feral queens also sampled had no CEH. They concluded that colony queens showed a predisposition to CEH that was correlated with elevated serum estradiol concentrations. CEH is one of the most important causes of infertility in catteries.

Cats with advanced CEH are occasionally found with mucometra or hydrometra, characterized by variable amounts of mucus in the uterus. In hydrometra, the mucin is thin and watery. In mucometra, the mucin is thick or even semisolid. Queens with either condition do not have bacterial infections and are not systemically ill. The main symptom is abdominal distension, with or without a vaginal discharge.

The clinical signs of pyometra include a vulvar discharge, depression, dehydration, anorexia, fever, weight loss and a distended abdomen. Any abnormal vulvar discharge in an intact queen should be assumed to be due to pyometra. However, 15-30% of queens have no vulvar discharge (closed cervix). Queens are often very meticulous in grooming, however, so evidence of the discharge may be hard to find. A surprising number of queens with open cervix pyometras have little or no signs of systemic illness. Very occasionally, pyometra is found during a routine annual health examination. Polyuria and polydipsia are far less frequent in queens with pyometra than bitches. Most queens with pyometra will have a leukocytosis with a left shift. The diagnosis can be affirmed by finding an enlarged uterus on radiographs or ultrasound. In some cases, the uterine enlargement is segmental, mimicking a pregnancy. Occasionally, only one horn of the uterus is involved.
 
Cats who have CEH but not pyometra may be normal on physical examination. Their blood and urine tests are normal. Ultrasound of the abdomen is very sensitive in detecting uterine enlargement. Radiographs are not as useful, but being able to see the uterus on a radiograph usually indicates the uterus is enlarged. The final diagnosis is often not made until exploratory surgery is performed and the uterus is removed and/or biopsied.

c) Treatment:
There is no specific treatment for CEH. Theoretically, a prolonged period of anestrus may allow for some normalization of the endometrium. Progestagens must be avoided. Mibolerone is effective in inducing anestrus in cats, but is associated with serious adverse effects. Maintaining queens in less than 10 hours of daylight may induce a photoperiod anestrus.

Initial treatment for pyometra may involve intravenous fluids and antibiotics. Since E. coli is the most common bacterium involved, good antibiotic choices are enrofloxacin (Baytril®), trimethoprim-sulfa (Tribrissen®), or clavulanate-amoxicillin (Clavamox®). It is not usually necessary to perform a culture and sensitivity test on the uterine discharge. Antibiotic therapy alone for pyometra is not often successful. Douches using antiseptic or antibiotic solutions are also not effective. One series of 183 queens (Kenney et al, 1987) with pyometra found an 8% mortality rate, most commonly associated with a ruptured uterus and peritonitis.

Two approaches to treatment of pyometra may be taken: ovariohysterectomy and prostaglandin therapy.

i) Ovariohysterectomy provides the most consistent results as the source of the problem is permanently removed and cats recover quickly. For queens who are not valuable to a breeding program, this is probably the best choice.

ii) Prostaglandin therapy has been the most successful treatment for open-cervix pyometra where it is desirable to preserve the future fertility of the queen. Success rates for return to fertility may be as high as 86%. Prostaglandin F2  (PGF2) has been used both for pyometra and for metritis postpartum. The best queens for this therapy are under 6 years of age, in good health, and have no retained fetal material if they are postpartum (ultrasound is very helpful in determining this). PGF2 therapy is contraindicated in queens with some medical conditions such as asthma. PGF2 therapy should not be used if the queen is in poor condition or is critically ill. Careful assessment of the patient is critical for ruling out conditions that could preclude the use of PGF2. For example, in rare cases, pyometra is associated with uterine torsion, a contraindication for PGF2 treatment. Treatment of closed cervix pyometra should only be undertaken with caution, and only in medically stable, young and otherwise healthy queens. If the cervix does not open after a few days of therapy, or if the queen becomes ill, she should be spayed.

Only natural prostaglandin is used since a dose has not yet been established for use of synthetic prostaglandins for this purpose in the cat. Queens are treated with 0.1 mg/kg of dinoprost (Lutalyse) SC, once or twice daily for 5-7 days. The main purpose of the PGF2 is to cause the uterus to contract and expel its contents. The luteolytic effects of PGF2 seen in other species have not been documented in the queen. If the feline CL does responds to PGF2 , it seems to take several days of treatment to effect luteolysis. Queens need to be watched closely during PGF2 therapy and may be hospitalized for the part of each day which follows administration of the drug. Queens must be monitored for rising fevers, abdominal pain, or other symptoms of systemic illness or rupture of the uterus (which could lead to peritonitis). Monitoring with radiographs or ultrasound may be needed in addition to blood counts. The rate of complications with this treatment is very low.

Side effects are noted often, usually within minutes of the injection, and will be worse in the first 2 days. The contractile effects of PGF2 on the smooth musculature of the myometrium, GI tract, respiratory tract, and bladder account for these reactions.  Common side effects include restlessness, vocalizing, panting, vomiting, diarrhea, salivation, and intense grooming of the flanks and vulva. These effects usually last only a few minutes, rarely lasting longer than 15-20 minutes. The reactions become less obvious with each treatment. Usually by the fifth day, little or no side effects are seen. Antibiotics should be given throughout the course of PGF2 therapy and for some time afterward.

Queens should be followed up by the veterinarian one and two weeks following PGF2 treatment. The vaginal discharge should change to a clear fluid by the seventh day following treatment. This clear discharge may last for up to 10 days. Most cats are back to normal 2 weeks after treatment. If a purulent or bloody discharge is persistent, a second course of therapy may be necessary. Most queens will come back into estrus within several weeks and they should be bred at the first opportunity. It may be valuable to treat the queen with antibiotics during this estrus and into the first 4 weeks of any resulting pregnancy. An antibiotic safe for use in pregnancy, such as amoxicillin/clavulanic acid (Clavamox®), should be chosen. Occasionally, a queen has a second episode of pyometra after a pregnancy, but repeating the PGF2 treatment may still enable her to have a litter in the future.

After treatment with PGF2, pregnancy rates of 71-86% have been reported. Davidson et al (1992) reported recurrence of  pyometra within 1 year in 14% of treated cats. Some cats (4%) will have subclinical generalized peritonitis associated with pyometra which may contribute to ongoing problems with ill health and eventually necessitate ovariohysterectomy. There are no reports of successful treatment of closed pyometra in the cat although in the dog the success rate is reported to be 34%.

References:

Davidson AP, Feldman EC, Nelson RW. Treatment of pyometra in cats, using prostaglandin F2alpha: 21 cases (1982-1990). J Amer Vet Med Assoc 200(6): 825-828, 1992
Gudermuth DF, Newton L, et al. Incidence of spontaneous ovulation in young, group-housed cats based on serum and faecal concentrations of progesterone. J Repro Fert Suppl 51:177-184, 1997
Kenney KJ, Matthiesen DT, et al. Pyometra in cats: 183 cases (1979-1984). J Amer Vet Med Assoc 191(9): 1130-1132, 1987
Lawler DF, Evans RH, et al. Histopathologic features, environmental factors, and serum estrogen, progesterone, and prolactin values associated with ovarian phase and inflammatory uterine disease in cats. Am J Vet Res 52(10): 1747-1753, 1991
Lawler DF, Johnston SD, et al. Ovulation without cervical stimulation in domestic cats. J. Reprod. Fertil Suppl. 47:57-61, 1993
Perez JF, Conley AJ, Dieter JA, et al. Studies on the origin of ovarian interstitial tissue and the incidence of endometrial hyperplasia in domestic and feral cats. Gen comp Endocrinol 116(1): 10-20, 1999
Potter K, Hancock DH, Gallina AM. Clinical and pathologic features of endometrial hyperplasia, pyometra, and endometritis in cats: 79 cases (1980-1985). J Amer Vet Med Assoc 198(8): 1427-1431, 1991

Bonagura JD (editor). Kirk’s Current Veterinary Therapy XII: Small Animal Practice. W.B. Saunders Co., Philadelphia, 1995.
 Davidson AP. Medical treatment of pyometra with prostaglandin F2 in the dog and cat, pp. 1081-1083.
 Lawler DF, Johnston SD. Complications of noncopulatory ovulation in queens, pp. 1083-1085.

Feldman EC, Nelson RW. Canine and Feline Endocrinology and Reproduction. Second Edition. W.B. Saunders Co., Philadelphia, 1996, pp. 759-762. ISBN 0-7216-3634-9

Sherding RG (editor). The Cat: Diseases and Clinical Management, second edition. W.B. Saunders Co., Philadelphia, 1994. ISBN 0-7216-5936-5
 Johnson CA. Female reproduction and disorders of the female reproductive tract, pp. 1855-1876

Simpson GM, England GCW and Harvey M. (editors). BSAVA Manual of Small Animal Reproduction and Neonatology. British Small Animal Veterinary Association, Cheltenham UK, 1998. ISBN 0-905214-36-6
• Verstegen JP. Pharmacological control of reproduction in the cat, pp. 219-226

Strep G Infections – by Marva Marrow (Part 1)

G Strep (Group G Streptococcus bacteria): A Scary Story With a Happy Ending By Marva Marrow 7th Heaven Orientals

The beginning was very promising and I was excited. Sisa’s litter was a repeat breeding of a very successful previous litter. She had a huge belly, was healthy, eating well — all the signs of a normal pregnancy. Sisa went into labor and first gave birth to two stillborn kittens. I was sad, but not surprised as following that, she had eight healthy, good sized Oriental kittens. She was and always had been an excellent mother and got right to work cleaning babies, nipping cords, curling around them protectively and urging them to nurse. All was well.. That is, all was well until the kittens were ten days old.

That morning, I picked up the first baby, to check them as I usually did, first thing when I woke up. The baby’s little nostrils were clogged shut with mucous! I had never seen signs of URIs (upper respiratory infection) in such young babies, so, alarmed, I quickly picked up the next kitten. All the babies had clogged nostrils and it seemed to me that their breathing was labored. Panicked, I got my veterinarian quickly on the phone. We immediately initialized a program of Amoxy and I started supplementing the kittens, giving just a little bit of formula every couple of hours, so as not to stress their systems too much, cleaning off little noses with warm water and cotton.

By that evening at least one of the kittens was dead and a couple of others were dying. Round the clock for two weeks I gave sub-Q fluids, small amounts of formula and often, wiped little noses to keep them open. We changed their antibiotic to Clavamox, then added in injectible Baytril when that alone did not seem to be getting results – anything we could think of. My veterinarian and I were stumped and disheartened. I was emotionally exhausted. And the babies kept dying, one by one, despite my efforts. It was truly heartbreaking to watch and not be able to save them. Sisa, poor thing, was very confused and couldn’t understand what was going on with her babies.

I thought I had been hit with bordatella. I ordered the bordatella vaccine, found the most current information on treatment (no one else in my household showed any signs of illness), isolated Sisa and babies. No use, one by one I watched the babies die, struggling to breathe. And I couldn’t help them. Then the healthy litter of four who were in my bedroom with a different mother, also isolated, started to die and I lost all four of these babies…What was going on?? In the meantime, I had had a couple of kittens from Sisa’s litter posted with urgency and the request to see if it in fact had been bordatella. I also vaccinated everyone in the household with the bordatella vaccine and waited. The post mortem on the kittens was inconclusive, coming back “possible bordatella” and “cause of death, pneumonia.” Even I could see that, sides heaving and gasping for breath, pneumonia is what ultimately caused the death of these babies. As everyone was vaccinated and a couple of months had gone by without incident (and also without breedings or babies), I thought that the problems would be over. No such luck.. They were actually just beginning and I had no idea about this..

Over the next ten months or so I ALMOST got used to the idea that I would have breedings that wouldn’t take, litters of maximum one or two live kittens, litters with 4-5 stillborn kittens and only one that would survive, only to die at three weeks or so, too many pyometras, etc. etc. As all my girls (and boys) appeared totally healthy –no signs of URI, no digestion or other problems, my veterinarian and I were mystified. I wouldn’t be surprised if he was finally starting to think that my breed, the Oriental, was inherently fragile –or at least that is what I myself was starting to wonder! Where all these happenings just coincidence? Here are some of the problems I experienced: A girl (one of my DMs) who had had four healthy litters of 5-6 had a litter with five kittens, four of them stillborn. Only one lived. A young girl I had been showing, with over 160 points to her grand, on the morning of a show, she presented herself to me with a pyometra. I rushed her to the veterinarian. She was treated successfully with Baytril and prostaglandins. I bred her on the next heat. The breeding took. She aborted her kittens at eight weeks. I bred her again. It took. She AGAIN aborted her kittens at eight weeks into the pregnancy. My other DM girl who had had two good litters was bred to my stud THREE times and the breeding did not take.

 I had litters of one or two kittens where before I had had normal litters of 4-6. In two of these litters of one, the kitten was fine in the morning and suddenly dead in the evening –signs of a quick and intense pneumonia and nothing I could do. A girl who came for breeding (all tests and healthy) produced two kittens with spinal deformities that died at a few weeks of age. The sire had had many healthy litters with never any sort of deformity or problem. Needless to say, I couldn’t understand what was going on as all blood panels and other diagnostic tests came back totally normal, there were no signs of ill health: coats were shiny, eyes were bright, appetites were excellent, energy levels were great. I was getting really discouraged and depressed.

Then, a breakthrough… A breeder friend in Australia forwarded me an e-mail from an Australian feline health list. The post was from Dr. Sue Rodger-Withers PhD, a microbiologist and university lecturer in that country. She and her colleagues had done research on low grade uterine infections due to Gp G-Strep (Group G Streptococcus bacteria) and the use of Antirobe (clindamycin) for treatment. Here is what she said: “Symptoms: queens and kittens (males usually asymptomatic – they don’t have a uterus of course, but they can carry this bug) Some symptoms that might be caused by the Gp G-Strep: a.. Unexplained spontaneous abortions b.. All the signs of Chlamydia but negative on testing c.. Kittens doing ok then suddenly die from acute severe broncho-pneumonia (they are ok and you take a look a few hours later and some may already be dead) d.. Birth abnormalities e.g. intestines on outside e.. No live kittens (I know of one lady who in two years only had one live kitten out of ninety-two. After Antirobe treatment – everything is fine). f.. Problems don’t respond to the main stream antibiotics.

The manner in which this bacterium was found: after unexplained losses, a breeder who shall remain nameless, decided to treat a litter with severe bronchopneumonia (some about to die, others very ill) with Antirobe — at this time it was not scheduled for use in cats. Outcome: Some kittens died but several very ill ones were ok within hours. Decision: Treat all problems in cattery with Antirobe Outcome: Problems gone. I wanted to try to find out the cause (obviously microbial). I obtained aborted fetuses (sterile – still in their “plastic bags”): passed onto friends at Attwood Vet research lab (I used to work there). Result: Strep G – drug resistant to almost everything except Clindamycin (Antirobe). The bug was detected after incubation in a 10% oxygen environment for 10 days (called a facultative anaerobe). Question: Will samples sent to the usual vet diagnostic labs detect this? Answer: No. Requires specialized equipment to grow this bug and vet labs are reluctant to incubate something for 10 days (costs too much money).

Since this time, many breeders with similar unexplained problems have treated catteries with Antirobe and everything is now ok. Antirobe is now available for feline use (usually for gingivitis or osteomyelitis — involving facultative anaerobes). Many vets are still unaware of this bug….and say the problem is Chlamydia. Treatment plans: outlined in Truda Straedes book on breeding. Truda and myself have helped out many breeders (some wished to remain anonymous and that’s ok) – and passed the information onto the vets associated with the breeders.” Well, needless to say, receiving this information, which to me, described my situation exactly was like a bombshell! I immediately wrote to Dr. Rodger-Withers describing what I had experienced. As I compiled the letter to her, my list of “coincidental” fertility and reproductive problems grew longer and longer and I realized that in the past year, I really had not had ONE single, what I would call “normal” pregnancy and litter! Dr. Rogers-Withers was kind enough to reply to me almost immediately.

She said that what I was describing did indeed sound like Gp G-Strep. She described the treatment, which I was very eager to begin: All cats in the household, including spays/neuters, males, older kittens (especially those to be used in a breeding program) should be treated with Antirobe (clindamycin) 25mg per cat, twice daily for THREE WEEKS. This can also be given safely in pregnancy!! Now, Antirobe is one of the most foul tasting (bitter) medications on the planet. The idea of dosing ALL my cats (about 15, including spays/neuters, older kittens) with this twice daily for three weeks was pretty daunting!! I opted to get the 25 mg capsules instead. I got pretty good at popping those suckers down the “hatch,” although I did catch the odd tooth on my fingers at time and had plenty of nicks from the process.

However, get through it, we did. As I had one girl at four weeks pregnant at the time I started, for assurance, I also had my veterinarian make me up syringes of penicillin to give to the mother and babies at birth, as Dr. Susan Little advises on her website (G-Strep article, site address is http://www.catvet.homestead.com . The direct link to the specific article is http://catvet.homestead.com/Strep.html .).

Hopeful, I decided to breed several girls right after they had the treatment. All the breedings took! Bellies started to look rounded and promising! Even my girl who had had the two miscarriages at eight weeks started to look very pregnant and she felt nice and hard –- I felt kittens moving. Happy ending…the Antirobe treatment worked, big time!! I now have large, healthy litters from all my girls – including Tierra, the girl that lost the two litters, gave birth to six healthy, vigorous babies last week! All kittens in all the litters are growing and doing fine and I have more kittens than I have EVER had at once. But as I work at home, I am just happy that I will be taking care of them and crazy for a couple of months with the sound of little paws running through the house.

One more thing…one little girl in the litter where the mother started treatment at four weeks into the pregnancy was not weaning. She was nine weeks old and her brother was twice her size. I was worried. A veterinary exam showed nothing at all wrong with her, but every kind of food I tempted her with or tried, failed. Then we decided to try the Antirobe with her, just on a hunch. After only two doses, she started eating!! The next day, it took very little coaxing to get her interested in the food and her outlook is now promising whereas before, I was starting to think I might lose her. If there are any “poor doer” kittens in the resulting litters of queens who have been treated with the Antirobe – no matter their age, consider treating those as well with the drug. Dosage instructions follow. I have used this for a week or more with no problems. Note: I have found since a good way to give the oral Antirobe, seems to cut the taste and make it more acceptable…draw up your amount into the oral syringe and then draw up a few tenths of a cc of liquid (pediatric) Vitamin C. The Vitamin C has its own benefits as well. This is an especially effective way to give the medication to young kittens.

 I would HIGHLY recommend that anyone experiencing these fertility/reproductive problems try the Antirobe treatment. You really do need to treat ALL the cats in your household though and for the full three weeks. I gave my two older kittens (around 3-4 lbs at the time) half the dose, or 25 mg ONCE daily, but everyone else had the twice daily dose of 25mg. Note: Dr. Kristi Fisher recommends that to be effective the dosage be on the high end: 11 mg/kg twice daily. She says, “Depending on the concentration at the tissue site, Antirobe can be either bacteriostatic (meaning just keep the bacteria from increasing) or bacteriocidal (meaning killing off all of the bacteria). Signs of overdose are basic – vomiting or diarrhea.”

 As I am mathematically impaired, Dr. Fisher also offered this useful information on calculating dosage: “The best way to break down a dosage is to remember that 1kg (kilogram) = 2.2 lbs (I really like to be weighed in kgs!). So, weigh the cat in pounds and divide it by 2.2 to give you the kgs. Then multiply that by the dose you want. In this case, lets say a 1 pound cat.. 1 lb/2.2kgs = 0.45kgs we want 11 mgs/kg twice daily, so 11mgs x 0.45 = 5mgs The Antirobe is 25mg/ml, so divide 5mg by 25mg/ml to get 0.2ml. That is your dose for a one pound cat.” Thankfully, following the treatment should knock out the Gp G-Strep problem for good, so even though it is quite an ordeal, it is DEFINITELY worth it. Take it from one satisfied…and relieved…breeder…

For those of you who need more information, Dr. Sue Rogers-Withers has checked this article for accuracy and has permitted me to publish her e-mail address. She would be pleased to hear from you: qihai@optushome.com.au You may also e-mail me: mmarrow@earthlink.net.

Strep G Infections – by Marva Marrow (Part 2)

G Strep Updates: The Continuing Story: Part 2 – Marva Marrow

Since I wrote my first article in 2002, describing my experiences with G Strep in breeding cats and young kittens, I have received an unprecedented quantity of feedback, both from breeders and veterinarians around the world. These were either breeders who had experienced to varying degrees the problems I had witnessed, were interested in the results of treatment or wanted to try it themselves, or from veterinarians who were familiar with these heartbreaking symptoms and events in their own feline patients. Veterinarians confirmed that this phenomenon occurs in virtually every breed and the feedback I received – from the US and other countries confirms to me that G Strep problems are much more widespread than I would have imagined.

Although my initial, radical treatment with dosing all the cats in the house with clindamycin for three weeks produced dramatic, positive results – live litters of kittens, breedings taking successfully, reduced numbers of pyometras and such, I was somewhat disheartened to see that the signs of G Strep had NOT been totally eliminated. Problems started creeping back, little by little and I was at a loss of how to handle this. Through the feedback I received from veterinarians and the additional research, I am now using an updated, slightly modified protocol, which seems to finally really be working.

Since I am gun shy, having seen far too much of the problems this elusive bacteria can cause, I will be treating my own cats for at least the next year, to attempt to control and rid myself of the problem. Again, I must state that to my observation and through my experience, there are virtually NO SYMPTOMS obvious in the adult cats. No sneezing, coughing, watery/teary eyes or discharge, no diarrhea, no weight loss, no failure to thrive, etc. My breeding cats are and always have been the picture of health – gleaming coats, good weight, etc. That is what has made this problem so very frustrating. In addition to this visual confirmation of good health, every test, every blood panel and even posts on dead kittens have come back inconclusive and normal. The ultimate nightmare!! In any case, because of the dramatically positive results using the clindamycin (and sometimes clindamycin/clavamox) treatment, I have concluded that this IS G Strep I am dealing with. So…I would like to share with you some ideas and the new protocol I am using with success. This information is based on the advice of several veterinarians I have queried and on my own personal experience. I have tried this new protocol for the past six months or so and am very happy with the results. This will be a clear, non-technical explanation. I hope it will make sense and, more than anything else, I hope it will help others as it has helped me.

First the bad news: After clindamycin treatment, the G Strep will most likely still be retained in the normal flora at a very low level. Therefore, the cat could always be a potential G Strep carrier with respect to breeding only. In other words, we should be concerned with the breeding aspects of the Strep G rather than whether the cats do not have any G Strep at all, since the clindamycin will most likely not get every last bit of it — even at a 3 week dose. The other thing (which you may already know) is that a culture will take about 10 days, and will most likely come back with “normal flora”, because the G Strep is at such a low level that it won’t “register” on the lab tests.

OK, so if we can’t consider the Strep G gone completely, then what to do? The good news (hopefully) is this: The key is to treat just before breeding, during breeding, right before delivery of the babies and immediately following the delivery! The feeling is that the only time the G Strep is really active is when the girls are cycling and at birth/delivery. And the male will also pass on/infect the female or other females afterwards, so it is imperative to treat the boy as well. None of the cats will be symptomatic in any way, as I mentioned. This treatment will kill the G Strep in the girl at this crucial time and also protect the boy.

Before Breeding: The first day a girl starts calling, give her clindamycin 25mg 2X daily for 3 days. THEN put her with the tom, giving the meds to BOTH cats until she is done cycling, or one week. I leave my girls with the boy until he isn’t interested anymore, but however you choose to do it, continue the meds for the whole week.

Before Delivery: One week before her projected due date, give the clindamycin (antirobe) 25mg 2X daily. You may or may not also give clavamox. I have given the additional clavamox before with good results in girls that had what I considered pretty severe problems (multiple breedings not taking or absorption of kittens, etc. in spite of giving the antirobe only). In a couple of girls I also gave the clavamox at the beginning, for the breeding. The clavamox is the usual dose, 1cc/ml 2X daily. Give these meds for the week before birth and also continue for 3-5 days afterwards as the mother can pass on the G Strep to the kittens through grooming.

At Time of Delivery: As soon as the kittens are born (I do this even before they are dry), dip the cords in iodine and administer long lasting penicillin (injectible – instructions follow). You can get the long lasting penicillin without prescription through vet supply houses. Make sure it is “long lasting penicillin” ((benzathine/procaine pen G) and NOT Pen G. Be sure to shake the bottle well as the liquid is thick. Give the mother 1cc subQ immediately following the birth. Give the babies an injection as well using this dilution and method: Draw up 1.5 cc sterile water or saline into a 3cc syringe. Then draw up .25cc/ml long lasting penicillin. Shake the syringe. Take off the needle. Insert the needle of a 1cc (tuberculin) syringe into the 3cc syringe (where you took off the needle) and draw off .25cc/ml of this mixture into separate syringes for each kitten. Prepare this solution no more than a couple of hours before the kittens are born (refrigerate). Give each kitten this injection subQ.

Fading Kittens: In the case of fading kittens, I give a “cocktail” of clavamox and liquid clindamycin. For very tiny kittens (up to a week or two, 5 oz. approximately) I would give .1ml of each medication, twice daily. You can either give this with a tube feeding or orally with a syringe. For a kitten of one pound, I would give about .2ml of each. Additional Tips A friend gave me a VERY helpful suggestion of how to get those pesky capsules down a very reluctant cat (you know the kind!!)! She simply opens the capsule into a tiny dish, adds a small spoon of baby food and lightly mixes, serves it immediately. Believe it or not, most cats will eat it this way! I guess it isn’t all that bad tasting in the powder form.

Although this new protocol seems a bit complicated and time consuming, in actuality, it really isn’t that difficult. And the results have been very promising. If you are one who has been experiencing the frustrating and heartbreaking problems of G Strep, I think you will find the time and energy put into following these instructions to be worth every minute. For comments, feedback and additional questions, please feel free to write to me: marva@kittykouch.com I do hope this information will help you to have healthy babies – please do let me know!

Marva Marrow 7TH Heaven Orientals

Vaccines

Vaccination Recommendations for Catteries – by Lorraine Shelton

Vaccination Recommendations for Catteries

by Lorraine Shelton for the Fanciershealth Yahoogroup

There is no “one protocol fits all” when it comes to vaccinating your cats. Each home/cattery must be evaluated individually and vaccinated according their past history of upper respiratory infections (URI) and current husbandry practices. Cats must be healthy to adequately respond to a vaccine. If a cat or kitten is running a fever, vaccination failure may result.

In a small, closed cattery with no history of URI, vaccinate kittens with an injectible three-way killed vaccine at 6 weeks, followed by an injectible modified live calici/rhinotraceitis with killed panleukopenia vaccine at 9, 12, and 16 weeks. You may want to use a vaccine with modified live panleukopenia for the last vaccine of this series if there has been a recent outbreak of this virus in your area.

An alternate protocol for small catteries who practice strict isolation of kittens and have no history of URI (or for catteries with a history of adverse vaccine reactions in young kittens) is to skip the vaccination at 6 weeks and start the series at nine weeks as above. The purpose of the vaccination at six weeks is to try and stimulate an immune response in kittens at the point that maternal immunity (antibodies ingested from the mother’s milk in the first 18 hours of life) starts to wane. Maternally derived protection generally does not last longer than five to six weeks for rhinotracheitis (herpesvirus), and seven to eight weeks for calicivirus and paneleukopenia.

For catteries with a history of URI, queens can be vaccinated with a three-way vaccine (all killed or modified live with killed panleuk) in their last trimester and the kittens vaccinated with a bivalent (NEVER trivalent, NO panleukopenia!) intranasal vaccine at ten days of age (when their eyes open). One drop of IN vaccine is given in each nostril with neonates. In catteries with a history of herpesvirus with corneal involvement, applying one drop to each eye may also be beneficial. However some catteries have experienced adverse events following ocular use of the intransasal vaccine. Cats that will be shown, offered at stud, or otherwise exposed to “outside” cats may benefit from an additional bivalent intranasal vaccination given at 19-20 weeks or a trivalent IN given in place of the 16 week injectable. This helps to stimulate a cell-mediated immune response in the mucous membranes, where exposure to upper respirator viruses occurs.

Never administer modified live panleukopenia to a pregnant cat or expose a pregnant cat to cats that have been recently vaccinated with modified live panleukopenia. Never administer modified live panleuk vaccines and killed panleuk vaccines to individuals in the same population of cats within the same week. Theoretically, recombination between modified live and killed vaccine strains can result in an especially lethal, live strains.

After the initial kitten vaccination series, a booster at approximately one year of age with a three-way vaccine is prudent. Therafter, vaccination every three to five years is sufficient for spays, neuters, and whole males (unless used at public stud, where an intranasal vaccine a few weeks prior to the breeding season may be advised). Vaccinating queens in the last trimester of each pregnancy can help optimize antibody levels in the colostrum ingested by newborn kittens.

The “FIP vaccine” has not been proven to be of value and I do not recommend its use under any circumstances. The FeLV vaccine should only be used in cats that roam outdoors or in situations where cats are admitted into the household without performing adequate FeLV testing. All incoming cats should be tested for FeLV *twice*, at both the beginning and end of a quarantine period where the new cat is separated from the existing population for a period of greater than 3 weeks.

Rabies vaccines should only be used when mandated by law or in cats that roam outside, due to the risks of vaccine associated sarcomas (cancer at the injection site).

The above is solely my personal recommendation, based on a review of the literature, current recommendations from the American Association of Feline Practioners , communication with researchers in feline virology, and my personal experiences from 17 years of breeding pedigreed cats.

–Lorraine Shelton, copyright 2004