Pharoah tries stemcells for FIP and the cure for FIP is found!

One success story at a time

With FIP there is no point being conservative except for the sake of the cat's comfort. So it was no surprise to hear that yet another innovative therapy is being tried - adipose stemcell therapy for dry FIP. The cat is called Pharoah and his vet is Ed Pattison of City Vets, Exeter UK https://www.facebook.com/cityvets/photos/a.128542133823284.22418.128403317170499/957763074234515/

But how interesting is this - the vet who pioneered the use of adipose stemcells for arthritis in dogs in australia, Simon Craig, was the same chap who cured Dusty of wet FIP - see survivor's page

and how dull and unsexy is this - Hip arthritis in dogs by the way you can simply prevent with adequate vitamin C and a proper diet.
http://oneradionetwork.com/health/dr-r-geoffrey-broderick-world-renowned-veterinarian/

Dr Belfield has the word on vitamin c in animals and was kind enough to answer my emails when Mishka was diagnosed. he did try it for FIP of course and it was the one thing he had no success with after it was established :( That's what we are up against.
I have NO DOUBT this is the same with FIP - we can prevent it  simply - no rocket stemcell science required and finally someone in authority is brave enough to say it 

"The best treatment for FIP is not to get it in the first place: if you are going to buy a pedigree kitten, make sure your Vet sends a blood sample to the University of Glasgow Veterinary Diagnostic Services to get a certificate saying that the kitten tested negative for feline coronavirus (FCoV) antibodies: we need to put consumer pressure on bad breeders and reward good ones." Dr Dianne Addie rocks! http://www.theexeterdaily.co.uk/news/local-news/exeter-vets-pioneer-stem-cell-treatment

- see prevention page

• stop inbreeding 
• stop crowding 
• stop malnourishment of starvation and stop feeding COOKED CRAP & KIBBLE to cats - they weren't designed to eat cereal; they are not birds.

Mutant Ninja FIP

"Evolutionary plasticity can be purchased only at the ruthlessly dear price of continuously sacrificing some individuals to death from unfavourable mutations."

~Theodosius Dobzhansky Genetics and the Origin of Species (1937)

Life does not stand still. Evidence of the mutation of Feline crossed Canine coronavirus to produce a virulent form that creates directly cat-cat transmissible FIP disease. Marleen from Facebook FIP fighters group posted this today -

"One of our members contacted Dr. Niels Pedersen from the UC Davic SOCK FIP team and he kindly sent her this lengthy reply (see below). She got his permision to share this with the FIP community.

Q: In a recent article by Wang et al (http://www.veterinaryresearch.org/content/44/1/57) an outbreak of FIP among cats in a Taiwanese shelter was described. This has caused some anxiety among cat owners concerning the potential of cat-to-cat transmission of FIPV. What are your views on this? 

A: I reviewed this paper and believe that this was a case that started with cat-to-cat transmission. However, the virus in this outbreak is what we call type II FIPV, which is a hybrid that occurs between feline and canine coronavirus. The primary strain of coronavirus in most cats is serotype I. Serotype II FIPV are more virulent than type I viruses and there is an old report of possible cat-to-cat transmission with another FIP virus of this serotype. However, this is a very rare occurrence and should not be taken as a universal finding. Cat-to-cat transmission of FIPV is extremely uncommon, even with serotype II virus, and when it occurs the outbreaks are self-limiting because the virus rapidly mutates to a form that does not go cat-to-cat. It is likely that the virus in this outbreak came from a cat or cats that were housed with dogs in another shelter and had not yet had time to fully adapt to cats. 

At this point, we need to define the difference between epizootic (epidemic=human) and enzootic (endemic=human) disease. An epizootic occurs when a new pathogen such as a virus enters a group of susceptible animals for the first time. There is a very rapid spread with a high morbidity (prevalence of diseased individuals) and often a high mortality (death from that disesae). An example would be the appearance of parvo virus enteritis in dogs in the 1970s, an epizootic disease that is now enzootic. Enzootic disease occurs when a pathogen lurks continuously in the environment and only targets individuals that become susceptible. For instance, feline enteric coronavirus is shed by a majority of older cats in a cattery but it is the kittens that take the brunt of disease. Enzootic disease is sporadic in nature and the morbidity and mortality waxes and wanes depending on the presence or absence of disease cofactors. People often mistake epizootic for enzootic disease when several cases occur close together. Epizootics usually get far more attention than enzootics, because they hit like a hammer. Enzootic disease is frequently tolerated, as is the case with feline upper respiratory and intestinal infections and even with FIP. However, the tap-tap-tap of enzootic disease is in the long run far more damaging and causes far more deaths than epizootic disease. 

Q: How can an epizootic of FIP, such as occurred in this Taiwan shelter, be differentiated from the enzootic type disease that causes almost all FIP deaths? Or another way to ask the question in the case of FIP is how can you differentiate cat-to-cat transmission of an FIP virus from the normal pattern of infection, which involves cat-to-cat transmission of the parent feline enteric coronavirus followed by internal mutation of the disease causing FIP virus?

A:  The epizootic of FIP that occurred in Taiwan was easy to characterize, because it could be traced to the introduction of a specific hybrid cat/dog virus that came in with a cat from another environment. This virus then rapidly spread to susceptible cats by contact. The virus that caused the epizootic was also genetically unique from normal enteric coronaviruses that were enzootic to the shelter, confirming that it was indeed a new introduction. As would be expected from an epizootic, the introduced virus changed as it rapidly spread cat-to-cat in the shelter. With subsequent cat passages, the infecting virus started developing mutations in one of the coronavirus-related genes associated with production of a protein called 3c. Coronaviruses that do not produce normal 3c protein will no longer infect enterocytes and are therefore not shed in the feces. This same type of mutation is common to the FIP viruses isolated from cats with enzootic disease. This occurrence of 3c gene mutations was probably the major reason why the Taiwanese outbreak was self-limiting, and not just because a simple quarantine was initiated.

Q: We can all understand that cases of FIP commonly occur in large catteries where FECV is prevalent, and where there is a genetic relationship between affected cats. However, there are also cases where 3-4 genetically unrelated cats in the same household (not a large cattery) develop FIP one after the other during a time period of 6-12 months. Assuming that all of these cats developed FIP due to internal mutation of FECV, this seems a bit strange considering that only a small proportion of cats are supposed to go on and develop FIP after FECV infection. How do you explain this?

A: The morbidity to FIP can range from less than 1% to more than 5-20% in the enzootic form, depending on many factors. In catteries, genetics play an important role, but it is not the sole factor. With random bred cats, non-genetic factors are even more important. We know that the age at exposure to FECV and stressors of many types that occur during primary FECV infection (starting around 9 weeks) are very important. Resistance develops with age and the younger they are exposed the more likely to come down. The problem is that in shelters and catteries the exposure occurs much earlier in life than if cats are running free at a reasonable density. There is no accident that over 70% of FIP cases come from catteries, shelters and kitten/cat foster and rescue organizations. We also know that 20% or more of FECV infections can generate FIP-causing mutants, but yet only a fraction of cats get sick. This means that many cats actually resist the disease. The question then becomes - why do some get the disease when others do not?

Q: Which are the most important stress factors that can influence the development of FIP in young cats?

A: In principle anything that interferes with a kitten’s immune response in that critical period between 9 weeks when they usually first see FECV and 16 weeks or so when their immune system really starts to become mature can potentially tip the balance towards disease. Vaccinations, deworming, early neutering, moving to a new family – all of these things can affect the immune system, plus all of the common kittenhood respiratory and enteric disorders that occur during this period. However, it is impossible to weight the influence of one or another, or any combination. I like to use the term “perfect storm” from the famous movie. You get FIP when enough bad things come together at the wrong time.

The Bottom Line - House your cats in small groups. Do not stress them when they are young. Protect kittens from encountering FeCoV until their immune system is strong and don't inbreed.

Leap of Faith

"Healing takes courage, and we all have courage, even if we have to dig a little to find it." - Tori Amos

I wrote this just before Mishka died on Feb 1st but I've decided to post it unchanged. Update: a few edits and see the comment from Dusty's mum below!
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Dusty is the reason we are treating Mishka. Dusty survived wet FIP of the lungs in part thanks to injections of feline interferon and oral prednisone in 2007. I first wrote about him in a post about Hope http://onecatlife.blogspot.com/2012/10/hope-is-black-swan.html

Virbac sent me the case history and amazingly here was a cat I could believe in because I knew the vet practice in Sydney (I think my mum even took our old cat there on occasion. Chloe was a stray my brother took in who lived to be 17 on a commercial diet without ever getting regular vaccinations btw)  so I phoned the vet, Simon Craig who verified the cat was still kicking and had made it off the interferon. Based on Dusty's outcome we did the math and decided we could afford the treatment on the basis of expecting a dead cat or a cure in a little over two weeks - but there you have it, each case is unique and Mishka has not progressed as well - but she's not dead either, so the budget is completely blown by five months worth of extra drugs. We have apparently converted an acute illness into a chronic one - as allopathic medicine does so well.

Possibly due to her more advanced disease ( she has abdominal FIP as well) her own genetic challenges (she is a Birman, Dusty is a Scottish Fold) or that two week delay or not using the steroids first up. Dr Addie does mention in her wet fip case study, which I only recently read, that the wet FIP response to FOI is higher for cats with FIP of the lungs, and doesn't seem to work as well on abdominal FIP.

My suspicion is this is because abdominal FIP can be cryptic for longer in that area without causing distress. Mishka had abdominal fluid for a few weeks to a month perhaps before we knew she was sick.

It wasn't until her lungs really filled up that we rushed to the vet. Perhaps she was also dehydrated somewhat and thirstier than usual. Here she is the night before, mucking about and looking ok:

She may have been sick for much longer as the earliest signs are so hard to detect as abnormal, if indeed they were - she started being more sleepy (thought that was natural as a cat growing older and not being a kitten any longer), more cuddly and purry - well she got to know us and that's a nice thing, she was very hungry and insisted on 4 am snacks - well she's a growing cat. She got so chubby she was stuck in her cat door - that was cute (ok my son had at that stage twigged something was up. "mum Mishka is not a cat anymore" ? "Definition of a cat - fits anywhere the head fits" ??!!! )

Definition of a cat - fits anywhere the head fits

 Mishka's Leap of Faith

 
and so we followed the example of Dusty. I feel like a cartoon character that's headed over the cliff - can't stop running to look down now or gravity will reassert itself. Hoping to make it to the other side on pure momentum. Courage kitty - leap!

Death and taxes

"In this world nothing can be said to be certain, except death and taxes." ~ Benjamin Franklin

FIP is not an illness the general cat owning public are aware of though breeders and vets are well acquainted with the general hopeless picture, if not the finer points since they tend to treat those affected as disposable, as do the bean counters - the insurance companies.

There were breed premiums mentioned in the brochure I picked up while waiting at the vet last november with little Mishka - all runny nose and feverish mystery. I was moved to pick up a brochure as it felt really odd to have a sick cat who was so young. Birmans weren't considered one of the dodgy breeds by the insurers. In fact prior to accepting Mishka a little investigation had falsely assured me the breed was considered a very hardy, healthy one. A much better tool found too late: This web page contains a list of genetic or inherited conditions which have been reported and lists the cat breeds affected. It's long and Birmans are frequently mentioned.

www.dr-addie.com/Conditions.htm

It didn't seem worth the premium based on the past record of First Cat - two vet visits in 19 yrs. With 20/20 hindsight it was a minor saving as in the teeny print you can only get off the interwebs FIP is specifically excluded including euthanasia for FIP. Neither PI nor interferon nor Moducare would be acceptable even if it was covered, being experimental or non-prescription treatments.

The current purchasing system for medications and nutriceuticals resembles a MLM Ponzi scheme, and I expect asking the government to release the most expensive of these treatments for FIP, the feline interferon, from GST is talking to stone. Mishka also takes a fair few nutritional supplements since she won't eat raw meat - colostrum and whey powder - full of growth factors, vitamin C, rutin and fulvic minerals and we have tried a heap more curcumin, pentoxifylline, prednisolone to name a few.

but restoring my faith in human nature are a bunch of people who give of their time and resources freely; I'll just mention someone here: Jevgenia sent Mishka her left over polyprenyl which amounts to nearly a full months course to try. It made it through customs without the stupid $325 AQIS clearance form we truly didnt need - we could have imported via Tanja who already had one for her cat (deceased) but the information given to her incorrectly said each cat had to have a separate permit. This butt covering delay has seen more than one cat die already waiting for their chance. If you want other cats in australia to have this chance too then donate to Mishka's fighting fund (right) so I can bring in enough boxes of PI on the one form to have spares ready to send out.

Mishka was knocked back months ago by the PI people because she has wet fip and their initial study showed it was ineffectual but possibly because most cats only survive a few days with the disease and PI needs about 2 -4 weeks to effect a change. It's still an off label use for FIP, dr Legendre himself is calling it a delaying treatment not a cure but what else is there except hope? Now it's approved for rhinotracheitis and not a freeby experimental drug you just need deep pockets, a vet's prescription (and for non US cats someone with the import clearance) in order to have a go.

Mishka has fought on for nearly 4 months now - i think largely due to having her own physician ( my husband) careful nursing, FOI and Moducare. The vets have been a mixed bag - choose with care!