"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.