Feline coronavirus causing FIP is a treacherous plot of antibodies

You can find the original article at veterinarni-lekari.cz
19. 8. 2020


It is typical for a coronavirus that the particular form of the disease it causes depends on the circumstances. He can be compared to a paratrooper who associates with local guerrillas in the body and, in cooperation with them, undertakes destructive sabotage. However, the virus causing infectious feline peritonitis (FIP) is proof that antibodies from an infected animal can also be used to harm.

Has the cheetah coronavirus decimated?

FIP, with its dry and wet forms, is the best known coronavirus disease in animals (Wolf and Gresemer, 1966). However, more than 20 coronavirus strains are known in cats (Knotek, Freedom, 1996).

All felines are susceptible to coronaviruses. But cheetahs are probably the most sensitive. 10,000 years ago, coronavirus FIPs are thought to have decimated the cheetah population to such an extent that cheetahs are genetically significantly less variable than other felines (Knotek, 1996).

Ability to mutate in the gut of cats

In addition to classic FIP, there are agents of enteral coronavirus infection (FECoV - feline enteric coronavirus) and coronavirus-like particles (CoVLP - coronavirus-like particles). The individual strains cross-immunologically react with each other, but differ in both virulence and mortality. Mortality ranges from 0 to 100 %. An interesting feature is their variability and probable mutation ability in the intestines of cats that have undergone viral enteritis.

Up to 7 weeks

The coronavirus enters the cat's body by the nasal or oral route, even indirectly. All you need for the infection is a shared bowl, a transport box or bringing it into your home on your shoes. The feline coronavirus normally stays in the environment for up to 7 weeks.

After entering the mucosa of the upper respiratory tract or the oral cavity, the virus replicates in the epithelium of the tonsils and small intestine. Secondary infection occurs in enterocytes, but also in other visceral organs (liver, spleen, kidneys and lymph nodes). Antibodies appear 7. − 10. the day after infection, but excretion of the virus by oronasal secretion occurs on day 2 after infection.

Macrophages as a means of transport

However, antibodies do not protect against FIP, vice versa they form complexes with the virus, allowing the virus to enter cells, including macrophages. Damaged macrophages then spread the virus around the body. This condition is exacerbated by stress, immunosuppressive factors (corticoids?) And especially by concomitant feline infectious leukosis (FeLV).

The incubation period depends on many factors, especially the active cell-mediated immune response and its ability to remove infected macrophages from the bloodstream.

Influence of interferon suppression on disease development

Macrophages are involved in the formation of perivascular lesions and the release of inflammatory mediators during the course of the disease. Vascular endothelial damage, blood clotting disorders, thrombocytopenia and excessive vascular permeability occur. Due to the action of prostaglandin E2 (PGE2) from damaged macrophages and neutrophils occurs interferon suppressionwhich normally prevents the virus from multiplying. Under these conditions, however, the virus uses the macrophages of the infected organism for its replication and transport throughout the body. The most massive manifestations of the virus take place in organs that contain large numbers of macrophages - in the liver, spleen, lymph nodes (Knotek, Freedom, 1996).

The effect of interferon suppression on disease development corresponds to my experience with the control of (not only) coronavirus diseases impulse therapywhose principle is stimulation of interferon by the body itself, ie endogenous. This method is both cheaper than the administration of exogenous interferon does not cause the side effects typical of exogenous interferon.

The clinical picture of FIP depends on the form of the disease

Clinical manifestations of 2 main forms of FIP - exudative and non-fusible (ie dry) - is different. In the first case (wet form), fibrin exudate is present on the peritoneum and there is a massive thickening of the mesentery with a watery or gelatinous consistency. The omentum forms a contracted formation in the cranial part of the abdomen. Similar fibrinous effusions may also occur in the thoracic cavity and pericardium, corresponding to the pattern of the disease in humans.

In the dry form, inflammatory diseases of the liver, spleen, lungs, CNS and eyes occur. Hyperbilirubinemia and jaundice may occur in the terminal stages.

Beware of seemingly cured carriers

Incubation time depends on the strain of FIP, the type and massiveness of exposure, the health status and age of the patient and his immunocompetence, especially mediated cellular immunity. It can move from 3-6 weeks to 6 months. A seemingly cured patient can be a hidden vector of the disease.

An intranasal vaccine was used to vaccinate cats, which stimulated the production of local mucosal immunity. However, it is no longer available in the Czech Republic and possibly in the European Union.

MVDr. Zdeněk Cvrček
Veterinary clinic and clinic Liberec

Literature by the author.

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