Feline Infectious Peritonitis (Feline Coronavirus)

Chapter 10 Feline Infectious Peritonitis (Feline Coronavirus)



Robert G. Sherding


Feline infectious peritonitis (FIP) is a progressive and highly fatal systemic disease of cats caused by feline coronavirus. Feline coronavirus most frequently causes inapparent enteric infection with fecal shedding of virus. Mild enteritis and diarrhea are seen rarely (see Chapter 14). A mutation of feline coronavirus during intestinal replication enables it to infect macrophages and cause FIP. Despite its name, the lesions of FIP are widespread and not restricted to the peritoneum. Effusive and non-effusive forms of FIP occur. Since its recognition in the 1950s, FIP has been one of the most studied diseases of cats, yet a definitive diagnostic test, an effective treatment, and a reliable vaccine are lacking. With the decline in prevalence of feline leukemia virus from vaccination, FIP has become the deadliest infectious disease of cats.



ETIOLOGY



Feline Coronavirus



• Feline coronavirus (FCoV) is a single-stranded enveloped RNA virus with distinctive petal-shaped peplomers projecting from the surface. There are two serotypes of FCoV that differ in cell culture characteristics. Serotype I predominates in North America and Europe, whereas Serotype II is more closely related to canine coronavirus (CCV) and predominates in Japan.

• Coronaviruses are found in many animals and are generally adapted for infecting epithelial cells of the respiratory or gastrointestinal tract. FCoV is closely related to CCV, swine transmissible gastroenteritis virus (TGEV), porcine respiratory virus, and some human coronaviruses. The CCV that causes enteritis and diarrhea in dogs (see Chapter 14) can infect cats and cause antibodies that crossreact with FCoV. Experimentally, CCV can cause enteritis, diarrhea, and even FIP in cats.


Pathogenesis of Feline Infectious Peritonitis




Key Point


FIP-causing coronaviruses are genetic mutants of harmless enteric FCoV.



• It was previously thought that cats were infected by two similar but distinct coronaviruses, the innocuous feline enteric coronavirus and the deadly FIP virus, but these are now considered phenotypic variants (biotypes) of the same virus. The non-mutated enterotropic FCoV typically causes a clinically inapparent infection of intestinal epithelial cells with fecal shedding of virus. During replication in the cat’s intestinal tract, FCoV mutates frequently, especially in kittens, and this sporadically results in critical genetic mutations that enable FCoV to infect and replicate in macrophages.



Key Point


Any cat with inapparent FCoV infection has the potential to develop FIP if the virus mutates during replication to allow the mutated FCoV variant to infect macrophages. Viral replication in macrophages is the defining event in FIP.



• Macrophages then replicate the mutated coronavirus and carry it to target tissues such as the peritoneum, pleura, kidney, uvea, and nervous system, resulting in widespread immune-mediated vasculitis, disseminated perivascular pyogranulomatous inflammation, and exudative fibrinous polyserositis. These are the characteristic lesions of FIP.

• The pathogenesis involves circulating immune complexes, complement fixation, cytokine release, apoptosis of activated T lymphocytes, and vascular damage with necrosis and increased permeability.



Key Point


It is not the virus that causes widespread damage in FIP. The disease is a consequence of the cat’s immune reaction to the virus.



• Natural immunity to FCoV is poorly understood but is presumed to be cell mediated rather than antibody mediated. Circulating FCoV antibodies can actually enhance progression of the disease.


EPIDEMIOLOGY



Prevalence



• FCoV is ubiquitous in cats worldwide. In many regions, 50% of cats are positive for coronaviral antibodies (i.e., seroprevalence). The majority of these seropositive cats represent current or past inapparent infection with non-mutated FCoV. Only some of these develop into mutated FIP-causing infections; thus, the prevalence of FIP is much lower.

• The prevalence of FCoV infection is highest in cats confined in crowded groups, such as catteries, shelters, and multiple cat households, where the seroprevalence ranges from 50% to 90%.

• In endemic catteries where the seroprevalence approaches 90%, most FCoV-infected cats remain healthy and only 5% develop FIP.

• The seroprevalence of FCoV in free-roaming feral and stray cats is 12% to 15%. The lower prevalence is presumed to relate to less social interaction and less exposure to fecally excreted virus than cattery cats.

• The seroprevalence in single-cat households is 15% or less.

• In a large survey of North American veterinary teaching hospitals, FIP was diagnosed in 1 of every 200 new feline accessions. This population mostly represents sick cats seen by veterinarians.

• FCoV can infect most wild felids, including the lion, cougar, cheetah, jaguar, leopard, bobcat, sand cat, caracal, serval, and lynx. Cheetahs are especially susceptible to developing FIP.


Risk Factors




Key Point


Whenever FCoV exists in a cat, so does the potential for developing FIP.



• FCoV infection occurs most often in young kittens after maternal antibodies dissipate, between 6 and 16 weeks of age; thus, the infection rate is highest in catteries where kittens are raised in association with virus-excreting adult cats.

• Young cats have increased risk for developing FIP. The peak incidence for FIP is between 6 months and 3 years of age, although cats of any age can be affected.

• Crowded group confinement (multicat households, purebred catteries, shelters) increases risk.

• Factors intrinsic to the shelter experience increase fecal shedding of FCoV up to 1 million-fold after 1 week.



Key Point


Most cats with FIP come from catteries and shelters.



• Any factor that increases FCoV replication in the intestines of an infected cat will increase the probability of the virus mutating to a form that can cause FIP. Thus, viral load, stress, immune impairment, corticosteroids, surgery, and concurrent disease (e.g., feline leukemia virus or feline immunodeficiency virus) can be risk factors for FIP.

• Inherited genetic susceptibility to FIP is a factor in some purebred cats and in cheetahs.


Transmission



• FCoV is primarily excreted in feces from cats with inapparent enteric infection. Healthy carriers often shed FCoV in their feces for at least 10 months, and some cats shed persistently for many years, possibly for life. One-third of healthy FCoV-seropositive cats are actively shedding virus. In high-density endemic catteries, up to 60% of healthy cats may be shedding virus at any given time.

• FCoV is usually inactivated in 24 to 48 hours at room temperature, but the virus can survive up to 7 weeks in dried fecal debris; thus, environmental contamination with small particles of used litter is an important source of infection. Contaminated surfaces, food and water dishes, and human clothing, shoes, and hands can act as fomites. Most disinfectants and detergents easily destroy FCoV.

• Transmission to uninfected cats most frequently occurs through oronasal contact with virus-containing feces or contaminated material from the environment. Contaminated litter and dust particles deposited on the fur are ingested during normal grooming activity.



Key Point


Indoor confinement in crowded groups increases exposure to large doses of infectious virus in feces in shared litter boxes.



• In catteries, kittens are most frequently infected as they lose maternal-derived immunity after 6 weeks of age through contact with feces from virus-shedding adult cats. Removing kittens from contact with adult cats at 5 to 6 weeks of age prevents infection (see “Prevention”).

• FCoV can also be excreted in saliva, respiratory secretions, and urine, but these are unlikely to be important sources of infection.

• Transplacental transmission is possible but uncommon.

• Cats with FIP shed mostly the avirulent non-mutated FCoV, not the virulent mutated virus that causes FIP; thus, FIP itself is not directly contagious. Cats with FIP also excrete less FCoV than healthy carriers.


CLINICAL SIGNS


Cats with non-mutated FCoV infection of the intestinal tract infrequently develop clinical signs (see Chapter 14). This section describes the clinical manifestations of mutated, FIP-producing FCoV infection. Cats with FIP often present initially with nonspecific and non-localizing signs, such as fever, anorexia, inactivity, weight loss, vomiting, diarrhea, dehydration, and pallor (anemia). As the disease progresses, these signs worsen and additional clinical signs develop that indicate either body cavity effusions in the “wet” form of the disease or organ-specific abnormalities in the non-effusive or “dry” form (Table 10-1). Approximately 75% are effusive and 25% are non-effusive. Some cats manifest features of both effusive and non-effusive disease or change over time from one form to the other.



Table 10-1 CLINICAL SIGNS AND LABORATORY ABNORMALITIES IN FELINE INFECTIOUS PERITONITIS



Nonspecific Signs


Chronic unresponsive fever of unknown origin


Unexplained anorexia, lethargy, and weight loss



Effusion Signs


Fluid distension of the abdomen


Dyspnea due to pleural effusion


Muffled heart sounds due to pericardial effusion


Scrotal swelling



Organ-Specific Signs


Abdominal disease


Enlarged, firm, irregular kidneys


Icterus and hepatomegaly


Intestinal pyogranulomatous mass


Splenomegaly


Pancreatitis


Mesenteric lymphadenopathy


Omental adhesions and mass


Neurologic signs (multifocal and progressive)


Uveitis (iridocyclitis; chorioretinitis)


Pyogranulomatous interstitial pneumonia


Testicular enlargement (orchitis)



Laboratory Abnormalities


Anemia (nonregenerative)


Neutrophilic leukocytosis or leukopenia; lymphopenia


Elevated serum protein (hyperglobulinemia)


Elevated serum liver enzymes and bilirubin (also bilirubinuria)


Azotemia of primary renal origin


Proteinuria of renal origin


Pyogranulomatous or fibrinous body cavity effusion


Elevated CSF protein and leukocytes (neutrophils)


CSF, cerebrospinal fluid; FIP, feline infectious peritonitis.



Incubation and Clinical Course



Incubation and Onset of Feline Infectious Peritonitis



• The natural incubation period is extremely variable, ranging from a few weeks to several years. Cats are at greatest risk for developing FIP within the first 6 to 18 months after initial infection with FCoV.

• This encompasses the unpredictable but often prolonged period of time it takes a carrier of the harmless, non-mutated FCoV to develop the critical viral mutation and then the time it takes the mutated virus to produce clinical disease.

• The onset of clinical signs is often insidious, but occasionally it is sudden, especially in young kittens.



Key Point


Chronic fluctuating fever that is unresponsive to antibiotics is a frequent early sign of FIP.



Clinical Course



• Once viral dissemination occurs and clinical illness develops, FIP is virtually always progressive and fatal. However, there is considerable variation in the duration of clinical illness before death; 3 to 6 weeks is typical, but prolonged illness exceeding 6 months can occur, as can intermittent illness punctuated by periods of remission.

• For effusive FIP, the clinical course is usually acute (days to weeks).

• For non-effusive FIP, the course is often chronic and insidious (weeks to months).

• Cats with only ocular involvement sometimes survive for a year or more.


Effusive (Wet) Form of Feline Infectious Peritonitis




Key Point


In cats with the effusive (wet) form of FIP, the predominant location of the inflammatory fluid is the abdominal cavity in 62%, the thoracic cavity in 17%, or both cavities in 21%.



Abdominal Effusion (Peritonitis)



• Effusive FIP involving the peritoneal cavity causes progressive, non-painful, fluid distension of the abdomen.

• Effusion is detected by palpation and percussion of a fluid wave. In the early stages, a small amount of abdominal fluid may be detected by palpation of intestinal loops that feel excessively slippery, as though the serosal surfaces are highly lubricated. Pain on palpation is infrequent.

• Extension of the peritoneal inflammation may involve the gastrointestinal tract (vomiting, diarrhea), hepatobiliary system (jaundice), or pancreas (vomiting due to pancreatitis).

• Scrotal swelling may occur in intact males as a direct extension of the peritoneal inflammation and effusion into the testicular tunics.

• Adhesions may organize the mesentery, omentum, and viscera into an irregular, firm mass that is palpable in the cranioventral abdomen.

• Abdominal effusion is confirmed by radiography, ultrasonography, or abdominocentesis, and the results of fluid analysis are highly indicative of FIP (see “Diagnosis”).


Thoracic Effusion (Pleuritis)



• Dyspnea, tachypnea, and exercise intolerance are the major presenting signs because lung expansion is restricted by compression from fluid in the pleural space.

• Cats with pleural effusion may prefer a sitting or sternal recumbent posture to facilitate breathing. Increased respiratory distress may occur with exercise, with physical restraint in the hospital, or with repositioning in lateral recumbency (i.e., orthopnea).

• Thoracic effusion may cause muffled heart and lung sounds on auscultation and hyporesonance and a horizontal fluid line on thoracic percussion.

• Thoracic effusion is confirmed by radiography or thoracocentesis (see Chapter 164). The results of fluid analysis are highly indicative of FIP (see “Diagnosis”).


Pericardial Effusion



• Pericardial effusion due to fibrinous pericarditis may occur in FIP, with or without other effusions. In one survey, FIP was the second most frequent cause of feline pericardial effusion, accounting for 14% of cases.

• Pericardial effusion in FIP does not usually cause overt clinical signs. It may be suspected from auscultation (muffled heart sounds), thoracic radiography, or electrocardiography, and it is confirmed by echocardiography (see Chapter 151).


Non-effusive (Dry) Form of Feline Infectious Peritonitis




Key Point


The non-effusive (dry) form of FIP is characterized by multifocal pyogranulomatous inflammation and necrotizing vasculitis in various organs, such as the abdominal viscera (e.g., liver, spleen, kidneys, pancreas, and intestines), eyes, central nervous system (CNS), and lungs.


Pyogranulomas appear as multiple discreet or coalescing gray-white nodular masses of variable size on the surface and within the parenchyma of affected organs. These are often mistaken for tumors. Effusion is often minimal or absent. The specific organs affected and the degree of resulting organ failure determine the presenting clinical signs.



Kidney Disease



• Pyogranulomatous nephritis causes the kidneys to become palpably enlarged, firm, and irregular (“lumpy”), associated with pyogranulomas scattered over the surface and infiltrating throughout the renal cortex.

• Extensive renal involvement occasionally causes renal failure with polyuria-polydipsia and azotemia (increased blood urea nitrogen [BUN] and serum creatinine).

• Proteinuria is a frequent laboratory finding in renal FIP. In addition, large quantities of circulating immune complexes may lead to subclinical glomerulonephritis with any of the other forms of effusive and non-effusive FIP.


Liver Disease



• Pyogranulomatous hepatitis (hepatomegaly, jaundice, and signs of hepatic failure) may occur in FIP.

• The most consistent laboratory abnormalities are bilirubinuria and hyperbilirubinemia. Mild to moderate elevations of serum liver enzymes (alanine aminotransferase, alkaline phosphatase) and serum bile acids also may occur.


Disease in Other Abdominal Organs



• Pyogranulomatous lesions may cause palpable enlargement of the visceral lymph nodes, spleen, or omentum.

• Pyogranulomatous enterocolitis may cause diarrhea and diffuse or masslike intestinal thickening, especially in the ileocecocolonic region.

• Pancreatic involvement can occasionally cause pancreatitis and, rarely, diabetes mellitus.


Ocular Disease



• Ocular lesions of FIP are usually bilateral and affect the vascular tunic or uvea (uveitis). Lesions may sometimes cause blindness.

• Manifestations of exudative anterior uveitis (iridocyclitis) may include miosis, aqueous flare, keratic fibrinocellular precipitates, hypopyon (“mutton-fat” deposits of cells and fibrin), hyphema, anterior chamber adhesions (synechia), corneal edema, and deep neovascularization of the cornea (see Chapter 136).

• Chorioretinitis from posterior uveal involvement is detected by ophthalmoscopic examination and may include perivascular cuffing, exudative retinal detachment, and retinal hemorrhages (see Chapter 138).


Neurologic Disease



• Multifocal pyogranulomatous meningoencephalitis and myelitis are frequent in FIP. Inflammatory lesions are perivascular and often involve the meningeal and ependymal layers. In one report, 29% of cats with FIP developed neurologic signs. In a retrospective survey of 286 cats with neurologic disease, lesions indicating FIP of the CNS were found in 16%. In another large survey, FIP was the most common spinal disease in cats.

• The neuroanatomic distribution of the lesions determines clinical signs; some of the most common are ataxia, tremors, vestibular dysfunction, seizures, posterior paresis, hyperesthesia, and behavioral changes. The relentless progression and multifocal nature of the signs are characteristic features of neural FIP.

Related posts:

  1. Feline Infectious Respiratory Disease
  2. Mammary Gland Neoplasia
  3. Keratinization Defects
  4. Canine and Feline Demodicosis

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Aug 27, 2016 | Posted by in SMALL ANIMAL | Comments Off on Feline Infectious Peritonitis (Feline Coronavirus)

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