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Feline Infectious Peritonitis And Pleuritis

Source : http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/56900.htm&word=Feline%2cInfectious%2cPeritonitis

Source Date : 2006

Merck Vet Manual

Feline infectious peritonitis (FIP), caused by a feline coronavirus, is seen worldwide. Although a large number of cats may be infected with the feline coronavirus, only a few develop clinical FIP. The disease is progressive and may manifest clinically as a continuum between the effusive (serositis or wet) and noneffusive (granulomatous or dry) forms. A distinct clinical form of noneffusive FIP affecting only the eyes or brain (or both) may be seen. Mortality, even with therapy, approaches 100%. Although primarily a disease of domestic cats, FIP has been recognized in exotic Felidae, including the large and small wild cats. Among larger cats, FIP is seen in lions, leopards, jaguars, mountain lions, and especially cheetahs. Smaller cats susceptible to FIP include the sand cat, lynx, caracal, and pallas cat.

Etiology:

Field strains of feline coronavirus vary in their ability to induce FIP. Some isolates cause FIP (feline infectious peritonitis virus [FIPV]); others cause more localized GI disease ( Feline Enteric Coronavirus). Mutations from feline enteric coronavirus to FIPV occur. The exact relationship between low virulence FIPV strains and feline enteric coronavirus, which is relatively nonpathogenic, is not clear. FIPV is antigenically related to and serologically cross-reacts (by current ELISA and immunofluorescent antibody tests) with a subgroup of mammalian coronaviruses, including transmissible gastroenteritis virus of swine, human coronavirus 229-E, canine coronavirus, and feline enteric coronavirus. FIPV and canine coronavirus are very closely related antigenically and may have crossed between hosts. Strains of FIPV may differ considerably in antigenicity.

Feline coronaviruses are fairly stable in the environment and, once dry, can survive for 4-6 wk. They are enveloped viruses and are destroyed by most household disinfectants, particularly household bleach at a 1:32 dilution.

Transmission, Epidemiology, and Pathogenesis:

Most FIPV infections probably result from ingestion of the virus; however, aerosol transmission is also possible. Close contact with an infected cat or its excreta, most likely feces and saliva, is required for virus transmission. Because cats shed viral particles in feces, litter box exposure and mutual grooming are important sources of infection. Cats living in multiple cat households are at greater risk of contracting feline coronavirus and developing FIP because of sharing multiple strains of the virus and stress-associated immunosuppression. Transplacental transmission is suggested by the occasional observation of FIP in stillborn kittens, but the frequency with which this occurs is unknown. In the past, up to 50% of cats with FIP were co-infected with feline leukemia virus (FeLV); FeLV potently suppresses cell-mediated immunity, which is required for resistance to FIP. Currently, the co-infection rate is only 5%, due to FeLV testing and vaccination.

Cats of all ages and either sex can develop the disease, but incidence is highest in cats 6-24 mo old, decreased in cats 5-13 yr old, and increased in those 14-15 yr old. Kittens raised in infected colonies may contract the virus from their mothers or asymptomatic carriers when their maternal immunity wanes at 5-10 wk of age. These kittens typically may develop FIP weeks or months after they are placed in new homes. The prevalence of clinical FIP is <1% of cat-containing households, even though 20-35% of cats are infected with coronavirus. Losses are often sporadic and unpredictable, and morbidity and mortality may be greatly increased, sometimes up to 35% or more in some breeding catteries and households with multiple cats. Generally, the morbidity rate in cattery-bred kittens is 10%. The prevalence of FIPV infection in the general cat population is difficult to determine because current serologic tests for detecting FIPV antibodies cannot discriminate between FIPV and other feline coronaviruses that do not produce disease and that may be more prevalent.

After ingestion of virus or aerosol exposure, FIPV initially replicates in tonsil or intestinal epithelium and then is transported via macrophages and monocytes to primary target organs such as liver, spleen, and visceral lymph nodes. The development of FIP, and the particular clinical form of disease (ie, effusive or noneffusive) depends on the intrinsic immune responses of the cat. Cats with a strong humoral immunity and a weak or absent cell-mediated immune response against FIPV develop a persistent viremia and effusive FIP. The effusive disease results from widespread formation and deposition of immune complexes in blood vessels and from complement activation leading to vasculitis, vessel damage, and leakage of serum and protein into body cavities. Cats with partial cell-mediated immune responses along with humoral immunity develop the more chronic noneffusive FIP, which is characterized by immune-mediated (delayed hypersensitivity-like), granulomatous, frequently perivascular lesions in abdominal viscera, lungs, eyes, and brain. Cats with strong cell-mediated immune responses with or without humoral responses can either completely recover or become persistently infected asymptomatic carriers. The latter may infect contact cats and may themselves later develop FIP, usually after periods of stress or co-infection with FeLV. Some asymptomatic, seropositive carrier cats subsequently may become seronegative and stop excreting virus.

Clinical Findings:

The acute or primary infection often is asymptomatic, but in some cases, fever of unknown origin, conjunctivitis, and other upper respiratory signs and diarrhea may occur. This stage may last several days or weeks or longer before signs of effusive or noneffusive FIP develop. Cats with effusive FIP are often presented after the owner notices progressive distention of the abdomen due to ascites. About one-third of cats with effusive FIP have pleural involvement and dyspnea, often accompanied by chronic fluctuating fever (102-106°F [39-41°C]) lasting 2-5 wk, anorexia, weight loss, and depression.

Cats with noneffusive FIP may have a history of vague illness, including chronic fever, malaise, weight loss, and occasionally major organ system failure (renal, hepatic). Overt ocular and CNS signs may occur simultaneously or independently. About 50% of all cats with noneffusive FIP have signs related to intra-abdominal involvement (kidney, liver, spleen, pancreas, lymph nodes); ~60% of cases exhibit either CNS or ocular signs, or both; and ~15% present with ocular signs only. Only 10-15% of noneffusive cases have lesions of the pleural cavity. Many cats have elements of both the effusive and noneffusive forms of FIP.

Ocular disease may manifest as a bilateral anterior uveitis with iritis or iridocyclitis, hyphema, aqueous flare, hypopyon, or keratic precipitates in the anterior chamber. Posterior chamber involvement may include chorioretinitis with subretinal fluid exudation or hemorrhage and secondary bullous or linear retinal detachment. Fundic lesions may include perivascular cuffing, engorgement of retinal veins, and retinal hemorrhage.

Involvement of the CNS in the noneffusive form may cause focal or diffuse lesions in the brain or spinal cord; ~40% of these cases have CNS signs occurring either alone (25%) or in combination with other organ involvement. Clinical signs are variable and may reflect primary spinal cord, cranial, or cerebellar disease. The most common neurologic signs, in order of decreasing frequency, are posterior incoordination and paresis progressing to generalized ataxia, dorsal hyperesthesia, convulsions, personality changes, and hyperesthesia.

Lesions: In classic effusive FIP, there is diffuse peritonitis or pleuritis (or both) characterized grossly by variable amounts of viscous abdominal or thoracic fluid, deposition of gray-white exudate, and disseminated necrotic plaques (0.5-3.0 mm) on the visceral and parietal peritoneum or pleura. Fibrinous adhesions, particularly between the liver and diaphragm and between loops of bowel, can develop in protracted cases; occasionally, the omentum may be contracted into the anterior abdomen as a thickened mass of fibrinous adhesions. Histologically, lesions are characterized by perivascular necrosis and fibrinonecrotizing or pyogranulomatous inflammation; FIPV particles are seen within macrophages at the periphery of lesions.

Gross lesions in noneffusive FIP consist of multiple, gray-white, raised nodules (0.5-2 cm or larger) in kidneys, visceral lymph nodes, liver, intestines, lungs, eyes, and brain. A single, obstructive, granulomatous intestinal mass is seen in some cases. Histologically, the lesions are perivascular granulomas or pyogranulomas with systemic vasculitis or thrombovasculitis. Ocular lesions may affect either anterior or posterior chambers causing anterior uveitis and iridocyclitis or chorioretinitis, retinitis, retinal hemorrhage and detachment, and optic neuritis. Lesions in the CNS affect the brain and spinal cord and can cause either focal granulomatous masses or more diffuse fibrinonecrotizing or pyogranulomatous meningitis and ependymitis. Occasionally, CSF flow is obstructed by inflammatory exudate, and obstructive hydrocephalus develops.

Diagnosis:

Presumptive diagnosis of FIP is based on history, clinical signs, and results of laboratory tests. Diagnosis of effusive FIP is based largely on analysis of the characteristic exudate. The fluid typically is sterile, viscous or ropey, and yellow to tan; it may contain fibrin strands, has a high specific gravity (1.017-1.047) and high protein content (5-12 g/dL), and is composed of variable amounts of mixed inflammatory cells (1,600-25,000/µL). Mixtures of neutrophils, lymphocytes, macrophages, and fewer mesothelial cells in a granular, eosinophilic, proteinaceous background are seen on Wright’s-stained smears. Protein determinations and electrophoresis of the exudate may be useful in diagnosis. Exudates with total protein >3.5 g/dL (of which >50% is gamma globulin) and cytology consistent with FIP have a positive predictive value of >90%. In addition, the albumin: globulin ratio of the effusion is usually <0.8; a ratio <0.45 is usually predictive of effusive FIP. Documentation of a coronavirus infection by either a positive titer or coronavirus RNA by reverse-transcriptase PCR support a diagnosis of effusive FIP.

About 50% of cats with effusive FIP (and up to 70% of cats with noneffusive FIP) have an increased total plasma protein (>7.8 g/dL), often with hyperglobulinemia (>4.6 g/dL) and a hypergammaglobulinemia. Serum protein electrophoresis may show increases in α2-globulins and polyclonal (occasionally monoclonal) increases in gamma globulin. Hematologic changes in both effusive and noneffusive FIP, although variable, most consistently show a neutrophilic leukocytosis (>19,000 cells/µL) and a relative lymphopenia (>1,500 cells/µL). Forty to 50% of cats develop a progressive normochromic, normocytic anemia (PCV <24%) that may be severe and nonregenerative if FIP is accompanied by FeLV or infection with Haemobartonella felis . Serologic tests (ELISA, immunofluorescent antibody) that detect antibodies against coronaviral proteins are not specific for FIPV and also detect antibodies against feline enteric coronavirus. The coronavirus titer in cats with FIP is usually increased (1:100 to 1:3,200); some cats with clinical FIP have negative or very low titers. PCR does not differentiate between feline coronaviruses and may be interpreted the same as a positive antibody titer.

Noneffusive FIP is a greater diagnostic challenge. Serum protein abnormalities in debilitated cats with nonresponsive fever, weight loss, multisystemic signs (including ocular and CNS signs), and increased coronavirus titers are suggestive of noneffusive FIP. Blood changes in the noneffusive form must be viewed collectively. Cats that have clinical signs of FIP, lymphopenia, and hyperglobulinemia of >5.1 g/dL have an almost 90% probability of having FIP. In cats that do not meet all 3 criteria, there is a 99% probability that FIP is not the diagnosis. A thorough ophthalmic examination is indicated because nearly 40% of noneffusive cases have ocular lesions. Other ancillary laboratory tests may be helpful; clinical chemistries may indicate organ dysfunction in liver, kidney, or pancreas. In cases of neurologic disease with diffuse meningeal involvement, CSF analysis may show increased protein content (90-2,000 mg/dL) and increased numbers of cells (90-9,250 cells/µL), predominantly neutrophils. The most definitive antemortem diagnostic technique is laparotomy and organ punch biopsy of lesions with subsequent demonstration of typical histopathologic changes.

FIP should be considered in the differential diagnosis of any condition that causes peritoneal or thoracic fluid accumulation and in any chronic wasting disease of cats. Effusive FIP with peritoneal involvement should be differentiated from ascites due to congestive heart failure or hypoproteinemia (renal and liver disease, glomerulonephritis, malabsorption, parasitism), neoplasia, bacterial peritonitis, pansteatitis, toxoplasmosis, tuberculosis, pregnancy, and trauma. Differential diagnoses of effusive FIP with pleural effusion include cardiac insufficiency, neoplasia (lymphoma), pyothorax, chylothorax, cryptococcosis, lung lobe torsion, diaphragmatic hernia, and trauma (hemothorax). Differential diagnosis of noneffusive FIP includes neoplasia and other systemic infectious diseases such as toxoplasmosis, nocardiosis, actinomycosis, tuberculosis, and deep mycotic disease (cryptococcosis, coccidioidomycosis, histoplasmosis, blastomycosis).

Treatment:

There is no known treatment that can cure FIP once clinical signs arise. Although spontaneous remission in treated cats has been reported, it is uncommon. The mortality rate of clinical FIP is 95%. Cats with the effusive form progress rapidly, usually within 2 mo. The noneffusive form usually is associated with a more prolonged clinical course, with many cats living several months to a year. Treatment with anti-inflammatory and immunosuppressive drugs, along with supportive care, can make the cat more comfortable; in some cats (probably ≤10%), therapy may extend survival time by several months. Treatment is best advised in cats that are in good physical condition, are still eating, have no neurologic signs, and that do not have concurrent FeLV-induced malignancy or bone marrow suppression.

Treatment is directed toward controlling the immune-mediated vasculitis and reducing viral load. The most effective treatments are combinations of prednisolone (4 mg/kg or 50-100 mg/m2 , PO, sid) and cyclophosphamide (2-4 mg/kg, PO, sid for 4 consecutive days of each week). Alternatively, the cyclophosphamide can be given at 50 mg/m2, PO, every 48 hr or 200-300 mg/m2, every 2-3 wk. Other cytotoxic agents may be substituted for the cyclophosphamide, such as chlorambucil at 10 mg/m2, PO, every 2-3 wk. Because this cytotoxic therapy may suppress bone marrow cells, the hemogram should be monitored weekly and the cat observed carefully for signs of sepsis. Supportive therapy for FIP is important and includes broad-spectrum antibiotics, adequate nutrition and fluid intake, and high doses of ascorbic acid (125-250 mg, bid). The use of low doses of aspirin (10 mg/kg every 48-72 hr) may be useful as an anti-inflammatory and possibly antithrombotic agent when used along with the steroids and cytotoxic agents. Treatment directed toward controlling the virus includes systemic interferon-a (10,000 U/kg, SC, sid or 1.3 million U/m2 , SC, 3 times/wk).

Prevention and Control:

An intranasal, modified live virus vaccine to help prevent FIP is available. It protects 60-90% of the cats vaccinated as determined by experimental challenge several weeks after vaccination. The protection afforded by the vaccine appears to be related to secretory IgA, which neutralizes the virus before entry. The duration of significant protection is unknown but is thought to be limited. Its use has not been associated with causing FIP or accelerated disease either in the general cat population or in catteries with endemic FIP, and it has shown efficacy in preventing FIP losses in large cat shelters with endemic FIP when given to uninfected cats. Because FIP in the general cat population is relatively rare, vaccination of individual pet cats that live mostly or entirely indoors appears to be unwarranted.

Vaccination alone cannot be relied on to control endemic FIP within a cat facility. Other measures to reduce exposure include frequent removal of feces (the primary source of coronavirus), early weaning, isolation of cats that test positive for coronavirus antibodies, isolation and testing of cats after shows, proper sanitation and cleaning using virucidal disinfectants, and immunization against other feline viruses. These should be combined in an overall preventive health program. Increasing the number of litter boxes to at least 1 litter box per 2 cats and reducing crowding stress will reduce FIP losses. A control program based on the presence of serum antibodies to coronaviruses is not warranted. No healthy cat should be euthanized on the basis of a positive coronavirus serum antibody test. The risk of developing FIP following FIPV infection has been shown to have a strong genetic influence. Thus, prevention programs in catteries should include pedigree analysis of disease incidence so that only FIP-resistant breeding stock are used.

Feline Enteric Coronavirus

Feline enteric coronavirus is an enveloped single-stranded RNA virus that is highly contagious among cats in close contact. Although the feline enteric coronavirus is antigenically similar to the virus of feline infectious peritonitis (FIP, Feline Infectious Peritonitis And Pleuritis: Introduction), the pathogenesis of each differs. The enteric form of infection is limited to the GI tract. Death from the enteric form of disease is uncommon.

Etiology and Pathophysiology:

The virus is shed in the feces of seropositive cats. Close contact between cats is required for effective transmission, although the possibility of transmission via fomites also exists. The close antigenic relationship of the enteric form of the virus and that causing clinical signs of FIP has led to speculation that FIP virus may be a mutated form of enteric coronavirus. Cross-protection is not induced by either virus to the other, and recent evidence refutes the supposition that preexisting infection with the enteric form of disease accelerates or enhances the severity of disease associated with FIP.

Feline coronavirus infects the apical columnar epithelium of intestinal villi of the duodenum, jejunum, and ileum, and causes the tips of villi to slough, fuse with adjacent villi, and atrophy.

Clinical Findings:

In catteries, the virus may be a cause of inapparent to mildly severe enteritis in kittens 6-12 wk old. Recently weaned kittens may exhibit fever, vomiting, and diarrhea that may last 2-5 days. More severely affected kittens may also be anorectic for 1-3 days. Adult cats often have subclinical infection. Transient neutropenia may appear with the onset of diarrhea in more severely affected kittens.

Diagnosis:

Most FIP infections result in seroconversion without progression to the fatal form of the disease. Positive coronavirus antibody titers are seen in ~10-40% of cats in the general cat population and in 80-90% of cats in catteries, but only 8% develop FIP. Serologic tests (serum ELISA and immunofluorescent antibody) do not differentiate the enteric form of the virus from that causing clinical signs associated with FIP. Furthermore, these tests do not differentiate between past exposure to the virus or an actively infected cat. Titers >1:3,200 are suggestive of FIP, as opposed to the enteric form of disease. Titers between 1:100 and 1:3,200 may be found in cats with effusive or noneffusive disease and in cats with the enteric form. Some commercial vaccines containing bovine serum components may induce antibody production that may react with antigenically similar bovine serum components in cell cultures used to propagate target FIP viruses for immunochemical tests, thus causing a false-positive test in recently vaccinated (<4 mo previously) cats. Consequently, antibody testing is only useful as a screening tool to detect the presence or absence of virus in a household, to recognize potential carriers or shedders when introducing new cats into an antibody-negative population, and as an aid in the clinical diagnosis of FIP.

Cytologic evaluation of effusions from cats with the wet form of FIP have a high protein content and a variable cell count consisting of neutrophils, macrophages, and lymphocytes. The neutrophils are nondegenerate and do not show signs of toxicity, and the lymphocytes are morphologically normal.

Treatment and Control:

The virus is ubiquitous in cats, and many cats that recover from the infection remain carriers. Enteric coronavirus infection can be prevented only by minimizing exposure to infected cats and their feces. Cats with the enteric disease do not progress to develop clinical signs of FIP. Most cats develop an effective immune response on exposure and recover from infection. However, once clinical signs of disease develop in cats with FIP, the disease is invariably fatal. Management consists only of supportive therapy, ie, fluids when indicated. Vaccination with the temperature-sensitive intranasal vaccine for FIP may protect against challenge with virulent enteric

Peritonitis

Inflammation of the peritoneum may be acute or chronic, local or diffuse, and most commonly is secondary to contamination of the peritoneal cavity. It is often accompanied by abdominal pain, fever, toxemia, and reduced fecal output.

Etiology:

Primary peritonitis is infrequent. It may be caused by infectious agents such as feline infectious peritonitis virus ( Feline Infectious Peritonitis And Pleuritis: Introduction), Nocardia spp , or Mycobacterium spp . Access to the peritoneal cavity is generally by the hematogenous route. Progression of primary peritonitis tends to be chronic (days to weeks).

Secondary peritonitis is often acute and results in rapid, progressive, systemic illness. It is most commonly associated with GI perforation or dehiscence of abdominal wound closure, or with perforation of other infected viscera (eg, prostatic or hepatic abscess, pyometra). Penetrating abdominal injuries may lacerate viscera or inoculate the peritoneal cavity with foreign material and microorganisms. Peritonitis may also occur secondary to chemical irritants (eg, bile, urine) and to other disease processes that allow transmural migration of bacteria (eg, neoplasia, visceral ischemia). Peritonitis from chemical irritation or foreign bodies (eg, sponge) may be septic or nonseptic. Septic peritonitis may remain localized if the omentum or mesentery contains the septic process, which sometimes results in formation of an abdominal abscess.

In large animals, peritonitis is most commonly seen in cattle, less often in horses, and rarely in pigs, sheep, and goats. As well, it is a serious and often fatal condition in small animals, with mortality suggested to be as high as 68%.

In large animals, peritonitis most commonly results from injury to the serosal surface of the GI tract, which allows intestinal contents to leak into the peritoneal cavity. Other causes include traumatic perforations of the abdominal wall or reproductive tract and introduction of pathogens or irritants via injection or surgery (Table: Common Causes of Peritonitis in Livestock).

Microorganisms associated with septic peritonitis reflect the source of contamination. A mixed bacterial population is seen in GI perforation (coliforms, anaerobes), whereas perforation of nongastrointestinal viscera (eg, gallbladder, uterus, prostate) may be associated with aerobic organisms including Escherichia coli , Staphylococcus , Proteus spp , and less commonly, Klebsiella , Enterobacter , Pseudomonas , and Corynebacterium . In horses, Streptococcus equi and Rhodococcus equi may be associated with peritonitis.

Pathogenesis:

Toxemia and septicemia, shock, hemorrhage, abdominal pain, paralytic ileus, fluid accumulation, and adhesions all contribute to the clinical signs and progression of peritonitis. Toxins produced by bacteria and tissue breakdown are readily absorbed through the peritoneum. Bacterial or chemical irritants increase serosal capillary permeability resulting in leakage of plasma proteins, solutes, and water into the peritoneal cavity. Exudation of protein-rich fluid can result in hypoproteinemia and bacterial proliferation. Endotoxins absorbed from the peritoneal cavity have systemic effects leading to hypotension, shock, and systemic inflammatory response syndrome (SIRS) and disseminated intravascular coagulation (DIC). Endotoxins, myocardial depressant factor, acid-base, and electrolyte disturbances directly affect the cardiac function, leading to reduced cardiac output. The combined effect of large fluid losses into the peritoneal cavity and vasodilatory effects of absorbed toxins can produce profound hypotension and hypovolemia. Rupture of the GI tract, with spillage of large volumes of intestinal contents, leads to acute peritonitis. Death due to endotoxic shock may occur suddenly with limited clinical signs or lesions. Shock and hemorrhage associated with rupture of the gut or uterus often lead to death in animals with infection of the GI or reproductive tracts; however, shock and hemorrhage may be minor following uterine rupture in cows. Peritonitis may not develop if the uterine contents are not contaminated, but it may follow if the uterus is not repaired or healed within a few days. Paralytic ileus is a frequent result of acute peritonitis and may also follow intestinal obstruction or surgery, leading to functional obstruction and increased mortality rate if it persists. Large volumes of inflammatory exudates may be secreted into the peritoneal cavity during peritonitis and may lead to impaired respiration by impinging on the diaphragm. Peritoneal trauma leads to secretion of fibrinogen and formation of fibrinous adhesions. Such adhesions help localize the inflammation but may cause mechanical or functional obstruction of the GI tract.

Clinical Findings:

Signs are nonspecific and vary depending on the type of peritonitis (primary or secondary). Abdominal pain may be generalized and severe, so that the animal guards the abdomen, walks with a stiff gait, or is recumbent. Cattle may have a shuffling, cautious gait, with a rigid, arched back; grunting when walking or when passing urine or feces is common. Deep, firm palpation of the abdominal wall results in an easily recognized pain response in cattle. Pain responses in all species are most evident in the early stages of the disease. Fever is common but may be suppressed by prostaglandin inhibitors. Fever (103.5-106°F [39.7-41.1°C]) is a common clinical finding in dogs with peritonitis, while cats may be hypothermic with peritonitis and concomitant shock. Abdominal distention, which may be inapparent, usually is due to accumulation of peritoneal exudate and may be accompanied by hemorrhage, septicemia, toxemia, paralytic ileus, shock, and adhesions. Fluid transudation sequesters electrolytes and protein in the abdominal cavity and atonic gut, and venous stasis leads to hypotension, acid-base disturbances, and circulatory collapse. Toxemia and bacteremia contribute to shock. Icterus may be present in generalized biliary peritonitis. Animals with secondary peritonitis may also exhibit signs of the primary illness.

In small animals, anorexia and depression are often accompanied by vomiting, and feces may not be passed. Dehydration, hypovolemia, and sepsis may result in hypothermia and death due to loss of extravascular fluid volume. In large animals, complete anorexia may be seen in acute, diffuse peritonitis, while decreased appetite may occur in less severe and chronic cases.

In horses, clinical signs include severe colic, ileus, distended intestines on rectal examination, gastric reflux, and occasionally diarrhea. Intestinal stasis leads to reduced peristaltic sounds but sounds of paralytic ileus may be audible and should be differentiated from normal gut sounds. The horse is restless and may lie down and roll intermittently. Tachycardia, weak pulses, poor peripheral perfusion, and fever are common. Septic peritonitis is frequently fatal, despite intensive treatment.

In cattle, rumination ceases and milk production drops. In chronic cases, ruminal contractions may be present but reduced in intensity. Abdominal percussion may detect ruminal tympany. Fever (103°F [39.5°C]) is typical during the first 24-36 hr in cattle with acute, local peritonitis. High fever (up to 106°F [41.5°C]) suggests acute, diffuse peritonitis.

Fecal output in large animals is reduced, although there may be an increased frequency of defecation in the early stages of peritonitis that gives the impression of increased production. Feces may be completely absent for as long as 3 days, even in animals that recover. Rectal palpation may reveal tacky, dry mucosa and fibrinous adhesions between intestinal loops.

Peracute, diffuse peritonitis is associated with extreme weakness, depression, and circulatory failure (tachycardia with a weak pulse). Body temperature is often subnormal (99-100°F [37-37.5°C]). Abdominal pain is not evident. In cases of cecal rupture during foaling, mares suddenly stop straining, and progress toward parturition stops. Shock develops, followed by death in 4-5 hr.

Chronic peritonitis is associated with development of fibrous adhesions. Cattle may have chronic indigestion and toxemia, with periods of acute, severe illness caused by partial intestinal obstruction. Liters of turbid, infected peritoneal fluid may be produced but may be difficult to distinguish from ruminal contents on physical examination. Weight loss, intermittent pain, and diminished gut sounds may be observed in horses with chronic peritonitis.

Diagnosis:

Diagnosis can be difficult because the clinical signs are nonspecific.The most reliable indicators of peritonitis include abnormal feces (in large animals, amount and composition), intestinal stasis, abdominal pain (diffuse or focal), fibrinous or fibrous abdominal adhesions, abnormal peritoneal fluid with an increased WBC count, and a normal or low peripheral WBC count with a degenerative left shift. Peritonitis is rarely diagnosed antemortem in pigs, sheep, or goats.

In dogs with septic effusion, peritoneal glucose concentration is often lower than blood glucose concentration. A blood-to-fluid glucose difference of >20 mg/dL has been found to be 100% sensitive and specific for diagnosis of septic peritonitis. In addition, a blood-to-fluid lactate difference of <2.0 mmol/L is equally sensitive and specific. In cats, blood-to-fluid glucose difference was 86% sensitive and 100% specific for septic peritonitis.

Abdominal radiographs may reveal GI obstruction (bowel dilatation, free abdominal air), ascites, or radiodense foreign material. Loss of serosal detail (a “ground glass” appearance) is indicative of abdominal fluid. Ultrasonography is a valuable adjunct test to evaluate size, shape, and contents of other viscera (eg, gallbladder, prostate gland) suspected to be the source of peritonitis. Rectal palpation in large animals is a useful means of evaluating the intestines. Abdominal paracentesis should be used in large and small animals to obtain fluid for cytologic examination and culture (Table: Characteristics of Adult Bovine and Equine Peritoneal Fluid, Table: Peritoneal Fluid Characteristics and Classification in Dogs and Cats). Diagnostic peritoneal lavage is used when small amounts of fluid cannot be obtained by paracentesis. Cytologic examination of abdominal fluid may reveal septic or nonseptic suppurative inflammation with one or more bacterial infections. Neutrophils are degenerative in the presence of sepsis.

The presence of intra- or extracellular bacteria confirms septic peritonitis. A number of serum biochemical abnormalities may accompany peritonitis. Anemia is commonly associated with any inflammatory disease process in dogs and cats. Hypoglycemia may develop but is not reliably present. Cats <6 mo of age appear more likely to present with a low blood glucose concentration (likely due to decreased glycogen and body fat reserves). Hypoalbuminemia and hyperbilirubinemia are frequently present in dogs and cats. Many septic dogs show cholestasis histopathologically, but this has not been found in septic cats. In contrast to reported findings in other species, cats rarely have an associated increase in serum alkaline phosphatase. Additional causes of icterus in septic animals might include hemolysis (immune-mediated, toxic, or secondary to electrolyte derangements), with or without a decreased capacity for hepatic hemoglobin metabolism.

Total and differential WBC counts are helpful in establishing a diagnosis and determining severity of peritonitis. Acute, diffuse peritonitis with toxemia is usually accompanied by leukopenia, neutropenia, and a marked increase in immature neutrophils (degenerative left shift). In less severe acute peritonitis, leukocytosis may occur as a result of increased neutrophil production. Acute, localized peritonitis may reveal a normal WBC count with a regenerative left shift. The total WBC count in chronic peritonitis may be normal, with an occasional increase in lymphocytes and monocytes.

Treatment:

Initial treatment must be directed toward stabilizing the metabolic consequences of peritonitis (electrolytes, acid-base, coagulation abnormalities) as well as determining the nidus of inflammation/infection and correcting or excising it. Replacement fluids, electrolytes, plasma, or whole blood may be necessary to maintain cardiac output. Broad-spectrum antimicrobial therapy should be initiated, usually by a parenteral route, once appropriate samples have been collected for cytologic evaluation and culture and sensitivity. Aminoglycoside or quinoline antibiotics are effective against gram-negative organisms, and penicillins or cephalosporins are effective against gram-positive organisms. The antimicrobial selected may be changed after sensitivity testing has been performed. There are no published clinical reports of the effectiveness of antimicrobials for treating peritonitis in cattle and horses. Cattle are typically treated with broad-spectrum antimicrobials; the specific choice depends on ease of use and drug withdrawal times. Antimicrobials used for peritonitis in horses include gentamicin (2.2-3.3 mg/kg, IV, bid-tid ), penicillin (22,000 IU/kg, IV or IM, bid-qid ), and metronidazole (15-25 mg/kg, PO).

In small animals, antimicrobial choice is often empirical initially. Multiple isolates are likely, including gram-negative, gram-positive, aerobic, and anaerobic organisms. For combination therapy, enrofloxacin or aminoglycosides (for gram-negative organisms) may be combined with penicillins, first-generation cephalosporins, or clindamycin (for gram-positive anaerobic organisms). Second- or third-generation cephalosporins or imipenum are good candidates for single-agent therapy. Appropriate antibiotics should be started once septic peritonitis is confirmed and fluid samples are obtained for culture and sensitivity.

Once the animal is stabilized, surgery is done to explore the abdomen and to repair any defects (eg, a ruptured viscus). This is followed by thorough peritoneal lavage with an isothermic, isotonic, balanced electrolyte solution. There is no proven clinical benefit in adding an antimicrobial to the lavage solution. Solutions containing antiseptics (eg, povidone-iodine) may induce chemical peritonitis and likewise have no proven clinical benefit. Abdominal drains to allow postoperative lavage and open peritoneal drainage (small animals) are sometimes used to treat severe peritonitis. Survival in dogs and cats managed with closed versus open drainage is very similar. The decision to manage a small animal patient with open peritoneal drainage is often based on experience level and severity of the case. Maintaining patency of drains can be difficult, especially in cattle. In animals treated by open peritoneal drainage, serum protein and electrolyte levels should be monitored periodically, because both are lost with drainage of exudate. Parenteral antimicrobials are continued postoperatively based on either empiric choice or culture and sensitivity data if available. Nutritional support should be anticipated, as many animals with peritonitis will not eat postoperatively. Enteral nutrition helps maintain the health of the intestinal mucosa; however, vomiting or anorexia may force the consideration of alternatives. Feeding tube placement in small animals (esophagostomy, gastrostomy, or jejunostomy tubes) at the time of surgical closure is easily performed. In certain patients, parenteral nutrition (total or partial) may be viewed as a way to provide a portion of the nutritional requirements while enteral nutrition is being initiated. Hyperalimentation, or alimentation by feeding-tube gastrostomy and catheter jejunostomy may be needed in anorectic animals.

In animals with toxemia and shock, IV fluids and electrolytes are crucial elements of treatment, especially during the first 24-72 hr following surgery in horses. Flunixin meglumine (0.25-1.1 mg/kg, IV, bid-tid ) is recommended for treatment of shock, although efficacy is unknown.

Fip Library

Source 1: Feline Infectious Peritonitis by Dr. Diane Addie

Source 2 : A Winn Foundation Health Article On Feline Infectious Peritonitis by Susan Little

Source 3 : Feline Infectious Peritonitis by Cornell University

Source 4: Feline Infectious Peritonitis FAQ by Erin Rebecca Miller

Source 5 : Feline Infectious Peritonitis, by Annette Hegyi, Andreas F. Kolb

Source 6 : Feline Infectious Peritonitis by Fred W. Scott, James R. Richards, Jeffrey E. Barlough

Source 7 : Feline Infectious Peritonitis by Chick Newman

Source 8 : Feline Infectious Peritonitis by Alice M. Wolf

Source 9 : WINN FOUNDATION COMPLETED STUDY REPORT Feline Infectious Peritonitis by Catherine Rokaw

Source 10 : Feline Infectious Peritonitis by Mark Schlatter, Class of 1998 edited by Tsang Long Lin

Source 11 : Feline Infectious Peritonitis by Wikipedia, the free encyclopedia