The most common physical examination findings are weakness, lethargy, and dehydration. Pain may be noted on palpation of the abdomen, or a hunched posture may be present. The perianal region may be contaminated with feces. Oral ulceration and mucosal pallor may be present in severely affected cats, and rarely, bacteremia may be accompanied by icterus.
Terminally, affected cats may be hypothermic, bradycardic, and comatose. Kittens with cerebellar signs are generally bright and alert but exhibit intention tremors, incoordination, ataxia, hypermetria, a broad-based stance, decreased postural reactions, a truncal sway, and absence of a menace response.
Cats with forebrain disease may show abnormal behavior, such as aggression or decreased mentation. Examination of the ocular fundus may reveal folding of the retina, evidence of retinal degeneration with discrete gray spots, and optic nerve hypoplasia. Retinal lesions may be an incidental finding in older, recovered cats, which includes surviving cats with cerebellar hypoplasia. The most common abnormality on the CBC in feline panleukopenia is leukopenia, which is due to a neutropenia and lymphopenia Box Recovery may be associated with lymphocytosis and leukocytosis.
Thrombocytopenia and mild anemia are also common. Thrombocytopenia may result from damage to the marrow or, possibly, disseminated intravascular coagulation DIC. Hyperglycemia or hypoglycemia may also be identified. As in dogs with parvoviral enteritis, abdominal radiography in cats with panleukopenia may show evidence of poor serosal detail and a fluid- and gas-filled gastrointestinal tract.
MRI of cats with neurologic signs due to FPV may reveal evidence of cerebellar agenesis or hypoplasia. Rarely, hydrocephalus, porencephaly, or hydranencephaly can be detected. Diagnostic assays available for feline panleukopenia are listed in Table Use of serology for diagnosis of feline panleukopenia is complicated by widespread exposure or immunization, so serologic assays that detect antibody against FPV are generally used to assess the need for vaccination rather than for diagnosis.
They can also be used in outbreak situations in order to determine which cats are at risk for development of disease and virus shedding, and which cats are protected and therefore at low risk.
The gold standard method for FPV serology is hemagglutination inhibition, which measures the ability of serum to prevent agglutination of erythrocytes by the virus see Chapter 2. Serum neutralization assays may also be used. The sensitivity and specificity of these assays varies from one assay to another and with the stage of infection, because virus shedding may be transient.
In general, false-negative results are common with these assays, but false positives are uncommon, so a positive test result in a cat with consistent clinical signs suggests a diagnosis of feline panleukopenia. Another study of 52 cats with diarrhea and healthy cats showed variability in the sensitivity and specificity of five different test kits when compared with fecal electron microscopy.
This study included only 10 cats with FPV as determined with electron microscopy. Additional studies are warranted that evaluate the sensitivity and specificity of these assays in larger numbers of cats with FPV infection when both real-time PCR and electron microscopy are used as the gold standard. False-positive fecal antigen assay results after vaccination with attenuated live viral vaccines appear to be uncommon, but again vary with the test used. Fecal electron microscopy is still offered by some institutions for diagnosis of viral enteritis.
It may also facilitate diagnosis of other infections such as rotavirus, astrovirus, torovirus, and coronavirus infections. Turnaround time may be slow. Generally speaking, large amounts of virus must be present for results to be positive, and technical expertise is required to accurately identify virus in the stool.
FPV can be isolated in feline cells, but as with CPV, isolation can difficult, and the virus shows minimal cytopathic effects. As a result, isolation of FPV is a specialized procedure that is uncommonly used for diagnosis. Clinicians should contact their laboratory to determine the specificity of the assay offered. The extent to which these assays detect attenuated live vaccine virus after vaccination requires further study.
Assays have also been developed that differentiate between field and vaccine strains of FPV. Gross pathologic findings in feline panleukopenia include thymic involution; thickening, distention, and discoloration of the intestinal wall with serosal hemorrhage Figure ; and enlarged, edematous mesenteric lymph nodes.
The intestine may contain bloody liquid contents, and mucosal hemorrhage may be identified. Hemorrhages may be visible on the surface of other organs as well. In some cats, mild pleural or peritoneal effusion is present. Cats infected prenatally may have cerebellar aplasia, or more commonly a small cerebellum often half to three-quarters normal size. Intestinal tract of a 2-year-old intact female domestic longhair cat with severe feline panleukopenia.
The intestinal loops are dilated and flaccid and discolored red to purple. Histopathologic findings in the intestinal tract are similar to those described for CPV-2 infection, with crypt dilation and necrosis of crypt epithelial cells, accumulation of cellular debris, neutrophil infiltration, loss of villi, and submucosal edema throughout the small and large intestines; the jejunum and ileum are usually most severely affected Figure , A.
Acutely affected cats show widespread lymphoid depletion and there may be hyperplasia of mononuclear phagocytes. Intranuclear inclusions are found in some cats Figure , B. Examination of the bone marrow may reveal bone marrow hypoplasia. Examination of the cerebellum shows cellular depletion; reactive astrocytosis may be present.
Immunohistochemistry or immunofluorescent antibody may be used to document the presence of the virus within tissues see Figure , C. A, Histopathology of the jejunum from a kitten with panleukopenia.
Villi are rounded and blunted with nearly complete epithelial loss and crypt dilation. B, Histopathology of the jejunum from a young barn cat that died after several days of profound weakness and neurologic signs.
Six other cats in the barn died with the same signs. Mucosal crypts are dilated and contain debris, and intranuclear inclusions are present small arrows. Another cell large arrow is foamy and degenerate and has a hyperchromatic nucleus. C, Same cat as in B. The presence of FPV in the intestinal tract is confirmed with immunohistochemistry brown stain. Treatment of cats with feline panleukopenia is with supportive care, especially intravenous crystalloids and parenteral antimicrobial drug treatment as for CPV-2 infections see Chapter Dextrose supplementation of the fluids may be required, and blood glucose concentration should be monitored.
Oral intake of food and water should be withheld until vomiting has ceased. Experience with early enteral nutrition has not been reported in cats, and extreme care is warranted to prevent aspiration pneumonia. Antiemetics such as metoclopramide or ondansetron may be effective. Cats with panleukopenia that survive the first 5 days of treatment usually recover, although recovery is often more prolonged than it is for dogs with parvoviral enteritis. In cats with feline panleukopenia from Europe, the survival rate was Only total leukopenia, and not lymphopenia, was correlated with mortality.
Hypoalbuminemia and hypokalemia were also associated with an increased risk of mortality. In contrast to dogs with parvoviral enteritis, mortality in cats does not appear to be correlated with age.
Cerebellar signs in kittens with cerebellar hypoplasia typically do not progress and may improve slightly as a result of compensatory responses from other senses such as vision.
Recovery from feline panleukopenia is thought to confer lifelong immunity. Effective vaccines are widely available, and include both parenteral inactivated and attenuated live viral vaccines.
An intranasal FPV, FHV-1 and feline calicivirus vaccine is available; its use has been controversial, because panleukopenia is a systemic disease. An outbreak of salmonellosis and panleukopenia occurred in one cattery that used an intranasal FPV vaccine.
Both inactivated and attenuated live vaccine types induce protective antibody titers after vaccination in a high proportion of cats, 5 although the attenuated live vaccine may be more likely to induce protective titers than the inactivated vaccine.
Two injections are always required for inactivated vaccines, and maximal immunity does not occur until 1 week after the second dose.
However, even with an inactivated vaccine, challenge 7. In shelter situations, the use of attenuated live vaccines is always recommended because of the slow onset of immunity with inactivated vaccines. The most common reason for vaccine failure is interference by MDA. Maternal antibody persists until at least 12 weeks, and possibly longer in some cats.
Virus neutralization titers above are likely to interfere with vaccination, and kittens with titers below are generally considered to be susceptible to infection by FPV.
Kittens should be vaccinated every 3 to 4 weeks from 6 to 8 weeks of age, and it is recommended that the last vaccine in the kitten series be given no earlier than 14 to 16 weeks of age. When there is a history of an outbreak situation, the final booster could be given no earlier than 18 to 20 weeks of age. Vaccination of pregnant queens with attenuated live viral vaccines can cause cerebellar hypoplasia or fetal losses. The frequency with which this occurs is unknown. As a result, it has been suggested that pregnant queens only be vaccinated with attenuated live FPV vaccines if they are being introduced into a shelter and quarantine while immunization with inactivated vaccines is performed is not possible.
Alternatively, assessment for protective antibody titers with an in-house test kit where available could be performed. New kittens should not be introduced into households that previously contained cats infected with FPV unless they are fully vaccinated. In the face of an outbreak, exposed and susceptible kittens may be effectively protected for 2 to 4 weeks through subcutaneous or intraperitoneal administration of 2 mL of type-matched serum from cats with a high antibody titer.
However, this is only effective when administered before the onset of clinical signs, and it can interfere with subsequent vaccination. For these kittens, it has been recommended that vaccination be withheld for 3 weeks after the serum has been administered. Repeated treatment with serum should be avoided because hypersensitivity reactions may occur. Prevention of feline panleukopenia should also include proper disinfection with disinfectants that are effective against parvoviruses, such as bleach, accelerated hydrogen peroxide, or potassium peroxymonosulfate see Chapter 11 and, in shelter situations, isolation or removal of cats that develop gastrointestinal illness, and separate housing for healthy kittens.
Callie was brought to an emergency clinic for acute onset of collapse and severe illness. The current owner had fostered the cat for 1 week after she was found as a stray. The cat had been nursing a litter of kittens. The kittens were 4 weeks old, being weaned and apparently healthy.
Since being fostered, the cat had exhibited a progressive decrease in appetite and thirst, and her feces had become soft and pasty. The night before she was brought to the emergency clinic, she had been bathed, and afterwards she vomited bile-stained fluid twice and was placed on a heating pad.
The following morning she was found laterally recumbent and minimally responsive. Fecal and urinary stains were present around the perineum and on the caudal aspect of the pelvic limbs. Diffuse muscle wasting was present. The cat was laterally recumbent and nonambulatory. The abdomen was soft and nonpainful on palpation. An abdominal ultrasound showed marked fluid distention of the small intestines. Callie was treated with active warming, and a central venous access line was placed.
The cat repeatedly vomited blood-tinged fluid, and so treatment with metoclopramide 0. When the CBC results were available, the cat was placed in the isolation ward. Pasty diarrhea that contained sloughed mucosa occurred every 1 to 2 hours, which transitioned to liquid red feces over 24 hours. Partial parenteral nutrition was initiated. That evening, pyrexia developed The owner elected euthanasia.
FPV can cause disease in all felids and in some members of related families eg, raccoon, mink , but it does not harm canids. Conversely, some currently circulating CPV strains CPV-2a, -2b, and -2c have been shown to cause feline panleukopenia in domestic cats and larger felids.
Virus particles are abundant in all secretions and excretions during the acute phase of illness and can be shed in the feces of survivors for as long as 6 weeks after recovery.
Being highly resistant to inactivation, parvoviruses can be transported long distances via fomites eg, shoes, clothing. Peroxygen disinfectants eg, potassium peroxymonosulfate are also highly effective. It is important that contaminated surfaces are thoroughly cleaned of organic material before disinfectants are applied.
Cats are infected oronasally by exposure to infected animals, their feces, secretions, or contaminated fomites.
Most free-roaming cats are thought to be exposed to the virus during their first year of life. Those that develop subclinical infection or survive acute illness mount a robust, long-lasting, protective immune response.
FPV infects and destroys actively dividing cells in bone marrow, lymphoid tissues, intestinal epithelium, and—in very young animals—cerebellum and retina. In pregnant queens, the virus may spread transplacentally to cause embryonic resorption, fetal mummification, abortion, or stillbirth. Alternatively, infection of kittens in the perinatal period may destroy the germinal epithelium of the cerebellum, leading to cerebellar hypoplasia, incoordination, and tremor.
FPV-induced cerebellar ataxia has become a relatively rare diagnosis, because most queens passively transfer sufficient antibodies to their kittens to protect them during the early period of susceptibility. Most feline panleukopenia infections are subclinical, as evidenced by the high seroprevalence of anti-FPV antibodies among unvaccinated, healthy cats. Those cats that do become ill are usually Physical examination typically reveals profound depression, dehydration, and sometimes abdominal pain.
Abdominal palpation—which can induce immediate vomiting—may reveal thickened intestinal loops and enlarged mesenteric lymph nodes. In cases of cerebellar hypoplasia, ataxia and tremors with normal mentation are seen. Retinal lesions, if present, appear as discrete gray foci. Mortality is highest in kittens There are typically few gross lesions due to feline panleukopenia, although dehydration is usually marked. Bowel loops may be segmentally dilated and may have thickened, hyperemic walls.
There may be petechiae or ecchymoses on the intestinal serosal surfaces. Perinatally infected kittens may have a noticeably small cerebellum. Histologically, the intestinal crypts are usually dilated and contain debris consisting of sloughed, necrotic, epithelial cells. Blunting and fusion of villi may be present. Eosinophilic intranuclear inclusion bodies are seen only occasionally in formalin-fixed specimens; use of Bouin's or Zenker's fixative will increase the likelihood of seeing these. There may be a notable lack of lymphocytic or inflammatory cell infiltration in the bowel walls because of destruction of these leukocytes by the virus.
Neutropenia develops earlier than lymphopenia. Salmonellosis Salmonellosis read more and infections with feline leukemia virus Feline Leukemia Virus and Related Diseases read more FeLV and feline immunodeficiency virus Feline Immunodeficiency Virus FIV In adult animals, immunodeficiencies often result from virus infections, malnutrition, stress, old age, or toxins. These are called secondary immunodeficiencies. Virus-induced secondary immunodeficiencies FPV infections combined with various salmonellae or feline calicivirus cause much more severe disease than FPV alone.
Successful treatment of acute cases of feline panleukopenia requires vigorous fluid therapy and supportive nursing care in the isolation unit. Electrolyte disturbances eg, hypokalemia , hypoglycemia, hypoproteinemia, anemia, and opportunistic secondary infections often develop in severely affected cats. Anticipation of these possibilities, close monitoring, and prompt intervention can improve outcome.
In addition to crystalloid infusion, transfusion of fresh-frozen plasma helps support plasma oncotic pressure and provides clotting factors to severely ill, hypoproteinemic kittens.
It also provides some anti-FPV antibodies. Whole blood is preferable for the occasional cat that is severely anemic. Parenteral, broad-spectrum antibiotic therapy is indicated; however, nephrotoxic drugs eg, aminoglycosides must be avoided until dehydration has been fully corrected. Because of the nephrotoxic potential of the gentamicin, urinary protein dipstick findings, sequential urine sediments, and serum SDMA or creatinine should be monitored.
Thus, FPV should be considered a cause for neuronal vacuolization in cats presenting with ataxia. Keywords: cat; central nervous system; feline panleukopenia virus; immunohistochemistry; next-generation sequencing; vacuolization.
Abstract Feline panleukopenia virus FPV infections are typically associated with anorexia, vomiting, diarrhea, neutropenia, and lymphopenia. Substances Capsid Proteins.
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