In a manner similar to all herpesviruses, FHV-1 enters a latent state in innervating sensory nerves after acute infection. In cats, this most commonly occurs in the trigeminal ganglion, and is estimated to occur in about 80% of infections.2 From this latent state, the virus can be reactivated, especially during stressful episodes, leading to replication in the epithelia, virus shedding, and, in a minority of cats, clinical disease (recrudescence). Reactivation can be stimulated by almost any stressor, including trauma, concurrent disease, parturition, boarding, or changes in social hierarchy. Recrudescent episodes are often asymptomatic and may be an important mechanism of maintaining the virus in a population. As new, immunologically naïve kittens are introduced, whether by birth (e.g., breeding cattery) or intake (e.g., shelter or home setting), asymptomatic shedders may expose them to FHV-1.

The typical presentation of FHV-1 infection is that of upper respiratory tract disease (URTD; see also Chapter 33: Respiratory and Thoracic Medicine): sneezing, nasal and/or ocular discharge, fever, depression, and decreased appetite following an incubation period of 2 to 6 days. Conjunctivitis is not uncommon, and can progress to severe hyperemia and chemosis, with mucopurulent ocular discharge (see Chapter 32: Ophthalmology). Infection may lead to corneal ulceration because of damage to the corneal epithelium. In fact, FHV-1 is believed to be the most common cause of feline ocular disease, and corneal ulceration in a cat should be assumed to be a consequence of FHV-1 infection until proven otherwise. This may manifest as a typical dendritic ulcer or may progress to involve the stroma, leading to a descemetocele. Occasionally, cats may manifest with stromal keratitis; this uncommon manifestation is a consequence of the immune response to herpesvirus antigen rather than direct destruction by the virus itself. The corneal stroma becomes infiltrated with mononuclear white blood cells, primarily lymphocytes, which may lead to blindness.

Less common manifestations of FHV-1 are ulcerative dermatitis (see Chapter 25: Dermatology), stomatitis (see Chapter 24: Dental and Oral Diseases), and pneumonia. Ulcerative dermatitis may be multifocal, often involving the face (Fig. 39.1) or planum nasale but may involve other areas of the skin such as the pinnae and flank.^3,4 Affected cats may not have concurrent or historical evidence of URTD. Cases of stomatitis associated with FHV-1 are also relatively uncommon and may involve the soft palate and tongue. An association with chronic gingivostomatitis has not been found.⁵ A necrotizing bronchopneumonia associated with FHV-1 infection is rare in adults but is sometimes seen in kittens where it is often fatal.^6–8

Diagnostic testing for FHV-1 infection primarily involves virus detection, because most cats are seropositive from either natural exposure or vaccination. In addition, studies have shown that the magnitude of the FHV-1-specific antibody level does not necessarily correlate with presence of either acute or chronic FHV-1 infection.9 Methods for viral detection include virus isolation, viral antigen detection, and detection of viral genetic material.

Virus isolation has traditionally been the gold standard diagnostic test because it identifies actively replicating virus. However, results may take several days, and virus isolation is not available everywhere. Virus isolation may be falsely negative in cats with chronic FHV-1 infection. This is due to the presence of locally produced neutralizing antibodies on the mucosal surface which prevent viral replication in cell culture. In addition, virus may be isolated from clinically normal cats.¹⁰ Viral antigen detection using immunofluorescence (IF) is fast and inexpensive; however, sensitivity is relatively low, especially in chronic infections. This test is performed on corneal, conjunctival, or oropharyngeal swabs or scrapings, and samples must be collected prior to fluorescein administration to avoid test interference.

Genetic detection using polymerase chain reaction (PCR) has become common, either as a standalone test or in a panel of pathogens. This assay amplifies viral genetic material through repeated rounds of DNA synthesis. It is performed on corneal, conjunctival, or oropharyngeal swabs or scrapings. The amplified viral material is identified using a probe (e.g., TaqMan real-time PCR). This technology has high sensitivity and specificity, and does not require viable virus, unlike virus isolation. However, the exquisite sensitivity of PCR is a double-edged sword because it may detect subclinical, recrudescent, and even latent infections; thus, positive results must be interpreted carefully.¹¹ Studies have shown that FHV-1 may be detected in many clinically normal cats using PCR,¹² as well as in normal corneas.¹⁰ In a study of shelter cats with acute conjunctivitis, the predictive value of PCR results for FHV-1 and Mycoplasma species were low. The researchers concluded that performing these tests to help formulate a treatment plan has minimal clinical utility in cats with suspected acute ocular infections.¹³ In addition, it appears that PCR assays may detect vaccine virus as well as field strains of FHV-1.¹² Therefore, an increase in test sensitivity does not necessarily equate with increased diagnostic sensitivity. Genetic detection by PCR may also be used to identify virus in ulcerative dermatitis lesions due to FHV-1 infection. The referral laboratory should be consulted for details of sample collection and submission.

Finally, histopathology may identify viral inclusions in skin biopsies, and immunohistochemistry (IHC) can be used for viral detection. Because lesions may contain eosinophils in addition to neutrophils, and intranuclear viral inclusions (Fig. 39.2) are not always found, misdiagnosis as eosinophilic granuloma complex is a concern.

Topical antivirals used in cases of FHV-1 ocular disease include trifluridine, vidarabine, and idoxuridine. These drugs are virostatic and should be considered an aid to the host’s ability to overcome the virus. They must be given often; thus, owner adherence to treatment may be a challenge. Ophthalmic formulations of cidofovir and ganciclovir require less frequent administration although limited data on efficacy and safety are available.14–16 Cats with FHV-1 ocular disease may also acquire bacterial superinfection so concurrent treatment with an antibiotic is often necessary. More information on treating FHV-1 ocular disease is in Chapter 32: Ophthalmology.

Systemic nucleoside analogs developed for human herpesvirus infections have shown some efficacy against FHV-1. Toxic side effects have been reported with some oral drugs, such as acyclovir and valacyclovir, but others, such as famciclovir, are safe in cats. Famciclovir appears to be effective for FHV-1 ocular disease, rhinosinusitis, and dermatitis.¹⁷ In a retrospective study of 59 cats with FHV-1 (ocular, respiratory, or dermatologic), oral dosages of 40 mg/kg every 8 hours and 90 mg/kg every 8 hours were compared using an owner survey.¹⁸ Most owners (91%) were satisfied with the treatment regardless of dosage. However, median time to improvement was significantly shorter and degree of improvement was significantly greater in the higher dosage group. Results of trials using famciclovir for FHV-1 disease in shelter cats have shown mixed, and often disappointing, results.^19,20 Adverse effects of famciclovir are most commonly gastrointestinal (GI; e.g., vomiting, diarrhea, dysrexia). Raltegravir, an integrase inhibitor, has shown promise for reducing ocular and respiratory signs associated with FHV-1 in a small placebo-controlled trial of experimentally infected cats.²¹

Interferons (IFN; both human IFN-alpha and recombinant feline IFN-omega) exert an antiviral effect through limiting cell-to-cell spread. Unfortunately, results of the few peer-reviewed, placebo-controlled, prospective clinical trials in cats are disappointing. As of this writing, recombinant feline interferon omega (rFeIFN) is not available in North America.

Oral lysine inhibits herpesvirus protein synthesis and restricts virus replication by antagonizing the growth promoting effect of arginine. It is optimal when used early in infection, or as a means to prevent recrudescence during stress, where it has been shown to reduce viral shedding in latently infected cats.²² However, studies evaluating its usefulness in preventing URTD in multicat settings, such as shelters, have not shown a positive effect from daily lysine supplementation.^23–25 For this reason, is it is difficult to recommend use of lysine in shelters. In pet cats, oral administration as a bolus (250 to 500 mg/cat/day) for acute infections and as prophylaxis in cats with recurrent signs has been recommended.²⁶ Lysine administration to cats appears to be safe, with no reports of adverse effects related to decreases in plasma arginine concentrations. More information on treating cats with FHV-1 URTD is in Chapter 33: Respiratory and Thoracic Medicine.

Protection following recovery is not long-lived and reinfections may occur. Antigenic variation is not a significant problem with FHV-1; thus, the antigenic coverage of available vaccines is adequate. However, currently available vaccines do not always prevent infection or production of the carrier state. Importantly, they do offer protection from disease and FHV-1 is considered a core component of feline vaccination programs. The nonadjuvanted modified live vaccines (MLV) that contain FHV-1 in combination with other agents have been shown to be both efficacious and safe when administered as directed. In multicat situations where FHV-1 infection is endemic, intranasal vaccination may be used in kittens for early protection from clinical disease and decreased viral shedding.27 Another benefit is that response to intranasal vaccination is not affected by the presence of maternal antibody. More information on FHV-1 vaccination is found in Chapter 8: Preventive Health Care for Cats.

Feline calicivirus is shed in secretions from the oropharynx, conjunctiva, and nose. Transmission is most efficient by direct cat-to-cat contact and by fomites. Aerosol transmission appears to be less important. A major source of infection is asymptomatic carrier cats that shed virus continuously. Unlike FHV-1, FCV shedding is not influenced by stress. There is a high prevalence of FCV infection in healthy cats. Carrier cats may shed for months to years (even lifelong), although one study showed that 50% of infected cats ceased shedding within 75 days.28 Long-term analysis of FCV shedding patterns in five naturally infected colonies revealed three distinct patterns of shedding in individuals: cats that shed virus consistently, cats that shed virus intermittently, and cats that never shed virus.²⁹ Re-infection after recovery is possible.

Feline calicivirus primarily targets epithelia of the upper respiratory tract, oral cavity, and conjunctiva. Unlike FHV-1, it is not associated with corneal infection and ulceration. Some strains appear to be quite pneumotropic, leading to severe interstitial pneumonia, especially in kittens. Co-infection with FHV-1 may be common in kittens with pneumonia.³⁰

Infection with FCV also produces a transient viremia, leading to widespread distribution of the virus. In most cases, this dissemination does not manifest clinically. Uncommonly, disease beyond the respiratory tract may occur. Lameness associated with acute synovitis may occur, and although the precise mechanism of disease remains unclear, viral antigen associated with joint macrophages has been identified.

Rarely, highly virulent FCV strains are associated with severe systemic infection (virulent systemic disease, VSD) that may occur, often as an outbreak within group-housed cats.^31–33 Outbreaks have also occurred in veterinary hospitals, presumably due to nosocomial infection.^33–36 Features of VSD include widespread vasculitis and multiorgan failure. Cases have occurred in vaccinated and unvaccinated cats.³² The underlying pathogenesis of VSD appears to involve viral mutations leading to hypervirulence, though the precise mutation remains unknown. In each documented outbreak where data is available, the virulent strain seems to have appeared spontaneously by mutation from caliciviruses already present in the group. Each isolate has been genetically unique. The FCV isolates causing VSD are not members of a single clade.³⁷ Instead, these mutant viruses are emerging from several different lineages intermixed with other field strains. In addition, the emergence of these variants seems to involve host and environmental conditions. Interestingly, many of the documented VSD outbreaks have occurred in shelter or rescue situations. One theory is that in these settings, FCV may be endemic in the population; in these situations, rapidly replicating virus that can attain high titers in a relatively short period of time is selected for because of the immunity of the endemically infected population.³⁸ Host parameters have also been speculated to play a role in VSD cases. In particular, immunopathologic mechanisms may contribute to the disease production.³⁹ Local modulation of cytokine levels have been found associated with lesions and may contribute to the vasculitis and increased vascular permeability seen.

Clinical presentations of FCV infection vary from mild URTD to viral pneumonia to lethal VSD. The typical presentation is similar to FHV-1 URTD although the ocular discharge usually remains serous, corneal ulcers do not occur, and oral ulcers are common. Cats may present with vesicular and ulcerative lesions of the oral cavity that may also involve the lips, nares, and even paronychial skin. Early signs include vesicular lesions that are commonly seen on margins of the tongue (Fig. 39.3). As the overlying epithelia necroses, the lesions ulcerate and become inflamed.

Sneezing, hypersalivation, fever, and serous ocular and nasal discharge may be seen. Ocular lesions include conjunctival hyperemia, chemosis, and blepharospasm. Most infections are mild and self-limiting. Acute lameness with joint and muscle pain may be seen in kittens accompanied by fever; about 25% also have oral ulceration. In these cases, clinical signs resolve quickly, usually within 72 to 96 hours. Feline calicivirus has been associated with chronic lymphoplasmacytic gingivostomatitis40 and it may also target alveolar epithelia of the lower respiratory tract.

Virulent systemic disease is typically more severe in adults than kittens. Epithelial infection and necrosis occur in skin as well as mucous membranes, leading to ulceration and crusting lesions that involve the ears, face, and paws (Fig. 39.4).⁴¹ Subcutaneous edema of the head and limbs may be seen. Clinical signs include jaundice, dyspnea, vomiting, and diarrhea. However, mild or subclinical infections may also occur, and asymptomatic cats are able to transmit fatal disease.⁴¹ Mortality rates as high as 60% have been reported.⁴² At necropsy, affected cats commonly have hepatocellular necrosis, interstitial pneumonia, and fluid in body cavities.^41,42

The presence of severe oral ulcerations is an important clinical indicator of FCV infection, even in cases of VSD. Confirmation of a diagnosis of FCV, as with FHV-1, relies primarily on detection of virus because the many cats are seropositive for FCV. Viral identification is particularly important in multicat settings. Virus isolation from samples collected from conjunctival, oropharyngeal, and nasal swabs has been considered the gold standard because it detects replicating virus, but it may not be practical or readily available. As with FHV-1, detection of FCV nucleic acid by PCR is being used more frequently for diagnosis and is done on the same samples as for virus isolation. The genetic variations of FCV may make PCR testing difficult, potentially leading to false-negative results. It is also possible that PCR assays may detect vaccine virus in addition to field strains.43 The referral laboratory should be consulted for details of sample collection and submission.

Clinicopathologic abnormalities associated with VSD are generally nonspecific, such as neutrophilia, hyperglobulinemia, and elevated liver enzymes. At this time, no assay can distinguish FCV strains causing VSD from those causing more classic disease; this classification is currently based on clinical presentation. In cases of suspected VSD, samples should be collected from the same sites as for typical presentations. In addition, tissue samples from those animals that die should be submitted for histopathology and IHC or PCR. These samples should include parenchymal organs and ulcerated lesions (e.g., skin, foot pads, lingual areas).

As for FHV-1, interpretation of positive results from antemortem assays must consider that asymptomatic carrier states are not uncommon; thus, finding FVC in a sick cat does not necessarily prove causation of disease.

Treatment of FCV infection primarily involves symptomatic and supportive care. Fluid therapy and nutritional support (e.g., esophagostomy or gastrostomy tube feeding) are important for anorectic cats, and oxygen therapy for dyspneic cats is critical. Broad-spectrum antibiotics should be used if secondary bacterial infection is suspected. Currently, no specific antiviral medication for FCV exists. For cats with VSD, intensive care is often needed; corticosteroids for the immunopathologic component may be beneficial.41

Vaccination for FCV is a core component of feline vaccination programs. As for FHV-1, vaccination prevents disease but does not always prevent infection or the carrier state. Most vaccines contain one or two FCV strains and these strains have been shown to be broadly cross-reactive based on neutralization studies. However, it is not known if currently available dual-strain vaccines are protective against VSD. It is difficult to create a vaccine that provides protection against most strains in circulation because of the antigenic variability of FCV, and continued evaluation of prevalent strains and their antigenic relatedness to vaccine strains will be critical. In a clinical setting, if vaccine breakthroughs are occurring within a cat population, using vaccines with a different FCV strain may enhance protection. More information on calicivirus vaccines is found in Chapter 8: Preventive Health Care for Cats.

Environmental decontamination is also important for control in multicat situations, including veterinary clinics. This virus can persist for days to weeks in the environment, and disinfection requires products with oxidizing activity, such as 5% sodium hypochlorite diluted 1:32 or potassium peroxymonosulfate.³⁸ Quaternary ammonium products are not effective against FCV.⁴⁴ Thus, decontamination following examination or housing of any cat with URTD should include cleaning with a detergent to remove organic matter, followed by disinfection with an appropriate product. During outbreaks of VSD, stringent quarantine measures and barrier nursing are required to prevent spread. All affected and exposed cats should be strictly isolated, and if possible, treatment away from the veterinary hospital is ideal.

While FPV is shed in all body secretions during active disease, it is most consistently found in feces, so the most common route of infection is fecal–oral and via contaminated fomites. The period of viral shedding is usually a few weeks but can be as long as 6 weeks. Asymptomatic recovered cats and those with subclinical infection can also shed virus. In one retrospective study of naturally infected cats, 62% were housed exclusively indoors and 15% had no contact with other cats; this highlights the role of fomites.50,51 Clinical or subclinical infection of pregnant queens may result in transplacental infection of kittens. The outcome may be aborted or stillborn fetuses if the queen is infected early in pregnancy or central nervous system (CNS) defects (mainly cerebellar hypoplasia) in live-born kittens if the queen is infected late in pregnancy.

After exposure, virus initially replicates in local lymphoid tissue. From there, it disseminates via lymphatics and blood to many tissues. Viremia can be detected within 2 to 7 days after infection and clinical signs appear in 2 to 10 days. As discussed later, successful viral replication leading to cell lysis occurs only in those cells that are actively replicating. Destruction of intestinal crypt cells leads to blunting or complete loss of intestinal villi, while bone marrow infection leads to profound leukopenia. In addition, destruction of lymphoid tissues can contribute to virus-induced immunodeficiency.

All parvoviruses share a tropism for cells of high mitotic index; that is, these viruses can only complete their replication cycle in cells that are rapidly dividing. With its small genomic coding capacity, much of the replication machinery for the virus must be provided by the infected cell. Parvoviruses, unlike larger DNA viruses, have no ability to “push” cells into the cell cycle; cells must be actively dividing to support parvovirus replication. In kittens and adult cats, this includes lymphoid tissue, blood cell precursors in the bone marrow, and intestinal crypt epithelia. In the neonate, this is primarily the cerebellum. The virus may also target a wide variety of cells in the developing embryo or fetus, causing reproductive loss. The virus causes a lytic infection in target cells, leading to cell destruction. The typical clinical presentation in kittens reflects bone marrow and intestinal epithelia involvement. For the former, because of the shorter half-life of white blood cells compared with red blood cells, this destruction manifests as severe leukopenia, though anemia can also occur. Anemia can also occur because of blood loss in the intestines.

Feline panleukopenia occurs most often in young, unvaccinated, or incompletely vaccinated cats. Kittens may receive maternally derived antibodies (MDA) in colostrum which maintain a protective titer until 6 to 8 weeks of age. Two studies showed that 50% to 67% of kittens born to immune queens became susceptible to challenge at 10 weeks of age, increasing to 100% susceptible by 12 to 16 weeks of age.52,53 In another study of FPL in kittens that had been vaccinated, none had received a vaccination after 12 weeks of age.⁵⁴ Finally, in a study of kittens from shelters and breeding catteries, almost 50% had no evidence of MDA to FPL at 6 weeks of age.⁵⁵In most countries, FPL is seen during the late spring to early autumn which corresponds to the time that large numbers of kittens with waning MDA enter adoption facilities. Unvaccinated cats are likely to acquire immunity to FPL through subclinical infection as they get older.⁵⁶

Infection with CPV or FPV may cause subclinical or clinical disease. The clinical presentation of FPL includes profound depression, anorexia, and a high fever. Signs referable to the GI tract may not be evident initially or may only include vomiting, but diarrhea that may be hemorrhagic is a hallmark sign in most cases. Hemorrhagic diarrhea is less common in infected cats than in infected dogs.50,51 Hypersalivation due to nausea may occur; it was observed in 20% of affected cats in a shelter study.⁵⁰ Physical examination often reveals severe dehydration; abdominal palpation may be painful and thickened intestinal loops and/or enlarged mesenteric lymph nodes may be found.

Kittens quickly become dehydrated and may be moribund with a subnormal body temperature. Sudden death can occur due to septic shock, especially in kittens less than 8 weeks of age. The classic disease presentation is most common in kittens at the time that maternal immunity wanes resulting in a high mortality rate. One study of kitten mortality in the United Kingdom (1986–2000) revealed that 25% of kitten deaths were due to FPL.⁵⁷

Infection of kittens in late gestation or in the neonatal period may result in cerebellar hypoplasia that manifests as permanent ataxia and intention tremors ( Video 39.1). Hydrocephalus, retinal dysplasia, and optic nerve hypoplasia may also be seen. While myocarditis is well recognized in puppies with CPV infection, there is no evidence that this occurs in cats.

Diagnosis of FPL is based on clinical presentation, the presence of severe leukopenia, and virus detection in feces. Leukopenia, characterized by neutropenia and lymphopenia, occurs in up to 75% of cases and may be severe (<2000 cells/µL).54,58 Fortunately, rebound leukocytosis can occur within 2 to 3 days of the nadir. Thrombocytopenia occurs in about half of cases and is due to megakaryocyte destruction or disseminated intravascular coagulation (DIC).^54,58 Anemia also occurs in about half of cases and is typically mild unless there is significant GI blood loss. Abnormalities on serum biochemistry panels include hypoalbuminemia, hypochloridemia, hyponatremia, hypoproteinemia, and elevated aspartate aminotransferase.^54,58

Virus detection can be accomplished with fecal antigen tests, PCR, and virus isolation. Fecal antigen detection is often performed with point-of-care (POC) fecal enzyme-linked immunosorbent assay (ELISA) kits. Typically, fecal antigen kits designed to detect CPV will also detect FPV.^59,60 The sensitivity of POC fecal antigen tests is variable; the range was 50% to 80% in a study that evaluated five different kits.⁶⁰ However, specificity was high, ranging from 94% to 100%. Evaluation of fecal antigen results must be interpreted considering vaccination history, especially in shelters. Fecal shedding of MLV virus from recently vaccinated cats is known to occur and may be detected by some assays.⁶¹ In one study of recently vaccinated kittens, the specificity of fecal antigen detection varied widely (80% to 98%) depending on the brand of kit.⁶¹ In addition, field and vaccine strains of FPV have been detected in the feces of clinically healthy adult cats.⁶²

When FPL is highly suspected but fecal antigen testing is negative, PCR can be used to confirm the diagnosis. Many PCR assays are sensitive and may detect vaccine virus; thus, positive results by PCR must also be interpreted considering other relevant clinical data. In addition, some PCR assays do not distinguish CPV from FPV.

At necropsy, findings typically include segmental enteritis with dilation, hyperemia, hemorrhage, and necrosis; lesions tend to be most severe in the jejunum and ileum. Mesenteric lymph nodes may be enlarged, hemorrhagic, and edematous. Histopathologic examination reveals crypt necrosis with villus blunting in the small intestines and cellular depletion in bone marrow and lymphoid tissues (Fig. 39.5). In severe cases, crypt epithelium may be completely sloughed leaving only the basement membrane.

Antiemetics may be necessary to control vomiting. The antiemetic of choice is maropitant; it can be combined with ondansetron if vomiting is intractable. If hematemesis or severe, intractable vomiting are present, a parenteral GI protectant may be indicated; proton pump inhibitors (e.g., pantoprazole, esomeprazole) are preferred in cats. In the past, it was common to recommend fasting for kittens and puppies with parvoviral enteritis. However, fasting may have a detrimental effect on the intestinal mucosa leading to a damaged mucosal barrier and increased risk of bacterial translocation. Early enteral feeding in patients with GI disease is now known to improve healing of enterocytes, promote more rapid clinical improvement, and decrease risk of sepsis.63 An attempt should be made to encourage food intake (or provide nutritional support through nasoesophageal tube feeding) even while patients have vomiting and diarrhea.

Bacterial septicemia due to leukopenia and intestinal epithelial necrosis is an important complication; thus, broad-spectrum antibiotics with activity against gram-negative and anaerobic bacteria (e.g., monotherapy with a cephalosporin or amoxicillin/clavulanic acid combined with a fluoroquinolone) are an important management tool.

Feline recombinant interferon–omega may have benefit in treating dogs with parvovirus infection,⁶⁴ but no studies have been published in cats. Use of feline recombinant interferon–omega has been recommended in pregnant queens and neonatal kittens prior to introduction to a potentially contaminated environment to enhance antibody production.⁶⁵ In some European countries, passive immunotherapy products are available that contain FPV antibodies. However, no prospective clinical trials have been published.

Fecal microbiota transplantation (FMT) has been used with success in puppies with parvoviral enteritis. In a study of 66 affected puppies, half were given FMT with standard supportive care and the remainder were given standard supportive care without FMT.⁶⁶ Although there was no difference in survival, treatment with FMT was associated with faster resolution of diarrhea and shorter hospitalization time than supportive care without FMT. As of this writing, no studies have been published on the use of FMT in cats with FPL.

Mortality rates may be high in unvaccinated kittens; death is often due to complications such as bacteremia, dehydration, and DIC. Few studies have evaluated prognostic factors in cats with FPL. In one European study, the records of 244 cats with FPL were retrospectively evaluated.⁵⁴ The overall survival rate was 51%. While some cats had been vaccinated, none had received a vaccine after 12 weeks of age. Increased risk of death was associated with low leukocyte (<1000/µL) and thrombocyte (<135,000/µL) counts at presentation. Other negative prognostic factors were hypoalbuminemia (<30 g/L) and hypokalemia (<4 mmol/L [<4 mEq/L]). In a retrospective study of shelter cats with FPL in Europe, risk of death was associated with lethargy, rectal temperature <37.0°C (<100.2 °F), and low body weight at diagnosis.⁵⁸ In a third retrospective study of 70 cats with FPL presented to a veterinary clinic in Italy, serum total thyroxine concentration <0.82 µg/dL (<10.55 nmol/L) was associated with increased risk of death (sensitivity 74%, specificity 83%).⁶⁷ Variables that did not influence mortality were age, neuter status, serum concentrations of amyloid A, haptoglobin, and cholesterol, and presence of systemic inflammatory response syndrome.

Panleukopenia is most common in kittens, especially unvaccinated kittens. It is a major concern in shelters where it may contaminate the environment and survive disinfection. Thorough cleaning with a detergent to remove all organic matter, followed by disinfection with an appropriate product with oxidizing activity (e.g., 6% sodium hypochlorite, potassium peroxymonosulfate) is needed to inactivate the virus.44 The virus survives disinfection with 70% alcohol and quaternary ammonium compounds. Contaminated fomites and caretakers can be an important mode of transmission; stringent precautions to prevent spread must be taken in veterinary hospitals and multicat environments.

Vaccination is recommended for every cat, given the severity of disease and the ability of the virus to persist in the environment. A MLV is recommended as early as 6 weeks of age with re-vaccination continuing through 16 weeks to ensure maternally derived immunity has not interfered with vaccine response. In the face of an outbreak, kittens can be vaccinated as early as 4 weeks with a MLV to provide rapid onset of immunity. Vaccination guidelines should be consulted for re-vaccination protocols in adult cats (Box 39.1). Vaccination of pregnant queens or neonates (<4 weeks) with a MLV is not recommended because live attenuated virus may infect and produce lesions in the fetus or neonate. Immunity after recovery from FPL is likely lifelong.