Feline Infectious Flashcards

A 2-year-old intact male DSH cat from a multi-cat household presents with progressive weight loss, anorexia, and a palpable abdominal mass. Abdominal effusion is present, and fluid analysis reveals a protein concentration of 5.8 g/dL, a Rivalta test that is positive, and a cell count of 4,200 cells/μL (predominantly non-degenerate neutrophils and macrophages). An immunofluorescence assay on the effusion detects coronavirus antigen within macrophages. Which statement BEST describes the pathogenesis underlying this cat's condition?

Answer: A biotype shift from enteric coronavirus to FIP virus occurs via two key mutations in the spike protein receptor-binding domain and the 3c accessory gene, enabling macrophage tropism and systemic spread.

FIP arises from in-host mutation of feline enteric coronavirus (FECV), most critically in the spike protein (affecting cell tropism) and the 3c gene (disrupting immune evasion), converting FECV into FIP virus (FIPV) with macrophage-tropic capability. This internal mutation model—not horizontal transmission of a FIPV strain—is the current consensus. Co-infection with FeLV/FIV is a risk factor but not a prerequisite. Antibody-dependent enhancement may play a contributory role but is not the sole or primary mechanism.

A 6-week-old kitten from an unvaccinated litter presents in lateral recumbency with intention tremors, broad-based ataxic gait, and dysmetria. The dam had an unknown vaccine history. The kitten otherwise appears normally developed and alert. Which of the following MOST accurately explains the timing of viral injury required to produce this neurological syndrome?

Answer: Feline panleukopenia virus (FPV) infected the kitten in utero or within the first two weeks of postnatal life, targeting rapidly dividing granule cell precursors in the external germinal layer of the cerebellum.

Feline panleukopenia virus is highly mitotropic and requires actively dividing cells. Cerebellar hypoplasia results from FPV infection during late gestation or within the first 1–2 weeks of life when the external germinal layer (EGL) of the cerebellum—a transient population of proliferating granule cell precursors—is present. Viral destruction of these precursors results in a hypoplastic cerebellum with characteristic non-progressive ataxia and tremors. After EGL involution (~2–3 weeks postnatal), FPV no longer produces cerebellar hypoplasia. FHV-1 and FCV are not causative agents of this syndrome.

A shelter veterinarian is investigating a cluster of cats with a highly virulent calicivirus (VS-FCV) outbreak. Affected cats exhibit facial and limb edema, ulceration of the nasal planum, pinnae necrosis, jaundice, and a mortality rate approaching 60%. Which of the following distinguishes VS-FCV from classical FCV strains and has the MOST direct implication for infection control?

Answer: VS-FCV is significantly more resistant to commonly used disinfectants, including quaternary ammonium compounds, and requires 1:32 dilution household bleach with extended contact time; it also causes high mortality in vaccinated adult cats.

VS-FCV (virulent systemic FCV) is notable for causing severe systemic disease and death even in vaccinated adult cats, highlighting the limitations of current vaccines against divergent strains. Like classical FCV, it is non-enveloped and highly environmentally stable, resistant to many disinfectants; dilute bleach (1:32) with adequate contact time remains effective. Fomite transmission is a critical route, making environmental decontamination and isolation essential. Vaccines do not provide sterilizing immunity against VS-FCV. Immunocompetent vaccinated adults can and do die.

A 4-year-old spayed female cat tests positive on an ELISA for FeLV p27 antigen. She is clinically healthy. A proviral PCR on peripheral blood leukocytes is also positive, but a repeat ELISA 12 weeks later is negative, and a subsequent proviral PCR on bone marrow is negative. What is the MOST accurate classification of this cat's infection status, and what is the recommended management?

Answer: The cat experienced a regressive (previously called 'abortive' or 'latent') FeLV infection; proviral DNA is absent from bone marrow, indicating viral clearance; she is likely not infectious and can be managed as a healthy cat with periodic monitoring.

FeLV infection outcomes include progressive infection (persistent antigenemia, high viral load, immunosuppression) and regressive infection (transient antigenemia that resolves, with proviral DNA integrated but not actively replicating—detectable in blood but not bone marrow). A cat with an initial positive ELISA that reverts to negative, combined with negative bone marrow proviral PCR, has most likely achieved regressive infection with viral clearance. These cats are generally not infectious, have a near-normal life expectancy, and do not require antiviral treatment—only periodic wellness monitoring. Focal/compartmentalized infection is a separate category involving persistent antigen in specific tissues despite negative blood tests.

A 9-year-old FIV-positive cat presents with a chronic, non-healing ulcer on the dorsal tongue. Cytology reveals large lymphoid cells. A biopsy confirms diffuse large B-cell lymphoma (DLBCL). Which of the following BEST characterizes the relationship between FIV and feline lymphoma development?

Answer: FIV does not directly transform lymphocytes; rather, chronic immune dysregulation, persistent B-cell antigenic stimulation, and impaired immune surveillance create a permissive environment for spontaneous oncogenic mutations, most commonly yielding B-cell lymphomas in older FIV-infected cats.

Unlike FeLV, FIV is not a directly transforming retrovirus—it lacks an oncogene and does not cause insertional mutagenesis at proto-oncogene loci. Instead, FIV-associated lymphomagenesis is indirect: chronic immune dysregulation, loss of tumor immunosurveillance, and persistent antigenic stimulation of B cells create conditions favorable for malignant transformation. Both B- and T-cell lymphomas occur in FIV-infected cats, with B-cell lymphomas (including DLBCL) becoming more prevalent in older cats. Tax is an HTLV-1/BLV oncoprotein, not an FIV protein. The CD4:CD8 ratio inversion is a feature of FIV disease progression but does not define lymphoma immunophenotype.

A 7-month-old DSH kitten presents with acute onset of corneal ulceration, periocular alopecia with facial dermatitis, and sneezing. Fluorescein staining reveals a classic dendritic (branching) corneal ulcer. Treatment with topical idoxuridine is initiated. Three weeks later, despite apparent resolution of acute signs, the owner reports persistent squinting and a new corneal opacity in the same eye. Slit-lamp examination reveals stromal vascularization and haze without epithelial staining. What is the MOST likely mechanism and appropriate management?

Answer: The stromal opacity represents immune-mediated keratitis (eosinophilic or stromal keratitis) driven by viral antigen persistence or recurrent subclinical reactivation; treatment should include topical corticosteroids (used cautiously) combined with antiviral prophylaxis such as topical cidofovir.

After resolution of the acute dendritic ulcer phase of FHV-1 keratitis, some cats develop stromal keratitis—a non-ulcerative immune-mediated inflammation triggered by persistent viral antigen or low-level viral reactivation in the stroma. It presents with stromal vascularization and haze without active epithelial defects (negative fluorescein stain). This phase has an immune-mediated component and paradoxically benefits from judicious topical corticosteroids combined with antiviral cover (e.g., topical cidofovir BID or oral famciclovir) to prevent viral flare during immunosuppression. Using antivirals alone is insufficient. The lesion is not simply a scar—active vascularization indicates ongoing inflammation. Antiviral resistance developing to idoxuridine within 3 weeks is not a primary concern here.