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Feline Panleukopenia Virus (FPV)

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1. Etiology

Greene's Infectious Diseases of the Dog and Cat (5th ed., p. 80): FPV is one of the most environmentally stable animal viruses known, making contamination of the environment a major epidemiological concern.

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2. Transmission

• Cats shed virus in all secretions during the acute viremic phase and up to 6 weeks post-recovery in feces.
• No long-term carrier state has been conclusively demonstrated.
• The virus can persist in the environment for >1 year under favorable conditions (Sykes' Canine and Feline Infectious Diseases, p. 187).

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3. Pathogenesis

Cellular Tropism

• Transferrin receptor 1 (TfR1) is the primary receptor used for cell entry.
• Target tissues: intestinal crypt epithelium, bone marrow, lymphoid tissue (thymus, lymph nodes, spleen), cerebellar Purkinje and granular cells (in neonates/fetal infection).

Sequence of Events

1. Oronasal inoculation → initial replication in oropharyngeal lymphoid tissue (tonsils, lymph nodes)
2. Primary viremia (Days 1–2) → hematogenous spread; virus infects circulating lymphocytes and monocytes
3. Systemic dissemination → bone marrow, lymphoid organs, intestinal crypts
4. Bone marrow suppression → destruction of myeloid and erythroid precursors → panleukopenia (most notably neutropenia and lymphopenia)
5. Intestinal crypt necrosis → collapse of villous architecture → malabsorption, diarrhea, protein-losing enteropathy, breakdown of mucosal barrier → bacterial translocation and sepsis
6. Secondary bacteremia/endotoxemia → systemic inflammatory response → multi-organ dysfunction

Special Populations

ABCD Guidelines on Feline Panleukopenia (Truyen et al., 2009): The hallmark lesion is collapse of intestinal villi with dilation and necrosis of crypts of Lieberkühn, resulting in a "ghost crypt" appearance on histopathology.

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4. Clinical Signs

Incubation Period

Peracute Form

• Found dead with no premonitory signs
• Common in kittens and immunocompromised cats

Acute Form (Most Common)

Subclinical Form

• Seen in adult cats with partial immunity; seroconvert without obvious illness

Cerebellar Hypoplasia (Neonatal/In Utero)

• Non-progressive cerebellar ataxia, dysmetria, intention tremors
• Head bobbing
• Signs apparent when kittens begin to ambulate (~3–4 weeks)

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5. Diagnosis

Clinical Suspicion

Hematology — Hallmark Finding

Ettinger & Feldman, Textbook of Veterinary Internal Medicine (8th ed., p. 2387): A WBC < 2,000/μL in a young, unvaccinated cat with vomiting and diarrhea is highly suggestive of FPV.

Point-of-Care / In-Clinic Tests

Advanced / Reference Laboratory Tests

Differential Diagnoses

• Feline panleukopenia must be distinguished from:
  • Salmonellosis, other bacterial gastroenteritides
  • Feline leukemia virus (FeLV) — bone marrow suppression
  • Feline immunodeficiency virus (FIV)
  • Feline infectious peritonitis (FIP)
  • Toxin ingestion
  • Other causes of leukopenia (immune-mediated, drug-induced)

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6. Treatment

Fluid Therapy (Cornerstone of Treatment)

Antiemetics

Antibiotics (for Secondary Bacterial Infection / Sepsis Prophylaxis)

Nutrition

• NPO (nothing by mouth) only if vomiting is uncontrolled
• Early enteral nutrition is strongly encouraged once vomiting is controlled — maintains gut mucosal integrity
• Nasogastric or esophagostomy tube feeding with liquid diets if anorexic
• Parenteral nutrition (TPN) if enteral route not tolerated

Blood Products / Immunotherapy

Antiviral Considerations

• CPFU-1 (2'-deoxyadenosine analog), HPMPA, and other antivirals have been tested in vitro but are not clinically established.
• Recombinant feline interferon-omega is the closest to an evidence-based specific therapy.

Nursing Care

• Strict barrier nursing and isolation to prevent nosocomial spread
• Warm environment (avoid hypothermia)
• Soft bedding, frequent turning if recumbent
• Monitor blood glucose (hypoglycemia in kittens)
• Monitor for septic shock

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7. Prognosis

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8. Prevention and Management

Vaccination — Primary Prevention

WSAVA/AAFP Vaccination Schedules

WSAVA Vaccination Guidelines (Day et al., 2016, J Small Anim Pract): FPV vaccination provides robust, long-lasting immunity; serologic testing (titer checks) can be used to assess protection and extend revaccination intervals.

Environmental Decontamination

• Clean all surfaces with detergent first (remove organic material)
• Apply 5% sodium hypochlorite (1:32 dilution of household bleach) contact time ≥10 minutes
• Quaternary ammonium compounds and alcohols are NOT effective against parvoviruses
• Potassium peroxymonosulfate (Trifectant/Virkon-S) is an alternative

Outbreak Management in Shelters / Catteries

1. Immediate isolation of affected animals
2. Cohort management — separate incoming animals from resident population
3. Emergency vaccination of all unvaccinated animals (MLV provides fast protection within 3–5 days)
4. Quarantine period — minimum 14 days for exposed animals
5. Thorough environmental decontamination of all areas
6. Fomite control — dedicated equipment per animal, no sharing
7. Suspension of intake if outbreak is severe

Management of Pregnant Queens

• Avoid exposure to FPV
• Do NOT use MLV vaccines during pregnancy (risk of fetal cerebellar hypoplasia)
• Use killed vaccines if vaccination during pregnancy is unavoidable

Cerebellar Hypoplasia Management

• No treatment reverses cerebellar damage
• Affected kittens can often lead good quality lives if ataxia is mild–moderate
• Provide safe environments (no heights, padded areas)
• Prognosis depends on severity; non-progressive nature means adaptation improves over time

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Summary Table

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• Greene, C.E. (Ed.). Infectious Diseases of the Dog and Cat, 5th ed. Elsevier, 2012. pp. 80–88.
• Sykes, J.E. Canine and Feline Infectious Diseases. Elsevier, 2014. pp. 187–196.
• Ettinger, S.J. & Feldman, E.C. Textbook of Veterinary Internal Medicine, 8th ed. Elsevier, 2017. pp. 2385–2390.
• Truyen, U., et al. "ABCD guidelines on prevention and management of feline panleukopenia." Journal of Feline Medicine and Surgery 11 (2009): 538–546.
• Day, M.J., et al. "WSAVA guidelines for the vaccination of dogs and cats." Journal of Small Animal Practice 57 (2016): E1–E45.
• de Mari, K., et al. "Therapeutic effects of recombinant feline interferon-omega on feline leukemia virus (FeLV)-infected and FeLV/FIV-coinfected symptomatic cats." Journal of Veterinary Internal Medicine 17 (2003): 477–482.
• Morgan, R.V. Handbook of Small Animal Practice, 5th ed. Elsevier, 2008.
• AAFP. Feline Vaccination Advisory Panel Report. Journal of Feline Medicine and Surgery 15 (2013): 785–808.

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Feline Calicivirus (FCV)

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1. Etiology

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2. Transmission

Carrier State — Critical Epidemiological Feature

• After resolution of acute signs, many cats become persistent oropharyngeal carriers — shedding virus in oral secretions for months to years, sometimes lifelong
• Estimates: 25–50% of recovered cats remain chronic carriers (Greene, p. 145)
• Carrier cats are the primary reservoir maintaining FCV in the population
• Stress, concurrent illness, immunosuppression, and corticosteroids may increase viral shedding
• Continuous viral evolution within the carrier cat can produce new antigenic variants

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3. Pathogenesis

Initial Infection and Replication Sites

1. Oronasal inoculation → initial replication in oral and upper respiratory epithelium (tongue, hard and soft palate, tonsils, nasal turbinates, conjunctiva)
2. Virus causes vesicle formation and ulceration — characteristic oral ulcers arise from vesicle rupture
3. Lower respiratory tract involvement: some strains replicate in type I and II pneumocytes → interstitial pneumonia
4. Viremia: limited but documented; enables dissemination to joints (synovitis/limping syndrome) and systemic organs in VS-FCV

Cellular and Molecular Mechanisms

• FCV uses junctional adhesion molecule-1 (JAM-1) as its primary cell surface receptor
• RNA replication occurs in the cytoplasm via a VPg-linked 5' cap system
• Rapid mutation → immune evasion; explains re-infection with heterologous strains despite prior immunity

Tissue Damage Mechanisms

VS-FCV Pathogenesis

• Vascular endothelial cells are primary targets → systemic vasculitis
• Perivascular edema, skin and mucosal hemorrhage, necrosis
• Disseminated intravascular coagulation (DIC)
• Multi-organ dysfunction (liver, pancreas, lungs, skin)

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4. Clinical Signs

Incubation Period

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A. Classic FCV — Upper Respiratory / Oral Form

Sykes' Canine and Feline Infectious Diseases (p. 212): FCV is responsible for approximately 50% of feline upper respiratory tract infections (URTIs); FHV-1 accounts for another 40%, with the remainder due to Chlamydia felis, Bordetella bronchiseptica, and others.

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B. Limping Syndrome (Transient Febrile Limping Syndrome)

• Fever (often high, 40–41°C), sudden onset lameness, joint swelling/pain
• Most commonly in kittens after MLV vaccination (within 1–2 weeks) but also with natural infection
• Self-limiting; resolves within 2–4 days
• Mild oral ulceration may or may not be present
• Mechanism: immune-complex synovitis

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C. Virulent Systemic FCV (VS-FCV)

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D. Chronic Stomatitis / Gingivostomatitis

• FCV (along with FHV-1 and other agents) implicated as a trigger for Feline Chronic Gingivostomatitis (FCGS)
• Severe, painful inflammation of the caudal oral mucosa (caudal stomatitis / faucitis)
• Immune-mediated component; FCV may perpetuate antigen-driven inflammation
• Chronic carrier cats with persistent oropharyngeal shedding most commonly affected

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5. Diagnosis

Clinical Diagnosis

• Combination of oral ulcers + upper respiratory signs in a cat is highly suggestive of FCV
• VS-FCV suspected in outbreak with facial edema, skin necrosis, jaundice, high mortality

Laboratory Diagnosis

Sample Collection

• Oropharyngeal swab — primary sample for culture and PCR
• Swab from ulcer edge/base is preferred
• Both dry swabs (PCR) and viral transport media (culture) required depending on test

Hematology / Biochemistry (especially VS-FCV)

Differential Diagnoses

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6. Treatment

Supportive Care

Antimicrobials (Secondary Bacterial Infection)

Pain Management

Antiviral Agents

Management of VS-FCV

Chronic Gingivostomatitis (FCGS)

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7. Prognosis

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8. Prevention and Management

Vaccination — Core Vaccine (WSAVA / AAFP / ABCD)

AAFP Vaccination Guidelines (2013): Because of high antigenic diversity among FCV strains, vaccination does not prevent infection or shedding but significantly reduces severity of clinical disease.

Vaccination Schedule

Environmental Control

• Disinfect with sodium hypochlorite 1,000 ppm (1:50 dilution of 5% bleach) — removes 4.5 log₁₀ infectivity in 1 minute (Disinfection and Sterilization in Healthcare Facilities, p. 25)
• Accelerated hydrogen peroxide and chlorine dioxide also highly effective (Ibid.)
• FCV survives up to 1 month dried on surfaces; thorough cleaning before disinfection is essential
• Quaternary ammonium compounds alone are insufficient (Ibid., p. 25–26)

Outbreak Control in Shelters / Catteries

1. Immediate isolation of all clinically affected cats
2. Quarantine all exposed animals (minimum 10–14 days)
3. Immediate vaccination of all unvaccinated/incompletely vaccinated cats with MLV — provides partial protection within 24–48 hours (mucosal IgA)
4. Environmental decontamination with bleach — all cages, bowls, litter boxes, surfaces
5. Suspension of adoptions until outbreak is controlled
6. Cohort management — do not mix new intakes with resident population
7. Staff PPE — gloves, gowns, dedicated footwear per ward
8. VS-FCV outbreak: notify other veterinary practices and shelters in the area; extreme contagiousness documented in hospital outbreaks

Management of Carrier Cats

• Test oropharyngeal swabs by RT-PCR in multi-cat households to identify shedders
• Separate chronic shedders where possible
• Stress reduction (Feliway, environmental enrichment) minimizes shedding
• Regular vaccination of in-contact cats
• No treatment reliably clears the carrier state

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Summary Table

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• Greene, C.E. (Ed.). Infectious Diseases of the Dog and Cat, 5th ed. Elsevier, 2012. pp. 140–151.
• Sykes, J.E. Canine and Feline Infectious Diseases. Elsevier, 2014. pp. 209–221.
• Ettinger, S.J. & Feldman, E.C. Textbook of Veterinary Internal Medicine, 8th ed. Elsevier, 2017. pp. 2391–2396.
• Radford, A.D., et al. "ABCD guidelines on prevention and management of feline calicivirus infection." Journal of Feline Medicine and Surgery 11 (2009): 556–564.
• Day, M.J., et al. "WSAVA guidelines for the vaccination of dogs and cats." Journal of Small Animal Practice 57 (2016): E1–E45.
• Hurley, K.F. & Sykes, J.E. "Update on feline calicivirus: new trends." Veterinary Clinics of North America: Small Animal Practice 33 (2003): 759–772.
• Pedersen, N.C. Feline Husbandry: Diseases and Management in the Multiple-Cat Environment. Goleta, CA: American Veterinary Publications, 1991.
• McDonagh, P., et al. "The feline calicivirus viroporin: a review." Viruses 2015.
• Rutala, W.A. & Weber, D.J. Disinfection and Sterilization in Healthcare Facilities. CDC Guidelines, pp. 25–26.

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Feline Herpesvirus Type 1 (FHV-1)

Feline Viral Rhinotracheitis (FVR)

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1. Etiology

Greene's Infectious Diseases of the Dog and Cat (5th ed., p. 151): FHV-1 is the most important cause of feline upper respiratory tract disease and is responsible for the majority of feline ocular surface disease.

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2. Transmission

Shedding Dynamics

• Approximately 80% of recovered cats establish latency (Sykes, p. 226)
• 45–97% of latently infected cats reactivate and shed virus following stress (corticosteroids, surgery, transportation, parturition, overcrowding, introduction of new cats)
• Reactivation can occur without overt clinical signs — subclinical shedders are epidemiologically significant

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3. Pathogenesis

Primary Infection Sequence

1. Oronasal/conjunctival inoculation → virus binds to mucosal epithelial cells via heparan sulfate proteoglycan and herpesvirus entry mediator (HVEM) receptors
2. Viral replication in epithelial cells of nasal turbinates, nasopharynx, tonsils, conjunctiva → cytolytic infection with direct cell destruction
3. Rhinitis and rhinotracheitis — mucosal necrosis, ulceration, hemorrhagic to fibrinous exudate
4. Anterograde axonal transport → virus travels along sensory nerve fibers to the trigeminal ganglion (and olfactory bulb)
5. Latency establishment — viral DNA circularizes and persists as an episome in neuronal nuclei; only a subset of latency-associated transcripts (LATs) expressed; no viral protein production → immune evasion

Tissue Damage Mechanisms

Latency and Reactivation

• Sites of latency: Trigeminal ganglia (primary), olfactory bulb, ophthalmic branch of trigeminal nerve
• Reactivation stimuli: Corticosteroid administration, surgery, transportation, lactation/parturition, introduction of new animals, intercurrent illness, immunosuppression (FIV, FeLV)
• Reactivation is governed by VP16-mediated transactivation of lytic genes
• Each reactivation episode can lead to fresh mucosal damage, further scarring

Maggs, Slatter's Fundamentals of Veterinary Ophthalmology (5th ed., p. 187): FHV-1 is the most common infectious cause of feline corneal ulceration and the primary differential for any cat presenting with conjunctivitis and corneal surface disease.

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4. Clinical Signs

Incubation Period

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A. Primary Acute Infection

Respiratory Signs

Ocular Signs

Systemic Signs

• Fever (40–41°C), profound lethargy, anorexia
• Hypersalivation (oral pain)
• Weight loss in prolonged cases

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B. Neonatal / Kitten Infection

• Kittens < 4 weeks particularly susceptible
• Neonatal conjunctivitis — purulent ocular discharge before eyelid opening; adhesion of eyelids
• Symblepharon — permanent adhesions; leads to entropion, corneal opacity
• Severe systemic illness; hepatitis, encephalitis (rare) in very young kittens
• High mortality possible

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C. Recurrent / Reactivation Disease

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D. Chronic Rhinosinusitis

• Consequence of severe primary infection with permanent turbinate and mucosal damage
• Chronic nasal discharge (mucopurulent), sneezing, stertor
• Secondary bacterial colonization (Pseudomonas, Pasteurella, Bordetella) drives ongoing inflammation
• CT imaging reveals turbinate lysis, mucosal thickening, fluid in sinuses
• Difficult to cure; managed long-term

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E. Dermatological FHV-1

• Ulcerative facial dermatitis — nasal, perioral, periocular skin ulcers
• Associated with FHV-1 reactivation; affects immunocompromised or stressed cats
• Biopsy + IHC or PCR confirms FHV-1 in skin lesions

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5. Diagnosis

Clinical Diagnosis

• Classic presentation: sneezing + conjunctivitis + corneal dendritic ulcers in a cat is highly suggestive
• Fluorescein staining essential for all cats with conjunctivitis to reveal ulcers

Fluorescein Stain — Corneal Ulcers

Laboratory Diagnosis

Cytology

• Conjunctival scraping: neutrophils, lymphocytes, necrotic epithelial cells
• Intranuclear inclusions rarely seen on cytology but diagnostic when present
• Eosinophils suggest eosinophilic keratitis (FHV-1-associated)

Advanced Imaging (Chronic Rhinosinusitis)

Differential Diagnoses

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6. Treatment

A. Antiviral Therapy — Cornerstone of FHV-1 Management

Topical Ocular Antivirals

Maggs, Slatter's Fundamentals of Veterinary Ophthalmology (5th ed., p. 192): Cidofovir 0.5% BID is favored for its efficacy and simplified dosing schedule in cats.

Systemic Antivirals

Sykes' Canine and Feline Infectious Diseases (p. 235): Famciclovir at 40–90 mg/kg q8–12h is the recommended systemic antiviral; owners must be cautioned that commercial 500 mg tablets require compounding for appropriate feline dosing.

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B. Lysine Supplementation — Controversial

• Historically recommended (500 mg PO q12h) based on the premise that L-lysine competitively inhibits arginine, which is required for FHV-1 replication
• 2015 systematic review (Bol & Bunnik, JFMS): no convincing clinical evidence that lysine supplementation reduces FHV-1 shedding, disease severity, or recurrence; some studies showed no benefit or potential harm (reduced appetite)
• Current consensus: Lysine supplementation is not recommended by ABCD and most current guidelines
• Arginine restriction is what theoretically matters, but dietary arginine restriction is dangerous (causes hyperammonemia in cats) — not clinically pursued

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C. Immunomodulatory / Supportive Antivirals

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D. Supportive Care

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E. Antibiotics (Secondary Bacterial Infection)

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F. Management of Eosinophilic Keratitis

• FHV-1-triggered immune-mediated condition
• Treat FHV-1 first (topical antiviral, famciclovir)
• Topical corticosteroids (prednisolone acetate 1% q8–12h) — use only after active ulceration has resolved; never with active corneal ulcers
• Topical cyclosporine 0.2% ointment q12h — immunomodulatory; safer alternative to steroids
• Long-term maintenance often required to prevent recurrence

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G. Chronic Rhinosinusitis Management

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7. Prognosis

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8. Prevention and Management

Vaccination — Core Vaccine

WSAVA Vaccination Guidelines (Day et al., 2016): Vaccination does not prevent FHV-1 infection or latency but significantly reduces severity and duration of clinical signs. Reactivation can still occur in vaccinated cats.

Vaccination Schedule

Prevention of Reactivation

• Minimize stressors: stable social groups, adequate space, environmental enrichment
• Avoid unnecessary corticosteroids — most potent iatrogenic trigger for reactivation
• Feliway (synthetic feline facial pheromone) — reduce stress in multi-cat environments
• Prophylactic famciclovir — consider before anticipated stressors (surgery, travel, introduction of new cats): 40 mg/kg PO q12h for 7 days

Environmental Decontamination

• FHV-1 is environmentally fragile — inactivated within 18 hours on dry surfaces
• Most standard disinfectants effective: sodium hypochlorite, chlorhexidine, quaternary ammonium compounds, alcohols, iodophors
• Despite fragility, thorough cleaning is still important in hospital/shelter settings

Outbreak Control in Shelters / Catteries

1. Immediate isolation of clinically affected cats
2. Emergency vaccination of unvaccinated cats (intranasal MLV for rapid mucosal immunity)
3. Quarantine all exposed animals — minimum 10–14 days
4. Standard disinfection of all areas (most disinfectants effective)
5. Stress reduction protocols — primary driver of disease amplification
6. Cohort management — avoid mixing new intakes with residents
7. Identify and segregate known chronic shedders/reactivating cats

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Summary Table

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• Greene, C.E. (Ed.). Infectious Diseases of the Dog and Cat, 5th ed. Elsevier, 2012. pp. 151–162.
• Sykes, J.E. Canine and Feline Infectious Diseases. Elsevier, 2014. pp. 224–237.
• Ettinger, S.J. & Feldman, E.C. Textbook of Veterinary Internal Medicine, 8th ed. Elsevier, 2017. pp. 2396–2402.
• Maggs, D.J. In: Slatter's Fundamentals of Veterinary Ophthalmology, 5th ed. Elsevier, 2013. pp. 185–197.
• Thiry, E., et al. "ABCD guidelines on prevention and management of feline herpesvirus-1 infection." Journal of Feline Medicine and Surgery 11 (2009): 547–555.
• Day, M.J., et al. "WSAVA guidelines for the vaccination of dogs and cats." Journal of Small Animal Practice 57 (2016): E1–E45.
• Bol, S. & Bunnik, E.M. "Lysine supplementation is not effective for the prevention or treatment of feline herpesvirus 1 infection in cats." Journal of Feline Medicine and Surgery 17 (2015): 1–5.
• Thomasy, S.M. & Maggs, D.J. "A review of antiviral drugs and other compounds with activity against feline herpesvirus type 1." Veterinary Ophthalmology 19 Suppl 1 (2016): 119–130.
• Gould, D. "Feline herpesvirus-1: ocular manifestations, diagnosis and treatment options." Journal of Feline Medicine and Surgery 13 (2011): 333–346.