Feline Viral Diseases Flashcards
Test for making a dx
Histopathology
IHC- specific Ag
ELISA - AG
PCR
Screening test for infection
Serology
ELISA-Ag
PCR
Certification that an animal is free of infection
Serology
PCR
2 primary methods for dx infectious diseases
Detection of organism (cx, cytology, fecal, PCR, immunologic techniques)
Detection of Ab against organism
Reasons for false positive PCR
Sample contamination during collection and analysis
Cross reaction without other organisms
Lack of lab quality control
Immunization of suspected Ag
Reasons for false negative PCR
Inappropriate handling during collection or transport
Abx therapy prior to sample collection
Early dz v late dz
Most common detection method
Detects Ab:
Indicated exposure, not necessarily active infection
Immune ystem needs time to develop Abs
Abs come too late to be of clinical value
Method of action for Ab detection
IgM ( 1st Ab produced after exposure) → IgG (days to weeks
Reasons for positive Ab test
Previous exposure to pathogen or immunization against a pathogen
Cross reaction with other organism
Technical error
Reasons for negative Ab test
No exposure to the organism of interest
Too early in the course of infection
Severe immunosuppression
Poor sensitivity (prone to false negatives)
Ab detection characteristics
Large pops of animals may have Abs to infectious agents but dz may not occur
Vx induce Abs
Magnitude of tier doesn’t = magnitude of dz
Feline Coronavirus
Large, enveloped, single stranded RNA
Serotypes 1 and 2
Enteric Dz (FECV)
Kittens, mild self-limiting diarrhea
Benign, virus replicating in enterocytes
Feline Infectious peritonitis (FIP)
Fatal and progressive, systemic
Most common deaths from infectious
Pathogenesis of Feline corona virus
Internal mutation theory: 2 distinct circulating strains (virulent and avirulent)
Immune Dysregulation
Internal Mutation Theory
Initial infection: low pathogenicity
Mutation and multiply in macrophage: spike protein gene and pyogranulomatous infection
Immune dysregulation
Depletion of CD4 and CD8 cells
Production of TNF alpha, GM-CSF and G-CSF
Hypergammaglobulinemia
Impaired IFN alpha production
FIP dry form
Granulomatous infection of LN, kidneys, eyes, brain, liver and lung
Ileocolic junction
Wet form of FIP
No immune response (seen the most)
Pleural/ abdominal effusion (↑ protein and low cells)
↑ vascular permeability
Pyogranulomatous
Coronavirus signalment
Young <2y or old >10y
Abyssinians, bengals, burmese, ragdolls, rexs
Multiple cat housing
Coronavirus transmission
Oronasal infection
Shed from 1 w, chr. carriers
CS of coronavirus
Leth. and inappetence with fluctuating fever
10% effusions and 10% neuro signs
Coronavirus lab tests
Eosinopenia and lymphopenia
Hyperproteinemia (↓ albumin and ↑ globulins)
Rads, effusions, rivalta test (glob formed)
Coronavirus effusions
High protein >3.5 g/DL
Low cells <5,000
Coronavirus
Rt- PCR with CSF
Serology with blood, effusion or CSF
Pathology: histopath is gold standard
Coronavirus tx
Pred, antiviralsm immunomodulators, pentoxyphyline
Remdesivir (newer meds)
Prognosis of coronavirus
Grave with effusive form
Neg prog factors: lymphopenia and hyperbilirubinemia
FIP vx
Lipid nanoparticle (LNP) encapsulated mRNA
Not proven to be effective, interferes with testing
FELV and FIV
Retroviruses
Most common infectious dz
Risk factors: outdoor, male, adult, aggressive
Easily disinfected
FeLV
FeLV-A (transmitted between animals)
Transmission: close contact
Tumors, myelosupression, opportunistic infections
Regressive infection of FeLV
Infection → replicating virus spreads systemically → shed in saliva → BM infected → persists for life
Early Ag (+) and late Ag (-)
Reactivation during stress
Abortive stage of FeLV
Infection → replication in LN → good immunity
No viremia
Regressive Infection of FeLV
Infection → replicating virus spreads systemically → shed in saliva → BM infected → persists for life
Early Ag (+) and late Ag (-)
Reactivation during stress
Focal infection of FeLV
No virus in blood or marrow
Persistent replication of virus
Progressive infection of FeLV
Development of FeLV associated dz
Marrow involved
Ag (+)
Viral load ↑
FeLV opportunistic infection manifestations
Immunosuppression, URI, UTI
FIP stomatitis, fading kitten syndrome
Anemia (non-regen)
FeLV neoplasias
FeLV-B
Insertional mutagensis (activation of proto-oncogenes)
Lymphoma, leukemia or fibrosarcoma
Diagnostic testing for FeLV
Serology: p27 Ag
PCR: FeLV RNA or proviral DNA
IFA: FeLV Ag in blood cells
Tx for FeLV
Avoid steroids
Tx lymphoma, opportunistic infections
Blood transfusions
Immunomodulators and antivirals
Prognosis of FeLV
Good (ave 3y)
Negative prognostic indicator: lymphoma
FeLV vx
Adjuvanted inactivated whole virus
Non-adjuvanted canary pox*
Recombinant subunit
FIV
6 subtypes (A-F)- A and B widely distributed
Neuro dz, tumors and opportunistic infections
Bite wounds (saliva)
Acute stage of FIV
3-6m, primary infection
Inoculation → replication → high viral load 2w post infection → ↓ T cells → transient illness
Persistent replication of virus
Asymptomatic stage of FIV
T cells ↑, ↓ viral load
Slow progressive ↓ in T cells
T cells present but unable to respond
Terminal phase of FIV
Disease presentation
Tumors (B cell lymphoma), neurological dz and opportunistic infection
Chr. Stomatitis
More common in FIV cats
Invasion of plasma and lymphocytes → anprexia and emaciation
+/- calicivirus
Dx testing for FIV
Serology: Ab to FIV (p24)
PCR: proviral DNA or viral RNA
Tx of FIV
Oral hygiene (stomatitis), extractions
Pain: opioids, NSAIDs
Same tx as FeLV
Prognosis of FIV
Good (ave 5y)
More aggressive in neonates and geriatrics
