Canine Viral Diseases Flashcards
(19 cards)
Pathogenesis of parvovirus
non-enveloped ssDNA virus - faeco-oral route.
1-2 weeks incubation
(viral shedding before onset of signs). Replicates first in oropharyngeal lymphoid tissues then disseminates
Cannot change cellular replication so infects rapidly dividing cells and uses cellular machinery for its replication (during S phase)
Tropism: thymus, BM, enterocytes
Causes BM reversible injury to stem cells resulting in severe immunosuppression (neutropaenia) that is usually transient. Also affects thymus so impairs adaptive immune response in puppies –> immune suppression
May also see anaemia - can be non-regen due to BM arrest or due to acute GI blood loss.
Infection of enterocytes in intestinal crypts –> sloughing of mucosa and increased intestinal permeability resulting in bacterial and endotoxin translocation with severe impairment to barrier function. Also malabsortive and maldigestive diarrhoea with high fluid loss.
Parvo risk factors in AVJ 2020 review and reported prevalence
Low socioeconomic areas
Summer
Recent high rainfall
<16weeks of age
Survey of Aust vet clinics estimated a prevalence of 4/1000 dogs
Outcome of inutero CPV infections
Early in gestation -> loss of pregnancy
> 2 weeks foetal viral myocarditis (neonate CHF)
Neonate - also see mycoarditis and subsequent fibrosis resulting in ventricular heart failure
Classical findings of CPV and definitive Dx
Fever
GI blood loss
Vomiting and diarrhoea
Leukopaenia
Hypercoagulability
Evidence of sepsis
Malabsorption causing hypoglycaemia
Typical signalment <16weeks (as mAb wane)
Detection of virus in faeces or oropharyngeal swabs. PCR based methods considered most sensitive
Cage-side ELISA and PCR are most available, haemagglutination and electron microscopy limited to research
Sens/Spec of CPV diagnostics
Antigen ELISA - Sensitivity 82%; specificty 92-98%
False + post-vaccination within 4-8d
May miss shedding in faeces if present late in disease course (shedding occurs before clinical signs)
Viral DNA PCR - remains positive longer than ELISA.
Some assays able to differentiate vaccine from field infection strains.
JVIM 2022 - compared sampling sites of faeces, blood and pharyngeal swab. Faecal samples had poorest sensitivty in sick dogs, with all sick dogs positive at at least 1 site and 83% all sites.
Highest positivity after vaccination was in faeces with pharyngeal PCR only having 12% positivity after vaccination
Antibody detection - not considered useful for Dx due to mAb and prior vaccinations. Also delay in seroconversion. Useful for demonstrating vaccine efficacy
Histo and IHC used for necropsy diagnosis in most cases
Haemagglutination test - virus in stool agglutinates porcine erythrocytes. requires high viral load in faeces but is considered specific for disease
Faecal electron microscopy - not widely available. Can also differntiate from other viral infections but has slow turnaround. Again need large amount of virus to be present in sample
Treatment of CPV - broad considerations and recent recommendations
- Restore fluid and electrolyte balance
- Correct hypoglycaemia
- Antinausea
- Monitor for sepsis and correct hypotension to prevent MODS
- Early enteral nutrition: improves barrier and faster clinical improvement
- Antihelminth therapy (common comorbidity)
- IV ABx: broad spectrum incl anaerobe and G- coverage (base selection on severity/evidence of sepsis)
- JVIM 2017 study reported faster diarrhoea resolution and shorter hospitalisation in dogs recieving faecal transplant. Though did not affect mortality
- Probiotics also shown to improve clinical scoring though no effect seen in subsequent studies (need to compare same probiotic)
CRP correlates with disease severity and response to treatments
- Immune plasma: may provide improved recovery and survival benefit. repeated treatments may cause hypersensitivty reactions
-G-CSF: may improve neutrophil count but conflicting evidence on whether this confers survival benefit
_Oseltamivir - neuramidase inhibitor antiviral prevented neutropaenia in one trial, but did not effect hosp tim eor clinical scores. Probably best avoided.
CPV Prognosis reported in Aust studies
reports range from 60-90% survival depending on treatment regime
42% estimate case fatality in 2012 Aust survey. These are surveys so affected by lack of reporting and variability in treatment.
Causes of CPV vaccine failure
Vaccination before 14-16weeks resultin gin mAb inhibition.
WSAVA reccomends final booster beyond this time to ensure protection/mounting of appropriate immune response
Infection during window of susceptibility when mAb wanes and vacc immunity not emerging
Possible reversion to virulence
Different CPV strain infection - may be failure of cross protective immunity
Canine Distemper - epidemiology, transmission, pathogenesis
Can infect a variety of canine hosts resultin gin wild population of reservoir
Spread by oronasal route but also in fomites. See outbreaks in dense housing and poor cleanliness.
Shed in respiratory exudates, saliva, urine faeces, vomit
Incubation 1-3 weeks, shed from 7days post exposure
Virus replicates in macrophages in URT and LNs (uses SLAM membrane protein to enter cells - expressed on macrophages and immature lymphocytes)
Then viraemia develops and virus spreads to LN, Spleen, Liver causing fever, immunosuppression and lymphopaenia. Severity of viraemia determines which tissues end up affected.
Outcome determined by host immunity:
- no immunity -> severe disease in multiple organs often culminating in CNS signs
- Intermediate response - recover from acute illness but fail to clear virus from skin/footpads, CNS or eye (so may be subclinical lung/skin lesions) so develop chronic disease manifestation often uveitis, CNS dysfunction; foot pad lesions
- Strong immune response clears infection, but still carries risk of CNS disease development
CNS infection causes demyelination in acute form (due to metabolic derangement), or chronic inflammatory encephalitis
(secondary to CDV induced immune response)
Clinical signs of CDV
Dogs that present with respiratory signs consistent with CIRD that also have GI signs, ocular discharge, neurologic signs, and/or an unknown vaccination history should be considered at high risk of having distemper
Approx 50% of infections are subclinical.
Most common in unvaccinated dogs at waning of mAb 12-16 weeks
Acute infection - fever, lethargy, conjunctivitis and respiratory (mucopurulent discharge)
Often see secondary opportunistic infections due to virus induced immunosuppression (replication in T cells and suppress cytokine production).
Can also see skin and eye lesions as well as metaphyseal osteopathy in large breed dogs.
1-3 weeks later see neurological signs develop due to demyelination (infection of neurons by virus) or secondary to virus induced inflammation. Predilection for the cerebellum (ie intention tremor and vestibular signs)
There is strain dependent variation in ability to cause CNS signs
Diagnostic tests for CDV
Demonstration of intracellular viral inclusion bodies in macrophages - usually performed on tissue samples, sensitivity improved by testing multiple sites (blood, csf, urine, conjunctival smears, BALF)
IFA can enhance sensitivity, specificity generally good but false positives occur after vaccination. False negatives in low virus levels within samples
ELISA antigen - sensitivity and spec not established. False positives with vaccination
RT PCR - cannot differentiate vaccine from virus. but highly sensitive. Sensitivity improved by testing multiple sites
Serology Ab - acute and convalescent sera. False positive with vaccination. Retrrospective Dx
Serum titres correlate well with protection
Can see high levels in dogs with delayed onset encephalomyelitis
Hist and FISH - latter being most sensitive method of detection.
Immunostaining can improve detection of intracytoplasmic inclusion bodies
CDV vaccination protection, type of vaccine
attenuated live virus or recombinant vaccines available
mAb can interfere with immunity so recommend vacc at 14-16 weeks
Duration of immunity thought to be 3-5y based on Ab titrres. Seems to be good cross neutralisation with various field strains.
Post-vaccinal encephalitis was associated with earlier vaccines
Canine Adenovirus - transmission, pathogenesis
Can cause disease in other canids which are a reservoir for infection
Oronasal transmission to contaminated saliva, faeces, urine
4-9 day incubation, shed for
9 months
Virus replicates in oral lymphoid tissue then disseminates with predilection for endothelial cell invasion resulting in DIC/SIRS and liver, kidney and eye damage (due to direct cytotoxic effects)
Can cause a severe centrilobular to panlobular hepatic necrosis and subsequent fibrosis. Also pyelonephritis.
Generation of large amounts of Ag:Ab complexes results in type II hypersensitvity disease - ICGN, uveitis, vasculitis within 1 month of infection.
Anterior uveitis also reported via type III hypersensitivity
May also be persistent glomerular endothelium infection causing interstitial nephritis.
Clinical signs and prognosis of Canine adenovirus hepatitis
Peracute - circulatory collapse and rapid death
Acute - most common.
Mortality of 10-30%
fever, tonsilitis, PD, vomiting, haematemesis, diarrhoea, cough (laryngitis/tracheitis), icterus. Hepatomegaly. Corneal oedema
Chronic - hepatic failure weeks to months after infection. In dogs with partial immunity.
Dx based on acute hepatitis in dog with unknown vacc history, often <1y and concurrent respiratory, GI upset with corneal oedema.
10-30% mortality in acute form. Survivors may go on to die from hepatic failure in several months time.
Diagnosis of CAV1
Histo: hepatocellular necrosis and intranuclear viral inclusion bodies within Kupffer’s cells and hepatocytes
PCR - may not differentiate from vaccine strain. Low prevalence of disease reduces PPV but improves NPV.
Serology - would be retrospective documentation of 4fold rise, cross reaction with vacc Ab makes single measurement difficult to interpret.
Virus isolation - can be performed on any tissue and likely has high sensitivity in acute disease. Not widely available
Infectious components of CIRDC and recent prevalence studies in NZ
Canine Pi 2
Canine ADenovirus 2
Canine respiratory coronavirus
Bordetella Bronchiseptica
Mycoplasma cynos - maybe
Canine herpes virus - maybe
Prevalence in recent NZJ study reported 17% M cynos, 6% CPiV and B.b and 13% CAV2. Though convenience sampling meant no case controls and small sample size so inference on disease causality cannot be made.
Another study found seroprevalence of CCoV in NZ was 53% with respiratory signs only reported in 2.8% of dogs sampled - thoguh CCoV had higher prevalence in these dogs compared to those without resp signs
Multiagent, complex pathogenesis likely involving repeated damage to MCC via various mechanisms and predisposition to concurrent infections
Host immune status, environment and exposure to pollutants can all impair local immune defences and predispose to disease
JVIM 2021 pooled URT samples tested on 295 asymptomatic dogs found prevalence of at least 1 component of CIRDC in 11%. Higher among shelter dogs than privately owned.
ISCAID recommendations for acute tracheitis work up
None unless outbreak in facility, severe progressive symptoms in an individual or symptoms not improving with supportive care/doxycycline after 10 days of treatment
In outbreak sample multiple animals both sick and healthy.
Rabies - Transmission, pathogenesis, common CS, incubation length, tests, prevention
Reservoir species in most of world, transmitted by bite of infected animals (or saliva contamination of wounds)
Cats have increased risk of contracting infection
Variable incubation, up to 6 months. Shorter if closer to CNS - transport takes time!
Local viral replication then neurotropic and infects local peripheral nerves -> retrograde transport to CNS where it then undergoes massive viral replication which profoundly alters function of brain
Virus leaves CNS in somatic and autonomic nerves to infect salivary glands as well as other tissues. New virion production occurs predominantly in salivary glands.
No period of systemic viraemia occurs. Virus is only shed in saliva and not urine or faeces.
Phases: prodromal (fever, licking, chewing bite site)
furious (forebrain dysfunction, anxiety/excitability, hyperaesthesia, hypersalivation, roaming, aggression)
Paralytic phase (1-10 days after onset of signs, flaccid paralysis and dropped jaw) finishing in coma and death
Direct IFA of brain tissue is gold standard PM diagnosis.
RT PCR of CNS tissue or CSF may be highly specific and sensitive
Saliva testing can be considered antemortem but not recommended due to safety.
Serology for antibodies not considered useful, often false negatives
