Adenoviridae Flashcards
Describe the morphology, genome & replication, and general characteristics of Adenoviridae.
- Morphology
-non enveloped
-hexagonal
-12 vertex penton capsomers each w fiber protrude from surface of capsid - Genome & replication
-intranuclear inclusion body w lg # of virions in para-crystalline arrays - General characteristics
-agglutinate RBC
>hemagglutination when tips of penton fibers bind to surface receptor on RBC
-some oncogenic in lab animals
-stable in environment but inactivated by disinf
-narrow host range
Describe the pathogenesis of Adenoviruses.
-cause acute respiratory or gastroenteritis dz (most subclinical but vary in severity)
-immunosuppresion
-long period of latency
>virus persist in lymphoid & other tissues like tonsil, adenoids, peyer patch
>reactivated in immunocompromised
>highly pathogenic in immunodeficienct
-oncogenesis
>under special conditions
Describe infectious canine hepatitis.
‘ICH, Rubarths Disease’
1. Etiology
-canine adenovirus 1 (CAV1)
2. Transmission
-acute inf: CAV1 in all secretion & excretion
>after, virus shed in urine for 6-9mo
3. Route
-oronasal
>contact w:
A) secretions/excretion of inf dog
B) contam fomites
C) ectoparasites harbor CAV1
Describe the sites of virus replication of ICH.
Mac, kupffer cells, hepatocytes, vascular endothelium of diff organs (incl CNS), parenchymal cells of organs & tissues
LIVER, KIDNEYS, SPLEEN, LUNGS = main target organs
Describe hepatitis pathogenesis of ICH in dogs.
- At time of inf dogs have Ab titer of >500 & show little clinical evidence of dz
- Acute case = sufficient Ab response by day 7 post inf (>500 Ab response by day 7 PI) clear virus from blood & liver & restrict hepatic damage
- Persistent low Ab titer (<4) -> widespread centrilobular to panlobular hepatic necrosis
- Partial immunity (Ab titer >16 but <500) -> chronic active hepatitis & hepatic fibrosis
Describe other pathogenesis of ICH in dogs.
- Chronic case = cirrhosis in liver or kidney
- Acute inf = kidney glomerulonephritis
- Immune complex reaction after recovery from acute or subclinical dz = chronic kidney lesions (chronic glomerulonephritis)
- Ocular lesions (corneal edema) ‘blue eye’
-occur in 20% natural inf
-less than 1% dogs after S/C MLV-CAV1 vacc
-dogs during recovery, or chronic cases
Describe how corneal edema develops in ICH.
CAV1 Ab prod inc & form viral Ab immune complex -> complement activation (neutrophil chemotaxis) -> damage to corneal endothelium -> disrupt intact corneal endothelium & allows aqueous to enter cornea -> accumulate edematous fluid in corneal stroma = corneal edema
Describe the complications from ICH.
- DIC from:
-damage to endothelium
-inability of dz liver to remove activated clotting factors - Bacterial pyelonephritis from renal damage
Describe the clinical signs of ICH.
-freq in dogs <1yr
-concurrent parvoviral or distemper inf worsens prognosis
-unvaccinated dogs of all age sus
-most inf asymp
-signs from fever to death
Describe ICH peracute VS acute cases.
- Peracute
-severely inf dogs moribund & die in few hrs after CS - Acute
-CS in dogs that survive acute viremic phase
-fever >104 (40c), depression, anorexia
-vomiting
-ab pain, tenderness, hepatomegaly
-hyperemia or petechiae hemorrhage of oral mucosa
-pale MM, jaundice
-enlarged tonsil, swollen LN
-SQ edema of head, neck, trunk
-CNS involvement unusual & result of vascular injury
-icterus uncommon in early acute phase
-corneal edema & anterior uveitis when clinical recovery begins ‘blue eye’
Describe the diagnosis of ICH.
- CS
- Necropsy & histopath
-paint brush hemorrhage on gastric serosa, LN, thymus, pancreas, SQ tissue
-centrilobular necrosis in liver, w neutrophilic & monocytic infiltration, & hepatocellular intranuclear inclusions
-grayish white foci in kidney cortex of recovered dogs or dogs w chronic dz - Biochem & hematology
-leukopenia persist thruout febrile period
-inc ALT & AST due to hepatic injury
-proteinuria
-prolonged prothrombin time, thrombocytopenia - Virus isolation: urine, blood, tissue homogenates
Describe the treatment & immunity of ICH.
- Treatment
-symptomatic & supportive
-limit secondary bacterial invasion, support fluid balance, & control hemorrhage - Immunity
-recovered immune to systemic form of dz
-maternal Ab interfere w active immunization until puppies are 9-12weeks
-attenuated CAV1 live vacc = make transient unilateral or bi lateral opacities of cornea
>cause mild subclinical interstitial nephritis & shed in urine
-CAV2 attenuated live virus strain = cross protection against CAV1, CAV2
>little tendency to make corneal opacities or uveitis & virus not shed in urine preferred
Describe canine infectious tracheobronchitis.
‘ITB, Kennel Cough’
self limiting URT dz of dogs
1. Etiology
-multiple
-CAV2, bordetella bronchiseptica
2. Transmission
-contagious (aerosol droplets)
-stress, unfavorable conditions inc severity of dz
3. Treatment
-antitussives + bronchodilators
4. Immunity
-MLV vacc against distemper, parainfluenza, CAV2 (provides protection against CAV1)
Describe complicated VS uncomplicated ITB.
- Complicated
-severe pneumonia or bronchopneumonia
-life threatening - Uncomplicated
-paroxysms of harsh, dry cough, etching, gagging
-coughing = high pitched honking sound
-rhinitis, serous nasal discharge, conjunctivitis
Describe equine adenovirus general characteristics & clinical signs.
GC:
-EAV1 & EAV2
-asympt or mild upper or lower respiratory tract dz
-EAV1 = severe respiratory dz in SCID foals
-maternal Ab wanes = foals sus to adenovirus inf
>inf progressive & foals die within 3mo of age
CS:
-severe bronchiolitis & pneumonia + respiratory distress
