Family: Adenoviridae Flashcards
Morphology of family Adenoviridae
Non-enveloped
Hexagonal
Icosahedral symmetry
12 vertex penton capsomers each with a fiber protruding from the surface of capsid
Genome and replication of family Adenoviridae
Non-segmented, linear double-stranded DNA
Replication takes place in the nucleus by a program of early and late transcription (before and after DNA replication)
Intranuclear inclusion bodies are formed, containing large numbers of virions, often in para-crystalline arrays
Immunosuppression achieved by Adenoviruses
Adenoviruses encode proteins hat suppress host immune and inflammatory responses
- Inhibition of class I major histocompatibility antigent transport by E3/19K
- TNF induced apoptosis is inhibited by adenoviral E3/14.7K
- Blocking of IFN produced protein kinase R-mediated inhibition of viral protein synthesis
- Modulate antiviral inflammatory responses by inhibiting nuclear factor kB transcriptional activity
Oncogenesis of Adenoviridae family
E1A and E1B gene products are associated with cell transformation
E1A - inactivate Rb protein
E1B - inactivatep53 protein
Mammalian Adenoviruses
Genus: Mastadenovirus
A single penton fiber projects from each vertex
Avian Adenoviruses
Genus: Aviadenovirus
Each penton fiber is bifurcated, appear as two fibers extending from each penton base
Canine adenovirus-1
-common names
Infectious Canine Hepatitis
Rubarth’s Disease
CAV-1 (ICH) transmission
CAV-1 is found in all secretions and excretions with acute infection
Virus is shed in urine for 6-9 months
Oro-nasal transmission
Sites of replication and target organs of CAV-1
Macrophages, Kupffer cells, hepatocytes
Vascular endothelium of different orgnans, including CNS
Parenchymal cells of organs and tissues
Liver, kidney, spleen, and lungs are main target organs
3 main pathogenesis of CAV-1 (ICH)
Hepatitis
Ocular Lesions
Disseminated intravascular coagulation
Hepatitis pathogenesis of CAV-1
Dogs with sufficient antibody titers (>500) show little clinical evidence of disease
In acute cases, sufficient Ab response by day 7 post-infection (>500 Ab by day 7) clears virus from blood and liver, and restricts hepatic damage
Persistently low Ab titer (16 but
Pathogenesis of ocular lesions of CAV-1
Corneal edema (Blue eye)
Seen in dogs during recovery or chronic cases
CAV-1 enters eye via uveal tract during viremia
CAV-1 localizes in endothelium of chorid
4-6 days post-infection, virus enters aqueous humor
Disruption of intact corneal endothelium allows aqueous to enter the cornea
Accumulation of edematous fluid within corneal stroma results in corneal edema
Pathogenesis of DIC of CAV-1
Results from damage to endothelium and inability of diseased liver to remove activated clotting factors
Clinical signs of CAV-1
Most frequent in dogs less than 1 year old
Concurrent parvoviral or distemper infection worsens the prognosis
Most infections are asymptomatic
Clinical signs in peracute cases of CAV-1 (ICH)
Severely infected dogs become moribund and die within a few hours after onset of clinical signs
Clinical signs in acute cases of CAV-1 (ICH)
In dogs that survive acute viremic phase
Fever, depression, anorexia, vomiting, abdominal pain and tenderness
Hepatomegaly
Jaundice (icterus is uncommon in ICH)
Corneal edema and anterior uveitis occur when clinical recovery begins
Necropsy and histopathology findings of CAV-1 (ICH)
“Paint-brush” hemorrhage on gastric serosa, lymph nodes, thymus, pancreas, and subcutaneous tissue
Centrilobular necrosis in liver with neutrophilic and monocytic infiltraiton, and hepatocellular intranuclear inclusions
Grayish white foci in kidney cortex of recovered dogs or dogs with chronic disease
Immunity of CAV-1
Maternal antibodies interfere with active immunization until puppies are 9-12 weeks of age
Vaccination for CAV-1
Attenuated CAV-1 live vaccines can produce transient unilateral or bilateral opacities of the cornea, can cause interstitial nephritis, and may be shed in urine
CAV-2 attenuated live virus strains provide cross-protection against CAV-1 and CAV-2; preferentially used because they have little tendency to produce corneal opacities or uveitis, and virus is not shed in urine
Canine Infectious Tracheobronchitis
- common name
- disease
- etiology
ITB
Kennel cough
A self-limiting upper respiratory disease
CAV-2 and Bordetella bronchiseptica (primary pathogen) are the most prevalent
Transmission of kennel cough
Highly contagious, via aersolized droplets
Stress, unfavorable conditions increase severity of disease
Uncomplicated ITB clinical signs
Prominent clinical signs are paroxysms of harsh, dry coughing, followed by etching and gagging
Coughing causes a high pitched “honking” sound
Rhinitis, serous nasal discharge, sometime conjunctivits
Complicated ITB clinical signs
Severe penumonia or bronchopneumonia
Life threatening
Diagnosis of ITB
Coughing is easily induced by gentle palpation of the larynx or trachea
Treatment of ITB
Antitussives (cough suppressant), when used in conjunction with bronchodilators, are considered the standard treatment
Antitussive drugs interrupt the cough cycle
Immunity of ITB
Modified live vaccine against distemper, parainfluenza, and CAV-2, which also provides protection against CAV-1
Equine Adenovirus
EAV-1 is associated with severe respiratory disease in severe Combined ImmunoDeficiency (SCID) in foals
Immunodeficiency in SCID foals
V(D)J recombination is essential for expression of antigen receptors on B and T lymphocytes
Without these receptors, B and T lymphocytes do not differentiate and lymphoid tissues fail to develop
In SCID foals, there is a mutation in the allele encoding for a DNA-dependent protein
As a result there is severe immunodeficiency
Clinical signs in SCID foals
Severe bronchiolitis and pneumonia
Respiratory distress
Avian Adenoviruses
Chickens - Inclusion body hepatitis; egg drop syndrome
Ducks - Hepatitis (rare)
Qual - Bronchitis
Turkeys - Hemorrhagic enteritis; egg drop syndrome
Pheasants - Marble spleen disease
