Family: Adenoviridae Flashcards
Family: Adenoviridae - Morphology
Non-enveloped, hexagonal, icosahedral symmetry, capsid is 720 hexon subunits arranged as 240 trimers, 12 vertex penton capsomers each with a fiber protrude from the surface of capsid.
Family: Adenoviridae - Genome and replication
Non-segmented, linear double-stranded DNA of 35-36 kb, replication takes place in nucleus, virions released by cell lysis, intranuclear inclusion bodies, containing large number of virions.
Family: Adenoviridae - General properties
Agglutinate RBC. Hemagglutination. Tips of penton fibers bind to surface receptors on RBC. Some viruses are oncogenic in laborator animals. Relatively stable in environment, but are inactivated easily by common disinfectants, Most narrow host ranges.
Family: Adenoviridae - Pathogenesis
Many adenoviruses cause acute respiratory or gastroenteric disease. Mostly subclinical infections. Penton and fiber proteins, capsid are toxic to cell.
Family: Adenoviridae - Immunosuppression
Inhibition of class I MHC antigen transport by E3/19K. Apoptosis in inhibited by adenoviral E3/14.7K. Blocking of IFN induced protein kinase R-mediated inhibition of viral protein synthesis. Modulate antiviral inflammatory, inhibiting nuclear factor kB NF kB transcriptional activity.
Family: Adenoviridae - Long periods of latency
Virus persists in lymphoid and other tissues. Reactivated immunocompromised animals. Highly pathogenic in immunodeficient animals.
Family: Adenoviridae - oncogenesis
E1A: Inactivated Rb protein
E1B: Inactivated p53 protein
Family: Adenoviridae involve 2 genera
- Genus: Mastadenovirus
2. Genus: Aviadenovirus
Genus: Mastadenovirus
Mammalian adenoviruses. A single penton fiber projects from each vertex.
Genus: Aviadenovirus
Avian adenoviruses, penton fiber is bifurcated.
Canine Adenovirus-1
Infectious Canine Hepatitis (ICH, Rubarth’s Disease)
ICH - Transmission
All secretions and excretion. Afterwards, virus shed in urine for at least 6 to 9 months. Oronasal transmission. Contact with secretions/excretions/ fomites, and ectoparasites.
ICH - Pathogenesis
Replicates in macrophages, kupffer cells, hepatocytes and vascular endothelium
ICH - Kidney
Acute infection, glomerulonephritis. Basophilic inclusion bodies. Chronic kidney lesions may result from immune complex reactions after recovery from acute or subclinical disease.
ICH - Ocular Lesions
Corneal edema (blue eye). Occurs in about 20% of natural infections. Less than 1% of dogs after S/C MLV CAV-1 vaccination. Seen in dogs during recovery of chronic cases.
How does corneal edema develop?
- During viremia, CAV-1 enters the eye via the uveal tract.
- CAV-1 localizes in endothelium of choroid and causes mild uveitis.
- By 4-6 days post infection, virus enters the aqueous humor from the blood and replicates in corneal endothelial cells.
By day 7, Severe anterior Uveitis and Corneal Edema (Blue Eye) develop
- CAV-1 antibody production increases, and formation of viral-antibody immune complexes.
- This result in Complement activation, neutrophil chemotaxis.
- Cause extensive damage to corneal endothelium.
- Disruption of intact corneal endothelium allows aqueous to enter the cornea.
- Accumulation of edematous fluid within corneal stroma results in corneal edema.
- From days 8-21, macrophages remove the immune complexes and corneal endothelium regenerates, re-establishing the hydrostatic gradient.
- Clearing of corneal edema.
ICH - DIC
Results from damage to endothelium and inability of diseased liver to remove activated clotting factors
ICH - Clinical signs - peracute cases
Severely infected dogs become moribound and die within few hours onset of clinical signs.
ICH - Clinical signs - acute cases
Fever, vomiting, abdominal pain, hepatomegally, icertus is uncommon. Corneal edema and anterior uveitis occur when clinical recovery begins. Encephalitis is more commonly seen in foxes.
ICH - Diagnosis
Clinical signs, necropsy and histopathology (“paintbrush” hemorrhageson serosa), virus isolation in urine, antigen detection using FAT, nucleic acid detection using PCR, paired serum tested.
ICH - Treatment
Treatment is symptomatic and supportive. The goals of therapy are to limit secondary bacterial invasion. support fluid balance, and control hemorrhagic tendencies.
ICH - Immunity
Maternal antibodies interferes with active immunization until puppies are 9 to 12 weeks of age. CAV-2 attenuated
ICH - Immunity - Attenuated CAV-1 live vaccines
Have produced transient unilateral or bilateral opacities of the cornea. Vaccine virus can cause mild subclinical interstial nephritis and may be shed in urine. Discontinued in many countries.
ICH - Immunity - Attenuated CAV-2 live virus strains
Provide cross protection against CAV-1. CAV-2 attenuated vaccines are preferentially used because they have very little tendency to produce corneal opacities of uveitis, and the virus is not shed in urine.
Canine Adenovirus-2 (CAV-2)
Canine Infectious Tracheobronchitis ITB or Kennel Cough
Incubation period 1-3 days
CAV-2 - Transmission
Highly contagious, via aerosolized droplets. Stress, unfavorable conditions increases severity of disease.
CAV-2 - Clinical signs - Uncomplicated ITB
The prominent clinical sign is paroxysms of harsh, dry coughing, followed by etching and gagging. Coughing causes a high pitched “honking” sound. Rhinitis, serous nasal discharges, sometimes conjunctivitis.
CAV-2 - Clinical signs - Complicated ITB
Severe pneumonia or bronchopneumonia and life threatening
CAV-2 - Diagnosis
Clinical signs, coughing is easily induced by gentle palpation of the larynx or trachea. Nucleic acid detection, serology, virus isolation same as CAV-1.
CAV-2 - Treatment
Anitussives, wen used in conjunctiong with bronchodilators, are often considered the standard treatment for dogs with ITB. Antitussive drugs serve to interrupt the cough cycle.
CAV-2 - Immunity
MLV against distemper, parainfluenza and CAV-2 which also provides protection against CAV-1.
Equine Adenovirus
EAV-1 and EAV-2. Most are asymptomatic or mild respiratory tract disease.
EAV-1
Associated with severe respiratory disease in severe combined immunodeficiency (SCID) foals
SCID
Mutation in the allele encoding for DNA-dependent protein kinase (DNA-PK) that is needed for lymphocyte V(D)J recombination. As a result, there is severe immunodeficiency.
Clinical signs in SCID foals
Severe broncholitis and pneumonia. Respiratory distress and related signs. May develop generalized EAV infections, as virus destroys cells of different organs, such as pancreas, GIT, renal and bladder.
Avian Adenoviruses - Chickens
Inclusion body hepatitis. Egg drop syndrome.
Avian Adenoviruses - Ducks
Hepatitis (rare)
Avian Adenoviruses - Quail
Bronchitis
Avian Adenoviruses - Turkeys
Hemorrhagic enteritis. Egg drop syndrome
Avian Adenoviruses - Pheasants
Marble spleen disease
ICH - Hepatitis
At time of infection, antibody titers (>500) show little clinical evidence of disease. Antibody response by day 7 post-infection clears virus from blood and liver and restricts hepatic damage. Persistently low antibody titer (16, but
