virology wk 2

  1. Bovine herpesvirus type I
    • most common viral infection in cattle
    • alphaherpesvirus
    • 2 forms = Respiratory: Infectious Bovine Rhinotracheitis (IBR) and abortion
    • genital: infectious pustular vulvovaginitis (IPV) in females, infectious balanoposthitis (IBP) in males
    • Highly infectious, rarely fatal
    • Entry through mucosal surfaces
    • genital stays localized (sacral ganglion)
    • IBR viremia, uterus, trigeminal ganglion.
  2. Infectious Bovine Rhinotracheitis (IBR)
    • bovine herpesvirus type I, respiratory
    • in through mucosal surfaces, systemic viremia to uterus (abortion) and trigeminal ganglion (latent)
    • ADR, c/s, lacrimation, conjunctivitis, oronasal ulcers/fetid breath, oronasal d/c, abortion, encephalitis in young calves.  
    • ELISA to detect antibodies in milk
    • serological to tell latent carriers
    • virus isolation from nasal swabs (not latent)
  3. Infectious Pustular vulvovaginitis (IPV)
    • female genital form of bovine herpesvirus I
    • mucous membrane transmission, stays localized, sacral ganglion
    • ADR, vesicles/pustules and ulcerations on vulvar skin, vaginal mucosa
    • frequent micturation
    • tail away from vulva (painful)
    • serological to tell latent carriers
    • virus isolation from vaginal swabs (not latent)
  4. Infectious Balanoposthitis (IBP)
    • male genital form of bovine herpesvirus I
    • mucous membrane transmission, stays localized, sacral ganglion
    • balanitis = inflammation of glans penis
    • posthitis = inflammation of prepuce
    • vesicles to ulcers
    • bulls refuse to breed (painful)
  5. prevention and control of bovine herpesvirus I
    • sterilize AI, test semen
    • steroids can cause reactivation (ID carrier bulls)
    • Stress causes reactivation
    • careful around pregnant cattle!
    • modified live vaccine and inactivated, marker vaccines--best to vaccinate calves
  6. bovine herpesvirus type II
    • alphaherpesvirus
    • USA: bovine mammilitis (BHM), transmit via biting arthropods and fomites (milking machines), possibly respiratory
    • Africa: bovine mammilitis (BHM) and pseudo-lumpy-skin-disease (lumpy is a poxvirus, PLSD).  Transmission via biting arthropods, wild bovids are reservoir
    • vesicles 7d post infection.  Latent period.
    • intracellular inclusions and hydropic degeneration of skin cells
    • NO VACCINE, just good hygiene
    • 2 years of immunity post-infection
  7. Pseudo lumpy skin disease (PLSD)
    • symptom of bovine herpesvirus II in Africa
    • painful edematous nodules in skin of neck, back, head, chest, tail
    • can develop necrosis, serous exudate and then scab on nodules
  8. Bovine mammalitis (BHM)
    • symptom of bovine herpesII in USA, Africa
    • skin lesions on teats and udder of lactating cows.  Teat and mammary swelling and ulceration prevents milking, decreased production
    • milk retention causes bacterial mastitis
  9. Malignant Catarrhal Fever (MCF)
    • fatal disease in cattle, deer, antelope and buffalo caused by several ruminant GAMMA HERPESVIRUSES
    • Don't cause disease in natural host (wildebeest - Alcelaphine herpesvirus I (AIHV-1)) (sheep (Ovine herpesvirus type 2 (OHV-2)))
    • Infect respiratory mucosa, lymphocytes (viremia), increase in T-cells, lymphadenopathy, lymph delivers virus to endothelial cells, vasculitis
    • ADR, nasal/ocular discharge, lymphadenopathy, mucosal erosions, CNS signs, bilateral ophthalmia (corneal opacity in center spreading to periphery, eventual blindness)
    • death in 2 days to 1 week
    • vasculitis with necrosis, hemorrhage, edema; lymph nodes edematous +/- hemorrhagic
    • erosions in nasal turbinates, gut, larynx
  10. differentials for malignant catarrhal fever (MCF)
    blue tongue disease, bovine viral diarrhea, foot and mouth disease
  11. Alcelaphine herpesvirus I (AIHV-1)
    • gammaherpesvirus that causes malignant catarrhal fever in cattle
    • circulates africa and zoos
    • no clinical signs in natural host (wildebeest, topi, hartebeest)
    • transmission to cattle upon close contact, esp around calving time
    • FATAL DISEASE morbidity low, mortality high
    • does not spread cattle to cattle
  12. Ovine herpesvirus 2
    • gammaherpesvirus that causes malignant catarrhal fever in cattle
    • circulates in Western USA
    • no clinical signs in sheep (natural host)
    • transmission to cattle upon close contact, especially around lambing time
  13. equine herpes (5)
    • 1 (abortion virus), 3 (equine coital) and 4 (equinerhinopneumonitis) are alpha
    • 2 and 5 (equine multinodular pulmonary fibrosis) are gamma
  14. Equine herpesvirus type I
    • alphaherpesvirus of domestic and (occasionally) wild horses, widespread (less than 4).  respiratory signs (worse than 4)
    • neurologic disease (equine herpes myeloencephalitis (EHM)) on racetracks
    • aka equine abortion virus, causes abortion storms
    • biphasic fever
    • primary respiratory, viremia to endothelial cells, vasculitis, thrombosis, disseminated ischemic necrosis.  Abortion (fetus may be - if severe enough), spinal cord (neuro ischemia = hind limb ataxia, NOT REPLICATION IN NEURONS--endotheliotropic)
    • quarantine/vax (killed not great, modified live are dangerous to pregnant) and supportive care
    • See intranuclear viral inclusions
  15. equine herpesvirus type 4
    • alphaherpesvirus, endemic worldwide (4>1), like 1 but less pathogenic
    • upper resp signs like 1 (nasal d/c) in young horses (2m - 1y), could move to lower.  
    • Vaccination (1 and 4 combination inactivated)
    • decrease stress, quarantine new, hygiene (enveloped).  MANAGEMENT
  16. Equine herpesvirus 3
    • alpha
    • equine coital exanthema, STD (maybe flies)
    • 2-day incubation
    • genital mucosa, no viremia.  Latent, stress causes reactivation.  Open sores/ulcerative lesions = shedding virus.  Lesions heal in 2 weeks.  
    • DON'T BREED WHILE SHEDDING.  disinfect AI equipment.  White scars = latent infection.  NO vaccine.
  17. Equine herpes 2
    • gammaherpesvirus
    • widespread (70-100%), pathogenic?  Herpetic keratoconjunctivitis, nonspecific signs, "poor performance"
  18. Equine herpes 5
    • gamma, less widespread than 2
    • equine multinodular pulmonary fibrosis
  19. adenovirus properties
    • non-enveloped, icosahedral medium sized ds DNA (stable in environment), fibers from capsid, species-specific
    • receptor-mediated endocytosis, cell lysis, replicates in nucleus, early and late genes
    • intracellular inclusion bodies
    • agglutinate erythrocytes for HA assays
  20. adenovirus genera (2)
    • mastadenovirus (mammals)
    • aviadenovirus (egg drop syndrome and hemorrhagic enteritis of turkeys)
  21. how adenoviruses overcome host antiviral defenses
    • interfere with Fas ligand death
    • interfere with Bcl-2 control of apoptosis
    • enhance proliferation (p53 and Rb), control translational initiation (PKR and interferon)
  22. diseases of canine adenovirus
    • CAV-1: infectious canine hepatitis virus (ICHV)
    • CAV-2: respiratory disease
  23. Infectious Canine Hepatitis (CAV-1)
    • Canine adenovirus I
    • dogs, foxes (encephalitis) (wolves, coyotes, skunks, bears)
    • mild/asymptomatic, respiratory
    • 4-9d incubation
    • 3 syndromes: peracute (dead in 3-4h, no signs), acute (fever, depression, inappetence, diarrhea, petechia, jaundice), mild (most common)
    • systemic replication of virus, necrotic foci (neutrophilic, mononuclear and plasma cell infiltration), hepatitis with necrosis, "blue eye" when virus-antibody complex deposits in ciliary body capillaries= corneal edema, resolves spontaneously
    • inclusion bodies diagnostic
  24. Infectious canine hepatitis (CAV-2)
    • respiratory disease (upper and mid, rarely lung or systemic = viral pneumonitis)
    • infectious tracheobronchitis (kennel cough) from co-infection with bordetella bronchiseptica, parainfluenza or canine influenza
    • persist, shed at low levels for months
  25. CAV (1 & 2) diagnosis and vaccines
    • virus isolation, immunohistochemistry, serology (HA inhibition, ELISA), antibodies or DNA (qPCR)
    • kidney infection = viruria, shed up to 6 months
    • shed in feces and saliva
    • vaccines: routine and effective!  From CAV-2 will cross-protect
    • maternal immunity ~9d
    • titers 1:100 = successful immunity
  26. equine adenovirus
    • asymptomatic or mild mid-to-upper respiratory: fever, nasal discharge, cough
    • spontaneous resolution (secondary bacterial)
    • combined immunodeficient foals die before 3 months
  27. adenovirus of deer
    • extremely severe/fatal
    • mule deer, occasionally black or white tailed
    • no treatment (management)
    • ulcers/absesses/hemorrhage in mouth/throat/GI, rapid breathing, foaming/drooling, diarrhea, weakness, third spacing, death 3-5d post-exposure
    • histology: widespread vasculitis with endothelial cell intranuclear inclusions
    • diagnosis via antigen in tissues, detection of virus or DNA
  28. avian adenovirus diseases (2)
    • egg drop syndrome
    • hemorrhagic enteritis of turkeys
  29. egg drop syndrome
    • avian adenovirus of chickens, wild and domestic ducks and geese
    • decreased egg production, soft or a-shellular eggs.  Otherwise chickens are healthy
    • lesions in pouch shell gland in eggs, necrotic epithelial and intranuclear inclusion bodies
    • Ha inhibition, PCR for viral DNA
    • control contaminated eggs, fomites, needles, droppings.  
    • Primarily eradicated in domestic in most countries
  30. hemorrhagic enteritis of turkeys
    • turkey adenovirus 2 (marble spleen disease of pheasants)
    • turkeys > 4w = splenomegaly, intestinal hemorrhage.  Acute onset, depression, bloody droppings, death, secondary bacterial infection
    • flock mortalities 1-3%
    • reticuloendothelial hyperplasia and intranuclear inclusion bodies in spleen
    • fomites, stable in droppings!!
    • attenuated vaccine via drinking water
  31. polyomavirus characteristics
    • dsDNA, icosahedral, smallish, non-enveloped, very stable in environment
    • many species, persistent infections but NO DISEASE IN IMMUNOLOGICALLY INTACT HOST.
    • may infect humans via vaccine and biologics made of bovine serum (contamination).  No evidence to date (SV-40)
    • causes budgerigar fledgling disease
  32. budgerigar fledgling disease
    • acute generalized disease in fledgling budgies
    • die acutely
    • abdominal distension and reddening of skin
    • virus in many tissues
    • intranuclear inclusions
  33. papillomavirus characteristics
    • dsDNA, icosahedral, smallish, non-enveloped, very stable in environment
    • lots of genotypes within species
    • PAPILLOMAVIRUS REPLICATION INTIMATELY LINKED TO TISSUE DIFFERENTIATION - expressed only in cells at certain stages of differentiation (terminally differentiated)
  34. papillomavirus in skin
    • virus can only enter basal cell layer and grow up.  Replicates in stratified squamous and mucosal epithelium
    • early genes = cellular hyperplasia (increased basal cells, slow maturation of spinosum and granulosum strata)
    • late genes = capsid proteins (stratum spinosum), particles in granulosum
    • virions shed from exfoliated skin
  35. canine oral papillomatosis
    • lip, buccal mucosa, tongue, palate, pharynx
    • incubation 4-8weeks, immune-mediated regression in 4-8 weeks.
  36. bovine papillomavirus with distinct lesions (1-6), general
    • common infection (though more in calves/yearlings)
    • BVP-1: teat front warts (equine sarcoids)
    • BVP-2: common cutaneous warts (equine sarcoids)
    • BVP-5: rice grain fibropapillomas
    • BVP-3,4,6: epithelial and cutaneous lesions without fibroblast proliferation (3 = broad base, last longer.  4=alimentary tract and bladder carcinomas.)
    • warts are fibrous core with stratified squamous epithelium, outer layers hyperkeritinized on udder, teats, head, neck, shoulders, vagina, vulva, penis
    • enter through abrasions
    • hyperplasia, hyperkeritinization 4-6w post-infection
    • 4-6m, then spontaneous regression
    • will not grow in culture (EM, viral DNA or PCR)
    • contact and fomites, sexual transmission.  Horses can get it.
  37. equine papillomatosis
    • small elevated keratinized papillomas.  Lip, nose, neck, belly, hind legs.  
    • 1-9 months.
  38. Equine sarcoids (general + 4 kinds)
    • BVP-1 or BVP-2, mostly not horse-to-horse transmission
    • skin tumors (fibrosarcomas), not metastatic
    • persist for life, locally invasive
    • 1. verrucous (flat), hairless, slow-growing
    • 2. fibroblastic - intradermal fibroblastic proliferative response, rapid growth and ulceration
    • 3. mixed
    • 4. occult - flat with rough thickened skin
    • injecting immune stimulators may help
    • surgery, cryosurgery, chemotherapy (may recur).  
    • More severe because NOT A HORSE VIRUS
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virology wk 2
IV wk 2