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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.
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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)
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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)
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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)
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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
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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
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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
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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
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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
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differentials for malignant catarrhal fever (MCF)
blue tongue disease, bovine viral diarrhea, foot and mouth disease
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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
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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
- FATAL DISEASE
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equine herpes (5)
- 1 (abortion virus), 3 (equine coital) and 4 (equinerhinopneumonitis) are alpha
- 2 and 5 (equine multinodular pulmonary fibrosis) are gamma
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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 careSee intranuclear viral inclusions
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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
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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.
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Equine herpes 2
- gammaherpesvirus
- widespread (70-100%), pathogenic? Herpetic keratoconjunctivitis, nonspecific signs, "poor performance"
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Equine herpes 5
- gamma, less widespread than 2
- equine multinodular pulmonary fibrosis
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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 genesintracellular inclusion bodies
- agglutinate erythrocytes for HA assays
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adenovirus genera (2)
- mastadenovirus (mammals)
- aviadenovirus (egg drop syndrome and hemorrhagic enteritis of turkeys)
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how adenoviruses overcome host antiviral defenses
- interfere with Fas ligand death
- interfere with Bcl-2 control of apoptosisenhance proliferation (p53 and Rb), control translational initiation (PKR and interferon)
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diseases of canine adenovirus
- CAV-1: infectious canine hepatitis virus (ICHV)
- CAV-2: respiratory disease
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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
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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
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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
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equine adenovirus
- asymptomatic or mild mid-to-upper respiratory: fever, nasal discharge, cough
- spontaneous resolution (secondary bacterial)
- combined immunodeficient foals die before 3 months
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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
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avian adenovirus diseases (2)
- egg drop syndrome
- hemorrhagic enteritis of turkeys
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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
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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
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polyomavirus characteristics
- dsDNA, icosahedral, smallish, non-enveloped, very stable in environmentmany 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
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budgerigar fledgling disease
- acute generalized disease in fledgling budgies
- die acutely
- abdominal distension and reddening of skin
- virus in many tissues
- intranuclear inclusions
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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)
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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
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canine oral papillomatosis
- lip, buccal mucosa, tongue, palate, pharynx
- incubation 4-8weeks, immune-mediated regression in 4-8 weeks.
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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.
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equine papillomatosis
- small elevated keratinized papillomas. Lip, nose, neck, belly, hind legs.
- 1-9 months.
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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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