Ross Univeristy Virus Families
Herpesviridae General Characteristics
Enveloped virion
linear dsDNA
replication in nucleus
presist indefinitely in host
very fragile
Herpesviridae Transmission
Close contact, mucosal contact or short distance droplet spread (oral, nasal or genital secretions)
Herpesviridae Immunity
neutralizing antibody is primarily directed at envelope glycoprotein peplomers
viral antigens on surface of infected cells are targets for cell-mediated immune lysis
Herpesviridae Diagnosis
viral antigens (immunofluorescence staining)
Viral nucleic acid (PCR)
Viral antibodies using ELISA, virus neutralization
Virus isolation (hen's egg or cell culture)
Gross and histopathy
Alphaherpesvirinae (main subfamily) Characteristics
grow rapidly, lyse infected cells, establish latent infections in sensory ganglia, low temperatures, lesions in skin, CNS, respiratory, genital
generalized infections in neonates
Pregnant animals: mononuclear cell-associated viremia leading to abortion
Bovine Herpesvirus 1
Infectious Bovine Rhinotracheitis, infectious pustular vulvovaginitis, infectious balanoposthitis, abortion
Infectious Bovine Rhinotracheitis Transmission
Aerosol derived from ocular and nasal secretionsCoitus and artificial insemination
Infectious Bovine Rhinotracheitis Pathogenesis
mononuclear cell-associated viremia
virus persists for years
latent virus is reactivated with injections of corticosteroids or other stresses (trigeminal nerve, sciatic nerve)
Infectious Bovine Rhinotracheitis Respiratory Disease
necrotic rhinitis, red nose, dust pneumonia, high morbidity(100%), low mortality (10%), fever, depression, anorexia, salvation, nasal discharge, death can be resultant of secondary bacterial bronchopneumonia
Infectious Bovine Rhinotracheitis Conjuctivitis
conjunctiva inflamed, edematous and mucopurulent discharge
Infectious Bovine Rhinotracheitis Generalized Disease of Neonatal Calves
fever, anorexia, depression, respiratory distress, diarrhea, incoordination and convulsions. Often fatal
Alphaherpesvirus diseases
infectious Bovine Rhinotracheitis
Bovine Mammillitis and Pseudo-Lumpy SKin
Pseudorabies
Equine Herpesvirus 1 (Equine Abortion storm)
Hemorrhage Disease of PUppies
Feline Rhinotracheitis
Infectious Laryngotracheitis
Marek's Disease
Bovine Mammillitis and Pseudo-Lumpy SKin
Bovine Herpesvirus 2
Mechanically transmitted and trauma to skin
Mammillitis: lesions on teats, reduction in milk
Pseudo-Lumpy Skin: high fever, skin nodules
Pseudorabies
REPORTABLE
swine, dogs, cats, ruminants, horses
Porcine Herpesvirus 1
Pigs are primary host and reservoirs - nasal secretions, saliva, milk, ingestion of carcasses
Rodents are minor resevoirs
Pseudorabies pathogenesis
oral, intranasal then replicates in nasopharynx and tonsils, spreads to lymph nodes and CNS, may be brief viremia
Pseudorabies in Cattle
effects CNS
"mad itch"
severe pruritis
Respiratory Failure
CNS, paralysis of pharynx, salivation
Pseudorabies in dogs/cats
Dogs: pruritis, paralysis of jaw and pharynx, no aggression
Cats: death too fast for signs
Pseudorabies Diagnosis
Virus isolation
Fluorescent antibody staining
serology
Vaccination of swine
vaccines don't prevent infection
Equine Herpesvirus 1 Characteristics
Equine abortion virus
most virulent equine herpesvirus
abortions, respiratory, perinatal foal disease, encephalitis
inhalation, direct/indirect contact with nasal discharges, aborted fetuses/placenta
Equine Herpesvirus 1 Pathogenesis
replicates in epithelial cells of respiratory tract, regional lymph nodes, circulating leukocytes and endothelial cells, inhibits antigen presentation by inhibits TAP protein
Equine Herpesvirus 1 Clinical signs
Macrophage associated viremia, virus can spread to fetus and late term abortion
Encephalomyelitis: present as primary disease, vasculitis
Perinatal foal: dead from septicemia and interstitial pneumonia, lower body temp, 100% mortality
Equine Herpesvirus 1 Control
Inactivated vaccine, short lived immunity, must vaccinate several times a year
Equine Herpesvirus 4 Characteristics
respiratory disease, inhalation, young foals, complete recovery, secondary infection causes death, short-lived immunity so need to multiple times
Hemorrhagic Disease of Puppies
Fading Puppy Syndrome characteristics
Highly fatal under 4 weeks puppies
Canine herpesvirus 1
Transmission in utero, infected nasal, oral or vaginal secretions
Hemorrhagic disease of puppies fading puppy syndrome pathogenesis
replicate in nasal epithelium, pharynx and tonsils, followed by macrophage-associated viremia and virus replication in endothelial cells. Large ecchymotic hemorrhages and necrosis are observed in kidney and liver.
Hemorrhagic Disease of Puppies Clinical Features
painful crying, abdominal pain, anorexia, dyspnea, sort odorless yellowish green stool, no fever
meningoencephalitis: CNS signs generally dont show due to quick death
Hemorrhagic Disease of Puppies Histopathology
perivascular necrosis and hemorrhage
acidophilic or basophilic intranuclear inclusions, depending on the stage of cellular infection and method of fixation
Feline Rhinotracheitis Characteristics
Feline herpesvirus 1
transmission: ocular, nasal, and oral secretions, stay dormant with intermittent shedding
Feline Rhinotracheitis Pathogenesis
replication occurs primarily in the mucosae of the nasal septum, turbinates, nasopharynx, and tonsils
Feline Rhinotracheitis Clinical Signs
Neonates: fever, sneezing, coughing, profuse serous nasal and ocular discharge, dypsnea, anorexia, weight loss, profuse frothy salivation
keratitis with punctate corneal ulcers
abortion in first trimester
Feline Rhinotracheitis Pathology
necrosis of epithelia of nasal cavity, pharynx, epiglottis, tonsils, larynx, and trachea
Infectious Laryngotracheitis (ILT)
acute highly contagious disease of chickens
severe dyspnea, coughing, rales
Gallid herpesvirus 1
inhalation or ingestion
severe laryngotracheitis charaterized by necrosis, ulceration, hemorrhage, and formation of diphtheritic membranes
death from asphyxiation
respiratory distress
morbidity 100%
vaccine with modified live virus
Very Virulent Marek's Disease (vvMDV)
high incidence of neural and visceral lymphomas
oncogenic in chickens vaccinated for HVT
prevented with bivalent vaccines
Very Virulent Plus Marek's Disease (vv+MDV)
associated with a high incidence of lymphomas
oncogenic in chickens vaccinated with bivalent vaccines
Marek's Disease Transmission
highly contagious disease
inhalation of infectious feather debris, dust or chicken dander
Marek's Disease Pathogenesis
genetic susceptibility traced to different MHC class II haplotypes (B21 genetically resistant)
replication in respiratory tract followed by macrophage associated viremia
Fully Productive INfection
production of fully infectious virions (enveloped virions) and cell death (cytolysis) in feather follicle epithelium
Productive restrictive infection
production of naked virions and viral antigens and cell death
occurs in B cells and activated T cells(profound immunosuppression)
Non-productive Latent Infection
viral genome persists in lymphoid cells but no antigens are expressed
Non-productive Neoplastic Transformation
latently infected T cells undergo neoplastic transformation
Marek's Disease Lesions
result from infiltration and in situ proliferation of the transformed T lymphocytes
cell lysis in productive infections results in a marked inflammatory response
Marek's Disease CLinical Signs
progressive disease with overlapping signs, mortality 80%
Neurolymphomatosis: enlargement of one or more peripheral nerve trunks - splayed legs
Visceral Lymphomatosis: lymphocytic tumors are present in heart, liver, kidney, spleen
Ocular Lymphomatosis: graying of the iris of one or both eyes resulting from T cell infilatration
Cutaneous Lmphomatosis: plucking of the feathers reveals round, nodular lesions
Marek's Disease Diagnosis
history, age, clinical signs
detection of viral antigen using, PCR
Detection of antibodies using AGID, IFA, and virus neutralization tests
Virus isolation
Marek's Disease Control
Reportable Disease
Vaccination
Avirulent turkey herpesvirus
Bivalent vaccines consisting of HVT and CV1988/Rispens strain of serotype 1 or HVT
Betaherpesvirus
slow-replicating and cell lysis does not occur until several days after infection
chronic infection
enlarged infected cells (cytomegaly)
latent form in secretory glands and lymphoreticular cells
continuous viral excretion
Inclusion Body Rhinitis
endemic in swine up to 90%
Porcine Herpesvirus 2
transmitted through inhalation, transplacental
Inclusion Body Rhinitis Pathogenesis
primary virus replication in nasal mucous glands and respiratory tract
viremia, macrophages, epithelial-type cells, endothelial cells
petechial hemorrhages and edema
anemia in neonates due to bone marrow damage
Inclusion Body Rhinitis Clinical Signs
piglets less than 3 weeks
sneezing, coughing, serous nasal and ocular discharge and depression
SMEDI
Inclusion BOdy Rhinitis Pathology
petechiae and edema
basophilic intranuclear inclusion bodies and cytomegaly
Inclusion BOdy Rhinitis Diagnosis
gross and histo
virus isolation from nasal mucosa, lung, and kidney
detection of antibodies using ELISA or IFA test
Inclusion Body Rhinitis Control
good management and abstention from introducing new stock during mating and first month
Gammaherpesvirinae
lymphotropic (replicate in T or B lymphocytes), lymphoid tumors
latency in lymphoid tissues
Malignant Catarrhal Fever (MCF)
sporadic but highly fatal disease of ruminants
lymphoid and epithelial cells of respiratory and GI
Alecelaphine herpesvirus 1
Alecelaphine herpesvirus 2
Ovine herpes virus 2
Malignant Catarrhal Fever Transmission
close contact esp in african form: cell free state
American form: close contact
Malignant Catarrhal Fever Pathogenesis
cell-associated viremia, immune mediated since virus is usually absent
widespread necrotizing vasculitis
Peracute form of Malignant Catarrhal Fever
1-3 days
severe inflammation of oral and nsal mucosa and hemorrhagic gastroenteritis