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110 Cards in this Set
- Front
- Back
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Poxviridae
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Largest and most complex of all viruses. Envelope may or may not be present. Eosiniphilic intracytoplasmic inclusions. Very resistant and can live for many years in scabs. Highly epitheliotrophic. CAM test. They are very resistant and can live in scabs for years.
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Orthopoxvirus disease
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Cowpox - Rodents are reservior hosts.
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Pseudocowpox
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parapoxvirus - infected cattle are the sources of infection. Causes milker's nodule
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Cowpox
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Only identified in Europe. infects cattle and wild/zoo animals. Rodents serve as reservior host. humans get Maculopapular lesions. Long lasting immunity.
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Psuedocowpox
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This is a chronic infection. Infected cattle are the source of infection. Hyperplasia of sqamous epithelium. Scabs drop off leaving red horseshoe-shaped rings of scabs surrounding small wart-like granulomas. 4-6 month immunity.
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Milkers nodule
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Pseudocowpox of the parapox diseases. Poxviridae
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Contagious ecthyma
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Acute infection of lambs and kids. Virus can live forever in the environment in scabs. Vesiculopapular eruptions. Verrucose mass under the scabs. Complications arise from contamination from larvae of screw worm, or frm Fusobacterium necrophorum. Non attenuated vaccine
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Capripox diseases
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Sheeppox is most important. Also Includes goatpox. There is cross infection and cross protection.
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Sheeppox
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Endemic in Africa, Asia, and europe. Aerosolization and direct transmission. Active in scabs for up to 6 months. mechanical transmission by stomoxys. Systemic disease. Inhalation - leukocyte associated viremia. Severe necrotizing vasculitis resulting in ischemic necrosis of the dermis and epidermis. Malignant form - lambs, signs include fever salivatio lacrimation, hyperpnea, edema of the eyelids, and serus discharge becoming mucopurulent later. Benign - in adults mostly skin lesions. Reportable. Lifelong immunity. Quarantine and slaughter. attenuated and inactive vaccines. 50% mortality
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Ovine Capripoxvirus
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Sheeppox
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Goatpox
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Africa, Asia, and Europe. Similar to sheeppox but has a low mortality (5%)
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Suipoxdiseases
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Swinepox. Similar disease is caused byt he vaccina virus. All age groups are suseptable, but infection occurs mainly in young growing pigs.
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Swinepox
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Worldwide. Direct contact transmission. Haematopinus suis transmits it. Transient low grade fever with development of macules, papules, vesicles, pustules, and crusts. Solid immunity. Eradicate lice from the piggery
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Avipoxvirus Diseases
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Cause disease in chickens, turkeys, guinea fowl, peacocks, pheasants, and other avian species.
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Fowlpox
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Worldwide. Avipoxvirus. chickens and turkeys. This was the first virus to be grown in an embyonated egg. bollinger bodies. Borrel bodies inside Bollinger bodies. Direct transmission. 2 forms of disease wet and dry. Dry form - cutaneous form. Small papules on wattles and combs. lesions around cloaca and feet. Nodules becoome yellowish and produce a think scab. Recovery in 4 weeks. Wet form - diptheritic form - mucous membranes of upper resp. lesions coalesce resulting in necrotic psuedomembrane causing death via suffication. Vaccine available
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Ulcerative dermatitis of Sheep
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Worldwide. Unclassified Ovine poxvirus. 2 forms - crusted ulcers of the mouth and nose and legs. The other is a venerally transmitted ulceration of the prepuce and penis or vulva. Lip n leg ulceration, ovine venereal disease, venereal balanoposthitis and vulvitis. Direct contact transmission.
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Circoviridae
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nonenveloped icosehedral virion. SS DNA.
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PMWS
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Post-Weaning Multisystemic Wasting Syndrome.
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Post-Weaning Multisystemic Wasting Syndrome
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Procine circovirus 2 (PCV2) Disease of growing pigs 4-14 weeks of age, characterized by wt loss, anroexia, diarrhea, and skin discoloration. Only effects swine. Very stable (ph 3-9 and 60C for 30 mins) Fecal oral route, but also in blood, saliva, urine, semen. Transplacental transmission (first and second trimester means fetal death and resorption. third trimester has minimal effects on fetus.) Monocytes/macrophages, hepatocytes, kupffer, dendritic, and cardiac myofibers effected. Lymphopenia. co-infection with parvovirus, arterivirus and mycoplasma hyopneumonia is common. Basopihilic Intracytoplasmic/intranuclear IB's. Vaccine available
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PDNS
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Porcine dermatitis and nephropathy syndome
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Porcine dermatitis and nephropathy syndome
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Associated with PCV2 (porcine circovirus 2) older pigs affected. you see necrotizing skin lesions in the perineal area and hind limbs. Systemic necrotizing and fibrinous glomerulonephritis
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CIA
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Chicken Infecctious Anemia
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Chicken infectious anemia
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Avian cirovirus. Disease occurs in chicks less then 3 weeks. This is characterized by growth redardation, aplastic anemia, and generalized lymphoid depletion. fecal oral transmission. principal cells effected are precursor T cells in the thymus, and hemoblasts in the bone marrow. Cell death caused by protein apoptin. Mortality btwn 10-50%. To Dx - PCR, in-situ hybridization using DNA probes, immunoperoxidases, and immunoflorescence staining. Ab detection IFA, ELISA. MLV vaccine available.
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Principal cells effected by CIA
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Precursor T-cells in the thymus and hematoblasts in the bone marrow
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Herpesviridae
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Enveloped. Icosahedral. Double stranded DNA. most produce eosiniphilic IB's (except betaherpesvirus) Persists forever in hosts. These are very fragile!
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Subfamily alphaherpesvirinae
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Grow rapidly, lyse infected cells, and establish latent infections primarily in sensory ganglia. Latent forms are maintained as episomes. Replication occurs at lower then normal body temp. Mononuclear cell associated viremia in pregnant animals.
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T or F Chickenpox is a pox virus?
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False, it is a herpes virus
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Infectious bovine rhinotracheitis
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Vovine herpesvirus 1. worldwide. Either aquired via aerosolization or through coitus. Latentcy in the trigeminal and sciatic nerves. with respiratory disease - seen 7-14 days after exposure toa feedlot. Low mortality, but death is associated with secondary bacterial bronchopnuemonia. you can see conjunctivitis. Abortion is seen. Generalized disease in neonatal calves. Often fatal in these calves. Genital disease - NO abortions seen. infectious pustular vulvovaginitis. You see pain, dysuria, tail swishing and edema/discharge of vulva. with bulls infectious blanopsthitis. Vaccine available - IM and intranasal. IM can cause abortion in pregnant cows, so intranasal should be used.
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Bovine mammillitis and psuedo-lumpy skin diseases are caused by what virus?
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Bovine herpes virus 2
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In most countries, what does BHV-2 cause?
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Mammillitis
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Mammillitis
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Ulcerative lesions observed at the teats, but in severe cases much of the skin can be effected.
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Psuedo-lumpy skin disease
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No scabs present - Bovine herpes virus 2. Mild fever followed by sudden appearance of skin nodules all over the body. healing without scarring is complete within a few weeks.
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Mad Itch
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Psuedorabies, Aujeszkys's disease
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Psuedorabies (main info)
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Porcine herpesvirus 1. it may survive in the environment for up to 2-3 days.The rabbit is the most suseptible to infection. Secondary hosts aer ruminants, dogs, cats, horses etc. Transmission of virus from swine to other species and swine to swine is paramount. it is shed from the pigs nasal secretion, saliva, and milk. Recovered swine will shed virus continuously in their nasal secretions. all animals must come in contact with the pig or its carcasses.
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Psuedorabies in swine
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Virus replicates in the nasopharynx and tonsils. A brief viremia is associated with virulent strains, however replication is primarily in URT. Virus spread continues in the CNs with a ganglioneuritis, nonsuppurative meningioencephalitis, and perivascular cuffing.
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Clinical features of psuedorabies in swine
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In weaned, growing, and adult pigs - sneezing coughing, fever, salivation, constipation, and vomiting. Pigs are listless, depressed and cns signs. low mortality. No pruritus in swine! Piglets born to nonimmune sows - sneezing coughing, encephalitis, prostration and death. mortality approached 100% nonimmune pregnant sows - SMEDI - 50% abort.
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Psuedorabies in secondary hosts besides swine
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Cattle (mad itch) Intense pruritus, and they can become frenzied. increased CNS signs and paralysis of the pharynx. Death from respiratory failure. Dogs - frenzy associated with pruritis. paralysis of jaws and pharynx. no agression. Cats - Disease is so rapid that no pruritis is noted.
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Control of psuedorabies
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Reportable. Vaccines do not prevent the establishment of a disease from the wild-type virus. There are 3 vaccines - modified live, inactivated, and gene deleted vaccine
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What is known as the Equine abortion virus?
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Equine Herpes Virus 1 (EHV-1)1
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Basic idea of EHV - 1
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it is the most virulent eqine herpesvirus, and is associated with abortion storms. it is also indicated in respiratory disease, perinatal foal disease, and encephalitis. Most important cause of viral abortion on horses.
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the predilection site for EHV-1
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Circulating leukocytes, and endothelial cells.
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How is EHV-1 transmitted?
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Via aerosols, or direct/indirect contact with contaminated nasal discharge or placental fluid/stroma.
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With the eqine abortion virus, what trimester do the pregnant mares tend to abort?
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it is equine herpesvirus 1, and they abort in the third trimester. Reproductive efficency is not compromised
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Encephalomyelitis caused by EHV-1
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The neurologic signs can be a primary issue, or can be combined with respiratory disease and/or abortion. Vasculitis of the small vessels of the CNS, followed by hypoxic degeneration (infarction) and hemorrhage through the brain and spinal cord. It is said that the vasculitis results from virus/antibody immune complexes. Severity can vary from slight incoordination to quadraplegia and recumbancy resulting in death.
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Perinatal foal mortality
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Caused by EHV-1 It is a fatal generalized disease and is accompanied by respiratory distress due to interstital pneumonia.
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T or F rhinopnuemonitis is caused by EHV-1
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True, occasionally.
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Immunity in EHV-1
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There is an inactivated vaccine, but immunity is short lived - 2-4 months
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Equine herpesvirus 4
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This is usually associated with rhinopnuemonitis but has been recovered from individual cases of abortion. It is worldwide and transmission occurs via inhalation of droplets from infected horses and older horses. Disease is mainly observed in foals over 2 months, weanlings and yearlings. In older animals, infections are subclinical
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Hemorrhagic disease of puppies is also known as?
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Fading puppy syndrome
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What age group is effected by Fading puppy syndrome?
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those puppies under 4 weeks of age.
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Etiologic agent of fading puppy syndrome
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Canine herpes virus 1
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How does transmission of hemorrhagic disease of puppies take place?
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It can occur in utero, from direct contact with effected littermates, or from nasal secretions from the dam.
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What is the pathogenesis of fading puppy syndrome?
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Initial replication takes place in the nasal epithelium, followed by a viremia and replication in endothelial cells. Large ecchymotic hemorrhages and necrosis are observed in multiple organ systems. this occurs in puppies bc the virus needs a lower temp of 33C to replicate, and neonates do not have temperature regulatory abilities yet.
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What are the clinical signs of puppies infected with hemorrhagic disease of puppies?
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Painful crying, anorexia, dyspnea, and soft odorless green stool. NO FEVER. You can see meningoencephalitis in oronasally infected puppies.
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Feline herpesvirus 1 is also known as?
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Feline rhinotracheitis virus
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Punctate corneal ulcers are pathognomic of what etiology
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Feline herpesvirus 1 (aka feline rhinotracheitis)
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What are the 3 major diseases of the URT of felines?
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Feline rhinotracheitis, Feline calicivirus, and feline pneumonitis
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ulcers of the tongue are pathognomonic of what feline virus?
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Feline Calicivirus
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ILT
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Infectious laryngotracheitis
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what animal is the host for infectious laryngotracheitis?
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Chickens and pheasants.
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What is the etiological agent for infectious laryngotracheitis?
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Gallid herpesvirus 1
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What is the pathogenesis of Infectious laryngotracheitis?
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Severe laryngotracheitis, characterized by necrosis, ulceraion and the formation of diptheritic membranes. The dipthetiric membrane may occulde the trachea, and therefor the cause of death is asphyxiation. Before death you see extension and slinging of neck and bloody mucus. 100% morbidity
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Where do you innoculate an embryonated egg when checking for gallid herpesvirus 1?
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To check for infectious laryngotracheitits, you inject the chorioallantoic membrane
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the "most important disease in chickens"
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Marken disease which is gallid herpesvirus 2
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Fowl paralysis, range paralysis, polyneuritis, and neurolymphomatosis are all synonyms for
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Mareks disease/gallid herpesvirus 2
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True or false Mareks disease is quickly cytopathic
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False - it is slowly cytopathic
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How is transmission of Mareks disease accomplished?
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Via inhalation - chicken dander can survive for many months in the litter. this is a very highly contagious disease. Vertical transmission has not been reported.
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there are 3 phases of in vivo infection with Mareks disease. What are they?
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Productive infection - you get a transient productive infection due to a macrophage associated viremia. Latent infection - this accounts for the long-term carrier states. This works with activated T cells. Neoplastic transformation - you can see in-situ proliferation of latently infected T-cells that have become neoplastic
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Neurolymphomatosis
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Classic Mareks disease - Splayed legs "hurdlers pose" with unilateral nerve enlargement. you can also see limberneck
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Visceral lymphomatosis
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Lymphocytic tumors are present in the heart, liver, kidney, and spleen. this is from Mareks disease which is an Alphaherpesvirus/gallid herpesvirus 2.
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Ocular lymphomatosis
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Greying of the eye of the chicken. also called cat eye, and pearl eye. This is from Mareks disease which is a gallid herpesvirus 2, and an Alphaherpesvirus
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Cutaneous lymphomatosis
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Happens with Mareks disease - round nodular lesions on the skin that become apparent after plucking feathers from the area. Productive infection of the epitheial cells is associated with the release of free virus
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there are 3 phases of in vivo infection with Mareks disease. What are they?
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Productive infection - you get a transient productive infection due to a macrophage associated viremia. Latent infection - this accounts for the long-term carrier states. This works with activated T cells. Neoplastic transformation - you can see in-situ proliferation of latently infected T-cells that have become neoplastic
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Neurolymphomatosis
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Classic Mareks disease - Splayed legs "hurdlers pose" with unilateral nerve enlargement. you can also see limberneck
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Visceral lymphomatosis
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Lymphocytic tumors are present in the heart, liver, kidney, and spleen. this is from Mareks disease which is an Alphaherpesvirus/gallid herpesvirus 2.
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Ocular lymphomatosis
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Greying of the eye of the chicken. also called cat eye, and pearl eye. This is from Mareks disease which is a gallid herpesvirus 2, and an Alphaherpesvirus
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Cutaneous lymphomatosis
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Happens with Mareks disease - round nodular lesions on the skin that become apparent after plucking feathers from the area. Productive infection of the epitheial cells is associated with the release of free virus
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there are 3 phases of in vivo infection with Mareks disease. What are they?
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Productive infection - you get a transient productive infection due to a macrophage associated viremia. Latent infection - this accounts for the long-term carrier states. This works with activated T cells. Neoplastic transformation - you can see in-situ proliferation of latently infected T-cells that have become neoplastic
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Neurolymphomatosis
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Classic Mareks disease - Splayed legs "hurdlers pose" with unilateral nerve enlargement. you can also see limberneck
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Visceral lymphomatosis
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Lymphocytic tumors are present in the heart, liver, kidney, and spleen. this is from Mareks disease which is an Alphaherpesvirus/gallid herpesvirus 2.
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Ocular lymphomatosis
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Greying of the eye of the chicken. also called cat eye, and pearl eye. This is from Mareks disease which is a gallid herpesvirus 2, and an Alphaherpesvirus
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Cutaneous lymphomatosis
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Happens with Mareks disease - round nodular lesions on the skin that become apparent after plucking feathers from the area. Productive infection of the epitheial cells is associated with the release of free virus
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How do you diagnose Mareks disease?
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PCR, Fluorescent antibody tes. Detection of antibodies using AGID, IFA and virus neutralization tests. CAM or Yolk sac
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Betaherpesvirus
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Slow growing where cell lysis does not occur for several days. This causes chronic infection lasting several months before clinical recovery. Infected cells are generally large - hence we call these viruses cytomegaloviruses. These diseases are often associated with continous viral excretion.
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Inclusion body rhinitis etiologic agent
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Porcine herpesvirus 2. Up to 90% of a herd may carry this disease.
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Pathogenesis of porcine herpesvirus 2
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AKA porcine cytomeglovirus - site of replication is the nasal mucous glands and other epithelial cells in the URT. You see a viremia and the endothelial damage accounts for the petichial hemorrhaging and edema. Anemia in neonates is attributed to bone marrow damage
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Anemia with procine cytomegalovirus is attributed to what?
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Bone marrow damage
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inclusion body rhinitis is most severe in what animals?
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Piglets less then 3 weeks old
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What color are the inclusion bodies of Porcine herpesvirus 2?
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Basophilic intranuclear IB's are observed.
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Gammaherpesvirinae
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Different members of this family replicate in T and B lymphocytes. these are slowly cytopathic. they are latent in lymphoid tissue. Some gammaherpesviruses are shed continuously from epithelial surfaces.
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MCF
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Malignant Catarrhal Fever
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What cells does Malignant catarrhal fever infect
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lymphoid tissue, and epithelial cells of the repiratory and GIT
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what is the mortality rate of malignant catarrhal fever?
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100%
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Wildebeest and hartebeest carry what highly fatal disease?
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It is the african form of Maligant catarrhal fever
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What is the european and North american form of malignant catarrhal fever?
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Sheep associated MCH
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What are the 2 etiologic agents of malignant catarrhal fever?
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Alcelaphine herpesvuris 1 (aka)Bovine herpesvirus 3 (african form) and Ovine herpesvirus 2 (american and European form)
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what form of malignant catarrhal fever does the widebeest/hartebeest harbor
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African form
cell free state |
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Cattle have what kind of malignant catarrhal fever?
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Cell associated virus form
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What is the pathogenesis of MCF
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Viral infection is followed by cell associated viremia. Damage to tissue appears to be immune mediated. CD8 T cells are the predominant cells associated with the widespread necrotizing vasculitis.
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The acute form of MCF is characterized by what?
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Fever, depression, profuse nasal and ocular discharge, general lymphadenopathy, and extensive mucosal erosions of GIT (bloody diarrhea) Bilateral opthalmia, photophobia, corneal opacity (blindness) Edema of the meninges
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Infectious bovine rhinotracheitis etiologic agent
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Bovine herpesvirus 1
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infectious vulvovaginitis, infectious balanoposthitis etiologic agent
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Boveine herpes virus 1
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Number one cause of abortion in horses
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Equine herpes virus 1
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Pseudorabies etiologic agent
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Porcine herpes virus 1
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Rhinopneumonitits in horses
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Equine herpesvirus 4
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What is the source of infection of parapox?
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Infected cattle transmit pseudocowpox
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Verrucose mass under scabs is a sign of what?
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Contagious ecthyma
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Stomoxys calictrans transmits what virus?
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Ovine capripox - sheep pox
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Haematopinus suis is an important vector is what disease?
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Suipox virus - swinepox
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Is there a vaccine for swinepox?
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No
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