Exam 2 - Family: Herpesviridae Flashcards Preview

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Flashcards in Exam 2 - Family: Herpesviridae Deck (140):
1

Herpesviridae Virus Morphology

- Enveloped, spherical to pleomorphic
- 150-200 nm in diameter
- Icosahedral capsid, T=16
- 162 capsomers surrounded by a layer known as tegument
- Glycoproteins embedded in lipid envelope

2

Herpesviridae Viral Genome

Monopartite (non-segmented), linear, double-stranded DNA genome. Fall in three categories.

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Herpesviridae Viral Genome: Three Categories

1. Those encoding proteins concerned with regulatory functions and virus replication
2. Those encoding structural proteins
3. A heterologous set of "optional" genes

4

Herpesviridae Viral Replication

- Occurs in the nucleus
- Viral envelope is acquired by budding and obtaining the nuclear envelope
- Mature virions are released by exocytosis or cytolysis

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Herepesviridae General Charcteristics

- Do not survive well outside the host
- Requires close contact transmission
- Latently infected animals serve as a reservoir
- Can be oncogenic
- Reactivation of latent herpesvirus infection is usually associated with stress and glucocorticoid drugs
- Characteristic eosinophilic intranuclear inclusion bodies
- Cell-to-cell fusion facilitates spread of infection and virus

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Herpresviridae Inclusion Bodies

Type A Cowdry bodies. Composed of nucleic acid and protein.

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Subfamily: Alphaherpesvirinae

This includes:
1. Bovine herpesvirus-1
2. Bovine herpesvirus-2
3. Equine herpesvirus-1
4. Equine herpesvirus-4
5. Porcine herpesvirus-1
6. Feline herpesvirus-1
7. Canine herpesvirus-1
8. Gallid herpesvirus-1
9. Gallid herpesvirus-2

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Alphasherpesvirinae Properties

Highly cytopathic, lyse infected cells. Short replication cycle. Episomes are integrated into the chromosomal DNA of latently infected neurons. Produce localized lesions in the skin and mucosae of respiratory and genital tract. Pregnant animals - abortion characteristically with multifocal areas of necrosis in several fetal organs.

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Bovine herpesvirus-1 (BHV-1) Diseases

Infectious bovine rhinotracheitis (IBR), pustular vulvovaginitis. Balanoposthitis, conjunctivitis, abortion, enteritis, and generalized disease of newborn calves.

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BHV-1 serotype and subtype

Only a single serotype of BHV-1 is recognized

3 subtypes:
1. BHV-1.1 = respiratory subtype
2. BHV-1.2 = genital subtype
3. BHV-1.3 = encephalitic subtype

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BHV-1 Transmission

Droplet transmission and either coitus or artificial insemination

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BHV-1 Pathogenesis

In both genital and respiratory form of the disease, the lesions are focal areas of epithelial cell necrosis in which there is ballooning of epithelial cells.

Intense inflammatory response within the necrotic mucosa, frequently with formation of an overlying accumulation of fibrin and cellular debris (pseudomembrane).

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Site of Latency - Trigeminal Nerve

Respiratory disease with BHV-1

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Site of Latency - Sciatic Nerve

Genital disease with BHV-1

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BHV-1 Clinical signs - Respiratory form

Red nose, Necrotic rhinitis, dust pneumonia

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BHV-1 Clinical signs - Ocular form of IBR

Conjunctivitis is a common finding with "red nose"

DO NOT misdiagnose as pink eye. IBR lesions are confined to the conjunctiva and no lesions on cornea except diffuse edema.

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BHV-1 Abortion

Can result from MLV vaccines given to pregnant animals. Higher incidences with fetuses infected in the second half of gestation.

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BHV-1 Systemic Disease of Newborn Calves

Typically less than 10 days. Calves develop a generalized disease with pyrexia, diarrhea, respiratory distress, ocular discharge, incoordination, eventually convulsion and death.

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BHV-1 Genital Disease - IPV`

Infectious Pustular Vaginitis. Vaginal discharge, vulva swollen, red spots, and discrete pustules

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BHV-1 Genital Disease - Balanoposthitis

Inflammation and pustules in the mucosa of the penis and prepuce

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BHV-1 Control (Vaccination)

MLV, subunit and inactivated vaccines. Subunit vaccines contain the major surface glycoproteins that elicit antibody response.

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Bovine herpesvirus-2 (BHV-2)

Causes bovine ulcerative mammillitis and Pseudo Lumpy Skin Disease

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Bovine ulcerative mammillitis - Host

Cattle, heifers, usualy within 2 weeks after calving

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Bovine ulcerative mammillitis - Transmission

Direct contact and mechanical transmission

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Bovine ulcerative mammillitis - Clinical signs

Swollen, painful teat. Skin is bluish, exudes serum, formation of raw ulcers.

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Pseudo Lumpy Skin Disease - Distribution

Southern Africa

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Pseudo Lumpy Skin Disease - Transmission

Mechanical Transmission

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Pseudo Lumpy Skin Disease - Clinical Signs

Sudden appearance of skin nodules. Nodules are flat with slightly depressed center and can undergo necrosis.

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Porcine herpesvirus-1/ Suidherpesvirus-1

Causes Pseudorabies (Aujesky disease, Mad itch)

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Pseudorabies - Hosts

Primary host: Pigs
Secondary host: horses, cattle, sheep, goats, dogs, cats, etc.

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Pseudorabies - Transmission Primary Host

Typically are reservoirs from pigs and rodents that are latent carriers shedding the virus. Can be be through saliva, nasal discharges and milk.

VIRUS DOES NOT SHED IN URINE OR FECES.

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Pseudorabies - Transmission Secondary Host

Dogs & Cats - ingestion of infected pig meat or rodents
Cattle - direct contact with pigs

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Pseudorabies - Pathogenesis

Primary site of viral replication is upper respiratory tract.

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Pseudorabies - Spread of Virus

Via the lymphatics to regional lymph nodes, where replication continues

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Pseudorabies - Spread of Virus CNS

Spread to CNS via axons of cranial nerves. Preference for neurons of the pons and medulla.

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Pseudorabies - CNS Lesions

Ganglioneuritis, non-suppurative meningoencephalitis, perivascular cuffing

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Pseudorabies - Clinical signs

Depend on the age of the affected pig.

Pruritus, a dominant feature in secondary hosts, is rare in pigs.

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Pseudorabies - Necropsy Findings

Gross lesions are often absent or minimal. Liver and spleen have yellow-white necrotic foci.

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Pseudorabies - Cattle (Mad Itch)

Intense pruritus, frenzied, progressive CNS involvement, stage or paralysis, ataxia, death from respiratory failure, self trauma, profuse salivation.

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Pseudorabies - Dogs

Frenzy, pruritis, self mutilation, paralysis of jaw and pharynx, drooling, plaintive howling. THEY DO NOT ATTACK.

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Pseudorabies - Cats

Disease progress so rapidly that pruritus may not be observed

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Pseudorabies - Diagnosis

History and clinical signs. Histopathology - intranuclear eosinophilic inclusion bodies. PCR, ELISA.

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Pseudorabies - Vaccination In Pigs

In enzootic areas. Recombinant DNA deletion mutant, live-attenuated and inactivated vaccines available. DO NOT PREVENT INFECTION, but cal alleviate clinical signs in pigs.

(def. Enzootic: relating to, or denoting a disease that regularly affects animals in a particular district or at a particular season.)

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Equine herpesvirus-1 (EHV-1)

Most virulent equine herpesvirus.

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EHV-1 Transmission

Inhalation of infected aerosols, direct or indirect contact with nasal discharges, aborted fetuses, placenta or placenta fluids.

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EHV-1 - Latency

Maintains the virus. Can reside in tissues of CNS specifically the trigeminal nerve. Can also reside in lymph system (specifically lymphocyte).

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EHV-1 Pathogenesis

Cell-associated viremia. Principal route is through the respiratory tract. Infects endothelial cells in lamina propria.

The central lesion caused by EHV-1 responsible for the three types of conditions seen (respiratory, reproductive & CNS).

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EHV-1 Immunosuppression

Codes a protein that inhibits TAP protein, thereby blocking delivery of antigen to class I MHC molecules.

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EHV-1 Respiratory Disease

Affect mostly younger horses. Rhinopneumonitis. Fever, bilateral nasal discharge, coughing, inappetence, and depression.

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EHV-1 Encephalomyelopathy

EHM, Equine Herpesvirus Myeloencephalopathy

Characterized by immune mediated vasculitis leading to infarction and hemorrhage within the brain and spinal cord.

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EHV-1 Reproductive Form

Abortions can occurs between 8-10 months of gestation. Reproductive efficiency is not compromised.

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Equine Herpesvirus-4

Equine Viral Rhinopneumonitis

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EHV-4 - Transmission

Observed in horses under two years of age, causes life long latent infection. Droplet infection from infected horses and older horses in which inapparent viral shedding occurs.

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EHV-4 Pathogenesis

Causes less severe tissue destruction than EHV-1. Rarely causes abortions and rarely results in viremia. Death is rare.

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EHV-4 Clinical signs

Results primarily in upper respiratory tract disase (rhinoparhyngitis and tracheobronchitis). Also include nasal discharge, mild coughing, fever and lung sounds.

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EHV-4 Vaccination

Live attenuated and inactivated commercial EHV-1 vaccines are available, including combined products that include both EHV-1 and EHV-4

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Canine Herpesvirus -1 (CHV-1)

Hemorrhagic disease of puppies (fading puppy syndrome)

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CHV-1 Transmission - Neonates

Contact with infected oral, nasal or vaginal secretion of dam. In-utero transmission.

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CHV-1 Transmission - Older dogs

Venereal transmission. Contact with saliva, nasal discharge, or urine of infected dogs or puppies.

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CHV-1 Pathogenesis - In-utero

Abortion, stillbirth, infertility. Most pups develop systemic infection within 9 days from birth.

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CHV-1 Pathogenesis - Systemic Neonatal Infection

Less than 1 week. Replication occurs in nasal epithelium, tonsils and pharynx. Leukocyte associated viremia. Virus replication in endothelial cells. Diffuse necrotizing vasculitis, multiple hemorrhagic necrosis in several organs.

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CHV-1 Pathogenesis - CNS infection

Meningoencephalitis commonly occurs in oro-nasally infected neonatal puppies.

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CHV-1 Factors governing systemic neonatal infection

Body temperature & Maternal immunity.

Body temperature: CHV-1 replicates optimally at 33oC (the temperature of upper respiratory and genital tracts.) If pups aren't warm enough they can be more susceptible to this disease.

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CHV-1 Clinical signs in puppies

Painful crying, abdominal pain, anorexia, dyspnea, passing soft odorless, greenish stool, no elevation in body temperature. Persistent neurological signs such as ataxia and blindness.

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CHV-1 Adult female genital infection

Generally asymptomatic or limited vaginal hyperemia. Vesicular vaginitis with discharges. In-utero infections.

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CHV-1 Adult male genital infection

Balanoposthitis

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CHV-1 Clinical signs in adults

respiratory infections and ocular infections

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CHV-1 Diagnosis

Focal area of necrosis and hemorrhages in multiple organs. Intranuclear inclusion bodies may be present. Causative virus can be isolated readily in canine cell cultures. Nucleic acid detection.

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CHV-1 Control

Keeping puppies in warm temperature. Isolation of infected mother and pups. Lack of available vaccines.

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Feline Herpesvirus-1

Causes feline rhinotracheitis

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FHV-1 Transmission

Spread is largely by direct contact with an infected cat OR by aerosol route (not considered important).

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FHV-1 Pathogenesis

Replication takes place in mucosae of nasal septum, turbinates, nasopharynx and tonsils. Restricted to low temperature (upper respiratory tract)

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FHV-1 Clinical signs - Kitten

up to 4 weeks. Severe upper respiratory disease. Extensive rhinotracheitis. Fatal bronchopneumonia may develop. Conjunctivitis and ulcerative keratitis.

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FHV-1 Clinical signs - Cats

> 6 months; mild or subclinical disease in older kittens

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FHV-1 Clinical signs - Pregnant Queen

Abortion around 6th week of pregnancy. No evidence that the virus crosses the placenta. Conjunctivitis, hyperemia and serous ocular discharge, ulcerative keratitis.

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FHV-1 - Diagnostics - Ophthalmic strips

Detection of corneal ulcers using Fluorescein. A break in the corneal epithelium allows water-soluble fluorescein to be absorbed by the hydrophilic corneal stroma. The exposed, and now stained, corneal stroma will therefore fluoresce.

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How to differentiate FHV-1 with Feline Calicivirus (FCV) infection

Ulcers on tongue of cat are common with FCV. Oral ulcers are rare in cats with FHV-1 infection.

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FHV-1 Diagnosis

Histopathology: lesions include necrosis of epithelia of nasal cavity, pharynx, epiglottis, tonsils, larynx and trachea. Virus isolation with ocular or pharyngeal swab. Serology.

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FHV-1 Vaccination

MLV parenterally, MLV intranasally, and inactivated vaccine parenterally.

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Gallid Herpesvirus-1

Infection Laryngotracheitis (ILT)

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Gallid Herpesvirus-2

Marek's Disease

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ILT- Host

Chickens, most common in ages 4-18 months. Also pheasants, partridges and peafowl

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ILT-Transmission

Inhalation, droplets to conjunctiva, and occasionally ingestion. Mechanical transmission through scavengers.

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ILT- Pathogenesis

Necrosis, hemorrhagic, ulceration and formation of the diphthertic membrane. Second tube formation, can block air passage. Trigeminal ganglion is the latency site.

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ILT - Clinical signs

Mild coughing, sneezing followed by nasal and ocular discharge, dyspnea, loud gasping, coughing and depression.

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ILT - Incubation period

6-12 days

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ILT- Clinical signs - Severe form

Severe respiratory distress. Head shaking with coughing. Raised neck and head "pump handle respiration". Cough of blood mucus.

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ILT-Clinical signs - low virulence

Conjunctivitis, ocular discharge, swollen infraorbital and nasal sinuses, and decreased egg production.

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ILT - Diagnosis

Tracheal plug, detection of typical intranuclear inclusions in respiratory tissues. Virus grows well in CAM of embryonated eggs.

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ILT - Control

Complete depopulation and culling of infected birds and premises.

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ILT- Vaccination - 3 types

1. Chick Embryo Origin (CEO)
2. Tissue Culture Origin (TCO)
3. Pox vectors recombinant

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CEO Vaccine

Vaccines have the capability of reverting to virulence and causing full blown ILT signs. Induce better immunity.

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TCO

Vaccine is only given by eye drop and does not spread significantly or revert to virulence. Level of induced immunity is limited.

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ILT vaccines can backfire

Veterinary vaccines have been found to combine into new infectious viruses.

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Marek's disease - Synonym

Fowl paralysis, range paralysis, polyneuritis, neurolymphomatosis.

Very important disease of poultry

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Marek's disease - Hosts

Chickens, turkeys, quails, pheasants

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Marek's disease - Transmission

Cell free viruses release from the feather follicles are highly infectious but labile. Viruses in desquamated cells (dander) are less infectious, but can survive in poultry house dust or litter for several months.

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Marek's disease - 4 Pathotypes

1. mMDV
2. vMDV
3. vvMDV
4. vv+MDV

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mMDV

Mild Marek's disease. Most associated with neural MD. Disease is preventable with HVT (Turkey's herpesvirus vaccine

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vMDV

Virulent Marek's disease. Associated with high incidence of neural and visceral lymphomas. Disease is preventable with HVT (Turkey herpesvirus vaccine)

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vvMDV

Very Virulent Marek's disease. Associated with high incidence of neural and visceral lymphomas. Viruses are oncogenic in HVT vaccinated chickens. Disease preventable with bivalent vaccines.

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vv+MDV

Very Virulent Plus Marek's disease. Associated with high incidence of neural and visceral lymphomas. Viruses are oncogenic in chickens vaccinted with bivalent vaccines.

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Marek's disease - Pathogenesis

Various overlapping virus-cell interactions have been observed.

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Marek's disease - Fully productive infection

Production of enveloped virions and cell death (lysis). Occurs only in feather follicle epithelium. Infected T cells appear to be the "trojan horse" by which MDV enters the feather-follicle epithelium.

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Marek's disease - Productive-restrictive infection

Production of naked virions (not infectious) and viral antigens. Cell death due to lysis. Occurs in B-cells and activated T-cell (primarily CD4+ cells). Profound immunosuppression.

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Marek's disease - Non-productive infection

Viral genome persists in T-cells undergo neoplastic transformation. A new antigen, MATSA (Marek's Disease Associated Tumor Specific Antigen), appears in transformed T-cells.

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Marek's Disease Virus is slowly cytopathic and remain associated with cells.

Cell free infectious viruses are almost impossible to obtain, except in dander from feather follicles. Lesions in Marek's Disease result from infiltration and in situ proliferation of transformed T lymphocytes.

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Marek's disease - Genetic susceptibility

Varies depending on different MHC class II haplotypes

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B19 haplotype

Chickens are highly susceptible to Marek's disease

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B21 haplotype

Chickens are genetically resistant to Marek's disease

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Marek's disease - Clinical features - Neurolymphomatosis

Enlargement of nerve trunks. Vagus, brachial, and sciatic nerves. Usually unilateral. Edematous, grey or yellowish. Lameness, droopy wings, paresis legs, limberneck, torticollis (twisted neck) and incoordination

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Marek's disease - Clinical features - Visceral lymphomatosis

Diffuse or nodular lymphoid tumors may be seen in various organs, particularly the liver, spleen, gonads, heart, lungs, kidney, muscle, and proventriculus. Bursa is only rarely tumorous and more frequently is atrophic. The absence of bursal tumors helps distinguish this disease from lymphoid leukosis.

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Marek's disease - Clinical features - Ocular lymphomatosis

Graying of the iris (aka gray eye, cat eye, or pearl eye). Interference with normal pupillary constriction and dilation. Due to T-cell infiltration and partial or total blindness.

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Marek's disease - Diagnosis

Cell culture, CAM inoculation

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Marek's disease - Control (Vaccination)

REPORTABLE DISEASE!

Most widleyused vaccine consists of Turkey Herpesvirus (HVT). Bivalent vaccines consists of HVT and either SB-1 or 301B/1 strains of Gallid herpesvirus 3 (Serotype, avirulent strain). Most protective commercial vaccine is CVI988/Rispens.

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Subfamily: Betaherpesvirinae

Porcine Herpesvirus-2

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Subfamily: Betaherpesvirinae - Properties

- Slow replicating virus
- Associated wit chronic infections
- Infected cells are often enlarged (cytomegaly)
- Maintained in latent form in secretory glands and lymphoreticular cells
- Often associated with continuous viral excretion

118

Porcine Herpesvirus-2

Inclusion Body Rhinitis also known as Porcine cytomegalovirus (PCMV)

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PCMV - Hosts

Pigs from ages 2 to 10 weeks old or piglets less than 3 weeks old

120

PCMV - Transmission

Inhalation and transplacental

121

PCMV - Pathogenesis

Primary site of replication is the nasal mucous glands and epithelial cells of upper respiratory tract. Endothelial cell damage and necrosis: petechial hemorrhages and edema.

Infected cells are enlarged and possess intranuclear inclusion bodies, especially in nasal glands. Hence, known as Inclusion Body Rhinitis.

122

PCMV - Clinical signs - piglets

Less than 3 weeks old. Mucopurulent rhinitis. Violent sneezing, respiratory distress, conjunctivitis, shivering, mouth breathing and variable death loss. Appear weak, anemic or stunted and there may be edema around the throat and tarsal joints.

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Subfamily: Gammaherpesvirinae

Malignant Catarrhal Fever (MCF). Includes

1. Alcephaline herpesvirus-1 (AHV-1)
2. Ovine herpesvirus-2 (OvHV-2)

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Subfamily: Gammaherpesvirinae - Properties

Lymphotrophic (replicate in B or T cells). Slowly cytopathic for epithelial and fibroblastic cells, causing death without production.

125

MCF- Synonyms

Bovine Malignant Catarrh, Malignant Head Catarrh

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MCF - Host

Highly fatal disease of cattle and some wild ruminants (deer, bison, antelope)

127

MCF - Alcephaline herpesvirus-1

Wildebeest associated. Transmits to cattle. Occurs in most African countries. DOES NOT CAUSE DISEASE TO WILDEBEEST. Epizootic and seasonal (based on wildebeest calving season)

(def. epizootic - denoting a disease that is temporarily prevalent and widespread in an animal population.)

128

MCF - Ovine herpesvirus-2

OvHV-2 is transmitted from sheep to cattle. Occurs year round.

129

REMEMBER!

In Africa, MCF is predominantly found where cattle are in close contact with blue or black wildebeest, while outside Africa, it is usually associated with contact between sheep and susceptible species.

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MCF - AHV-1 - Transmission

Wildebeest to cattle. Present in nasal and ocular secretion of young wildebeest in a cell free state. Ingestion of pasture contaminated with nasal or ocular secretions from young wildebeest. Direct or close contact, inhalation or aerosol with young wildebeest. Direct or close contact with wildebeest during calving (virus in cell-free state in young). Virus in cell-associated form in adult wildebeest, so rarely transmitted from adults.

131

MCF - OvHV-2 - Transmission

Not known. Presumably by inhalation or ingestion.

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MCF - Cattle

Cattle are dead end hosts. Cattle have cell-associated virus, but not cell-free virus, in secretions. this may explain the noncontagious nature of MCF when contact occurs with MCF affected cattle.

133

MCF - Pathogenesis

Infection followed by cell-associated viremia. Lymphoid proliferation and infiltration. Necrotizing vasculitis. CD8+ T cells are predominant cells associated with vascular lesions.

134

MCF - Clinical signs - Peracute

Sudden death. "Head and eye" form may not appear. High fever, acute gastroenteritis.

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MCF - Clinical signs - Head and eye form - Early stages

Reddened eyelids, bilateral corneal opacity, crusty muzzle, nares, nasal discharge, salivation.

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MCF - Clinical signs - Head and eye form - Later stages

Erosions on the tongue and hard palate. Necrosis and erosion of the buccal papillae.

137

MCF - Other Clinical signs

Joints, superficial lymph nodes swell, horn, hoof, coverings slough, nervous signs, incoordination, head pressing, nystagmus, hyperesthesia (extreme sensitivity to touch), enlarged prescapular lymph node, sloughing of hoof coverings.

138

MCF- Alimentary/Intesinal form

Death occurs from severe diarrhea. Diarrhea is rarely observed in wildebeest derived MCF, but is more commonly in sheep associated MCF.

139

MCF - Mild form

inoculated animals, recovery expected

140

MCF - Necropsy findings

Zebra striping: bovine colon. Severe longitudinal linear congestion of the mucosa.