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S20656, S20154, S21456, S20995, S21597, S21579, S21158, S21135

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Erosions and hemorrhages

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Focally erosion and ulceration

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Erosions

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Corneal opacity

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Entry stage- occurs through the sheep’s nasal cavity and enters into the lungs where it replicates. The virus undergoes a tropic change and infects lymphocytes, also known as white blood cells, which play a role in the sheep’s immune system.

Maintenance stage- The virus remains on the sheep’s lymphocytes and circulates the body.

Shedding stage- The virus undergoes another change and shifts its target cells from lymphocytes to nasal cavity cells, where it is then shed through nasal secretions.

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No treatment has been found to provide any consistent benefit. Stress reduction of subclinical or mildly affected animals is indicated.
* There is a vaccine available  to treat this  disease. But it is not internationally recognized yet.

HOW TO PREVENT?

Early weaning and isolation.

Separation of carriers from susceptible species.

When large numbers of potent shedders are present, such as in lamb feedlots, distances >1 km may be necessary to protect highly susceptible species.

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Presumption diagnosis:

History

clinical sign

*presence of bilateral corneal opacity

Direct:

PCR

*the most often method as confirmation

*spleen & lymph nodes = optimal

Microscopic lesions in tissues

Immunofluorescence

Indirect:

virus inoculation in cell culture

Serology:

ELISA

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Necropsy (post-mortem)

1. Corneal opacity

2. Vast erosions, edema (swelling), and hemorrhage throughout the gastrointestinal tract, including the oral cavity,

3. Lymphadenopathy: all lymph nodes are enlarged, edematous, and sometimes hemorrhagic.

4. Focally disseminated erosions and ulcerations in the GIT.

5. Erosions and hemorrhages within the mucosa of the turbinates, larynx, and trachea

Histologically

1. Widespread proliferation of lymphocytes (lymphoblast).

2. Multifocal areas of necrosis, centered on small blood vessels, and small arteries may exhibit characteristic fibrinoid necrosis of their muscular walls

3. lesions are present in all affected tissues, including brain and eye

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Common symptoms

Fever

Depression

In appetence

Diarrhea

Discharge from eyes and nose

Malignant catarrhal fever (MCF): head and eye syndrome in cow (Devon)

Lesions of buccal cavity and muzzle

Swelling of the lymph nodes, opacity of the corneas leading to blindness.

Skin/ gum ulceration

Malignant catarrhal fever: dry necrosis and ulceration on gums and dental pad

Neurology sign of MCF

ataxia

nystagmus

head pressing

Head pressing (http://www.nadis.org.uk/bulletins/nervous-diseases-in-cattle.aspx)

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1. The epidemiology of the two major viruses (alcelaphine herpesvirus 1 and ovine herpesvirus 2 within their natural, well adapted hosts differs significantly.

2. Intense virus shedding from the wildebeest occurs predominantly during first 90 days of life

3. Wildebeest-associated malignant catarrhal fever of cattle most frequently in Africa during calving season

4. Sheep-associated form occurs year-round in cattle, with only one modestly increased incidence during lambing season

5. In American bison, it is a winter disease

6. Outbreaks of the sheep-associated form of malignant catarrhal fever have occurred amongst farmed deer, particularly red deer (Cervus elaphus)

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1. Is an infectious systemic disease.

2. Lymphoproliferative disease of cattle and some wild ruminants (deer, bison, antelope)

3. Primarily affecting:

Lymphoid tissues

Mucosal lining (respiratory and gastrointestinal tracts)

4. Caused by Herpesvirus :

Alcelaphine herpesvirus 1

Ovine herpesvirus 2

5. The principal carriers:

sheep (ovine herpesvirus-2)

wildebeest (alcelaphine herpesvirus-1)

goats (caprine herpesvirus-2)

6. Can be transmitted by:

Inoculation of large volume of animal blood from a clinically affected animal or by aerosol