Malignant Catarrhal Fever Virus

Also know as: MCFV - MCF

Introduction

Severe oculo-nasal Discharge of MCF (Courtesy of Alun Williams (RVC))

Fissures on tongue (no vesicles) in MCF (Courtesy of Alun Williams (RVC))

This virus is of the Herpesviridae family and the reservoir species are wildebeest and sheep, each transferring different forms of the virus. Each virus is innocuous to the reservoir host, but can sometimes cause a peculiar and fatal over T-cell division in dead end hosts. Dead end hosts include cows, kudu and some deer.

MCFV is endemic as a latent infection in Blue Wildebeest and the virus is excreted in large amounts in the periparturient period.

The disease is not all that common in UK, but is present. Outbreaks are usually sporadic and are often seen in animals mixing with sheep (carriers). In parts of Africa, you will see longer duration outbreaks, caused by different serotypes carried by Wildebeest. In deer, very serious outbreaks occur and this is probably due to infection with the sheep virus.

Signalment

Latent infection in Blue Wildebeest and sheep of all ages, breeds and sex. In dead end hosts, it can affect any sex or age, but is often seen most in youngish animals around 6 months to 1 year of age.

Clinical Signs

Clinical signs in cattle are severe and include necrotising lesions in  the upper respiratory tract and eye: conjunctivitis and corneal oedema / opacity (keratitis or "blue eye" - characteristic feature). Pyrexia and diarrhoea with severe oculo-nasal discharge and inappetance also occurs. The animal will appear dull with ulcers on its muzzle, which exude a brown exudate. These may spread to the rest of the face and occasionally the whole body. There may also be ulcers on the tongue, dental pad, and cheeks that regularly become secondarily infected. Lymphocyte proliferation to viral antigen in the blood vessels of lymph nodes, spleen lungs, liver and kidneys progresses until death occurs. The lymph nodes eventually become completely replaced by lymphoblasts, which is a similar pathogenesis to lymphosarcoma. There may also be vasculitis with medial necrosis of blood vessels throughout body with infiltration of walls of vessels by lymphocytes.

Diagnosis

History (where and what has the animal been stocked with), signalment (deer, cattle etc) and clinical signs are quite characteristic and will lead to a preliminary diagnosis of the disease. Definitive diagnosis can be achieved by performing PCR for detection of the herpesvirus DNA.

Treatment and Control

The main control measures is to not stock Wildebeest in zoos, where possible as they are latent innocuous carries of the disease. Sheep and deer should also not be housed together.

References

Bridger, J and Russell, P (2007) Virology Study Guide, Royal Veterinary College

Divers, T.J. and Peek, S.F. (2008) Rebhun's diseases of dairy cattle Elsevier Health Scieneces

Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial

Radostits, O.M, Arundel, J.H, and Gay, C.C. (2000) Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses Elsevier Health Sciences