DISEASE RISK MANAGEMENT: MALIGNANT CATARRHAL FEVER - THE FACTS PART 1
Malignant catarrhal fever (MCF) is a fatal lymphoproliferative disease caused by a group of ruminant gamma herpes viruses, including Alcelaphine Herpes Virus 1 (AlHV-1) and Ovine Herpes Virus 2 (OvHV-2). These viruses cause unobvious infection in their reservoir hosts, (sheep with OvHV-2 and wildebeest with AlHV-1) but are usually fatal in cattle and other ruminants such as antelope and buffalo (Wikipedia).
Malignant catarrhal fever is also referred to as malignant catarrh, malignant head catarrh, gangrenous coryza, catarrhal fever and in South Africa as ‘snotsiekte’ a colloquialism meaning "snotting sickness“. This disease is characterised by profuse mucopurulent oculo-nasal discharge, kerato conjunctivitis with corneal opacity and peripheral lymphomegally.
Due to its high mortality rate and no available treatment, MCF poses a high risk threat within the South African game breeding industry.
Malignant Catarrhal Fever in South Africa
Malignant catarrhal fever is generally fatal and occurs following infection with certain herpes viruses of the genus Macavirus. Five herpes viruses have been recognised as causing this disease, the most prominent being AIHV-1 and OvHV-2. MCF usually appears sporadically and affects few animals, although both AlHV-1 and OvHV-2 can give rise to rapidly spreading outbreaks.
Approximately 90 % of MCF cases in South Africa are caused by alcelaphine herpes virus-1
(AlHV-1) and the remaining 10 % by ovine herpes virus-2 (OvHV-2). MCF caused by AHV-1 is carried by wildebeest, hartebeest, and topi and is found primarily in the wild in South Africa.
For relevance to game breeding in South Africa, we will focus on MCF - alcelaphine herpes virus-1 (AlHV-1) and the natural host species that carry this virus, the wildebeest.
AlHV-1:
All wildebeest calves become infected with MCF (AlHV-1) within the first few months of life and remain carriers for life.
The blue wildebeest (Connochaetes taurinus) is the major reservoir host of MFC (AlHV-1), but black wildebeest (Connochaetes gnou) are also known carriers. Transmission to susceptible hosts occur only from wildebeest; there is no definitive evidence that MCF-affected animals transmit the disease horizontally.
Transmission of Malignant Catarrhal Fever
AlHV-1 in wildebeest occurs in both cell-free and cell-associated forms. These animals will shed the cell-free virus in nasal and ocular secretions for a short period of time after they have become infected where after the virus occurs mainly in the cell-associated form - transmitted very rarely to other animals.
AlHV-1 is spread mainly by wildebeest calves and virus shedding is most intense during the first 3-4 months of life. Contamination of pastures and feeding trophs may also contribute to the transmission of this disease. Transmission also occurs after close contact, however transmission has been reported when animals were separated by at least 100 meters.
Neutralising antibodies will usually develop by approximately 3 months of age after which shedding declines. After six months of age, wildebeest shed little virus except when they are stressed or during labour.
Inhalation is thought to be the primary means of transmission for all MCF viruses, although ingestion might also be possible. Cell-associated AlHV-1 is very fragile and infectivity disappears after 72 hours in the environment. The cell-free virus has been reported to survive for more than 13 days in humid environments. MCF viruses die rapidly when exposed to sunlight.
Clinical signs and pathology of Malignant Catarrhal Fever
Sudden, persistent pyrexia
Severe congestion, necrosis and erosion of nasal and oral mucosae
Serous, later mucopurulent, discharges
Scleral and conjunctival congestion; centripetal corneal opacity; hypopyon
Generalized enlargement of lymph nodes
Muscular tremors (meningo-encephalomyelitis)
Diarrhoea or dysentery (especially deer)
Dermatitis and laminitis
Natural incubation periods are often difficult to determine and can be very variable, but are reported to range from two weeks to nine months. The clinical course of the disease is also highly variable in individual animals and may be per acute, acute or chronic.
Per acute disease is characterized by sudden death with very few clinical signs observed beforehand. Clinical signs may include: rapid onset of depression, high fever and diarrhoea, which may become haemorrhagic, usually followed by death within 12 to 24 hours.
Generally, the onset of clinical signs in all forms of the disease are characterized by fever (rectal temperature of >42°C), in appetence, photophobia, lachrymation and a serous nasal exudate.
The ocular and nasal discharges may become profuse and mucopurulent. Such exudates may cause matting of the facial hair and may block off the nostrils resulting in difficulty in breathing. Ocular lesions are typically bilateral with corneal opacity developing from the periphery of the eye and progressively affecting the entire cornea. The cornea may become oedematous and blindness, corneal ulceration and hypopyon may result.
In the early stages of clinical disease, hyperaemia of the oral epithelium may be present, progressing to erosion of the mucosa. The latter is mostly seen on the ventral tongue surfaces, hard palate, gums and the tips of the buccal papillae.
Skin lesions may develop in affected animals and affected areas may show exanthema, exudation and encrustation. Such lesions are often restricted to the perineum, udder, teats, interdigital spaces and skin at the base of the horns and hooves. Hyperaemia may be seen in affected, unpigmented skin. The muzzle epithelium may become severely encrusted, necrotic and may slough.
Superficial lymph nodes may enlarge and a drop in milk production may be seen in lactating animals.
In some cases, clinical signs of meningoencephalitis may be observed.
Nervous signs including hyperaesthesia, lack of co-ordination, nystagmus, behavioural changes and head pressing may occur. These may be observed without any other clinical signs present or, may be part of a more typical clinical picture.
Aggression may be seen in some clinically affected animals. In a recent report by Mitchell et al (2009), the authors described nervous signs in calves which they considered unusual as only young calves were involved; with an unusually high morbidity (five out of a group of 20 affected); and neurological signs predominating.
Ocular and other signs were not prominent in these calves, occurring only in one calf.
More severe clinical signs may develop in the more protracted cases and death may be seen 9 to 10 days after the first clinical signs are noticed.
In general, disease in the more susceptible species follows an acute or per acute course. The clinical outcome of MCF is almost invariably fatal, however recovery or mild infection has been known to occur in MCF caused by AlHV-1, but the frequency with which this occurs is not clear at present.
To Be Continued
Sources *http://www.oie.int/fileadmin/Home/fr/Health_standards/tahm/2.04.16_THEILIERIOSIS.pdf *http://www.oie.int/fileadmin/Home/eng/Animal_Health_in_the_World/docs/pdf/Disease_cards/THEILERIOSIS.pdf *http://www.afrivip.org/sites/default/files/theileria_4_control.pdf *https://en.wikipedia.org/wiki/East_Coast_fever *http://www.merckvetmanual.com/mvm/circulatory_system/blood_parasites/theileriases.html *A review of Theileria diagnostics and epidemiology Ben J. Mans a,b,c,*, Ronel Pienaar a, Abdalla A. Latif a,b *SAVA WILD LIFE GROUP: Theileriosis in Roan antelope
