Animals which have suffered from chronic, protracted disease may be emaciated and dehydrated. The mucous membranes of the upper and lower respiratory tract are usually congested. In some cases they may become oedematous with small haemorrhages, multiple foci of epithelial necrosis, erosions and ulcerations, mucopurulent inflammation and pseudo membrane formation. The nasal passages, particularly between the turbinate’s, may be partially blocked by exudates. A patchy bronchopneumonia may be present in animals that suffered from more protracted disease.
The mucosa of the mouth may be hyperaemic. Petechiae and ecchymoses, foci of epithelial necrosis, erosions and, in some cases, diphtheritic exudates may be observed. Similar lesions may be found in the oesophagus, particularly its more cranial parts, the forestomaches and abomasum. In the latter organs, erosions and/or ulcers are frequently present - particularly on the margins of the mucosal folds. The small and large intestines may exhibit a catarrhal to haemorrhagic enteritis with their contents, particularly in the more acute cases, watery and blood-stained. Similar erosions or ulcerations to those in the abomasum may be present along the ridges of the mucosal rugae of the ileocaecal valve, caecum, colon and rectum.
Most of the lymph and haemolymph nodes usually become enlarged due to the lymphoid hyperplasia, oedema and sometimes congestion.
The spleen may, or may not, be enlarged and on cut surfaces, white pulp is generally prominent.
The liver is usually slightly enlarged and exhibits diffuse greyish-yellow colour and mottling. The gall bladder may show lesions of oedema, petechiae, ecchymoses in its walls and few, small mucosal erosions.
Characteristic lesions are usually seen in the kidneys as varying numbers of greyish – white foci which are 1 to 5mm in diameter. These are seen the cortices and they may bulge above the renal surface. In some cases, the presence of small, scattered renal haemorrhages may be observed.
The mucosa and wall of the urinary bladder may frequently be oedematous with petechiae and ecchymoses in the mucosa and serosa and occasionally erosions or ulcers on the mucosal surface.
Haematuria may sometimes be present. Increased amounts of cerebrospinal fluid are formed and the meninges may appear more moist than usual and the subarachnoid spaces may be slightly cloudy.
Diagnosis of Malignant Catarrhal Fever
A presumptive diagnosis of MCF can be made on a herd’s history, clinical signs and pathology. Histopathological examination can confirm MCF, but cannot confirm whether the cause of death was the wildebeest-associated alcelaphine herpes virus-1 (AlHV-1) or sheep-associated virus ovine herpes virus-2 (OvHV-2).
Confirmation of the diagnosis of wildebeest-associated MCF requires either isolation of the virus from blood or tissues of the affected animal, or detection of viral nucleic acid in blood cells and tissues by means of the polymerase chain reaction (PCR) method.
Organ specimens for viral isolation should be collected as soon as possible after death as infectivity in wildebeest-derived MCF is associated with viable host cells. Blood should be collected in an anticoagulant such as heparin preferably before death.
Serology is of limited value in the diagnosis of wildebeest-associated MCF, as humoral antibody responses only develop late in the course of the disease. Serological cross-reactions occur with other bovid herpesviruses when serological tests using AlHV-1 as the capture antigen are performed. This does not apply to the virus neutralisation test.
For legal purposes, both PCR tests and histopathological examinations are recommended to confirm that the animal did indeed succumb to the effects of clinical MCF. If only PCR test results are available, it can be claimed that the animal may have been latently infected and died of a disease with gross lesions similar to that of MCF.
Control of Malignant Catarrhal Fever
No treatment has been found to provide any consistent benefit for the treatment of MCF and most cases prove fatal. At present no vaccine is available.
Stress reduction of subclinical or mildly affected animals is suggested whilst the only other effective control strategy is separation of carriers from susceptible species.
As a means of control at Purple Rain Game Breeding, we are currently in the process of moving/isolating our Golden/Split wildebeest herds, to ensure they are separated from other susceptible animals by more than1km.
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