An evaluation of melarsomine hydrochloride efficacy for parasitological cure in experimental infection of dairy cattle with Trypanosoma evansi in Thailand.

Melarsomine hydrochloride can cure Trypanosoma evansi infection in camels at a dose of 0·25 mg/kg, but at that dose relapses occur in cattle. In our study, the efficacy of an intramuscular injection of melarsomine hydrochloride at 0·5 mg/kg was assessed in 3 normal and 3 splenectomized dairy cattle experimentally infected with a stock of T. evansi from Thailand. The animals were monitored for 5 months by haematocrit centrifugation, blood- or cerebrospinal fluid-mouse inoculation, polymerase chain reaction, the card agglutination test (CATT) for T. evansi, and the enzyme-linked immunosorbent assay­T. evansi. Parasitological and DNA tests became and remained negative just after treatment. By the end of the experiment, CATT was negative and ELISA scores were below or very close to the cut-off value. One of the splenectomized cattle died from anaplasmosis during the experiment, but tested negative for surra. It was concluded that the parasites had been cleared from the cattle, and melarsomine hydrochloride at 0·5 mg/kg can be recommended for treatment against T. evansi infection in dairy cattle in Thailand. Further work is necessary to validate the efficacy of the treatment in the event of confirmed CSF-infection.

Experimental infection of cattle with Trypanosoma brucei rhodesiense.

Infection of cattle with various stocks of Trypanosoma brucei rhodesiense indicated that 49% developed a fatal CNS disease comparable to that found in man. Duration of disease ranged from 85 to 1613 days post infection. All eight stocks of T. b. rhodesiense tested, including those from Ethiopia and Tanzania, induced CNS disease. Blood became positive three to five days after inoculation, and after an initial peak of parasitaemia remained positive for three to five months. Subinoculation of blood into rodents subsequently became negative, although trypanosomes persisted in the lymph nodes for at least 56 to 1613 days. Only animals with CNS disease had detectable parasites in the CSF, usually after the animals had undergone severe deterioration. At post mortem examination trypanosomes could usually be found in the lymph nodes and CSF, and occasionally in the blood. Clinical signs included fever, hyperkinesia, weight loss, cerebellar ataxia, tremor, salivation and hyperaesthesia. A mild to moderate anaemia accompanied a transient thrombocytopenia and leucopenia. Animals subsequently developed leucocytosis. A pleocytosis and elevated total protein in the CSF was found, which persisted in some animals for long periods. Histopathological examination of the brain showed prominent generalized perivascular infiltrates consisting mainly of lymphocytes and plasma cells. Mott's cells were regularly observed. Vascular changes were characterized by swollen endothelium, infiltration of the vascular wall by inflammatory cells, and in some instances perivascular oedema. In the most severe cases evidence of ischaemia consisted of large numbers of astrocytes, rarefaction of the parenchyma, and areas of necrosis with loss of normal architecture. Demyelination was limited to perivascular areas. Occasionally a moderate to severe pancarditis was found.

Cerebral trypanosomiasis in naturally-infected cattle in the Lambwe Valley, south Nyanza, Kenya.

Surveys in Zebu cattle in the Lambwe Valley in 1980 indicated that many (up to 70%) were infected with trypanosomes. The predominant parasite was Trypanosoma brucei sspl followed by T. congolense. Cerebrospinal fluid (CSF) analysis showed a high proportion of animals with pleocytosis and elevated total CSF protein. Trypanosomes were detected in CSF and signs of a central nervous system (CNS) disease were observed. Histopathological lesions in the CNS were identical to those found in experimentally-infected cattle and consisted of perivascular infiltrations, swollen endothelium of vessels, infiltration of the vascular wall, and perivascular oedema. The severest cases showed rarefaction, astrocytosis and areas of necrosis. Infected cattle transported to the Veterinary Research Laboratory were studied for up to four years. Absence of trypanosomes from the peripheral blood was common, and even subinoculation of lymph node aspirates and CSF were usually negative. Death was preceded by a period of weight loss and the development of severe CNS signs. An attempt to cure animals with Mel-B treatment failed. Serum from naturally-infected cattle neutralized T. b. rhodesiense stocks collected in the same area.