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Central nervous system involvement in goats undergoing primary infections with Trypanosoma brucei and relapse infections after chemotherapy

Published online by Cambridge University Press:  06 April 2009

D. D. Whitelaw ,
J. E. Moulton ,
W. I. Morrison  and
M. Murray
D. D. Whitelaw
Affiliation:
International Laboratory for Research on Animal Diseases, P.O. Box 30709, Nairobi, Kenya
J. E. Moulton
Affiliation:
International Laboratory for Research on Animal Diseases, P.O. Box 30709, Nairobi, Kenya
W. I. Morrison
Affiliation:
International Laboratory for Research on Animal Diseases, P.O. Box 30709, Nairobi, Kenya
M. Murray
Affiliation:
International Laboratory for Research on Animal Diseases, P.O. Box 30709, Nairobi, Kenya
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Extract

Relapse of infection after trypanocidal drug treatment of trypanosome infections is normally attributed to drug resistance on the part of the parasite, under-dosage of the drug, or reinfection of the host. We have demonstrated relapse infections in goats arising from none of these. Fourteen goats infected with Trypanosoma brucei suffered severe illness and 3 died within 45 days. Despite treatment with the trypanocidal drug Berenil, a 4th goat died 2 days later. Recovery of the remainder followed chemotherapy, and in 2 goats, necropsiecl 45 days after treatment, no trypanosomes or abnormalities were detected. However 2–3 months after Berenil chemotherapy, despite trypanosomes being undetectable in the blood during the intervening period, infections in 4 of the remaining 8 animals relapsed. At all stages of the primary and relapse infections, trypanosomes isolated from the blood of the goats were completely susceptible to Berenil when tested in mice, as were parasites isolated from cerebrospinal fluid and brain tissue at necropsy. At the time of treatment, only minimal cellular infiltration was found in the central nervous system (CNS), but death from the relapse infection was associated with a very severe meningoencephalitis. We conclude that the relapse infections were caused by the re-emergence of trypanosornes from the CNS, where sequestered parasites were inaccessible to the trypanocidal effects of the drug.

Type
Research Article
Information
Parasitology , Volume 90 , Issue 2 , April 1985 , pp. 255 - 268
Copyright
Copyright © Cambridge University Press 1985

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References

REFERENCES

Astrom, K. E., Webster, H. De F. & Arnason, B. G. (1968). The initial lesion in experimental allergic neuritis; a phase and electron microscopic study. Journal of Experimental Medicine 128, 469–96.CrossRefGoogle ScholarPubMed
Brightman, W. M. & Reese, T. S., (1969). Junctions between intimately apposed cell membranes in the vertebrate brain. Journal of Cell Biology 40, 648–77.CrossRefGoogle ScholarPubMed
Emery, D. L. & Moloo, S. K. (1980). The sequential cellular changes in the local skin reaction produced in goats b. Glossina morsitans morsitans infected with Trypanosoma (Trypanozoom) brztcei. Acta Tropica 37, 137–49.Google Scholar
Fiennes, R. N. T. W. (1970). Pathogenesis and pathology of animal trypanosomiasis. In The African Trypanosorniases (ed. Mulligan, H. W.), pp. 729–750. London: George Allen-Unwin.Google Scholar
Fink, E. & Schmidt, H. (1979). Meningoencephalitis in chroni. Trypanosoma brucei rhodesiense infection of the white mouse. Tropenmedizin und Parasitologie 30, 206–11.Google Scholar
Fink, E., Sayer, P. D. & Schmidt, H. (1983). IgG and IgM levels in serum and CSF of T. rhodesiense-infected vervet monkeys. In From Parasitic Infection, to Parasitic Disease, Contributions to Microbiology and Immunology, vol. 7 (ed. Gigase, P. L. and van Marek, F. A. E.), pp. 183–189. Basel: Karger.Google Scholar
Fruit, J., Santoro, R., Afohain, D., Duvallet, G. & Capron, A. (1977). Les immuns-complexes circulants clans la trypanosomiase aifricaine humain et experirnentale. Annales de la Société belge de Medecine tropicale 57, 257–63.Google Scholar
Galvao-Castro, B., Hochmann, A. & Lambert, P. H. (1978). The role of the host immune response in the development of tissue lesions associated with African trypanosomiasis in mice. Clinical and Experimental Immunology 33, 12–24.Google ScholarPubMed
Gutteridge, W. E. & Coombs, G. H. (1977). Biochemistry of Parasitic Protozoa. London: MacMillan.CrossRefGoogle Scholar
Jenni, L., Rudin, W. & Schell, K. F. (1983). Extravascular and vascular distribution of Trypanosonia brucei gambiense in Microtus montanus after cyclical transmission. In From Parasitic Infection to Parasitic Disease, Contributions to Microbiology and Immunology, vol. 7 (ed Gigase, P. L. and van Marck, E. A. E.), pp. 95–102. Basel: Karger.Google Scholar
Jennings, F. W. & Gray, G. D. (1983). Relapsed parasitaemia following chemotherapy of chronic T. brucei infections in mice and its relation to cerebral trypanosomes. In From Parasitic Infection to Parasitic Disease, Contributions to Microbiology and Immunology, vol. 7 (ed. Gigase, P. L. and van Marck, E. A. F.), pp. 103–119. Basel: Karger.Google Scholar
Jennings, F. V., Whitelaw, D. D. & Urquhart, C. M. (1977). The relationship between duration of infection wit. Trypanosoma brucei in mice and the efficacy of chemotherapy. Parasitology 75, 143–53.CrossRefGoogle Scholar
Jennings, F. W., Whitelaw, D. D., Holmes, P. H., Chizyuka, H. G. B. & Urquhart, G. M. (1979). The brain as a source of relapsin. Trypanosoma brucei infection in mice after chemotherapy. International Journal for Parasitology 9, 381–4.CrossRefGoogle Scholar
Killick-Kendrick, R. (1971). The low pathogenicity o. Trypanosoma brucei in cattle. Transactions of the Royal Society of Tropical Medicine and Hygiene 65, 104.CrossRefGoogle Scholar
Lambert, P. H. & Houba, V. (1974). Immune complexes in parasitic diseases. In Progress in Immunology II, vol. 5 (ed. Brent, L. and Holborow, J.), pp 57–65. Amsterdam: North Publishing Company.Google Scholar
Losos, G. J. & Ikede, B. O. (1972). Review of the pathology of diseases in domestic and laboratory animals caused by Trypanosoma congolense, T. vivax, T. brucei, T. rhodesiense and T. gambiense. Veterinary Pathology 9, (Suppl.), 1–71.CrossRefGoogle Scholar
Lowry, O. H., Rosebrough, N. V., Farr, A. C. & Randall, R. J. (1951). Protein measurement with the Folin phenol reagent. Journal of Biological Chemistry 193, 265–75.CrossRefGoogle ScholarPubMed
MacClennan, K. J. R. (1971). The aparasitaemic interval following diminazene aceturate therapy of a relapsing strain o. T. vivax infecting cattle. Tropical Animal Health and Producton 3, 208–12.CrossRefGoogle Scholar
Manuelidis, E. E., Robertson, D. H. H., Amberson, J. M., Polar, J. M. & Haymaker, W. (1965). Trypanosoma rhodesiense encephalitis; clinicopathological study of 5 cases of encephalitis and one of Mel B haemorrhagic encephalopathy. Acta Neuropathologica 5, 176–204.CrossRefGoogle Scholar
Masake, R. A., Nantulya, V. M., Akol, G. W. O. & Musoke, A. J. (1984). Cerebral trypanosomiasis in cattle with mixe. Trypanosoma congolense and T. brucei brucei infections. Acta Tropica 41, 137–46.Google Scholar
Morrison, W. I., Murray, M., Whitelaw, D. D. & Sayer, P. D.. (1983). Pathology of infection with Trypanosoma brucei: disease syndromes in clogs and cattle resulting from severe tissue damage. In From Parasitic Infection to Parasitic Disease, Contributions to Microbiology and immunology, vol. 7 (ed Gigase, P. L. and van Marck, E. A. E.), pp. 103–119. Basel: Karger.Google Scholar
Mott, F. W. (1907). Histological observations on the changes in the nervous system in trypanosome infections especially sleeping sickness and their relation to syphilitic lesions of the nervous system. Archives of Neurology 3, 581–646.Google Scholar
Murray, M. (1974). The pathology of African trypanosomiasis. In Progress in Isnncnnology II, vol. 4 (ed. Brent, L. and Holborow, T.), pp. 181–192. Amsterdam: North-Holland Publishing Company.Google Scholar
Murray, M., Murray, P. K. & McIntyre, W. I. M. (1977). An improved parasitological technique for the diagnosis of African trypanosomasis. Transactions of the Royal Society of Tropical Medicine and Hygiene 71, 325–6.CrossRefGoogle Scholar
Murray, P. K., Murray, M., Wallace, M., Morrison, W. I. & McIntyre, W. I. M. (1979). Trypanosomiasis in N'Dama and Zehu cattle I. An experimental investigation of susceptibility to Trypanosoina brucei, T. congolense and mixed infections. In International Scientific Council for Trypanosonciasis Research and Control, 15th meeting, Banjul, The Gambia, 1977, pp. 470–481. (OAU/STRC No. 110) Nairobi: Scientific Publications Division of Eleza Services.Google Scholar
Ormerod, W. E. & Venkatesan, S. (1971 a). The occult visceral phase of mammalian trypanosomes with special reference to the life cycle of Trypanosorna (Trypanozoon) brucei. Transactions of the Royal Society of Tropical Medicine and Hygiene 65, 722–35.CrossRefGoogle Scholar
Ormerod, W. E. & Venkatesan, S. (1971 b). An amastigote phase of the sleeping sickness trypanosome. Transactions of the Royal Society of Tropical Medicine and Hygiene 65, 736–41.CrossRefGoogle ScholarPubMed
Peruzzi, M. (1928). Final Report of the League of Nations an Human Trypanosomiasis. Section 5, 245.Google Scholar
Poltera, A. A., Hochmann, A., Rudin, W. & Lambert, P. H. (1980) Trypanosoma brucei brucei – a model for cerebral trypanosomiasis in mice: an immunolo and electron – microscopic study. Clinical and Experimental Immunology 40, 496–507.Google Scholar
Rudin, W., Poltera, A. A. & Jenni, L. (1983). An EM study on cerebral trypanosomiasis in rodents and primates. In From Parasitic Infection to Parasitic Disease, Contributions to Microbiology and Immunology, vol. 7 (ed. Gigase, P. L. and van Marck, E. A. E.), pp. 165–172. Basel: Karger.Google Scholar
Schmidt, H. & Sayer, P. D. (1982). Trypanosoma brucei rhodesiense infection in vervet monkeys. II. Provocation of the encephalitic late phase by treatment of infected monkeys. Tropenmedizin und Parasitologie 33, 255–9.Google ScholarPubMed
Stevens, P. R. & Moulton, J. E. (1977). Experimental ineningoencephalitis i. Trypanosoma brucei infection of deer mice (Peromyscus maniculatus). A light, immunolluorescent and electron microscopic study. Acta Neuropathologica 38, 173–80.CrossRefGoogle ScholarPubMed
Van Marck, E. A. E., Le Ray, P., Beckers, A., Jacob, W., Werry, M. & Gigase, P. L. J. (1981). Light and electron microscope studies on extravascula. Trypanosoma brucei gambiense in the brain of chronically infected rodents. Annales de la Société belge de Medecine tropicale 61, 57–78.Google ScholarPubMed
Wellde, B. T., Kovatch, R. M., Hockmeyer, W. T., Owiti, S., Masaba, S. C. & Arap Siongok, T. (1980). Trypanosoma brucei rhodesiense: experimental infections in cattle. In Recent Developments in Medical Research in Eastern African (ed. Njogu, A. R., Tukei, P. M. and Roberts, J. M. D.), pp. 187–203. Kenya Medical Research Institute and Kenya Trypanosomiasis Research Institute, Nairobi.Google Scholar