Hostname: page-component-8448b6f56d-m8qmq Total loading time: 0 Render date: 2024-04-15T18:37:29.724Z Has data issue: false hasContentIssue false
  • English
  • Français

Extravascular foci of Trypanosoma vivax in goats: the central nervous system and aqueous humor of the eye as potential sources of relapse infections after chemotherapy

Published online by Cambridge University Press:  06 April 2009

D. D. Whitelaw ,
P. R. Gardiner  and
M. Murray
D. D. Whitelaw
Affiliation:
International Laboratory for Research on Animal Diseases, P.O. Box 30709, Nairobi, Kenya
P. R. Gardiner
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
Get access Rights & Permissions [Opens in a new window]

Summary

Relapse of parasitaemia after 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. In addition, inaccessibility of parasites to drug through sequestration in privileged extravascular sites has been shown in the past to occur with Trypanosoma brucei, and we have obtained evidence that extravascular foci of T. vivax can also serve as a source of relapsing infections. Infection of goats with a West African stock of T. vivax resulted in severe illness, which was fatal if untreated. During the terminal stage of an acute infection, clinical signs of central nervous system involvement were apparent. Histologically, the choroid plexus was swollen and oedematous, and in some cases meningitis or meningoencephalitis was seen. Trypanosomes could be detected in the cerebrospinal fluid, and also extravascularly in the choroid plexus and meninges. In three cases they were present in the aqueous humor, associated with corneal cloudiness or opacity. Treatment of 2 goats with the trypanocidal drug diminazene aceturate eliminated parasitaemia, but infections in both relapsed about 6 weeks later, despite trypanosomes being undetectable in the bloodstream during the intervening period. We conclude that the relapse infections were caused by re-emergence of trypanosomes from the CNS and/or the eye, where sequestered parasites may have been inaccessible to the trypanocide.

Type
Research Article
Information
Parasitology , Volume 97 , Issue 1 , August 1988 , pp. 51 - 61
Copyright
Copyright © Cambridge University Press 1988

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

REFERENCES

Adams, A. R. D. (1936). Trypanosomiasis of stock in Mauritius III. The diagnosis and course of untreated T. vivax infections in domestic animals. Annals of Tropical Medicine and Parasitology 36, 521–31.CrossRefGoogle Scholar
Barry, J. D. (1986). Antigenic variation during Trypanosoma vivax infections of different host species. Parasitology 92, 51–65.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
Bungener, W. & Mehlitz, D. (1977). Extravasales Vorkommen von Trypanosoma vivax bei Rindern Tropenmedizin und Parasitologie 28, 8–10.Google Scholar
Emery, D. L., Barry, J. D. & Moloo, S. K. (1980). The appearance of Trypanosoma (Duttonella) vivax in lymph following challenge of goats with infected Glossina morsitans morsitans. Acta Tropica 37, 375–9.Google ScholarPubMed
Emery, D. L. & Moloo, S. K. (1981). The dynamics of the cellular reactions elicited in the skin of goats by Glossina morsitans morsitans infected with Trypanosoma (Nannomonas) congolense or T. (Duttonella) vivax. Acta Tropica 38, 15–28.Google ScholarPubMed
Gardiner, P. R., Thatthi, R., Gathuo, H., Nelson, R. & Moloo, S. K. (1986). Further studies of cyclical transmission and antigenic variation of the ILDar 1 serodeme of Trypanosoma vivax. Parasitology 92, 581–93.CrossRefGoogle ScholarPubMed
Gardiner, P. R., Webster, P., Jenni, L. & Moloo, S. K. (1986). Metacyclic Trypanosoma vivax possess a surface coat. Parasitology 92, 75–82.CrossRefGoogle ScholarPubMed
Gutteridge, W. E. & Coombs, G. H. (1977). Biochemistry of Parasitic Protozoa. London: Macmillan.CrossRefGoogle Scholar
Hornby, H. E. (1952). Animal Trypanosomiasis in Eastern Africa, 1949. London: His Majesty's Stationery Office.Google Scholar
Ilemobade, A. A. & Schilhorn van Veen, T. W. (1974). The presence of Trypanosoma vivax in the ocular discharge of an experimentally infected calf. Transactions of the Royal Society of Tropical Medicine and Hygiene 68, 410.CrossRefGoogle ScholarPubMed
van den Ingh, T. S. G. A. M. & de Neijs-Bakker, M. H. (1979). Pancarditis in Trypanosoma vivax infection in cattle. Tropenmedizin und Parasitologie 31, 239–43.Google Scholar
Jennings, F. W., Whitelaw, D. D. & Urquhart, G. M. (1977). The relationship between duration of infection with Trypanosoma brucei in mice and the efficacy of chemotherapy. Parasitology 75, 143–53.CrossRefGoogle ScholarPubMed
Jennings, F. W., Whitelaw, D. D., Chizyuka, H. G. B., Holmes, P. H. & Urquhart, G. M. (1979). The brain as a source of relapsing Trypanosoma brucei infection in mice after chemotherapy. International Journal for Parasitology 9, 381–4.CrossRefGoogle ScholarPubMed
Leeflang, P., Buys, J. & Blotkamp, C. (1976). Studies on Trypanosoma vivax. Infectivity and serial maintenance of natural bovine isolates in mice. International Journal for Parasitology 6, 413–17.CrossRefGoogle ScholarPubMed
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
MacLennan, K. J. R. (1971). The aparasitiaemic interval following diminazene aceturate therapy of a relapsing strain of T. vivax infecting cattle. Tropical Animal Health and Production 3, 208–12.CrossRefGoogle Scholar
MacLennan, K. J. R. & Na'isa, B. K. (1970). Relapsing Trypanosoma vivax infections in Nigerian zebu cattle treated with diminazene aceturate. Tropical Animal Health and Production 2, 189–95.CrossRefGoogle Scholar
Masake, R. A. (1980). The pathogenesis of infection with Trypanosoma vivax in goats and cattle. Veterinary Record 107, 551–7.CrossRefGoogle ScholarPubMed
Morrison, W. I., Murray, M. & McIntyre, W. I. M. (1981). Bovine trypanosomiasis. In Diseases of Cattle in the Tropics (ed. M., Ristic and McIntyre, W. I.), pp. 469–97. The Hague: Nijhoff.Google Scholar
Morrison, W. I., Murray, M., Sayer, P. D. & Preston, J. M. (1981). The pathogenesis of experimentally induced Trypanosoma brucei in the dog. I. Tissue and organ damage. American Journal of Pathology 102, 168–81.Google ScholarPubMed
Morrison, W. I., Murray, M., Whitelaw, D. D. & Sayer, P. D. (1983). Pathology of infection with Trypanosoma brucei: disease syndrome in dogs 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
Murray, M., Murray, P. K. & McIntyre, W. I. M. (1977). An improved parasitological technique for the diagnosis of African trypanosomiasis. Transactions of the Royal Society of Tropical Medicine and Hygiene 71, 325–6.CrossRefGoogle ScholarPubMed
Murray, M., Morrison, W. I., Emery, D. L., Akol, G. W. O., Masake, R. A. & Moloo, S. K. (1979). The pathogenesis of trypanosome infections in cattle. In International Symposium on the use of Isotopes for Research and Control of Vectors of Animal Disease, publication IAEA-SM-240/19, pp. 15–32. Vienna: IAEA.Google Scholar
Nantulya, V. M., Musoke, A. J. & Moloo, S. K. (1986). Apparent exhaustion of the variable antigen repertoires of Trypanosoma vivax in infected cattle. Infection and Immunity 54, 444–7.CrossRefGoogle ScholarPubMed
Rapoport, S. I. (1976). Blood-Brain Barrier in Physiology and Medicine. New York: Raven Press.Google Scholar
Raviola, G. (1977). The structural basis of the blood-ocular barriers. Experimental Eye Research 25 (Suppl.), 27–63.CrossRefGoogle ScholarPubMed
Seed, J. R. (1978). Competition among serologically different clones of Trypanosoma brucei gambiense in vivo. Journal of Protozoology 25, 526–9.CrossRefGoogle ScholarPubMed
Seed, J. R. & Effron, H. G. (1973). Simultaneous presence of different antigenic populations of Trypanosoma brucei gambiense in Microtus montanus. Parasitology 66, 269–78.CrossRefGoogle ScholarPubMed
Tanner, M., Jenni, L., Hecker, H. & Brun, R. (1980). Characterization of Trypanosoma brucei isolated from lymph nodes of rats. Parasitology 80, 383–91.CrossRefGoogle ScholarPubMed
Whitelaw, D. D., Moulton, J. E., Morrison, W. I. & Murray, M. (1985). Central nervous system involvement in goats undergoing primary infections with Trypanosoma brucei and relapse infections after chemotherapy. Parasitology 90, 255–68.CrossRefGoogle Scholar