Central nervous system involvement in goats undergoing primary infections with Trypanosoma brucei and relapse infections after chemotherapy
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 in...
| Main Authors: | , , , |
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| Format: | Journal Article |
| Language: | Inglés |
| Published: |
Cambridge University Press
1985
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| Subjects: | |
| Online Access: | https://hdl.handle.net/10568/29433 |
| _version_ | 1855517094035062784 |
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| author | Whitelaw, D.D. Moulton, J.E. Morrison, W. Ivan Murray, M. |
| author_browse | Morrison, W. Ivan Moulton, J.E. Murray, M. Whitelaw, D.D. |
| author_facet | Whitelaw, D.D. Moulton, J.E. Morrison, W. Ivan Murray, M. |
| author_sort | Whitelaw, D.D. |
| collection | Repository of Agricultural Research Outputs (CGSpace) |
| description | 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 withTrypanosoma bruceisuffered 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. |
| format | Journal Article |
| id | CGSpace29433 |
| institution | CGIAR Consortium |
| language | Inglés |
| publishDate | 1985 |
| publishDateRange | 1985 |
| publishDateSort | 1985 |
| publisher | Cambridge University Press |
| publisherStr | Cambridge University Press |
| record_format | dspace |
| spelling | CGSpace294332024-11-15T08:52:11Z Central nervous system involvement in goats undergoing primary infections with Trypanosoma brucei and relapse infections after chemotherapy Whitelaw, D.D. Moulton, J.E. Morrison, W. Ivan Murray, M. infection nervous system trypanosoma brucei goats chemotherapy drug therapy disease control infectious diseases parasitology 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 withTrypanosoma bruceisuffered 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. 1985-04 2013-06-11T09:23:33Z 2013-06-11T09:23:33Z Journal Article https://hdl.handle.net/10568/29433 en Limited Access Cambridge University Press Parasitology;90: 255-268 |
| spellingShingle | infection nervous system trypanosoma brucei goats chemotherapy drug therapy disease control infectious diseases parasitology Whitelaw, D.D. Moulton, J.E. Morrison, W. Ivan Murray, M. Central nervous system involvement in goats undergoing primary infections with Trypanosoma brucei and relapse infections after chemotherapy |
| title | Central nervous system involvement in goats undergoing primary infections with Trypanosoma brucei and relapse infections after chemotherapy |
| title_full | Central nervous system involvement in goats undergoing primary infections with Trypanosoma brucei and relapse infections after chemotherapy |
| title_fullStr | Central nervous system involvement in goats undergoing primary infections with Trypanosoma brucei and relapse infections after chemotherapy |
| title_full_unstemmed | Central nervous system involvement in goats undergoing primary infections with Trypanosoma brucei and relapse infections after chemotherapy |
| title_short | Central nervous system involvement in goats undergoing primary infections with Trypanosoma brucei and relapse infections after chemotherapy |
| title_sort | central nervous system involvement in goats undergoing primary infections with trypanosoma brucei and relapse infections after chemotherapy |
| topic | infection nervous system trypanosoma brucei goats chemotherapy drug therapy disease control infectious diseases parasitology |
| url | https://hdl.handle.net/10568/29433 |
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