Behaviour of a Trypanosoma brucei brucei stock (STIB 348C) in mice. 4. Different course of primary parasitemia in trypanosome variants of different virulence.
{"title":"Behaviour of a Trypanosoma brucei brucei stock (STIB 348C) in mice. 4. Different course of primary parasitemia in trypanosome variants of different virulence.","authors":"W Büngener","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>In three types of trypanosomes with low virulence, trypanosome numbers increased by a factor of 18-21 per day on average during prepatency and by a factor of 70-219 on average from the first to second day of patency. By contrast, a very virulent trypanosome variant showed an average increase of trypanosome numbers per day by 32 and 28 during prepatency and early patency, respectively. --In detailed studies, trypanosomes of low virulence exhibited a rapidly rising parasitemia in early patency which lasted for 20-30 hours and was followed by a plateau of slowly rising and falling parasitemia. Trypanosomes of high virulence showed a constant logarithmic increase of their numbers, slowing down at concentrations above antilog 5.5 per microliters of blood. In mild trypanosomes with peak parasitemias of antilog 5-5.7 per microliters of blood, after low dose infections the primary parasitemia was abruptly terminated after 70-100 hours of patency, obviously by the action of antibody. After massive infections, the parasitemia was terminated at 109-122 hours after infection. --In trypanosomes with higher peak parasitemias, primary parasitemias were seen to last longer, in some cases for 7 to 12 days. --Mice infected with low doses of highly virulent trypanosomes died with high parasitemias after some 60-90 hours of patency, before antibodies could normally become effective. After massive infections they died at 40-60 hours after infection. There is clearly no need to invoke non-immunogenicity of these trypanosomes or immunosuppression by these trypanosomes to explain this course of the infection.</p>","PeriodicalId":76764,"journal":{"name":"Tropenmedizin und Parasitologie","volume":"35 2","pages":"115-8"},"PeriodicalIF":0.0000,"publicationDate":"1984-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tropenmedizin und Parasitologie","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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Abstract
In three types of trypanosomes with low virulence, trypanosome numbers increased by a factor of 18-21 per day on average during prepatency and by a factor of 70-219 on average from the first to second day of patency. By contrast, a very virulent trypanosome variant showed an average increase of trypanosome numbers per day by 32 and 28 during prepatency and early patency, respectively. --In detailed studies, trypanosomes of low virulence exhibited a rapidly rising parasitemia in early patency which lasted for 20-30 hours and was followed by a plateau of slowly rising and falling parasitemia. Trypanosomes of high virulence showed a constant logarithmic increase of their numbers, slowing down at concentrations above antilog 5.5 per microliters of blood. In mild trypanosomes with peak parasitemias of antilog 5-5.7 per microliters of blood, after low dose infections the primary parasitemia was abruptly terminated after 70-100 hours of patency, obviously by the action of antibody. After massive infections, the parasitemia was terminated at 109-122 hours after infection. --In trypanosomes with higher peak parasitemias, primary parasitemias were seen to last longer, in some cases for 7 to 12 days. --Mice infected with low doses of highly virulent trypanosomes died with high parasitemias after some 60-90 hours of patency, before antibodies could normally become effective. After massive infections they died at 40-60 hours after infection. There is clearly no need to invoke non-immunogenicity of these trypanosomes or immunosuppression by these trypanosomes to explain this course of the infection.