STUDIES IN HUMAN MALARIA .18. THE LIFE PATTERN OF SPOROZOITE-INDUCED ELIZABETH STRAIN VIVAX MALARIA
STUDIES IN HUMAN MALARIA .18. THE LIFE PATTERN OF SPOROZOITE-INDUCED ELIZABETH STRAIN VIVAX MALARIA
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DOI：
10.1093/oxfordjournals.aje.a119385
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发表时间：
1950-01-01
影响因子：
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通讯作者：
BURGESS, RW
中科院分区：
文献类型：
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作者：
COATNEY, GR;COOPER, WC;BURGESS, RW
本报告总结了圣伊丽莎白假单胞菌菌株感染的主要特征。 vivaxin 在四年半的时间里对 198 人进行了实验性蚊虫叮咬感染。每只感染蚊子唾液腺中的子孢子数量从1+到4+分级；叮咬每位患者的蚊子总数可以作为传染性接种物的粗略衡量标准。药物用作临床预防剂或治疗剂。有关其管理的详细信息已在本系列的前几篇文章中给出，并在本公告中进行了总结。使用的药物为磺胺嘧啶、磺胺吡嗪、奎宁、美帕林、帕马喹、SN1796、SN5241、SN6771、桑托钦、SN7266、氯喹、SN8557、间氯定、秋水仙碱和喷他喹。其中，只有帕马喹和五喹被列为治疗药物，因为与奎宁合用可以预防复发。在接触感染后 45 至 60 天内，每天检查厚血涂片，并在第一次感染期间至少每周检查一次； 18 个月。在 198 名受试者中，195 名患有明显的疟疾。未能做到这一点的 3 人中，有 2 人失踪。在延迟原发性发作之前进行观察。在这 195 人中观察到 429 次疟疾发作； 135 次发作发生在蚊虫叮咬后 2 个月内，294 次发作发生在叮咬后 6 至 14 个月内。78 名受试者没有接受预防药物；其中 75 人在初次接触后 11 至 20 天内患上明显的疟疾。其余 3 例初次发作延迟至暴露后 298、318 和 319 天；所有这三名男子都接种了相对较小的疫苗。在接受保护性药物治疗的 120 名男子中，41 人在暴露后 12 至 64 天出现原发性发作：76 人在暴露后 193 至 350 天出现原发性发作。 3 例从未患上明显的疟疾[见上文] 在所有 41 例病例中，药物未能预防早期原发性疟疾的原因可以解释为所采用的治疗方案不充分。只要治疗能够根除红细胞寄生虫，早期发作治疗后的潜伏期持续时间与所使用的药物无关。在早期原发性发作期间接受抗疟原虫治疗的 116 名男性中，有 10 人接受了喷他喹和奎宁治疗 14 天：这 10 人中没有一人出现晚期发作。只有一名经过充分观察并接受非治疗性药物治疗的患者未能出现晚期发作；他接受了奎纳克林 [mepacrine] 治疗。74 例延迟性初次发作中，蚊虫叮咬后发作的平均发作时间为 287.1 天； 79 例早期活动后复发的时间为 275.6 天。长期潜伏期不依赖于感染发生的月份或季节、子孢子剂量、早期明显寄生虫血症的程度或持续时间，或早期非治疗性治疗的性质。长期潜伏期亚接种呈阴性，可实现同源株重复感染。在活动后期，通常会发生几次急性发作，当使用缓慢消除的药物时，发作间隔会更长。未治疗病例的晚期活动总持续时间比治疗病例长得多。接受治疗的受试者明显疟疾的最终终止不太可能是对红细胞寄生虫获得免疫力的结果。诺曼·怀特。
This report is a summary of the chief characteristics of infections with the St. Elizabeth strain ofP. vivaxin 198 persons experimentally infected by mosquito bites during a period of four and a half years. The number of, sporozoites in the salivary glands of each infected mosquito was graded from 1 + to 4 +; the total number of pluses for the mosquitoes that bit each patient served as a rough measure of the infective inoculum. Drugs were used either as clinical prophylactics or therapeutically. Details concerning their administration have been given in previous papers of this series which have been summarized in thisBulletin. The drugs used were sulphadiazine, sulphapyrazine, quinine, mepacrine, pamaquin, SN1796, SN5241, SN6771, sontochin, SN7266, chloroquine, SN8557, metachloridine, colchicine, and pentaquine. Of these only pamaquin and pentaquine are classed as curative inasmuch as in combination with quinine they can prevent relapse.Thick blood smears were examined daily during 45 to 60 days after exposure to infection and at least once weekly through the first; 18 months.Of the 198 subjects, 195 developed overt malaria. Of the 3 who failed to do so 2 were lost from. observation before delayed primary attacks were due. Four hundred and twenty-nine attacks of malaria were observed in these 195 persons; 135 attacks occurred within 2 months after mosquito bites, and 294 in a period of 6 to 14 months after bites.Seventy-eight subjects received no prophylactic drug; 75 of these developed patent malaria 11 to 20 days from initial exposure. The remaining 3 had primary attacks delayed to 298, 318 and 319 days after exposure; all these three men had had relatively small inocula.Of 120 men given protective medication, 41 had primary attacks in from 12: to 64 days after exposure: 76 had primary attacks delayed to from 193 to 350 days after exposure. Three never developed overt malaria [see above] The failure of drugs to prevent early primary attacks could be explained in all the 41 cases by the inadequacy of the regimen adopted.The duration of latency after treatment of early attacks bore no relation to the drug used provided that the treatment was capable of eradicating erythrocytic parasites. Of the 116 men given antiplasmodial therapy during early primary attacks, 10 were treated with pentaquine and quinine for 14 days: none of the ten developed late attacks. Only one adequately observed patient treated with a non-curative drug failed to develop a late attack; he was treated with quinacrine [mepacrine].The mean time of onset of the attack after mosquito bites was in 74 delayed primary attacks 287.1 days; in 79 relapses after early activity it was 275.6 days.Long-termlatency was not dependent upon the month or season during which infection occurred, sporozoite dosage, degree or duration of early patent parasitaemia, or the nature of early non-curative therapy. During long-term latency subinoculation was negative and homologous strain superinfection could be accomplished. During the period of late activity several acute attacks usually occurred, the intervals between them being greater when slowly eliminated drugs were used. The total duration of late activity was much longer in untreated than in treated cases. It is unlikely that the final termination of overt malaria in the treated subject is a result of acquired immunity to erythrocytic parasites.Norman White.