Treatment and follow-up of the first case of human trypanosomiasis caused by Trypanosoma evansi in India

Joshi, Prashant; Chaudhari, Amol; Shegokar, Vijay R.; Powar, R. M.; Dani, VS; Somalwar, Ashutosh M; Jannin, J.; Truc, Philippe

doi:10.1016/j.trstmh.2005.11.003

Cited by 27 publications

(13 citation statements)

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“…Microscopical examination of blood smears showed high numbers of parasites confirmed as T. evansi by molecular techniques [23]. Additional examinations did not show central nervous system invasion by the parasites and the patient was successfully treated with suramin [24].…”

Section: Methodsmentioning

confidence: 96%

Atypical Human Infections by Animal Trypanosomes

et al. 2013

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The two classical forms of human trypanosomoses are sleeping sickness due to Trypanosoma brucei gambiense or T. brucei rhodesiense, and Chagas disease due to T. cruzi. However, a number of atypical human infections caused by other T. species (or sub-species) have been reported, namely due to T. brucei brucei, T. vivax, T. congolense, T. evansi, T. lewisi, and T. lewisi-like. These cases are reviewed here. Some infections were transient in nature, while others required treatments that were successful in most cases, although two cases were fatal. A recent case of infection due to T. evansi was related to a lack of apolipoprotein L-I, but T. lewisi infections were not related to immunosuppression or specific human genetic profiles. Out of 19 patients, eight were confirmed between 1974 and 2010, thanks to improved molecular techniques. However, the number of cases of atypical human trypanosomoses might be underestimated. Thus, improvement, evaluation of new diagnostic tests, and field investigations are required for detection and confirmation of these atypical cases.

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Section: Methodsmentioning

confidence: 96%

Atypical Human Infections by Animal Trypanosomes

et al. 2013

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“…635 The APOL1-deficient patient was treated successfully with suramin with complete cure. 636 Selective NK cell defects. Summary statement 191.…”

Section: Defects Of Innate Immunitymentioning

confidence: 99%

Practice parameter for the diagnosis and management of primary immunodeficiency

Bernstein¹,

Blessing-Moore²,

Khan³

et al. 2015

Journal of Allergy and Clinical Immunology

587

494

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The American Academy of Allergy, Asthma & Immunology (AAAAI) and the American College of Allergy, Asthma & Immunology (ACAAI) have jointly accepted responsibility for establishing the "Practice parameter for the diagnosis and management of primary immunodeficiency." This is a complete and comprehensive document at the current time. The medical environment is a changing environment, and not all recommendations will be appropriate for all patients. Because this document incorporated the efforts of many participants, no single individual, including those who served on the Joint Task Force, is authorized to provide an official AAAAI or ACAAI interpretation of these practice parameters. Any request for information about or an interpretation of these practice parameters by the AAAAI or ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma & Immunology. These parameters are not designed for use by pharmaceutical companies in drug promotion.

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“…Human serum devoid of Hp and Hpr [Hp(r) Ϫ/Ϫ HS] originates from anhaptoglobinemic patients lacking both Hpr and Hp as a result of homozygous gene deletion (Ϸ20 kb) from the Hp promoter region to exon 5 of Hpr (17). Human serum devoid of ApoL-I (apoL-I Ϫ/Ϫ HS) originated from an Indian patient found to be infected with trypanosomes closely related to T. b. brucei (Trypanosoma evansi) (18,19). The absence of apoL-I resulted from two independent frameshift mutations in the apoL-I alleles (20).…”

mentioning

confidence: 99%