Human Trypanosoma evansi Infection Linked to a Lack of Apolipoprotein L-I

The first case of Trypanosoma evansi infection in a human was recently identified in India. This report shows that infection was due to a host rather than a parasite factor. Specifically, the serum of the patient was devoid of trypanolytic activity because of frameshift mutations in both apolipoprotein L-I alleles. The first case of Trypanosoma evansi infection in a human was recently identified in India. This report shows that infection was due to a host rather than a parasite factor. Trypanosoma evansi is a widely distributed hemoflagellate parasite that affects domesticated mammals (e.g., horses, cattle, camels, and water buffalo). Since its adaptation to mechanical transmission by blood-sucking insects (tabanids), the parasite has spread beyond its original distribution in sub-Saharan Africa and is now also present in South America, North Africa, and large parts of Asia, including India. Normally, humans are resistant to infection with T. evansi, as well as to infection with the related African trypanosomes, the prototype of which is T. brucei brucei . 1 – 3 Human innate immunity against T. brucei brucei is due to the trypanolytic activity of . . .