Human African Trypanosomiasis (HAT) found only in sub-Saharan Africa is caused by the parasite Trypanosoma brucei, which is transmitted by tsetse flies. Only two sub-species of T. brucei are pathogenic for humans: T. b. gambiense and T. b. rhodesiense. HAT is endemic in 36 sub-Saharan countries, and 98% of all reported HAT cases are due to T. b. gambiense. Fifty-five million persons in Africa are at risk of HAT. The number of HAT cases reported globally decreased fivefold in the last decade, which encouraged WHO to set a target to eliminate HAT as a public health problem by the year 2020, aiming for zero transmission by the year 2030. Tsetse flies do not lay eggs, but the female fly deposits a single mature larva in humid soil. The larva pupates and emerges as an adult fly 20 to 80 days later. A female fly produces only 3–5 larvae during her lifetime that typically lasts for 3 months making the intrinsic growth rate of tsetse populations rather low. An infected tsetse fly injects the infective form of the parasites into the mammalian host when it feeds. These parasites undergo, and can switch, their antigenic variation of their variant surface glycoprotein (VSG) coat, allowing them to escape the host immune response. This phenomenon of antigenic variation makes the development of an effective vaccine unlikely. The disease affects mainly the lymphoid system, heart, lungs, and brain, manifesting as intermittent fever, general malaise, severe headache, joint pains and muscle aches, pruritus, urticaria, or facial oedema. Lymphadenopathy is common with the classical Winterbottom’s sign. Patients with the meningo-encephalitic stage suffer continuous headaches with poor response to painkillers and show more specific neurological signs of the rather typical sleep disturbances. Diagnosis of HAT is a three-step procedure: (1) screening test to identify HAT suspects, (2) confirmatory parasitological tests, and (3) staging. Treatment is based on the stage of illness, with current options being pentamidine, suramin, melarsoprol, eflornithine, fexinidazole, and the nifurtimox-eflornithine combination therapy (NECT). Two strategies are used for the reduction or interruption of HAT transmission: elimination of the parasite reservoir and vector control. This last decade has seen several breakthroughs in clinical R&D for HAT, bringing new diagnostics and drugs to patient care, but the effective and efficient implementation of these new tools in HAT control and proper treatment of patients will require further research.
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BT - Neglected Tropical Diseases - Sub-Saharan Africa DO - 10.1007/978-3-031-53901-5_4 LA - ENG M3 - Book N2 -Human African Trypanosomiasis (HAT) found only in sub-Saharan Africa is caused by the parasite Trypanosoma brucei, which is transmitted by tsetse flies. Only two sub-species of T. brucei are pathogenic for humans: T. b. gambiense and T. b. rhodesiense. HAT is endemic in 36 sub-Saharan countries, and 98% of all reported HAT cases are due to T. b. gambiense. Fifty-five million persons in Africa are at risk of HAT. The number of HAT cases reported globally decreased fivefold in the last decade, which encouraged WHO to set a target to eliminate HAT as a public health problem by the year 2020, aiming for zero transmission by the year 2030. Tsetse flies do not lay eggs, but the female fly deposits a single mature larva in humid soil. The larva pupates and emerges as an adult fly 20 to 80 days later. A female fly produces only 3–5 larvae during her lifetime that typically lasts for 3 months making the intrinsic growth rate of tsetse populations rather low. An infected tsetse fly injects the infective form of the parasites into the mammalian host when it feeds. These parasites undergo, and can switch, their antigenic variation of their variant surface glycoprotein (VSG) coat, allowing them to escape the host immune response. This phenomenon of antigenic variation makes the development of an effective vaccine unlikely. The disease affects mainly the lymphoid system, heart, lungs, and brain, manifesting as intermittent fever, general malaise, severe headache, joint pains and muscle aches, pruritus, urticaria, or facial oedema. Lymphadenopathy is common with the classical Winterbottom’s sign. Patients with the meningo-encephalitic stage suffer continuous headaches with poor response to painkillers and show more specific neurological signs of the rather typical sleep disturbances. Diagnosis of HAT is a three-step procedure: (1) screening test to identify HAT suspects, (2) confirmatory parasitological tests, and (3) staging. Treatment is based on the stage of illness, with current options being pentamidine, suramin, melarsoprol, eflornithine, fexinidazole, and the nifurtimox-eflornithine combination therapy (NECT). Two strategies are used for the reduction or interruption of HAT transmission: elimination of the parasite reservoir and vector control. This last decade has seen several breakthroughs in clinical R&D for HAT, bringing new diagnostics and drugs to patient care, but the effective and efficient implementation of these new tools in HAT control and proper treatment of patients will require further research.
This is a preview of subsc
PB - Springer International Publishing PY - 2024 SN - 9783031539008/2194-8275, 2194-8283 SP - 73 EP - 97 T2 - Neglected Tropical Diseases - Sub-Saharan Africa TI - Human African Trypanosomiasis (HAT) ER -