Human African trypanosomiasis (HAT) or sleeping sickness is a severe vector-borne disease, with marked involvement of the peripheral and central nervous system. Still endemic in sub-Saharan Africa, HAT is caused by transmission of subspecies of the protozoan parasites Trypanosoma brucei (T. b.) through bites of tsetse flies (genus Glossina). Foci of HAT are reported mostly in remote, resource-poor settings, and areas of political instability. The disease has a chronic form caused by T. b. gambiense in Western and Central Africa, and an acute form caused by T. b. rhodesiense in Eastern and Southern Africa. Both forms, almost invariably fatal without treatment, evolve from a first, hemolymphatic stage to a second, meningoencephalitic stage due to T. b. brain invasion. Clinical features involve a constellation of sensory, motor and neuropsychiatric signs and symptoms, with a characteristic sleep disorder leading to sleep-wake cycle disorganization and sleep structure alterations. Therapy currently available to cure the second stage of both HAT forms is toxic. Stage biomarkers and safer therapy are urgently needed. Clinical objective evaluation is essential for diagnostic purposes, treatment assessment and patients’ follow-up. The recent decline in the number of reported new HAT cases should not foster further neglect of this highly neglected nervous system infection.

Human African Trypanosomiasis: a highly neglected neurological disease

BENTIVOGLIO FALES, Marina
2014-01-01

Abstract

Human African trypanosomiasis (HAT) or sleeping sickness is a severe vector-borne disease, with marked involvement of the peripheral and central nervous system. Still endemic in sub-Saharan Africa, HAT is caused by transmission of subspecies of the protozoan parasites Trypanosoma brucei (T. b.) through bites of tsetse flies (genus Glossina). Foci of HAT are reported mostly in remote, resource-poor settings, and areas of political instability. The disease has a chronic form caused by T. b. gambiense in Western and Central Africa, and an acute form caused by T. b. rhodesiense in Eastern and Southern Africa. Both forms, almost invariably fatal without treatment, evolve from a first, hemolymphatic stage to a second, meningoencephalitic stage due to T. b. brain invasion. Clinical features involve a constellation of sensory, motor and neuropsychiatric signs and symptoms, with a characteristic sleep disorder leading to sleep-wake cycle disorganization and sleep structure alterations. Therapy currently available to cure the second stage of both HAT forms is toxic. Stage biomarkers and safer therapy are urgently needed. Clinical objective evaluation is essential for diagnostic purposes, treatment assessment and patients’ follow-up. The recent decline in the number of reported new HAT cases should not foster further neglect of this highly neglected nervous system infection.
2014
9781461480990
sleeping sickness; Trypanosoma brucei; parasitic brain infection; sensory disorders; neuroinflammation; sleep; pain; behavioral disorders
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/756763
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