Neurologic Infections in Travelers

Malveeka Sharma, MD, MPH; Joseph R. Zunt, MD, MPH


Semin Neurol. 2019;39(3):399-414. 

In This Article

African Trypanosomiasis (Sleeping Sickness)


Human African Trypanosomiasis (HAT) threatens millions of people in sub-Saharan Africa and has been linked to multiple epidemics over the past century.[8,9] Due to ongoing control efforts, the number of reported cases has dropped from 40,000 in 1998 to below 3,000 in 2015.[8] The estimated population potentially exposed to HAT is 65 million people.

Life Cycle, Ecology, Species

There are two subspecies of Trypanosoma brucei that cause human disease: T. brucei gambiense (West African or Gambian) and T. brucei rhodesiense (East African or Rhodesian). The tsetse fly is the vector for both Trypanosoma spp. and is unique to Africa. The tsetse fly transmits the parasite via bite. About 5 to 15 days after the bite, a superficial chancre develops. The parasite then migrates through the blood, lymph nodes, and other organs and can cross the blood–brain barrier.[9] Of note, the trypanosome has a remarkable ability to undergo antigenic variation that allows it to evade the host immune system.[5]

Clinical Manifestations

During acute infection or early stage of HAT, rash, intermittent fever, and lymphadenopathy are common. Late stages of disease are associated with several symptoms. The hallmark and namesake of this disease is the development of sleep abnormalities consisting of reversal of the normal sleep/wake cycle. Other neurologic manifestations include weakness, gait disturbance, tremor, abnormal movements, and speech disturbances. Death often results from coma or secondary infection caused by severe neurological damage, and most often occurs within a few weeks during T.b. rhodesiense infection, but may be delayed several months or even years with T.b. gambiense infection. Trypanosomal invasion of the heart can lead to fatal arrhythmias and is also a common cause of death.[5,9]


Clinical suspicion for HAT and a history of living or traveling to endemic regions should be present in the history. During the acute infection, the parasite can be identified within the chancre or bite site. Definitive diagnosis can be made by identifying trypanosomes in centrifuged CSF, blood, or biopsied tissue.[5] The WHO criteria for diagnosis include the presence of trypanosomes in the CSF, or a white blood cell (WBC) count in the CSF of >5/μL, although these diagnostic criteria are not well accepted.[8,9] The card agglutination test for trypanosomiasis (CATT) has been used widely, but has limitations, such as frequent equivocal findings. The polymerase chain reaction (PCR) of blood has 99% specificity and 97% sensitivity; however, access to this test in endemic regions is severely limited. No specific or pathognomonic findings have been described for diagnosis of HAT.[9]


If there is no CNS involvement, recommended treatment includes suramin and pentamidine isethionate. When CNS involvement is suspected, melarsoprol can be prescribed and is effective against both T.b. gambiense and T.b. rhodesiense. However, there is a severe side-effect profile and growing level of resistance. Eflornithine in combination with nifurtimox was introduced in 2009 and is effective against only T.b. gambiense.[8] Prevention has been largely based on surveillance programs to improve case reporting and treatment, as well as vector control and improved diagnostic techniques.[8]