With T. b. rhodesiense, symptoms are seen within 1-3 weeks of the infective bite and the symptoms include high fever, chancre at the site of penetration, skin rash, headache, thrombocytopenia, myalgia and on rare occasions, splenomegaly, cardiac dysfunction and renal failure may be seen [9].

T.b gambiense does not have a specific presentation but weight loss, lymphadenopathy, pruritus, facial edema, myalgia, malaise, headache and fever may be recorded. The CNS gets involved after months to years of infection and this is characterized by severe headaches, somnolence, range of neurologic manifestations, mood disorders, behavior change, focal deficits, endocrine disorders etc. The clinical course of disease caused by T. b gambiense is less severe than T. b rhodesiense but if left untreated, they can be very fatal.

Although general laboratory studies may be helpful in the diagnosis of African trypanosomiasis (sleeping sickness), a definitive diagnosis of T brucei infection requires actual detection of trypanosomes in blood, lymph nodes, cerebrospinal fluid (CSF), skin chancre aspirates, or bone marrow. In areas where diagnostic studies are not readily available, however, symptomatic improvement after empiric treatment is the usual confirmatory test. Buffy-coat preparations concentrate the parasite [9].

Prehospital care of African trypanosomiasis (sleeping sickness) centers on management of the acute symptoms of fever and malaise in conjunction with close monitoring of the patient’s neurologic status. In the emergency department, if central nervous system (CNS) symptoms are severe, airway management to prevent aspiration becomes important, along with an immediate blood smear, complete blood count (CBC), and lumbar puncture for trypanosome detection [10].

Patients of stage 1 trypanosomiasis recover fully after treatment. In stage 2 trypanosomiasis however, the manifestations in the CNS ultimately become fatal if left untreated. With drugs that work inside the CNS like melasorprol, the cure rate is more than 95% [8].

In humans, there are two subspecies that are responsible for the initiation of the disease. In west and central Africa, the disease is caused by Trypanosoma brucei gambiense [5]. Trypanosoma brucei rhodesiense has a limited geographical range and it is responsible for causing the disease in east and southern Africa. Additionally, Trypanosoma brucei brucei is responsible affecting animals bit it doesn’t affect humans.

In the United States, all cases of African trypanosomiasis is imported from Africa by travellers who go to areas that have been designated as endemic. Infections amongst travellers however, is around 1 case per year, with some years not getting any records. Most of the infections are of T brucei rhodesiense and these are acquired in game parks in Eastern Africa.

Internationally, this disease is confined to tropical Africa covering the north of South Africa to south of Algeria, Libya and Egypt. Outside this area, the prevalence of African Trypanosomiasis varies by country and region [4]. Major outbreaks occurred in Angola, DR Congo and Sudan in 2005. African trypanosomiasis remains a challenge in the Central African Republic, Chad, Congo, Cote d’Ivoire, Tanzania, Uganda, Malawi and Guinea.

In Zimbabwe, Zambia, Rwanda, Nigeria, Mozambique, Kenya, Gabon, Equatorial Guinea, Cameroon and Burkina Faso, less than 50 cases are reported each year. The transmission of T.Brucei seems to have stopped in Togo, Swaziland, Sierra Leone, Senegal, Niger, Namibia, Mali, Liberia, Guinea Bissau, Ghana, Gambia, Ethiopia, Burundi, Bostwana and Benin as no new case has been reported for decades now.

The African Trypanosomiasis condition is a threat to millions of people in 36 countries in sub Saharan Africa. The situation is difficult to assess presently because of the lack of diagnostic expertise and surveillance in these locations.

The parasites, trypanosomes are parasites known for a 2-host life cycle namely mammalian and arthropod. The life cycle begins when the trypanosome is ingested during the course of a blood meal from either an animal reservoir (East African trypanosomiasis) or a human reservoir (West African trypanosomiasis). The parasites multiply over a 2-3 week period in the mid gut of the fly from where they move to its salivary gland, developing into an epimastigote [6].

Humans get infected with T brucei following the bite of a fly. Occasionally this causes a skin chancre at the site of penetration. The injected parasites mature further and divide in the blood and lymphatic system causing malaise, intermittent fever, rash and wasting. Over time, the parasites spread into the Central Nervous System where behavioral and neurologic changes like encephalitis and coma. In extreme cases, death may occur.

The parasites escape the initial host defense mechanisms through extensive antigenic variation of parasite surface glycoproteins (major variant surface glycoprotein [VSG]). This evasion of humoral immune responses contributes to virulence. During the parasitemia, most pathologic changes occur in the hematologic, lymphatic, cardiac, and central nervous systems. This may be the result of immune-mediated reactions against antigens on red blood cells, cardiac tissue, and brain tissue, resulting in hemolysis, anemia, pancarditis, and meningoencephalitis [7].

Skin problems like persistent urticaria, puritus and facial edema are caused by hypersensitivity reaction. Infested lymph nodes and increased lymphocyte levels in the spleen lead to fibrosis but it rarely every gets to splenomegaly. When the monocytes, macrophages and plasma cells get into the blood vessels increased vascular permeability and endarteritis occur.

No vaccine is available for African trypanosomiasis. Chemoprophylaxis is unavailable.

Avoidance of travel to areas heavily infested with tsetse flies is recommended. Tsetse flies are attracted to moving vehicles and dark contrasting colors. They are not affected by insect repellants and can bite through lightweight clothing. At-risk travelers are advised to wear wrist- and ankle- length clothing that is made of medium-weight fabric in neutral colors.

More commonly known as sleeping sickness, African Trypanosomiasis is an ailment that is endemic in sub-Saharan Africa [1]. It is caused by Trypanosoma brucei, a flagellate protozoan that exists in two morphologically identical subspecies namely: T brucei gambiense (West African or Gambian African trypanosomiasis) and T brucei rhodesiense (East African or Rhodesian African trypanosomiasis).

Both parasites are passed on to human hosts via the bite of already infected tsetse flies. Glossina palpalis transmits T brucei gambiense and Glossina Morsitans transmits T brucei rhodesiense. Both are only found in Africa.

For West African trypanosomiasis, humans are the exclusive reservoir of infection. With East African trypanosomiasis on the other hand, there is a zoonotic infection with animal vectors. African trypanosomiasis must not be confused with American trypanosomiasis. The latter is caused by Trypanosoma Cruzi and has different vectors, clinical manifestations as well as therapies.
The main factor that is epidemiologic in African trypanosomiasis is the contact between humans and tsetse flies [2].

The interaction is further influenced by increase in tse tse fly density, feeding habits that have continued to change, continued expansion into tsetse fly infested by humans, and increasing number of immunologically naïve individuals in areas that were formally endemic. The major outbreak between 1920 and 1950 brought about extensive treatment and immunity for 50 years. Infection is now recurring though meaning that the same populatison are losing their immunity [3].

Following recovery from stage-2 disease, a lumbar puncture is required every 3 months for the first year in patients with East African disease and every 6 months for 2 years in patients with West African disease.

Relapse has occurred if symptoms return, CSF pleocytosis appears, or if trypanosomes are still present in blood or CSF. A persistently elevated CSF white cell count can be found in recovering patients, so a change in white cell count is more helpful as an indicator of relapse.

If relapse occurs, treatment with melarsoprol or eflornithine should be repeated.

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