Sleeping Sickness: Human African Trypanosomiasis

One can wonder how a protozoan (Trypanosoma) of size, not more than 30 micrometres can notoriously wreck up your central nervous system and push you towards death in not less than a few months. What makes it deadly that the symptoms are asymptomatic. The parasite has the power to sing you to your last sleep. Hence popularly known as sleeping sickness. 


The two main protozoans which are responsible for sleeping sickness are:-

Trypanosoma brucei rhodesiense(TBR) and Trypanosoma brucei gambiense(TBG). The latter is responsible for being more virulent. It accounts for more than 98% of the infected cases. Humans are the main reservoir for transmission of Trypanosoma brucei gambiense. Whereas Trypanosoma brucei rhodesiense  is mainly zoonotic with rarely causing any infection of human. The main vector for this contagious disease is Tse-Tse fly. Let’s get a detailed introduction to these parasites:

Trypanosoma Bruceli 

Geographical Distribution

Both the parasites have divided their reign of terror. While Trypanosoma brucei gambiense(TBG) has taken up the land in the west and central Africa, Trypanosoma brucei rhodesiense(TBR) causes disease has limited geographical access only to east and southern Africa. The third type of species is also responsible for affecting but only in animals not in humans. 

Trypanosoma brucei gambiense keeps it’s symptoms latent for a phase of a month or even years before the infection spreads and ultimately results in death. 

Trypanosoma brucei rhodesiense is the acute form of the disease and death can occur within months since the symptoms emerge within weeks. It is believed to be more virulent and faster development than Trypanosoma brucei gambiense.  


Trypanosomas have a protective covering  which is composed of variant surface glycoprotein(VSG). This glycoprotein prevents the trypanosomas from any lytics factors which are present in human plasma. The host’s immune system can recognize the glycoproteins present on the coat and produces antibodies in response (IgM and IgG). These antibodies then try to act and destroy the parasite  but it experiences changes in their coating and results in new VSGs. Now the antibodies which were produced in response  to the parasites will no longer be able to recognize the mutated glycoprotein cover. This results in the rise of infection. Moreover the glycoprotein cover keeps on changing. 


The tse-tse fly (both male and female fly can transmit) (genus Glossina) serves as both host and vector for Trypanosomas parasites. 


The parasites produces a chemical compound which is induces sleep in human. The compound is Tryptophol. 

Life Cycle

Life cycle of protozoans responsible for sleeping sickness.
Life cycle

A tse-tse fly which is carrying the parasite injects metacyclic trypomastigotes into skin tissue. After entering into the body the parasites first goes to the lymphatic system  and then into the    bloodstream. The parasites then move to other body fluids like lymph, spinal fluids and continue to replicate by Binary Fission. 

 One of the reasons why T. brucei acts so fast on CNS is that it can cross the blood brain barrier. 

Symptoms of Sleeping Sickness

 It is hard to differentiate the symptoms because these are similar to that of common cold. There are signs of headaches,  fever, weakness, pain in the joints. Other symptoms includes lymphadenopathy and stiffness.  

It has also been observed that people who are affected may not show signs of illness at all. But over time the parasite attacks central nervous system by crossing the blood brain barrier. Certain  neurological changes are observed in the body which includes the sleep disorder (hence named “sleeping sickness”) , deep sensory disturbances, abnormal tone and mobility, ataxia, psychiatric disorders, seizures, coma and ultimately death. 

Diagnosis of Sleeping Sickness

Diagnosis of the stage of the disease is necessary step to complete a diagnosis of HAT and is vital for appropriate treatment.HAT progresses in two stages. Diagnosis is the confirmation of presence of a particular parasite inside the blood and lymph. Early diagnosis is quite difficult because lack of specific signs. Moreover Trypanosoma brucei gambiense remains latent inside the  body . 

Initially in both the cases Trypanosomes disseminate and proliferate in lymph, blood and other tissues. The first stage is haemo-lymphatic period, the second stage is meningoencephalitic stage. During the second stage the trypanosomes crosses blood brain barrier and enter into central nervous system. Progression into the second stage occurs after a mean days of 300-500 in gambiense HAT while in rhodesiense HAT brain invasion is estimated to take place  after 3 to 2 weeks of invasion. 

The disease is finally confirmed by examination of Cerebrospinal fluid(CSF).Lumbar puncture for staging is usually performed immediately after strong serological suspicion. In case of T.b. rhodesiense infection staging is performed after a dose of suramin has been administered, as it is considered that blood parasitaemia should be cleared before a lumbar puncture in order to avoid the risk for introducing the parasite into CSF in case of traumatic lumbar puncture. 


Sleeping Sickness is notoriously difficult to treat due to its toxicity and it’s high resistance to the administered drugs. Only four drugs are administered in the case of human trypanosomiasis: pentamidine, suramin, melarsoprol and eflornithine.

There’s no test for confirming the cure of trypanosomiasis. After administration of drugs patients should be closely monitored for 24 months. Recurrence of symptoms will require examination of body fluids including CSF.


Since there is no such perfect cure for sleeping sickness, preventive measures are aimed at minimizing contact with tse-tse fly. Local residents in endemic countries shoud be fully aware and use repellent preventive against the flies.