By Jereaghogho Efeturi Ukusare
Sleeping sickness also known as African trypanosomiasis is an insect-borne parasitic disease of humans and other animals. It is caused by the protozoa of the species called Trypanosoma brucei. There are two known types that infect humans, Trypanosoma brucei gambiense (TbG) and Trypanosoma brucei rhodesiense (TbR). TbG is responsible for over 98% of cases that have been reported.
The tsetse fly (genus Glossina) a large, brown, biting fly is both a host and vector for the trypanosome parasites. While taking blood from a mammalian host, an infected tsetse fly injects metacyclic trypomastigotes into the skin tissue. Parasites first enter the lymphatic system and then pass into the bloodstream. In the mammalian host, they transform into bloodstream trypomastigotes and conveyed to other sites throughout the body, reaching other body fluids — lymph, spinal fluid – and continuously replicates by binary fission. Rural areas are prone to this insect bite and reports on this mostly come from these areas.
The disease can also be transmitted by:
Mother-to-child infection: the trypanosome can sometimes cross the placenta and infect the foetus.
Accidental infections: through the handling of blood of an infected person in a laboratory and organ transplant; however, this is rare. Blood transfusion and Sex are possible ways the disease is transmitted. Horse-flies (Tabanidae ) and stable flies (Muscidae ) possibly play a role in transmission of nagana (the animal form of sleeping sickness) and the human disease form.
African trypanosomiasis symptoms occur in two stages. The first stage, known as the hemolymphatic phase, is characterized by fever, headaches, joint pains, and itching. Fever is intermittent, with attacks lasting from a day to a week, separated by intervals of a few days to a month or longer. Invasion of the circulatory and lymphatic systems by the parasites is associated with severe swelling of lymph nodes, often to tremendous sizes. Winterbottom’s sign, the tell-tale swollen lymph nodes along the back of the neck, may appear. Occasionally, a chancre (red sore) will develop at the location of the tsetse fly bite. If left untreated, the disease overcomes the host’s defenses and can cause more extensive damage, broadening symptoms to include anemia, endocrine, cardiac and kidney dysfunctions.
The second phase of the disease, which is the neurological phase, begins with the parasite invading the central nervous system by passing through the blood–brain barrier. Disruption of the sleep cycle is a leading symptom of this stage and is the one that gave the disease the name ‘sleeping sickness.’ Infected individuals experience a disorganized and fragmented 24-hour rhythm of the sleep-wake cycle, resulting in daytime sleep episodes and night time periods of being awake.
Other neurological symptoms include: confusion , tremor, general muscle weakness, hemiparesis , and paralysis of a limb. Parkinson -like movements might arise due to non-specific movement disorders and speech disorders. The individual may also exhibit psychiatric symptoms such as irritability, psychotic reactions, aggressive behaviour or apathy which can sometimes dominate the clinical diagnosis.
Without the administration of any treatment, the disease is invariably fatal. This manifests with progressive mental deterioration leading to coma, systemic organ failure and finally death. An untreated infection with T. b. rhodesiense will cause death within months whereas an untreated infection with T. b. gambiense will cause death after several years. Damage caused in the neurological phase is irreversible.
The standard for diagnosis is identification of trypanosomes in a patient sample by microscopic examination. Patient’s samples that can be used for diagnosis include chancre fluid, lymph node aspirates, blood, bone marrow and during the neurological stage, cerebrospinal fluid. Detection of trypanosome-specific antibodies can be used for diagnosis, but the sensitivity and specificity of these methods are too variable to be used alone for clinical diagnosis.
Trypanosomes can be detected from patient’s samples using two different preparations. A wet preparation can be used to look for the motile trypanosomes. Alternatively, a fixed (dried) smear can be stained using the Giemsa ‘s or Field ‘s technique and examined under a microscope. Often, the parasite is in relatively low abundance in the sample. Hence, techniques to concentrate the parasites should be used prior to microscopic examination. For blood samples, these include centrifugation followed by examination of the buffy coat; mini anion-exchange/centrifugation; and the quantitative buffy coat (QBC) technique. For other samples, such as spinal fluid, concentration techniques include centrifugation followed by examination of the sediment.
At the moment, there are few medically related prevention options for African Trypanosomiasis. That is, there exists no vaccine for immunity. Although the risk of infection from a tsetse fly bite is extremely low, the use of insect repellants, wearing long-sleeved clothing, avoiding tsetse-dense areas, implementing bush clearance methods and wild game culling are the best options to avoid infection available for local residents of affected areas.
During the 36th summit of the Organization for African Unity in Lome, Togo, in July 2000, a resolution was passed to form the Pan African Tsetse and Trypanosomiasis Eradication Campaign (PATTEC). The campaign works to eradicate the tsetse vector population levels and subsequently the protozoan disease by use of insecticide-impregnated targets, fly traps, insecticide-treated cattle, ultra-low dose aerial/ground spraying (SAT) of tsetse resting sites and the sterile insect technique (SIT). The use of SIT in Zanzibar proved effective in eliminating the entire population of tsetse flies but was expensive and is relatively impractical to use in many of the endemic countries afflicted with African trypanosomiasis.
Very frequent active surveillance which includes detecting and prompt treatment of new cases and tsetse fly control is the thrust of the strategy used to control sleeping sickness. Systematic screening of communities is the best approach to tackling this disease.
Intravenous or intramuscular pentamidine for T. b. gambiense or intravenous suramin for T. b. rhodesiense is employed in treating the first stage of this disease.
For the second stage of T. b. gambiense a regiment involving the combination of nifurtimox and eflornithine, nifurtimox-eflornithine combination treatment (NECT), or eflornithine alone is apparently more effective and results in fewer side effects. These treatments may replace melarsoprol when available with the combination being first line. NECT has the benefit of requiring less injections of eflornithine. Intravenous melarsoprol was previously the standard treatment for second stage which is the neurological phase of the disease and is effective for both types. Melarsoprol is the only treatment for second stage T. b. rhodesiense. There are cases of resistance to this treatment. Sadly, it causes death in 5% of patients who take it.
The disease has occurred in 37 countries in sub-Saharan Africa. It occurs regularly in southeast Uganda and western Kenya. It is recorded to have killed more than 48,000 Africans in 2008 alone. The Democratic Republic of the Congo is the worst hit country in the world accounting for 75% of the Trypanosoma brucei gambiense cases.
African governments should step up their efforts at surveillance as this is the key to success in the fight against this disease.