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African trypanosomiasis

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Human African trypanosomiasis - also called sleeping sickness - is a parasitic disease of people and animals, caused by the microscopic parasite Trypanosoma brucei and transmitted by the tsetse fly. The disease is endemic in some regions of sub-Saharan Africa, covering about 37 countries and 60 million people. It is estimated that 50,000 to 70,000 people are currently infected. In 2009 the amount of reported cases was below 10,000 the first time in 50 years.

Many cases go unreported and it is estimated that about 48,000 people died of it in 2008.Approximately 10 000 cases are reported to the World Health organisation every year In Recent history four major epidemics have occurred: one from 1896–1906 primarily in Uganda and the Congo Basin, two epidemics in 1920 and 1970 in several African countries, and a recent 2008 epidemic in Uganda.

African trypanosomiasis should be distinguished from Chagas disease which is transmitted by the triatomine bug found in the Americas.

The Tsetse fly

The word ‘tsetse’ comes from Tswana, a language of southern Africa, and, in that language, the word means fly. Tsetse flies are crudely similar to other large flies, such as the housefly, but can be distinguished by various characteristics of their anatomy, two of which are easy to observe. Tsetse flies fold their wings completely when they are resting so that one wing rests directly on top of the other over their abdomen. Tsetse’s also have a long proboscis, which extends directly forward and is attached by a distinct bulb to the bottom of their head. They are attracted to dark colors, especially blue and black and most tsetse flies are physically very tough. Houseflies are easily killed with a fly-swatter but it takes a great deal of effort to crush a tsetse fly.

Four characteristics definitively separate adult tsetse from other kinds of flies:

Proboscis

Tsetse have a distinct proboscis, a long thin structure attached to the bottom of the head and pointing forward.

Description: A photograph of the head of a tsetse illustrating the forward pointing proboscis.

Folded wings

When at rest, tsetse fold their wings completely one on top of the other.

Description: A photograph of the whole body of a tsetse illustrating the folded wings when at rest.

Hatchet cell

The discal medial ("middle") cell of the wing has a characteristic hatchet shape resembling a meat cleaver or a hatchet.

Description: A photograph of the wing of a tsetse illustrating the hatchet shaped central cell.

Branched arista hairs

The antennae have arista with hairs which are themselves branched.

Description: A photograph and diagram of the head of a tsetse illustrating the branched hairs of the antenna's arista.

Signs and symptoms

There are two forms of African sleeping sickness, caused by two different parasites:

  • Trypanosoma brucei gambiense , which causes a chronic infection lasting years and affecting countries of western and central Africa (Gambian trypanosomiasis)

  • Trypanosoma brucei rhodesiense , which causes acute illness lasting several weeks in countries of eastern and southern Africa (Rhodesian trypanosomiasis)

  • In Gambian trypanosomiasis , Trypanosoma brucei gambiense is transmitted by tsetse flies of the riverine bush, mainly in focal areas of West and Central Africa. Man is the only important reservoir for T.b. gambiense, which cause a chronic lesion often lasting more than a year.

    In Rhodesian trypanosomiasis, T.b rhodesiense is transmitted by tsetse flies of the woodland savanna of East Africa. Antelope, other game animals and domestic cattle are natural reservoirs of T.b rhodesiense. Incidental infection of man is an occupational hazard of game wardens, fisherman and cattle herders. T.b rhodesiense causes a disabling, acute, fulminant infection in man, killing the patient in 3 to 6 months.

    After the bite of an infected Tsetse fly, a firm, tender, reddened nodule may develop in a matter of a few days at the site of the bite.

    The ulcerated nodule, or "trypanosomal chancre", is accompanied by swollen and painful glands that lasts 1or 2 weeks. This is followed within 1 to 5 weeks by the onset of fever, sweating, general malaise and a generalized lymphadenitis often involving primarily the glands at the back of the neck. Also called the Winterbottom’s sign, 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.

    Frequently there are transient skin eruptions characterized by erythema or edema. These symptoms and signs may progress to the 2nd stage called the neurological phase. This phase begins when the parasite invades the central nervous system by passing through the blood-brain barrier.

    The term ‘sleeping sickness’ comes from the symptoms of the neurological phase. The symptoms include confusion, reduced coordination, and disruption of the sleep cycle, with bouts of fatigue punctuated with manic periods leading to daytime slumber and night-time insomnia. Without treatment, the disease is invariably fatal, with progressive mental deterioration leading to coma and death.

    Damage caused in the neurological phase is irreversible. Although there is much overlap between the clinical manifestation of T. brucei gambiense (West African sleeping disease) and T. brucei rhodesiense (East African sleeping disease) infections , the latter usually follows a much more acute course. Untreated persons with T. brucei rhodesiense infection frequently die within 3 to 6 months after onset of the disease.

    Only rarely does the victim survive long enough for the trypanosome to invade the central nervous system and produce lesions characteristic of the third stage of T. brucei gambiense infection. The neurologic symptoms and signs, when present are similar to those of gambian trypanosomiasis. Gambian trypanosomiasis is characteristically a chronic disease. When untreated, trypanosomiasis gives no respite from suffering and ultimately ends in death.

    In addition to the bite of the tsetse fly, the disease can be transmitted in the following ways:

  • Mother to child infection: the trypanosome can sometimes cross the placenta and infect the fetus.

  • Laboratories: accidental infections, for example, through the handling of blood of an infected person and organ transplantation, although this is uncommon.

  • Blood transfusion

  • Sexual contact (This may be possible)

  • Life cycle

    Life Cycle of Trypanosma brucei gambiense and Trypanosma brucei rhodesiense

    The tsetse fly (genus Glossina) is a large, brown biting fly that serves as both a host and vector for the Trypanosome parasites. A tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected animal or human host. In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply, leave the midgut, and transform into epimastigotes. The epimastigotes reach the fly’s salivary glands and continue multiplication..

    While taking blood from an animal or human host, an infected tsetse fly injects metacyclic trypomastigotes into skin tissue. From the bite, parasites first enter the lymphatic system and then pass into the bloodstream. Inside the host, they transform into bloodstream trypomastigotes, and are carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue to replicate.

    The entire life cycle in the fly takes approximately 3 weeks.

    Diagnosis

    The simplest diagnostic test is the demonstration of the trypanosomes in the circulating blood during a febrile episode by microscopic examination of the blood. Lymph node aspirations may also be useful for the identification of the parasite.

    Examination of the cerebrospinal fluid reveals trypanosomes as the disease progresses and may serve as an index of the course of the disease.

    Serological testing can be used as a screening diagnostic test. This includes identification of antibodies directed against the parasite.

    Treatment

    The key drugs used for therapy of African trypanosomiasis are

  • pentamidine, for chemoprophylaxis.

  • suramin, for the treatment of the early disease in which trypanosomes are found in the blood, lymph, and lymph nodes .

  • melarsoprol, for the later disease in which trypanosomes are located in the brain.

  • Control

    The most effective approach for controlling sleeping sickness has three parts:

    • Mobile medical surveillance of the population at risk by specialized staff using the most effective diagnostic tools (serology and parasitology) available. Patients are sent to specific referral centres for determination of the stage of the disease and treatment, and for post-therapeutic follow-up

    • Fixed post medical surveillance delivered at dispensaries, health centres or hospitals where blood samples are taken and analyzed at reference centres. All patients or suspected cases are sent to special centres for confirmation of diagnosis, determination of the stage of the disease and treatment, and for post-therapeutic follow-up

    • Vector (Glossina ) control using screens and traps: simple, cheap and ecologically acceptable methods.

    • Slaughter of wild animals (Removing the host of the parasite)

    • Land clearing (Removing the habitat of the fly)

    • Pesticide campaigns

    • Trapping

    • Releases of irradiated males

    History

    The earliest recorded account of sleeping sickness comes from upper Niger during the 14th century in the historical writings of Ibn Khaldoun, who wrote about the disease in his account of the history of North Africa . The next report came from Guinea in 1734 (Atkins, 1978).

    In 1803, the diseases that caused visible swollen lymph glands in West Africa came to be known as Winterbottom’s sign, after the description of the disease by Winterbottom. Such signs were readily recognized by slave traders who avoided trading and buying slaves who displayed those symptoms.

    The earliest detection of trypanosomes in human blood was in 1902, when R.M. Forde discovered what was then thought to be filiaria in the blood of a steamboat captain who had traveled extensively along the River Gambia. Similar discoveries of filiaria-like organisms in the blood were made by J.H. Cook in East Africa, but confusion arose as to how filiaria worms could cause such varying clinical symptoms. It was J.E. Dutton who, during a visit to Gambia, first correctly identified the parasite as a trypanosome and subsequently named it Trypanosoma gambiense . In 1902, A. Castellani observed the presence of trypanosomes in cerebrospinal fluid taken from a sleeping sickness patient, but it wasn’t until 1903 that D. Bruce correctly recognized that trypanosomes were the causative agents of sleeping sickness transmitted to humans by tsetse flies, and that "trypanosome fever" and "sleeping sickness" - both thought to be different diseases at the time - were in fact the same.

    Morphologically indistinguishable from the West African species as well as the animal infecting species Trypanosoma brucei brucei, Trypanosoma brucei rhodensiense was first discovered in Zambia by J.W.W. Stephens and H.B. Fantham in 1910. By 1926, T.b. rhodensiense could be found along the fly-belt between Tabora and Kigoma, Tanzania . The difficulties in identifying this virulent form of sleeping sickness lead to uncertainties today regarding the evolution and progression of T.b. rhodensiense through the continent, although it is generally agreed upon that it originated from the West African form.

    The earliest recorded major epidemics of sleeping sickness took place in Uganda and Congo between 1896 and 1908, where roughly 500,000 people were estimated to have died in the Congo Basin, and approximately 300,000 died in Busoga, Uganda .

    Dr. Swart has been involved in Communicable disease control since 2004 and is an authority on Malaria, tropical and infectious diseases in Africa.

    With the Rift Valley transecting the country, Uganda is in the precarious position of having foci of both forms of diseases which resulted in two other major epidemics of sleeping sickness - one in the late 1940’s and another in 1980. Throughout West Africa, smaller epidemics of sleeping sickness rapidly spread from Senegal to Cameroon during the 1920’s, and died down by the late 1940’s.


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