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
African trypanosomiasis should be distinguished from
Chagas disease which is transmitted by the triatomine bug found in
The Tsetse fly
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:
have a distinct proboscis, a long thin structure
attached to the bottom of the head and pointing forward.
rest, tsetse fold their wings completely one on
top of the other.
discal medial ("middle") cell of the wing has a
characteristic hatchet shape resembling a meat
cleaver or a hatchet.
Branched arista hairs
antennae have arista with hairs which are themselves
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
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
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
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 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.
Sexual contact (This may be possible)
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
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.
The key drugs used for therapy of African
pentamidine, for chemoprophylaxis.
suramin, for the treatment of the early disease
in which trypanosomes are found in the blood, lymph, and lymph
melarsoprol, for the later disease in which
trypanosomes are located in the brain.
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
Land clearing (Removing the habitat of the fly)
Releases of irradiated males
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.
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 .
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.