Blood protozoa of major clinical significance
include members of genera Trypanosoma (T.
brucei and T. cruzi); Leishmania (L. donovani, L.
tropica); Plasmodium (P. falciparum, P. ovale, P.
malariae and P. vivax); and Toxoplasma gondii.
Although the symptoms of African sleeping sickness were documented
by Atkins in 1742, the association of the clinical syndrome with its
etiological agent, the trypanosome, was not documented until 1902 by
Forde. In The Journal of Tropical Medicine, Forde chronicles his
treatment of a 42 year-old European male colonialist who presented to
his practice in the Gambia Colony in May 1901.
The patient
complained of fever and malaise, leading Forde to make a preliminary
diagnosis of malaria. He initiated anti-malarial quinine treatment, but
days later the patient’s conditioned had yet to improve.
Slides of the patient’s blood were prepared. This
examination ruled-out malaria due to a lack of
malarial parasites found in the blood. Only later,
Dutton, a second physician from the Liverpool
School
of
identification
Tropical
of
patient’s blood.
Medicine,
Trypanasoma
made
brucei
in
the
the
Trypanosomiasis or trypanosomosis is the name of
several diseases in vertebrates caused by
parasitic protozoan trypanosomes. More than 66
million women, men, and children in 36 countries
of sub-Saharan Africa suffer from human African
trypanosomiasis. The other human form of
trypanosomiasis, called Chagas disease, causes
21,000 deaths per year mainly in Latin America.
 The
Tsetse fly
Two examples of tsetse fly habitat from
West Africa (A) and East Africa (B).

The distribution of African trypanosomiasis is completely linked to the
range of its vector, the tsetse fly.

According to the World Health Organization, countries where the
disease is currently epidemic include Angola, Democratic Republic of
the Congo, Uganda & Sudan.

Countries with high levels endemicity of
including Cameroon, Congo, Cote d’Ivoire, Central African
Republic, Guinea, Mozambique, Tanzania, & Chad.

African sleeping sickness can also be found in low endemic levels
in Benin, Burkina-Faso, Gabon, Ghana, Equatorial
Guinea, Kenya, Mali, Nigeria, Togo, & Zambia.
The disease is a threat to more 60 million people throughout
Africa. However, currently only 3 to 4 million of these people are
under surveillance, leading to the reporting of only 45,000 cases
in 1999.
Epidemiologists estimate that between 300,00 and
500,000 cases actually occurred during that same time
period. Surveillance is not only essential to track disease trends
to determine possible interventions, but also to identify infected
individuals so that treatment may be initiated before the disease
progresses to less treatable state.
Human trypanosomiasis

Human African trypanosomiasis.

Human American trypanosomiasis
There are two clinical forms of African trypanosomiasis:
1.
Slowly developing disease caused by Trypanosoma
brucei gambiense.
2.
A rapidly progressing disease caused by T. brucei
rhodesiense.
T. b. gambiense and T. b. rhodesiense are similar in
appearance:
The
organism
measures
10
-
30
micrometers x 1-3 micrometers. It has a single central
nucleus and a single flagellum originating at the
kinetoplast and joined to the body by an undulating
membrane (Figure). The outer surface of the organism is
densely coated with a layer of glycoprotein, the variable
surface glycoprotein (VSG).
Bite reaction: painful, itchy chancre forms 1-3 weeks after the
bite and lasts 1-2 weeks. It leaves no scar.
A teenage girl in Uganda with sleeping sickness exhibiting the
characteristic chancre on her leg at the site of tsetse fly
inoculation (A), and a woman in Uganda with a partially healed
chancre just above her elbow (B).
Although (C) may look
painful, chancres are generally painless with some associated
tenderness.
Parasitemia: Parasitemia and lymph node
invasion is marked by attacks of fever which
starts 2-3 weeks after the bite and is
accompanied
by
malaise,
lassitude,
insomnia, headache and lymphadenopathy
and edema.
CNS Stage: The late or CNS stage is marked by
changes in character and personality. They include
lack
of
avoidance
interest
of
and
disinclination
acquaintances,
to
morose
work,
and
melancholic attitude alternating, mental retardation
and lethargy, low and tremulous speech, tremors
of tongue and limbs, slow and shuffling gait, etc.
A history of travel within an endemic
region and especially a memory of a bite
from a tsetse fly are both key to a
clinician’s ability to consider African
sleeping sickness when encountering a
patient outside an endemic region. If
exposure history has been documented,
the definitive diagnosis of African
trypanosomiasis is made by identifying
the protozoa in the patient’s blood,
cerebrospinal fluid.
A doctor performing
a spinal tap to
examine the cerebrospinal fluid of a
patient suspected to have an infection
with African trypanosomiasis
To concentrate the trypanosomes in a sample, centrifugation is
often advised. An ELISA may also be used to identify antigens,
as well as a new serodiagnostic tool termed the Card
Agglutination Test for Trypanosomiasis (CATT). Another test
called card Indirect Agglutination Test (CIATT) tests for antigens
rather than antibodies. It has a high sensitivity and specificity
and can distinguish between the two species of trypanosomes.
This latter test will allow for rapid and reliable data concerning the
incidence of African trypanosomiasis—a key aspect of any
prevention and control program.
The Card Agglutination Test for
Trypanosomiasis (CATT). This
inexpensive
and
rapid
serodiagnostic test identifies
those patients with antibodies
against the organisms, indicating
infection
Unless treated, African trypanosomiasis is a
fatal illness.
The most effective treatment
intervention for this disease must begin
before the organism migrates into the CNS
because the most effective drug does not
cross the blood-brain barrier.
This drug,
Suramin, is administered intravenously and
most often results in the full recovery of the
patient.
Melarsoprol is the drug of choice should the disease have
progressed sufficiently to affect the central nervous system.
This drug is toxic and may lead to myocarditis, renal damage,
encephalopathy. Approximately 5% of patients die from this
treatment,
while
another
5%
relapse.
More
recently,
Eflornithine, has proven to more safely and efficaciously
eliminate the protozoa from the blood stream and has thus
been termed “the resurrection drug.
The most effective means of
prevention
is
to
avoid
contact with tsetse flies.
Vector
eradication
is
impractical due to the vast
area involved. Immunization
has not been effective due
to antigenic variation.
A woman caring for her comatose husband who is dying of African trypanosomiasis, Uganda, 1990