I.

INTRODUCTION
The name trypanosoma comes from two Greek
words trypano meaning borer and soma meaning
body. Trypanosomes have been around for more than
300 million years. They are microscopic unicellular
protozoa that are ubiquitous parasites of insects,
plants, birds, bats, fish, amphibians and mammals.
Because trypanosomes they have been found for so
long, they and their natural hosts have evolved
together to ensure their mutual survival.
Trypanosomes can be found from Nairobi to New
York, Sydney to San Francisco, and from Birmingham to
Buenos Aires. Fortunately, few species are not
pathogenic. Trypanosomes and other parasites mainly
cause disease when they are transferred to new hosts.
For a long time now, trypanosomes are generally
associated with diseases in Africa andsouth America.
African trypanosomiasis is commonly known as
sleeping sickness in humans and nagana in cattle
(nagana meaning loss of spirit in the Zulu language).
There are many species including T. cruzi, T. rangeli,
T. theileri, T. nabiasi, T. rangeli, T. theodori, T. lewisi, T.
rhodesiense, T. brucei, T. equiperdum and others but
those of interest are trypanosoma brucei gambiense
and trypanosoma brucei rhodesiense, which are
transmitted by the tsetse fly. There is also the American
trypanosomiasis or Chagas disease caused by
trypanosoma cruzi. It is transmitted by bugs. Some
Trypanosoma species harmful to humans are illustrated
in table 1 below:

Table 1; Trypanosoma species which are responsible for

human diseases.
Trypanosome
T. brucei
gambiense and
T. brucei
rhodesiense
Trypanosoma
cruzi

II.

vector
Tsetse fly

reduviid

Disease
African
trypanosomiasis
(sleeping
sickness)
American
trypanosomiasis
(chagas
disease)

Trypanosomes
II.1 Morphology:
T. gambiense and rhodiense are hemoflagelated
parasites that exhibit a corkscrew like motion in their
movement with the aid of a whip-like flagellum. They
either feed by pinocytic or phagocytic mechanisms.
These subspecies of T. brucei have typical
components of a eukaryotic cell i.e. they possess a
nucleus, microtubules, endoplasmicreticulum, golgi
bodies and a single mitochondrion through
protozoan in nature. They also have a kinetoplast, an
additional structure which is an extension of the
mitochondrion and contains mitochondrial genome
and is capable of self-replicating.
African trypanosomiasis shows two morphologic
forms:Trypomastigote and epimastigote forms.
Trypomastigote forms are found in both the blood of
human and in the fly, and can be pleomorphic

ranging in length from 12-40 mm. kinetoplast of

trypomastigote is in the posterior section of the
nucleus and has special organelles, like membrane
bound glycosomes which contain glycolytic enzymes.
Flagella, which are close to, but out of the
mitochondria,originate from the plasmatic basal
body. Flagellum is first enclosed by flagella pockets
and then emerges onto the surface of the organism
and runs to the anterior end of the organism as a
pulling flagellum. The flagellum adheres to the cell
surface locally so that an undulating membrane is
seen during movement which is visible under the
light microscope.
Epimastigote form is found in the salivary glands of
the fly. Here, the kinetoplast is anterior to the
nucleus with a short undulation membrane running
about half the length of the body.
Both these forms divide by binary fission.
See figure 1 below;
(kayser, medical microbiology, 2005 thieme).

Note; T. gambiense and rhodiense are closely

related morphologically indistinguishable and hence
are studied together.

II.2

Life cycle:

Both species that cause African sleeping

sickness are of the section Salivaria, which is they
are transmitted through the saliva of the vector,
tsetse fly, when it bits the vertebrate(humans) to
feed. When the vector feeds on an infected host,
trypomastigotes (short stumpy in shape) are
injected into it and they migrate into the mid gut of
the insect where they complete their mitochondrial
development and change to long slender procyclic
forms. These procyclic forms then develop further
and then migrate into the insects salivary glands
where they transform to epimastigotes and
multiply. Finally some epimastigotes complete their
final transformation stage forming non dividing
metacyclic trypomastigotes which detach from the
cells of the salivary gland and form a surface coat.
They are now infective and infect a vertebrate
bitten by the tsetse fly, see fig 2.0 below. The
trypomastigotes measure 12-25m while the
epimastigotes are 25-40m in diameter. The
promastigotes and amastigotes stages are absent
in the African species.

Fig 2: life cycle of Trypanosoma gambiense. (Kayser

Color Atlas of Medical Microbiology 2005 Thieme)

II.3

Pathogenesis:

One of the earliest signs is a swelling which

later develops into trypanosome chancre a at the
point of the insect bite. They then spread to the
blood stream and the lymph nodes where they
multiply in the trypomastigote stage. There can
also be invasion of the central nervous system
leading to the characteristic sleeping sickness. As
parasitic multiplication of T gambiense continues,
fever, joints and muscle pains are observed;
swelling of the lymph nodes referred to as
Winterbottom sign. In chronic state, mental
retardation occurs, meningoencephalitis,
convulsions, paralysis of one side of the
body(hemiplegia) ,incontinence and general
deterioration are seen.
For T.rhodesiense, the infection is acute but
fatal and the chronic infections seen in T
gambiense are not seen. In addition to causing
CNS problems, multiplication of the parasite causes
kidney damage and myocardiasis leading to death.

II.4

Epidemiology:

There are epidemiological differences between

T. gambiense and T. rhodesiense, the main one
being that T. rhodesiense persists
in a latent enzootic cycle in wild and domestic
animals and is normally transmitted by Glossina
from animal to animal, more rarely to humans. T.
gambiense, on the other hand,is transmitted
mainlyfrom humantohumanbythe tsetse flies,
althoughvariousanimalspecieshavealsobeenidentifi
edasreservoirhosts for T. gambiense strains.
(Kayser, Medical Microbiology 2005 thieme, pg.
488)

II.5

Clinical manifestation:

Sleeping sickness is, in the initial phase, a

febrile, generalized disease with lymphadenopathy
and is later characterized by meningoencephalitic
symptoms. The infection runs a two-stage course:
The febrile-glandular or hemolymphatic stage
1, and the meningoencephalitic, Stage 2.The
difference is therapeutically significant. In stage 1,
the trypanosomes multiply in the tissue fluid at the
inoculation site. Within 24 days an inflammatory,
edematousswellingcandeveloptheprimarylesion
ortrypanosomechancre,whichthen
disappearswithinaboutthreeweeks.
Withinaperiodofapproximatelytwoweeksthe
trypanosomesenterthe bloodstream
andlymphaticsystem.Later, in the second
stage,theyalso
invadethecentralnervoussystem.Table 2.0
summarizes further details of the disease.
Table 2.0; Infection Course and Clinical
Manifestations of Sleeping Sickness
Stage, course
T. gambiense
T. rhodesiense
and symptoms
1st stage: Febrile-glandular or hemolymphatic
phase
Trypanosome
In Africans: <5% Approximately
chancre
In Europeans:
50%
approximately
20%
Onset of
2-3 weeks
1-2 weeks
parasitemia
Type of
Low-level,
High-level, often
parasitemia
intermittent
persistent
ParasitemiaFever, chills, headache, joint and

associated
symptoms

muscle pain, transitory edemas,

weight loss, lymphadenopathy,
cardiac dysfunction, anemia,
thrombocytopenia, raised serum
IgM
course
Chronic (also acute persons without
immunity
nd
2 stage: meningoencephalitic phase
Penetration of
4-6 months or
Frequently after
trypanosomes
later
only a few weeks
into CNS
Symptoms
Signs of progressive
meningoencephalitis, epileptiform
convulsions, later somnolence,
apathy, coma, pleocytosis in CSF,
raised total protein and IgM levels
Duration of
Months to
Rarely > 3disease
>6years
7years
(Kayser, Medical Microbiology 2005 thieme, pg.
488,499)

II.6

Diagnosis:

Laboratory diagnosis best depends on

Demonstration of T. gambiense or T.
rhodesiense in blood, lymph node, aspirates or
in CSF. Both the trypanosomes are
morphologically identical.
Demonstration of specific antibodies in serum.
Preferred samples used during diagnosis are;
whole blood with anticoagulants preferably during
the febrile period when trypanosomes are
maximum in number, lymph node aspirates, CSF
and/or serum.
Techniques;
i.

ii.

iii.

Examination of blood for trypanosomes by

Thick or thin blood film stained by fields
or giemsas stains
Concentration of trypanosomes by buffy
coat technique or by micro haematocrit
method.
Smears of lymph node aspirates or CSF
prepared directly or from the sediment and
stained by the methods above.
Demonstration of specific antibodies in serum,
The test used should detect IgM antibodies
against the trypanosomes because the
population in endemic areas may rather have
high IgG levels of antibody. IgM antibodies in CSF
are diagnostic of the disease. Other techniques
used are; indirect immunofluorescence test
(IFAT), enzyme linked immunosorbent assay
(ELISA) and indirect haemaglutination test (IHA).

(Jochei, A. Kolhatkar, Med.lab.sc. theory and

practice)

II.7

Treatment:

Suramin sodium (Germanin) or Pentamidine

Isethionate (Lomidine) are principal drugs used in
the treatment of African trypanosomiasis. A
promising drug is Eflornithine which is used in the
treatment of the blood and CNS phases of T
gambiense infection and the Hemolymphatic
phases of T rhodesiense infection. In chronic cases
Melarsoprol is a drug of choice.

II.8

Prevention and control:

The prevention of tsetse fly bites is a principal

way of control. This is by the use of insecticides or
by the application of repellents when in risk of the
bite. Tourists should put on long clothes to cover
their skin.

III. Trypanosoma cruzi (American

trypanosome)
III.1 Morphology:
Trypanosoma cruzi is a pleomorphic trypanosome
that includes an additional form of amastigote in its life
cycle. The vectors for transmission are reduviid bugs. In
blood the parasite measures 16-22m long.
III.2 Life cycle:
The reduviid bugs when taking a blood meal on an
infected hostingest the trypomastigote of T cruzi.
In the intestines of the vector, they are
transformed to the multiplying epimastigotes
(flagellated) form and later on to the
trypomastigotes forms and then excreted in faeces
after six to seven days. In subsequent blood meals
the bugs excrete droppings that infect the host
with trypomastigotes through skin breaks (bites of
the bug) or mucosa ( e.g the conjunctiva of the
eye). When in the human host, they can either be
phagocytised or invade other cells e.g. heart,
muscle and neuroglia cells where they differentiate
into the amastigote form and divide by binary
fission, (see figure 3 below). A cell with up to 500
parasites is called a psuedocysts. After about five
days the parasites elongate reacquiring their
flagella and differentiating into trypomastigotes via
an intracellular epimastigote intermediate. The
slender trypomastigotes on escape from the cell
invade adjacent cells or enter blood and lymph in
which case they may begin to differentiate
extracellularly, to give broad trypomastigotes or

amastigotes which can be picked up by the kissing

bug during a blood meal and the cycle continues.

Fig. 3; life cycle of Trypanosoma cruzi(Medical

parasitology, Ethiopian Public Health Training Initiative,
pg. 58, 59)

III.3 Pathogenesis:
When the parasite gains entry into a host, there is
often an inflammatory dermal reaction called chagoma
at the site of entry. The parasite can also enter the host
via conjunctiva in which case conjunctivitis results with
eyelid edema. During these inflammatory reactions,
there is infiltration of mononuclear cell and necrosis of
infected cells occurs.In acute infection by
T.cruzi,psuedocysts(intracellular aggregation of
amastigotes)are often found in sections of infected
tissues. High parasitamia of the acute disease causes
lymphocytosis(increase in number of lymphocytes in
the blood) and mild elevations of transaminase may be
present .in some acute cases of the disease, the
parasite may move to the CNS. In chronic infections by
this parasite, the heart is the most commonly affected
organ where in it causes atrophy of myocardial cells
leading to bilateral ventricular enlargement typically
involving the right site of the heart, this may result to
apical aneurysm(an abnormal blood filled bulge of a
blood vessel especially d artery resulting from
weakening of the vessel wall) and mural thrombi.

III.4 Epidemiology:
The bloodsucking bugs of the family Reduviidae find a
hidingplace for the day and quest for food at night. The
natural habitats of theseinsects are nests, animal dens,
and other places frequented by vertebrate
animalswhose blood provides their sustenance. Some
species of reduviids (e.g. Triatoma infestans, Rhodnius
prolixus, Panstrongylus megistus) have
invadeddomestic habitats (also in urban areas!) and are
typically found in simple humandomiciles. Potential
carriers of T. cruzi include over 150 species of
wildTrypanosoma and domestic mammals. The most
important in epidemiological terms aredogs, cats,
rodents, chickens, opossums, and armadillos. Aside
from the reduviidvector, T. cruzi can be transmitted
between humans by blood transfusions,diaplacental
infection, or organ transplants.(Kayser, Medical
Microbiology 2005 Thieme, pg. 491,492)
T.cruzi occurs widely in both reduviid bugs and a
broad spectrum of reservoir animals in North, Central,
and South America. Human disease is found most
oftenamong children in South and Central America,
where there is direct correlation between infected wild
animal reservoir hosts and the presence of infected
bugswhose nests are found in human dwellings.
(Medical parasitology, degree and diploma program for
health science students, pg. 58, 59)

III.5 Clinical manifestation:

Acute illness typically develops about a week after
exposure and lasts up to 60 days. A chagoma may
develop at the site of infection; for example the
Romaa sign (edema of the eyelid and ocular tissues).
Most infected people never develop symptoms, but
remain infected throughout their lives. Approximately
30% of patients will develop chronic manifestations of
Chagas disease after a prolonged period without any
clinical manifestations.
Chronic Chagas disease usually affects the heart,
clinical signs include nervous system abnormalities,
ventricular arrhythmias, and in late-stage disease,
congestive cardiomyopathy. Less common chronic GIT
problems like megaesophagus or megacolon may
develop with or without cardiac manifestations. Reoccur
of disease can always occur in immune-compromised
patients.

III.6 Diagnosis:
Diagnosis of T. cruzi infection depends on
i.
ii.
iii.

Demonstration of trypomastigote in blood

Demonstration of amastigote In tissue
Detection of specific antibodies in serum
Specimens used include whole blood with
anticoagulants, collected during acute phase of
disease, aspirates from enlarged lymph nodes, and/or
serum.
Techniques:
i.

Demonstration of trypomastigote of T. cruzi in

blood by
Examination of thick or thin blood films;
blood smears stained by Giemsa stained
should be examined for C or U shaped
trypomastigote, they have a prominent dark
red kinetoplast at the posterior end and a
central nucleus. The trypomastigotes of T
cruzi are fragile and more easily damaged in
blood films. Moreover they are generally
very few in number in the peripheral blood
except in the febrile period.
Examination of wet film with a cover slit for
motile trypanosomes
Concentration of parasites by micro
haematocrit or test tube method (buffy coat
concentration)
Isolation of parasite from blood or tissue by
culture techniques in NNN medium. Incubate
the medium at 25o for up to 30 days for
epimastigote forms with kinetoplast closed
to the nucleus

 Xenodiagnoses; light infections can be

detected by allowing bugs which are free of
trypanosomes to feed on patients blood.

IV. BLIBLIOGRAPHY
(Kayser, medical microbiology, 2005 thieme).
(Kayser, Medical Microbiology 2005 thieme, pg. 488)
(Kayser, Medical Microbiology 2005 thieme, pg.
488,499)
(Jochei, A. Kolhatkar, Med.lab.sc. theory and practice)
(Kayser, Medical Microbiology 2005 Thieme, pg.
491,492
(Medical parasitology, Ethiopian Public Health Training
Initiative, pg. 58, 59)
World health organization media centre,fact sheet
number 259 updated may 2015.
S. Gillespie and Richard D,2001; Principles and Practical
of clinical Parasitology (page 315-335)