Trypanosomiasis, Sleeping sickness disease of Africa

Tropical disease

1. Trypanosomiasis.
Sleeping sickness.
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2. African trypanosomiasis
(Sleeping sickness)
•–protozoan disease transmitted to human
beings by the bite of infected tsetse flies.

3. Classification:
•Eukaryota(organisms with
nucleated cells),Kingdom
Protista, Phylum Protozoa.
•East African
trypanosomiasisis caused
by the parasite
Trypanosomabrucei
rhodesiense.
•West African
trypanosomiasisis caused
by Trypanosomabrucei
gambiense. The parasites
are spread by tsetse flies,
found only in Africa.

4. Morphology
Trypanosomes have a single central
nucleus and a single flagellum
originating at the kinetoplast and joined
to the body by an undulating membrane.
The outer surface of the organism is
densely coated with a layer of
glycoprotein, the variable surface
glycoprotein (VSG).
From the point of view of functional
and physiologic complexity, a
protozoan is more like an animal than
like a single cell.

5. Morphological Forms
TRYPOMASTIGOTE
•The kinetoplast (kt) is located on the
posterior end of the parasite. The
flagellum emerges from the posterior
end and folds back along the parasite's
body. This attachment of the flagellum
to the body forms an undulating
membrane (um) that spans the entire
length of the parasite and the free
flagellum emerges from the anterior
end. This is considered the anterior
end since the flagellum pulls the
organism and the end with the free
flagellum is the front in reference to
the direction of movement. The
undulating membrane functions like a
fin and increases the motility of the
organism.

6. Morphological Forms
EPIMASTIGOTE
•The kinetoplast (kt) is more
centrally located, usually just
anterior to nucleus (Nu). The
flagellum (fg) emerges from the
middle of the parasite and forms
a shorter undulating membrane
(um) than observed in
trypomastigotes. Epimastigotes
are noticeably less motile than
trypomastigotes.

7. Morphological Forms
PROMASTIGOTE
•The kinetoplast (kt) is
towards the anterior end and a
free flagellum (fg) with no
undulating membrane
emerges. The end that the free
flagellum emerges from in all
three motile forms is
designated as the anterior end
because they swim in that
direction. In other words, the
flagellum pulls the organism.

8. Morphological Forms
AMASTIGOTE
•The parasite is more spherical in
shape and has no free flagellum.
A basal body (bb) and the base
of the flagellum is still present.
The kinetoplast (kt) is usually
detectable as a darkly staining
body near the nucleus (Nu).
This form is a non-motile
intracellular stage.

9. Etiology.
There are two clinical
forms of African
trypanosomiasis:
•1) a slowly developing
disease caused by
Trypanosome brucei
gambiense and
•2) a rapidly progressing
disease caused by T.
brucei rhodesiense.

10. •The Gambian form tends to be more chronic
and sometimes takes several years to develop
central nervous system (CNS) involvement.

11. Major Differences Between African
Trypanosome Species
Attribute T. rhodesiense T. gambiense
tsetse vector G. morsitansgroup G. palpalisgroup
ecology dry bush, woodland rainforest, riverine, lakes
transmission cycle ungulate-fly-human human-fly-human
non-human reservoir wild animals domestic animals
epidemiology sporadic, safaris endemic, some epidemics
disease progression rapid, often fatal slow (~1 yr) acute ⇒chronic
parasitemia high low
asymptomatic carriers rare common

12. Life cycle of Trypanosomabrucei parasites

13. Epidemiology
•Human trypanosomiasis has caused massive
epidemics in the past. At the turn of the
century, in Zaire and around Lake Victoria,
large epidemics caused at least three-
quarters of a million deaths. Although only
approximately 20000 cases are reported
each year to the World Health Organization,
gross under-reporting, reduced surveillance,
and recent epidemics in Zaire, Uganda,
Tanzania, Mozambique, and Sudan underline
the continuing importance of human
trypanosomiasis in public health.
Trypanosomiasis of domestic animals and
man remains an important deterrent to
development in endemic areas and shows
increased prevalence associated with war,
civil disturbance, and refugee groups as well
as deteriorating health services and disease-
specific control programmes.

14. EPIDEMIOLOGY
•Genus : Trypanosoma
•Source : sick person
•Transmission:
1.Insect bites: the parasites that cause
sleeping sickness can be transmitted by
the bite of infected tsetse flies
2.Mother-to-child transmission
3.Sexual contact
•Risk group : rural areas

15. •Blood trypomastigotesenter the insect’s body
during the blood-sucking of invaded
vertebrates or humans, which multiply by
binary division in the intestinal lumen of the
tsetse fly.
•By day 3-4, trypomastigoticforms enter the
salivary glands, where they are transformed
into epimastigotes. In the salivary glands,
epimastigousforms undergo multiple divisions
and complex morphological changes, as a
result of which they turn into metacyclic
trypomastigotes, which are an invasive stage
of trypanosomes.

16. PATHOGENESIS
•When bitten again, the tsetse fly, along
with saliva, introduces metacyclic
trypomastigotesunder the human skin,
which after a few days enter the blood and
lymph, spread through the body, turning
into blood trypomastigotes.

17. КЛИНИКА
•Incubation period –1 week
•a local inflammatory reaction develops at the
entrance gate in the form of a painful itchy
chancre (trypanoma, or trypanosomal
chancre), which is a painful erythematous
nodule with a diameter of 1-2 cm,
resembling aboiland regional
lymphadenitis.
•Hemolymphaticstage in 1 –3 Weeks.
•late (meningoencephalitic)

18. •Trypanidson the trunk and limbs.
•swelling of face and hands.
•Lymphadenitis –posterior cervical
(Winterbottom’ssymptom), which become
dense and can reach the size of a pigeon’s egg

19. Clinical Symptoms
•A tsetse fly bite is often painful and
can develop into a red sore, called a
chancre.
•Usually on the head or upper limbs

20. Clinical Symptoms(Hemolymphatic)
•fever,
•severe headache,
•irritability,
•extreme tiredness,
•swollen lymph glands,
•aching muscles and
joints.

21. Clinical Symptoms
•Weight loss and a body rash
are also common.
•Infection of the central
nervous system causes
confusion, personality
changes, slurred speech,
seizures, and difficulty in
walking and talking. If left
untreated, the illness
becomes worse, and death
occurs within several weeks
to months

22. Laboratory Diagnostics:
•In the early stages of the disease,
the parasites can be
demonstrated in lymph nodes
and blood; later, they appear in
the cerebrospinal fluid. In the
Rhodesian type, lumbar puncture
is indicated because of early CNS
invasion. Culture or laboratory
animal inoculations can be useful.
Serologic tests, such as indirect
immunofluorescence, direct card
agglutination, and indirect
hemagglutination, are used
successfully for diagnosis.

24. Treatment
•Medicine for the treatment of African trypanosomiasis
is available. Treatment should be started as soon as
possible and is based on the infected person's
symptoms and laboratory tests results.
•Patients need to be hospitalized for treatment and
require periodic follow-up exams for 2 years.
•The current standard treatment for first stage disease
is: Intravenous pentamidine(for T.b. gambiense); or
suramin (for T.b. rhodesiense).
•The current standard treatment for second stage
disease is: Intravenous melarsoprol.
•In areas with melarsoprol resistance or in patients who
have relapsed after melarsoprol monotherapy, the
treatment should be: melarsopsol and nifurtimox, or
eflornithine.

25. Prevention
•There is no vaccine or drug to prevent African
trypanosomiasis.
•When traveling in areas where the disease
occurs, take these precautions against bites
from tsetse flies and other insects.