African

Trypanosomiasis
Causative agents:
Trypanosoma brucei
gambience
Trypanosoma brucei
rhodesience

Classification of
Trypanosomes`
Protozoa
Pylum
- Sarcomastigophora
Sub-Phylum - Mastigophora
Class
- Zoomastigophora
Order
- Kinetoplastida
Family
- Typanosomatidae
Genus
- Trypanosoma brucei
gambiense & Trypanosoma brucei
rhodesiense

Geographical Distribution

Gambian and Rhodesian Trypanosomiasis

Grouping Trypanosomes- I
Trypanosomes are grouped on the basis of
the site of Development in the
invertebrate host (Vector)
Salivarian Trypanosomes
- Infective stages develop in the Anterior
station (Salivary Glands)
Genuses: Trypanosoma brucei brucei
Trypanosoma brucei gambiense
Trypanosoma brucei
rhodesiense
Trypanosoma rangeli

Grouping Trypanosomes -II

Stercorian Trypanosomes
Infective stages Develop in the hind
gut of the Vector ( posterior station)
Genus: Trypanosoma cruzi
This trypanosome is Leishmania like and
have amastigote forms dividing in
tissue

General Morphology of
trypanosomes
-

Elongate spindle shaped body

Central nucleus
Undulating membrane
Single flagellum
Volutin granules

Morphology -1

Trypanosoma brucei complex

Morphology - 2
Trypomastigotes in blood

T.brucei brucei complex

Morphology -3

Morphology of hemoflagellates -4

Life cycle and Biology of

Trypanosomes - i

Development in Tsetse fly

Trypanosomes ingested as fly
feeds on man or animals
Move to the salivary glands and
transform to Epimastigotes
which undergo division
Epimastigotes transform into
infective metacyclic forms- these
are injected into man by Glossina

Life cycle and Biology of

Trypanosomes - ii

Development in Man
Metacyclic forms which are
injected by the tsetse fly transform
into long slender forms and divide
in tissue and blood
Short stumpy non dividing forms
survive in fly and are the ones
which develop in the fly
Trypanosomes in the blood exist in
different forms - PLEOMORPHIC

Lifecycle

T. b. gambience &
T.b.rhodensience

Life cycle - 2

Epidemiology -1

Transmission: man to man through

the bite of Glossina species
Male and female flies bite man
Direct mechanical transmission
through contaminated proboscis
Congenital transmission
Blood transfusion
Laboratory infections

Epidemiology -2

Vectors: T.b. gambiense

Glossina palpilis group the principal vector of
T. gambiense. Riverline tsetse flies frequent
vegetation along water courses and lakes,
forest edges and gallery forests
Speices: Glossina fuscipes, Glossina
tachinoides, Glossina palpalis
Feed on man and domestic animals, cattle,
sheep, horses , pigs and other game animals
Reservoirs: No proof that game animals are
reservoirs. Domestic animals, cattle pigs,
goats carry the infection without symptoms

Epidemiology - 3

Trypanosoma brucei rhodesiense

Zoonotic: Infect small numbers of people
compared to T. b. gambiense
Adapted to wild game animals and cattle.
Parasite has limited distribution. It is a
disease of hunters, fishermen and tourists
Health human carriers are uncommon
Parasite not well adapted to man

Epidemiology - 4

T.rhodesiense ( Cont.)
Vectors: Glossina morsitans group savanna flies, species include:
Glossina morsitans
Glossina swynnertoni
Glossina pallidipes
Glossina palpalis
Development in Fly: Mainly influenced
by moisture and Temperature
Development period: 12 to 30 days
about 10% of flies may be infected

African Trypanosomiasis II

Disease , Management and

Control

Pathology/Pathogenesis - 1

Site of inoculation:
Trypanosomes multiply in tissue spaces at
the site of the bite resulting in Chancre
Gradually parasites invade organs of the
host
Sequence of invasion:
Blood stream Lymphnodes arachnoid
spaces of the CNS Brain substance

Pathology/Pathogenesis -2

Gambian Trypanosomiasis
Chronic in nature
Incubation period 2 to 3 weeks
Begins with fever, develops slowly and
insidiously- kill victim several years later
Characterized by 3 progressive states:
A: Trypomastigotes predominantly in blood.
The blood stream is invaded after 1 to 2 weeks
Clinical signs mainly, high fever, weakness,
headaches, joint pains and pruritis

Pathology/Pathogenesis -3

B: Trypomastigotes predominantly in
lymphnodes.
Characterized by enlarged and painful
lymphnodes febrile and afebrile periods
Pronounced lymphadenitis in posterior
cervical triangle lymphnodes
(Winterbottoms sign)
Axillary and groin lymphnodes enlarge
Spleen, liver, heart, lungs, kidney are also
affected.
Bone marrow depression, anemia and other
blood changes ensue.

Winterbottom sign
Posterior neck Ln
enlargement

Pathology/Pathogenesis -4
Lymphatic system Changes (cont.)
- Initial symptoms become pronounced at
this stage and patient may die or
spontaneously improve.
C. Trpomastigotes invade the CNS
Sleeping sickness stage of the
infection is initiated
- Parasites primarily found in frontal
lobes, pons and medulla

Pathology/Pathogenesis - 5
Trypomastigotes invade the CNS ( Cont.)
Behavioral and personality changes are
seen at this stage
Gammbian trpanosomiasis is
characterized by: steady progressive
meningo-encephalitis, apathy(lack of
interest), confusion, fatigue, coordination
loss and somnolence(sleepy)
Patient cannot concentrate becomes
indifferent to environment, experience
insomnia during the night and exhausted

Pathology/Pathogenesis - 6

Invasion of CNS (Cont.)

In terminal phase the patient is emaciated,
progressing to profound coma and death
Indicators of CNS Invasion
Increased protein greater than or equal to
0.3mg/ml
More than 5 lymphocytic cells/ cu mm of
CSF (normal 2- 3 cells)
Cells: Lymphocytes, morula, mononuclears,
eosinophils and Trypanosomes
Raised IgM levels in CSF.

Pathology/Pathogenesis - 7

Rhodesian Trypanosomiasis
More acute course of the disease,
symptoms begin within 5 to 7 days
and death occurs in a few weeks to a
year.
Pathology/Pathogenesis is similar to T.
gambiense. Disease process is rapid
and fulminating. Patient dies before
CNS invasion

Pathology/Pathogenesis - 8

1.

2.
3.

4.

Rhodesian Trypanosomiasis (Cont.)

Characteristic symptoms
Headache, extreme weakness, febrile pa
roxysms and rapid loss of weight
Lymphnode enlargement not pronounced
Skin rashes, edema and myocardits may
be present
Marked nervous symptoms of sleeping
sickness NOT EVIDENT

Parasite Biology: Antigenic

Variation

Antigenic Variation: This is an inherent capacity of

the trypanosomes to vary the antigenic character
by varying the amino acid sequence in the
glycoprotein surface coat (VSG). This phenomenon
enables the trypanosomes to persist in blood. The
African trypanosome has thousands of
antigenically distinct VSG genes. Periodically blood
stream trypomastigotes switch expression from
one VSG gene to another VSG gene (the variants
evade immediate immune recognition and
elimination). The VSG switching results in recurrent
waves of parasitemia a characteristic feature of
African Trypanosomiasis.

Diagnosis- 1

Symptoms for diagnosis

Attacks of irregular fever
Enlargement of lymph nodes
Erythematous skin eruptions
Delayed sensation to pain (Kerandels sign)
Differential diagnosis
Malaria, relapsing fever, enteric fever,
undulant fever, ancylostomiasis, syphilis

Diagnosis -2

Demonstrate Trypanosomes in:

Blood, tissue fluid aspirates, lymph node,
borne marrow biopsy or spinal fluid
Techniques
Microhaematocrit buffy coat microscopy
Centrifuge finger prick blood in
hematocrit tube- cut tube 1mm below
the Buffy coat parasites will be found in
plasma and cell mixture
Anion Exchange method: Blood passed
through a column of cellulose- separate
trypanosomes and erythrocytes

Diagnosis - 3

Serology
Useful for surveys than case diagnosis:
IFAT, ELISA, etc.
High antibody titers in acute stage of
infection
Raised IgM levels are indicative of infection
Raised ESR 140 mm
Cultivation Cultures and Animal
inoculations

Treatment -1

Early Diagnosis
Pentamedine (Isethionate and
Methanesulphonate) : 3 -4 mg
pentamedine base/kg body wt/day (10%
solution in distilled water) Intramuscular
injections for 7 10 days
Suramin: Intravenous injections daily or
weekly to achieve 5 injections: 1g (10 ml
of 10% solution) on days 1, 3, 7, 14 and 21
Test dose 0.1 g
Both are useful in early phases of T.
gambiense and T. rhodesiense. For Tr there
may be potential resistance in some areas

Treatment -2
Late Diagnosis
For late stage arsenic based drugs are
recommended because they cross the
blood brain barrier and attack the
parasites in the CNS.
Melarsoprol (Mel B, Arsobal) 3.6 mg/kg
(maximum single dose 5ml) given in
3.6 % solution in propylene glycol
IV for 3 or 4 consecutive days repeat
after 1 week
Strict milk diet recommended.
May produce encephalopathic reactions

Treatment - 3

Alternative and safer drug:

Difluoromethylornithine (DFMO) or
Eflornithine effective in gambiense disease
but must be given in great volumes by
intravenous drip (second line drug)
can also be taken orally: 400mg/kg
once/day for 5 to 6 weeks late stage of
disease
Early stage 200mg/kg/day for 6 weeks

Prevention- 1

Gambian trypanosomiasis: Affects rural

populations, controlled by population
screening programmes: Approach to
prevention:
Clearing streams of under bush
Eliminating breeding grounds
Use insecticide fly traps
Release of sterile male flies
Clothing (long sleeved shirts and trousers)
Insecticide repellants, bed netting and
screens
Adopt an integrated approach to reduce
human reservoir of infection

Prevention - 2

Rhodesian trypanosomiasis: The

disease is an occupational hazard for
persons working in game reserves
and visitors. Prevention approach:
Reduction of human tsetse contact
in areas of endemicity
Reduction of vegetation around
human settlements
Insecticide spraying and Use of fly
traps
Prophylactic treatment of domestic
animals

Other trypanosomes

Trypanosoma congolense
Trypanosoma vivax
Trypanosoma simiae
Trypanosoma evansi
Trypanosoma equinum
Trypanosoma equiperdum
venereally transmitted in horses