• Trypanosoma

•Introduction
•The name is derived from Greek word,
trypano means (borer) soma means (body)
•They are unicellular flagellate protozoa.
• Have corkscrew like motion.
• Need more than one host to complete its
life cycle. Often transmitted by a vector.
• Teste fly
• Rhodnius Prolixus
•Generally found in intestine, but some time
found in blood stream or in heart.
• Intermediate host :
•Fly and bug
•Final host :
•Humans and animals
Species:
• T. brucei, which causes sleeping sickness in humans
and nagana in cattle.
• (Trypanosoma gambiense and Trypanosoma
rhodesiense)
• T. cruzi, which causes Chagas disease in humans
•T.vivx which causes the disease mainly in West
Africa.
•Types:
•There are two types of trypanosomes.
1. Salivarian
• These mostly develop in insects interior gut, and
after that transfer to other hosts or humans
2. Stercorarian
• These infections occurs through the contact of
vector's feces and the biting wound (or a mucosa
Transmission:
• Cyclical transmission - In the cyclical mode of transmission, the parasite is
transmitted by infected tsetse flies. Here, the parasite undergoes development
in the insect before being transmitted when the fly is feeding (through saliva).
• Mechanical transmission - In this mode of transmission, the parasite is
transmitted by a number of biting flies including tsetse flies. According to
studies, stomoxes and tabanids are the main biting flies involved in the
transmission of the parasites.
• Per-oral and vertical transmission - In per-oral transmission, transmission of
the parasite is as a result of ingesting contaminated fluids. Vertical
transmission, on the other hand, may occur during pregnancy or shortly after
birth (parent to offspring transmission).
• Morphological Forms
Several different morphological forms of kinetoplastids are
observed. These various morphological forms are associated with
different life cycle stages in the various species. The four major
morphological forms found in kinetoplastids which cause human
disease :
1. 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.
2. 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.
3. 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.
4. 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).
Life Cycle
 Clinical Sign
and symptoms

Blood lymphatic CNS

Chronic Stage:
Anorexia Acute Chronic
Progressive confusion • Intermittent Neurological
Lassitude fever symptoms appear
And severe neuorological •symptoms.
Severe such as
headache • lymphadenopathy • Anorexia
• Muscle fatigue • Convulsion
• Anemia • lassitude
• Weakness
• Pathogenesis of Trypanosomiasis in Animals

• Infected tsetse inoculate metacyclic trypanosomes into the skin of animals, where the
trypanosomes reside for a few days and cause localized inflammation (chancres).
• They enter the lymph and lymph nodes, then the bloodstream, where they divide rapidly by
binary fission. It
• It infection, the organisms attach to endothelial cells and localize in capillaries, small blood
vessels and can cause tissue damage
• The immune response is vigorous, and immune complexes cause inflammation, which
contributes to fever and other signs and lesions of the disease.
• Trypanosomes have a large family of genes that code for variable surface-coat glycoproteins
that are switched in response to the antibody response, evading immunity.
• Antigenic variation has prevented development of a protective vaccine and permits
reinfections when animals are exposed to a new antigenic type.
Diagnosis:
• Thin Blood Smear Examination
• Serological test
• ELISA
• Stilbamide test
• Mercuric test

Treatment:
• Suramin 10mg/kg @5 days
• Pentamidine 4mg/kg @ 10 days
• Melarsoprol 3.6 mg/kg @ 3days
• Eflornithine 400mg/kg@14 days

Prevention and control:

• Wear protective cloth
• Use insect repellent
• And control the fly by insecticide.