Trypanosoma

Mr. Ravi Kumar

Department of Zoology�Hans Raj Mahila Maha Vidyalaya�Jalandhar (Punjab)

​

Trypanosoma gambiense

• Trypanosoma gambiense is digenetic; i.e,

it completes its life cycle in two hosts.

• The primary or definitive host is man.
• The mammals, like pigs, buffaloes, antelopes often act as reservoir hosts harboring the parasite.
• The intermediate host is blood sucking insect called tsetse fly.

Trypanosoma gambiense

• Trypanosoma are unicellular, parasitic and flagellated protozoans that belong to the family Kinetoplastea.
• The word Trypanosoma has been taken from the Greek words trypano (borer) and soma (body) because of their corkscrew-like motion.
• All the members belonging to the zooflagellate, protozoan Trypanosoma genus are referred to as trypanosomes.
• They are obligatory parasites, meaning they require at least one host to complete their life cycle.
• Some species are heteroxenous that require more than one host to complete their life cycle.
• They are mostly transmitted by blood feeding invertebrates.

​

Classification:

• Eukaryota (organisms with nucleated cells),Kingdom Protista, Phylum Protozoa.
• East African trypanosomiasis is caused by the parasite Trypanosoma brucei rhodesians.
• West African trypanosomiasis is caused by Trypanosoma brucei gambiense.
• The parasites are spread by tsetse flies, found only in Africa.

Geographical Distribution

​

• Trypanosoma gambiense is endemic in West and Central Africa.
• Trypanosoma b. rhodesiense is restricted to East and Southeast Africa.
• Habit and Habitat�Trypanosoma gambiense lives as a parasite in the blood, lymph, lymph nodes, spleen, or cerebrospinal fluid of man and in the intestine of blood-sucking fly Glossina palpalis (Tsetse fly).
• The parasite causes a disease called Gambian or West-African sleeping sickness in human-beings.

Morphology

• They are unicellular, parasitic and flagellated protozoans.
• The mitochondrial genome of trypanosomes is known as kinetoplast DNA or kDNA.
• It is made up of catenated circles and minicircles and requires a different set of proteins during cell division
• The trypanosomes undergo a series of morphological changes during their transition from invertebrates to vertebrates. 
• Trypomastigote is identified by their flagella that is attached to the body by an undulating membrane and the kinetoplast lies in the posterior portion of the body.

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.

TRYPOMASTIGOTE

• The kinetoplast (kt) is located on the posterior end of the parasite.
• 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.
• The undulating membrane functions like a fin and increases the motility of the organism.

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.

​

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.

​

� 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.

​

Etiology.

• There are two clinical forms of African trypanosomiasis:
• A slowly developing disease caused by Trypanosome brucei gambiense and
• A rapidly progressing disease caused by T. brucei rhodesiense.

Major Differences Between African Trypanosome Species

Life cycle in man

• The metacyclic stage (infective form) of T. gambiense is introduced into the body of man by the bite of the tsetse fly.
• The tsetse fly harbours the metacyclic form in the lumen of its salivary glands.
• When the vector sucks human’s blood, it introduces the contained trypanosomes into his blood stream.
• During sucking through the proboscis, the fly releases metacyclic forms along with saliva.
• The saliva of tsetse fly contains an anticoagulant which prevents the clotting of blood.

​

Development within the Salivary Gland of Insect Fly

• Later the long slender forms make their way into salivary glands through the hypopharynx.
• Here they multiply and change their morphology, first into epimastigote and then into the metacyclic stage (short stumpy forms of trypo­mastigote) which are infective to man.
• It has been reported that the time taken for the complete evolution of the infective forms (metacyclic stage) inside the vector insect is about 20 days.
• These flies remain infective for the rest of their lives, a period extending upto 185 days. When the vector fly bites a healthy person, it transfers the metacyclic forms along with saliva into his blood where they initiate another infec­tion.

​

Development in the Midgut of Insect Fly

• Further change of trypomastigote occurs in the insect vector’s midgut within peritrophic membrane and the short stumpy forms of the parasites trans­form into long slender forms.
• Now these long slender forms appear which pass to posterior end of the extra peritrophic space (a space between the peritrophic membrane and epithelial cells),where they continue to multiply for some days.
• By the 15th day they escape from the peritrophic space and enter the lumen of the proventriculus (the periventricular form is the same as that of the midgut form)

​

Life cycle in tsetse fly

• When this insect vector sucks the blood of an infected person, it also takes short stumpy forms of trypomastigote along with the sucked blood.
• Now these stumpy forms continue development in the midgut of insect vector

Multiplication

• All stages of Trypanosoma in man are extracellular as the parasites are found in blood plasma and not inside blood corpuscles.
• Within the host’s blood the metacyclic forms (which are devoid of flagellum) become trans­formed into long, slender and flagellated forms.

​

Movement

• They swim within the human blood by the beating of their free flagella and the vibratile movements of the undulating membrane.
• The adult forms of the parasite multiply by longitudinal binary fission.
• The multiplication commences at the kinetoplast and is followed by the division of nucleus and cytoplasm. Sometimes multiple fission has also been observed but no syngamy occurs in the life cycle.
• It is to be noted that multiplying trypano­somes gets energy by anaerobic glycolysis 

​

Relapse of infection

• It is fact that some of the long and slender trypanosomes do not undergo metamorphosis but change the antigens of blood to which the host has produced antibodies so the slender forms of trypanosomes survive and continue to multiply in blood leading to future relapses of the infection.

​

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.

Pathogenesis

• Inflammatory changes (possibly autoimmune) cause CNS demyelination.
• Immunosuppression by the parasite facilitates secondary infections.

African trypanosomiasis �(Sleeping sickness)

• Protozoan disease transmitted to human beings by the bite of infected tsetse flies.

Clinical Symptoms

• A tsetse fly bite is often painful and can develop into a red sore, called a chancre.
• Fever
• severe headache
• irritability
• extreme tiredness
• swollen lymph glands
• aching muscles and joints.

​

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

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.

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.

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.