Species of Trypanosoma | Microbiology

The following points highlight the four important species of Trypanosoma for which man is host. The species are: 1. Trypanosoma Gambiense 2. Trypanosoma Rhodesiense 3. Trypanosoma Cruzi 4. Trypanosoma Rangeli.

Species # 1. Trypanosoma Gambiense:

It was discovered by Forde in 1901. Sir David Bruce reported that sleeping sickness is transmitted by tseitseily. T. gambiense is the causative agent of African sleeping sickness or Gambian trypanosomiasis. This species is confined to West and Central parts of Africa, particularly Nigeria and Congo.

T. gambiense in the blood of man is long and slender. It measures about 25 x 2 um with a flagellum. The parasite multiply by longitudinal binary fission. It migrates through the body by way of blood. Normal habitats are the blood plasma, cerebrospinal fluid, lymph nodes and spleen.

The chief vector hose which transmits the trypanosome from one man to another is the tse tse fly, Glossina palpalis, which bites man and feeds on his blood. Occasionally, Glossina tachinoides also acts as a vector. Domestic and wild animals like buffaloes, pig, antelopes and reed bucks serve as reservoir or temporary hosts.

There is no developmental cycle in these hosts, but simply waits for its introduction into the man. Tse tse fly is a common ectoparasite of both principal host and reservoir hosts. In the intestine of tse tse fly, Trypanosoma reproduces and forms both epimastigotes and trypomastigotes.

After two weeks or more in the gut of the fly the flagellates migrate to salivary glands where they become attached to the epithelium and develop into infective slender trypanosome forms, known as metacyclic forms.

Pathogenesis:

By the bite, tse tse fly inoculates trypanosomes into human blood. In addition to development in blood, parasite migrate to other parts. Chronic form of Gambien sleeping sickness primarily involves the nervous system and the lymphatic system. After an incubation period of one or two weeks, fever, chills, headache and loss of appetite occur.

As time goes on, enlargement of the spleen, liver and lymph nodes occurs, accompanied by weakness, skin eruptions, disturbed vision and reduced pulse rate. As the nervous system is invaded by the parasites, the symptoms include weakness, apathy, headache and definite signs of “sleeping sickness”. A patient readily falls asleep at almost any time. In advanced stage the patient falls in coma. Death is always the ultimate fate.

Sometimes congenital infection occurs through the damaged placenta of mother. The infection may also be transmitted through the mother’s milk. The parasite may also enter through the mucous membrane of the upper part of the alimentary canal.

Treatment:

Gambian trypanosomiasis can be treated successfully during early stages before the parasite invade cerebrospinal fluid. The drugs effective in the early stages are Atoxyl, Bayer 205, Suramin sodium, Antripol, Germanin, Tryparsamide, arsenic and antimony compounds. Pentamidine, Lomidine, butyric acid and Parsenophenyl are useful for prevention and treatment of human infection. If the central nervous system is affected by infection, Orsanine is quite effective. Melarsen oxide is quick in action without side effects. If proper treatment is not given to the patient, it will result in death.

Control:

1. Destruction of tse tse flies.

2. Reduce contacts between tse tse fly and human population.

3. Transmission should be checked.

4. Spraying of DDT over bushy areas in the vicinity of villages to control tse tse flies.

5. Sanitary conditions should be improved.

6. Susceptible persons should take injection of Suramin (dose 1 grm.) every two or three months.

Species # 2. Trypanosoma Rhodesiense:

It is closely related to T. gambiense. It is identical in appearance and has the same type of life cycle, but it also occurs in antelope and cattle. It is the causative agent of Rhodesian trypanosomiasis. This species is confined to East and Central parts of Africa, particularly Rhodesia. The insect vectors are tse tse flies mainly Glossina morsitans and G. pallidipes.

Pathogenesis:

T. rhodesiense cause the Rhodesian sleeping sickness. As compared to Gambien type, this is acute and more rapid type of human sleeping sickness. This disease usually results in death within a year. The incidence of infection is less than that with T. gambiense. The parasite is restricted to a much more limited area. Willett (1965) consider T. rhodesiense as a virulent type of T. gambiense.

Species # 3. Trypanosoma Cruzi:

This species is the causative agent of South American trypanosomiasis or Chaga’s disease. The adult flagellate lives in the blood and reticuloendothelial tissues of man, monkey, dog, cat, rat armadillos, opossum and other mammals. Within the mammalian host T. cruzi enters tissue cells especially muscle and glia and changes to amastigote forms (rounded, no external flagellum), that multiply rapidly.

Amastigotes develop into promastigote and epimastigote stages and finally to trypomastigote forms. They destroy the host cell and enter the blood and lymphatic vessels. Multiplication does not occur in the blood stream.

T. cruzi is transmitted by bugs of the family Reduviidate. The common vector bug in Brazil is Panslrongylus megistus. With a meal of blood the trypanosomes are taken to the posterior part of gut of bug. There they develop into amastigote forms with a short flagellum. These are spheromastigotes. They are infective stages to man.

When a man is bitten by a bug, the insect usually defaecates and thus deposits the infective metacyclic forms on the skin. Parasite enter the body by penetrating through skin. Animals and man are sometimes infected by eating bugs or bug faeces or by eating other infected animals.

Pathogenesis:

Chaga’s disease is found mainly in Central and South America, and is more common in children. At least seven million people have the disease. Symptoms of Chaga’s disease are varied. Mostly the bug bites the area of eye especially in children. The eye becomes puffy and is often closed. Both eyes and even the whole face may become involved.

As parasite invade body organs, enlargements of the spleen, lymph nodes and liver occur with head aches, fever and anemia. In serious condition, enlargement of oesophages and colon occur. The heart, urinary bladder muscles, striated muscles and nervous system may also be affected. Intramuscular forms are mostly amastigote stages. Anemia and injury to heart muscles lead to death.

Treatment:

There is no permanent cure of Chaga’s disease. Primaquine and Puromycin are used for temporary relief.

Control:

1. Destruction of vector bugs.

2. Reduce contacts between bug and human population.

3. Man should prevent themselves from contamination.

Species # 4. Trypanosoma Rangeli:

It occurs in man, monkeys, dogs and possibly opossums in Central and South America. The insect vector is the triatomid bug, Rhodnius prolixus. It transmits the flagellate during the act of biting the host, through saliva. In the vertebrate host, the parasite multiplies only in the trypomastigote stage. It is nonpathogenic to vertebrates, but damages it’s insect hosts.

Some species of Trypanosoma found in other animals:

Trypanosoma lewisi -Rat

T. theileri – Cattle

T. melophagium – Sheep

T. vivax – AH domestic animals

T. uniforme – Cattle, sheep & Goat

T. congolense – Horse, Camel & Sheep

T. simiae – Monkeys

T. bruci – Dog, sheep, mule etc.

T. evansi – Horse and Camel

T. equinum -Horse

T. equiperdum -Horse

T. avium – Birds

T. gallinarum – Chickens

T. hannai – Pigeon

T. giganteum -Fish

T. mega -Toad

T. rotatorium -Frog

T. suis -Pig