Trypanosoma of the Haemoflagellates Family | Protozoan Cell

In this article we will discuss about:- 1. Systematic Position and Distribution of Trypanosoma 2. Polymorphic Forms of Trypanosomes 3. Pathogenic and Non-Pathogenic.

The family of Trypanosomidae is the impor­tant groups among the Haemoflagellates. Members of this family, the Trypanosomes, are all parasitic and were originally parasites of the digestive canal of insects.

Now, many are found in the blood and/or tissues of mammals and birds. They are characteristically leaf like in shape; they have single flagellum and this is attached to the body of the organism by an undulating mem­brane.

During their life cycle at-least one further developmental stage undergoes, the various stages being morphologically distinct.

Systematic Position and Distribution of Trypanosoma:

Systematic position:

Subphylum – Sarcomastigophora

Superclass – Mastigophora

Class – Zoomastigophora

Genus – Trypanosoma

Species – gambiense, evansi.

Distribution:

T. gambiense occurs on the west coast of Africa between the latitudes of 15° north and 18° south with Lake Victoria as an eastern limit. Geographically T. evansi occurs typically in the Indian subcontinent. However, it is now widespread throughout the Far East; it also occurs in the Near East, in North Africa, north of latitude 15°north, and in the Philippines, and Central and South America.

Transmission is by bitting flies such as Tobanus, Stomoxys and Lyperosia. An essen­tial factor in mechanical transmission is interrup­ted feeding on the part of the flies which pass quickly from one host to the other in order to become replete. Trypanosoma evansi does not sur­vive for more than 10-15 minutes within the pro­boscis of a fly.

In case of T. gambiense, the areas near the rivers and lakes have the greatest incidence of infection, since the insect vector, the tsetse fly, live there in low and thick vegetation.

Polymorphic Forms of Trypanosomes:

The polymorphic forms (developmental stages) are as follows:

i. Trypanosome stage (trypanomastigote):

Blade like form with a kinetoplast poste­rior to the nucleus and usually near the posterior extremity. Undulating mem­brane conspicuous and often with a free flagellum.

ii. Crithidial stage (epimastigote):

Body elongate. Kinetoplast and axoneme ante­rior to the nucleus. Short undulating mem­brane.

iii. Leptomonad stage (promastigote):

Body elongate, nucleus large, anteriorly located kinetoplast and axoneme. Flagellum short and unattached.

iv. Leishmanial (amastigote) stage:

Round or oval form with a nucleus and kinetoplast. Flagellum absent or represented by a short fibril.

Principal Vector (host) and Temporary Vector of T. gambiense and T. evansi:

The chief vector which transmits T. gambiense from man to man is the tsetse fly, Glossina palpalis, but Glossina tachinoides is also known to be an important vector (Fig. 4.2).

  Occasionally, T. gambiense utilizes a wide range of domestic and wild mammals, such as monkeys, dogs, camel, cat, pigs, antelopes, buffaloes and reed bucks as reservoir hosts. It is noteworthy, the parasite does not undergo any developmental stage but simply waits for its administration into the human organism.

In case of T. evansi, the transmission is done by biting flies (chief vectors) such as Tabanus, Stomonys and Lyperosia. In Central and South America the vampire bat may also act as a reser­voir vector or transmitter, though the bat may die of infection about a month after an infected blood meal.

Pathogenic and Non-Pathogenic Try­panosomes:

(a) Trypanosoma equiperdum:

It causes “Stallion’s disease” (venereal disease) in Central and South America, Africa and parts of Asia including India and former U-S.S.R.

Habitat:

Genital system of horses and asses.

Life cycle:

Direct transmission from one animal to another during sexual intercourse.

Treatment:

Suramin injection (intravenous), 2 gm. twice or 2 mg per kg of quinapyramine.

(b) Trypanosoma brucei (human strains):

They cause “African trypanosomiasis” (Rhodesian, Gambian and Zambezi forms of sleeping sickness).

T. brucei (animal strains):

Cause “Nagana” in some domestic animals. They are found in wild games and domestic animals of tropical Africa; transmitted by Sand-fly, Glossina morsitans. Development occurs in the midgut and the sali­vary glands of the fly. Transmission may also be mechanical by biting-flies. T. brucei infection may also be acute in dogs.

Infections, usually result from bites of G. palpalis and G. tachinoides; the disease is rapid in onset and there is a marked intermittent rise in temperature, dullness and prostration. In cattle the infection is seldom severe and most infections are mild and transient.

Treatment:

i. Single intramuscular injection of pentami­dine for “Gambian disease” 4 mg/kg pro­vide prophylaxis for six months.

ii. Destruction of habitat of the vector.

(c) Trypanosoma cruzi:

Cause “Chagas disease” or American trypanosomiasis discovered by Dr. Chagas in Brazil. They are found from Southern USA to Argentina. The parasite inhabits blood and various tissues of man. T. cruzi infection occurs in children and infants and the parasite is trans­mitted by blood sucking bugs, Reduviid bugs in which the metacyclic infective form develops in hindgut.

The amastigote form is seen in brain, muscles, adrenals, thyroid etc. T. cruzi is a plemorphic trypanosome having two phases of life cycle—in man and other vertebrate hosts and in insect vectors (invertebrate hosts). The most important vectors are Panstrongylus megistus, P. geniculatus, Rhodnius prolixus. Triatoma infestans etc. Younger people suffer more than others.

The symptoms include nausea, vomiting, anorexia, high fever, diarrhoea, conjunctivitis with oedema of eyelids and face. Lymph nodes may be enlarged. In the chronic stage there is myocardial involvement, leading to heart failure.

Treatment:

i. No satisfactory treatment, one drug in use is Nifurtimox.

ii. Residually sprayed Dieldrin markedly reduces the infection.

iii. Personal prophylaxis is important by using mosquito net.

(d) Trypanosoma rangeli:

Trypanosoma rangeli is a non-pathogenic trypanosome found in the blood of man in Venezuela, Columbia, El Salvador and Costa Rica. The parasites inhabit blood and various tissues of man, dog, opossum and monkey.

The development of this parasite occurs in Reduviid bug, Rhodnius prolixus. Epimastigotes and metacyclic trypomastigotes occur in the hind gut. Metacyclic trypanosomes may migrate to the salivary glands and infection is either by inocula­tion or by contamination.

The parasite is non-pathogenic to vertebrates but it is reported to be pathogenic to insect host.

(e) Trypanosoma rhodesiense:

Causes “African sleeping sickness” of humans and antelopes. It inhabits blood. It is an acute disease. The parasite is distributed in Zambia, S. Rhodesia, Nyasaland, Tanzania, Bechuanaland in the Southern Sudan and around the shores of Lake Victoria.

The principal transmitting flies are the Glossina morsitans, G. swynnertoni and G. pallidipes.

The clinical disease is more acute than the Gambian form of the disease and cause more mor­tality. Central nervous system is involved earlier than in the case of the Gambian disease. A fatal termination is common in untreated cases, which may be a matter of months only.

Treatment:

i. In the first phase of the disease, Suramin (Antrypol, Moranyl) is given intravenously every 6 or 7 day intervals which is more effective. Initial dose should not exceed 0.3-0.5 gm., subsequent doses being 1.0 gm. and to be continued till the total of 7-10 gm. will be attained.

ii. Lomidine or Pentamidine may be adminis­tered orally which also give good result.

iii. Tryparsamide is effective in chronic and late cases of African sleeping sickness.

iv. New drugs like Melarsoprol and sodium melarsen are coming into prominence to resist the disease.