Trypanosoma and Its Classification | Protozoa | Zoology

In this article we will discuss about trypanosoma and its classification.

Trypanosomes are usually found in the body fluids of vertebrates, especially in the plasma, and in the digestive tracts of arthropod or leech vectors. Trypanosomes, however, may occur in any body organ, and some have a “preference” for certain organs such as the heart. The numbers of these parasites in one host may be enormous. For example, 20 million to 4 billion can be recovered from the blood of an animal 100hours after infection.

However, the relation between numbers and infectivity of trypanosomes varies during the normal development of these flagellates in the vector and in the mammal host. Host specificity also varies considerably.

Some species, especially Trypanosoma congolense, occur in practically all domestic animals; others are found almost exclusively in one type of host, for example, T. lewisi in rats. Feeding, apparently occurs by pinocytosis (“cell drinking”), which involves the passage of food down the cytostome and absorption through an«’ enlargement or vacuole that forms at the end of the cytostome.

Identification usually involves a study of the location and behaviour of the parasite in the insect vector; the morphologic types that occur in the vertebrate; the method of transmission; and the physiologic and biochemical characteristic. Parr and Godfrey stated:

“The measurements of the activities of a small series of different trypanosomal enzymes allows the computation of a relatively large number of ratios of the activity of one enzyme expressed relative to the activity of a second enzyme. Since the rate of enzyme synthesis within an organism is dependent on the genetic constitution of that organism, it would be expected that, in certain instances, different types of trypanosome would give different ratios. This principle is illustrated in the finding … that the ratios of alanine and aspartate aminotransferases differ between trypanosome species, and, clearly, if applied in extensor, will allow an elaborate series of parameters to be computed and used for identification, classification and taxonomic purposes”.

Relationships are revealed by cytologic hybridization of kinetoplast DNAs of different hemoflagellates with complementary RNA to study base sequence homology.

The pathology of trypanosome infection varies from host to host and with different species of parasite. Detailed information may be found in Lumsden. In general, at the site of infection, there may be edema due to lymph exudation and a cellular infiltration of lymphocytes associated with proliferation of histiocytes.

In blood vessels, the parasite may cause hypoglycemia, an increase in numbers of lymphocytes and monocytes, a rise in serum IgM, and a drop in erythrocyte count. Anemia is characteristic of all trypanosome infections. Disease of the lymph glands and enlargement of the spleen are common. Mild myocarditis may occur, and the central nervous system may be involved.

Trypanosomes are commonly placed in one of four groups:

i. Lewisi Group

ii. Vivax Group

iii. Congolense Group and

iv. Brucei Group.

i. Lewisi Group:

The posterior end of these parasites is pointed; the kinetoplast is large; not terminal; free flagellum always present; division occurs in amastigote, epimastigote, or trypomastigote stages; transmission is contaminative through feces (posterior station) (T. rangeli is also inoculative).

Trypanosoma lewisi, a common blood parasite of rats, occurs throughout the world. Although it is generally nonpathogenic in adult animals, it can cause lethal infection in suckling rats. It is a slender flagellate, pointed at both ends and averaging about 25 µm long. The life cycle is similar to that of T. cruzi, but the intermediate host is the rat flea, Ceratophyllus fasciatus.

Trypanosoma theileri is a large blood parasite of cattle, reaching 70 µm in length in the ordinary blood stage and up to 120 µm in length in animals suffering from chronic infection of the disease. The lowest limit of unaided human vision is about 100 µm, so this huge trypanosome can be seen without a microscope. The life cycle is similar to that of T.cruzi, and the insect vector is probably the horsefly (Tabanus).

Trypanosoma cruzi causes Chagas’s disease (South American trypanosomiasis). The species also appears in the literature with the subgenus Trypanosoma (Schizotrypanum) cruzi Chagas’s disease is found mainly in Central and South America. A 1970 Pan American Health Organization report estimated that at least 7 million people have the disease. It is lifelong disease, and spontaneous cures do not occur. Digestive and/or cardiac manifestations are common, and sudden death is frequent.

The infection has been described as the most important cause of myocarditis in the world. The incidence of infection may be as high as 50%, especially in children. Adult flagellates live in the blood and reticule endothelial tissues of man and of dogs, cats, rats, monkeys, armadillos, opossums, and other mammals.

Within the mammalian host, T. cruzi enters tissue cells, especially muscles and nerve, and changes to amastigote forms that multiply rapidly. Cells filled with amastigotes are pseudocysts. Amastigotes develop into promastigote and epimastigote stages, and finally to trypomastigote forms that destroy the host cell and enter the blood and lymphatic vessels. They may, however, infect another tissue cell immediately on escaping from the dead host cell. Multiplication does not occur in the blood.

A common insect vector of Trypanosoma cruzi is Panstrongylus megistus in Brazil, or other members of the insect family Reduviidae. With a meal of blood, the trypanosomes are taken to the posterior part of the insect gut, where they develop into amastigote-like forms with a short free flagellum. These are spheromastigotes.

They multiply and give rise to a type of spheromastigote with an undulating membrane and are then infective to man. The cycle in the insect requires about two weeks, but it varies with temperature and other factors. The parasites have no apparent effect on the bug. When man is bitten by the bug, the insect usually defecates while feeding and thus deposits the infective metacyclic forms on the skin.

Often, the irritated host rubs the bitten area, so there is considerable opportunity for the parasites to be rubbed into the wound made by the bug. The most likely infection route other than through abraded skin is via the mucosae, especially the ocular, and to a lesser degree, the oral. Infections may arise even from contaminated syringes.

A foetus may receive the parasite through the placenta, and the infection may be transmitted to babies by mother’s milk. Animals and man are sometimes infected by eating bugs or bug feces or by eating other infected animals. Infected bugs may infect “clean” bugs when they are kept together in the same chamber. The insect is apparently infective for life.

Symptoms of Chagas’s disease are so varied that a clear diagnostic picture is difficult to present. Often, however, the bug bites the area of the eye, especially in children. During the acute stage there occurs a unilateral swelling of the face (Romana’s sign), apparently due to the bite of the bug, not to the trypanosomes. The eyelid becomes puffy, and the eye is often closed. Both eyes and even the whole face and neck may become involved.

As parasites invade body organs, enlargements of the spleen, lymph nodes, and liver occur, with headaches, fever, anemia, and prostration. The “mega” condition of enlargement of the oesophagus or colon appears to be related to this disease. Urinary bladder muscles, striated muscles, and the nervous system may also be affected.

Chronic myocarditis is the leading cause of death by heart failure in endemic areas. Intramuscular forms are mostly amastigote stages. The existence of distinct immunologic types may explain clinical diversity. The disease is diagnosed by several kinds of serologic tests and by finding flagellates in the blood. Acute manifestations of the disease subside spontaneously in 2 to 3 months in 90 to 95% of cases.

Trypanosoma cruzi infects more than 100 species of wild and domestic animals. In some parts of the southwest United States, wood-rat nests are inhabited by triatomid bugs that are parasitized with T. cruzi, and the disease in man has been reported a few times.

See von Brand for a review of the physiology of T. cruzi and other Protozoa. For details on Chagas’s disease, see Ciba Found. Symp. 20; see also Congresso International Sobre Doenca DeChagas, Santos Buch; and for a bibliography, see Olivier et al.

Tyrypanosoma rangeli (T. ariaril) occurs in man, monkeys (Cebas fatuellus), dogs, and possibly opossums, in Panama, Venezuela, Brazil, Colombia, Guatemala, Chile, and French Guiana. The insect vector is the triatomid bug, Rhodnius prolixus, which transmits the flagellate during the act of biting the host.

To get into the salivary glands of the insect, the parasite must penetrate the midgut, pass through the hemocoel, and migrate to the head region, where it leaves the vector through the hypopharynx. This trypanosome is apparently not pathogenic to vertebrates, but damages its insect hosts.

Trypanosoma melophagium, a common blood parasite of sheep in England, is transmitted by the sheep ked (Melophagus ovinus), which is a wingless, bloodsucking fly. Probably up to 90% of British sheep are infected with this flagellate. A similar parasite, T. theodori, occurs in goats.

ii. Vivax Group:

These parasites occur in monomorphic forms; free flagellum is always present; the posterior end of the body is rounded; development in the fly, Glossina, occurs in the proboscis (anterior station) only; T. vivax is also transmitted mechanically by tabanid flies.

Trypanosoma vivax, an active blood parasite, occurs in practically all domestic animals in Africa, the West Indies, and part of Central and South America. Dogs and pigs are not easily infected. In Africa, the insect vector is the tsetse fly, but in other countries, transmission is by mechanical means, indicating that the parasites have been introduced to these countries and have been able to maintain themselves in spite of the lack of a suitable intermediate host. These parasites average 22 µm in length, with a range of 20 to 26 µm. The posterior end of the body is characteristically wider than the anterior end.

Trypanosoma uniformed shorter than T0. vivax and occurs in cattle, sheep, goats, and antelope. It is transmitted by tsetse flies.

iii. Congolense Group:

These parasites occur in monomorphic or polymorphic forms; free flagellum is present or absent; the kinetoplast is typically marginal; they are of medium size; there is development in Glossina in the midget and the proboscis; parasites of this group may enter midgut cells. In monomorphic forms, free flagellum is short or absent, the undulating membrane is inconspicuous; their length is usually 12 to 17 µm.

Trypanosoma congolense is a short flagellate that lacks a free anterior flagellum. It averages about 13 µm in length, with a range of 9 to 18 µm. It is carried by tsetse flies, from which infection occurs through the mouth parts. A wide variance in degree of virulence suggests the existence of several strains of T. congolense.

This species appears to be a parasite of the plasma rather than an invader of tissues. Usually, the infection is serious in cattle, in which it causes anemia and other symptoms common to other forms of trypanosomiasis. Host blood serum lipids are altered. With some strains, infection is almost always fatal. These parasites may also be found in horses, sheep, goats, and camels.

Trypanosoma simiae is a species similar to T.congolense but longer, averaging 14 to 24 µm. It is a common and virulent parasite of African monkeys and is also found in sheep, goats, pigs, and camels. It is the most important trypanosome of domestic swine, but apparently does not infect horses, cattle, or dogs. It is transmitted by the bite of tsetse flies and can be transferred mechanically by bloodsucking flies.

iv. Brucei Group:

Monomorphic or polymorphic forms occur; free flagellum is present or absent; the kinetoplast is small, subterminal, and in some species dyskinetoplastic; the undulating membrane is conspicuous; development in Glossina occurs in the midgut and salivary glands (except in the evansi subgroup).

Trypanosoma gambiense and T. rhodesiense cause African sleeping sickness (African trypanosomiasis of man) T. ganbiense is responsible for the variety that is endemic in the west and central portions of Africa.

This disease should not be confused with the virus-caused sleeping sickness found in the United States and elsewhere. T.gambiense in the blood of man may be long and slender, measuring about 25 × 2 µm with a flagellum, or short and broad without a flagellum, or intermediate in shape. The parasite multiplies by longitudinal splitting, and it migrates through the body by way of the blood plasma, cerebrospinal fluid, lymph nodes, and spleen. The disease occurs in men, women, and children.

The vector host of this flagellate is usually the tsetse fly, Glossina palpalis, which bites man and feeds on his blood. In the intestine of the fly, the parasite reproduces and forms both epimastigotes and trypomastigotes. After two weeks or more in the gut of the fly, the flagellates migrate to the salivary glands, where they become attached to the epithelium and develop into the infective stage.

Congenital infection may occur when the placenta is damaged. The infection may also be transmitted through mother’s milk. The parasites may also enter through the mucous membrane of the upper part of the alimentary canal. It is possible that Masai tribesmen become infected by drinking fresh blood. Laboratory workers have become infected through abraded skin.

These unusual portals of entry are possible with both T.gambienseand T.rhodesinse there is no evidence of natural T. gambiense infection in wild mammals, but such animals are possible reservoirs of infection. In guinea pigs terminally infected with T.gambiense, the level of glycogen and activity of glucose-6- phosphatase in the liver are decreased. This inhibition of enzyme function in dying guinea pigs is apparently the cause of hypoglycemia.

The Gambian or chronic form of sleeping sickness primarily involves the nervous and lymphatic systems. There may also be invasion of the dermis with the production of a local chancre. After an incubation period of one or two weeks, fever, chills, headache, and loss of appetite usually occur, especially in non-natives.

As time goes on, enlargement of the spleen, liver, and lymph nodes occurs, accompanied by weakness, skin eruptions, disturbed vision, and a reduced pulse rate. The infection leads to meningo-encephalomyelitis and hemolysis. 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. The possibility of immunopathologic involvement is being studied. Coma, emaciation, and often death complete the course of the disease, which may last for several years. The mortality rate is high.

Trypanosoma rhodesiense 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. The insect vectors are the tsetse flies, Glossina morsitans, G. pallidipes, and others. T. Rhodesians causes the Rhodesian or acute and more rapid type of human sleeping sickness, which usually results in death within a year.

Because of its rapid course, Rhodesian trypanosomiasis rarely if ever causes the symptoms normally associated with sleeping sickness. Compared with Gambian sleeping sickness, there is less involvement of the central nervous and lymphatic systems, but cardiac involvement is more severe.

The incidence of infection is less than that with T.gambiense, and the parasite is restricted to a much more limited area, being almost confined to the high tablelands of southeast Africa. A malignant variety of Rhodesian trypanosomiasis has arisen among tourists who have visited East African wildlife reserves and national parks. Mental depression, amnesia, impaired renal and liver function, anemia, and myocarditis are common clinical pictures.

There is some justification in considering Trypanosoma rhodesiense as a virulent type of T.gambiense. Certainly, the distinctions between the two types of sleeping sickness are difficult to recognize. The two parasites, however, seem to be antigenically different species. Much more knowledge about Glossina host relationships is needed, as well as more infectivity measurements and more research on the immunology of trypanosomiasis

Trypanosoma brucei causes nagana in livestock. This trypanosome is morphologically identical to T.gambiense and T. rhodesiense and is also transmitted by the tsetse fly; however, it is apparently a different species. T.brucei is widely distributed in Africa in dogs, sheep, goats, horses, mules, donkeys, and camels. Cattle and pigs suffer mild infections, whereas laboratory animals may be severely infected. The parasites range from 25 to 35 µm in length by 2 to 3 µm in width. Long, short, and intermediate forms may appear in the blood at the same time.

The parasites live mainly in connective tissue. As they spread throughout the body, host reaction is shown by edema, anemia, fever, nervous symptoms, conjunctivitis, keratitis, blindness, paralysis, and, especially in horse, death. T. brucei is present as a natural infection of many wild mammals in Africa. A related species, T. suis, is pathogenic to pigs.

Trypanosoma evansiis another serious parasite of horses and camels. It causes the disease known as surra. A small percentage of this species develops without a kinetoplast. The organism can be found in dogs, in which the disease is often fatal, and in donkeys, cattle, and elephants.

It is widespread throughout Asia and occurs in parts of Africa and parts of Central and South America. There is no cyclic development in the insect host. The principal vector is the horse fly, Tabanus, but other flies also mechanically transmit the flagellate. Ticks (Ornithodoros) and even the vampire bat have been implicated. The pathology of the disease is similar to that of T.brucei anemia is the commonest clinical sign of infection.

Trypanosoma epuinum infects horses in South and Central America and causes a disease known as mal de caderas. It may also infect bats, laboratory animals, and a South American rodent called a “capybara”. Biting flies cause a mechanical transmission of the protozoan. The flagellate resembles T.evansi, but appears to lack a kinetoplast.

Trypanosoma equiperdum causes the disease dourine in horse. It is transmitted during copulation and thus is a venereal disease. The flagellate is morphologically identical to T.evansi, and its length is about 25 µm. It does not exhibit the usual changes in morphology during its life cycle.

The parasite first affects the sexual organs of male and female horses and causes swelling and ulcers. Enormous numbers of parasites can be found in these ulcers. The nervous system may become involved, as evidenced by paralysis of the legs or parts of the face. The mortality rate is high, and there is no effective treatment. Dogs, mice, rats and rabbits may become infected with T. equiperdum, but the parasites remain largely in the blood of these hosts. A complement fixation test has been developed to identify the disease in horses.

Trypanosomes of Other Vertebrates:

Trypanosomes of birds have been reported primarily from domestic species, but undoubtedly many wild birds harbor as yet un-described forms. Trypanosome avium occurs in various birds; T.gallinarum is a parasite of chickens, and T. hannai may be found in pigeons. The names of other birds’ forms may be found in texts on protozoology

Trypanosomes of fish are transmitted by leeches. Many fish trypanosomes, such as Trypanosoma giganteum in the ray and T.percae in perch, are unusually large (e.g. up to 130 µm long).

Trypanosome mega lies in the toad, Bufo regularis. This parasite has been found to be a convenient and suitable flagellate for experimental studies. The taxonomy of anuran trypanosomes is in a much confused state. Many species have been described, but few with adequate care and detail. For a review of this neglected group, see Bardsley and Harmsen.

Endotrypanum schaudinni is found within the red blood cell of the sloth, where it usually occurs in the trypomastigote stage. Epimastigote stages may also occur. The vector is presumed to be an independent genus and probably is best placed between Trypanosome and Leishmania.