Genera of Trypanosomatidae | Protozoa | Zoology

The genus Leptomonas is morphologically indistinguishable from Phytomonas living in plants. Leptomonas is so similar to Herpetomonas that some authorities doubt the existence of two separate genera.

Genus Leptomonas:

Elongate trypanosomatids, these organisms are pointed at the posterior end and are pointed or narrowly rounded at the anterior end. A reservoir (flagellar pocket), whose depth does not exceed one-fifth of the body length, opens narrowly at the anterior end. The kinetoplast occurs below the base of the reservoir.

The flagellum emerges from the bottom of the reservoir, passes out of the cytostome, and continues freely. There is no undulating membrane. The nucleus occurs in the middle third of the body length. The species of this genus are parasites of protozoa, nematodes, molluscs, and insects. There is only one host in the life cycle. Sample species: L. buetschlii

Genus Herpetomonas:

Species of this genus are opistomastigote parasites of insects. The body is elongate and slender, pointed or truncate at the posterior end, and pointed or rounded at the anterior end. The nucleus occurs in the middle or posterior third of the body length. The reservoir opens narrowly in the anterior end and extends a variable distance into the body.

The kinetoplast is situated anywhere from a point one-fifth to about nine-tenths of the body length. The flagellum originates near the kinetoplast, passes through the reservoir, and emerges through the mouth of the reservoir. There is no undulating membrane. As in the leptomonads, development occurs only in one host. Sample species: H. muscarum.

Genus Crithidia:

These are small (4 to 10 µm long) choanomastigote parasites of insects, with a body usually shorter and wider than in other genera.

The anterior end is truncate. The body is often constricted in the anterior third, to produce a vase-like shape. The reservoir is wide, with its mouth (cytostome) occupying most of the truncate anterior end. The kinetoplast is large, lateral, and located posteriorly, sometimes near or beside the nucleus. The flagellum moves in a circular motion. These organisms are often clustered together or are attached like the pile of a carpet to the intestinal wall. There are no intermediate hosts. Sample species: C. fasciculata.

Genus Blastocrithidia:

Species of this genus are insect epimastigote flagellates (15 to 33 µm long) drawn to a long point anteriorly. The reservoir opens along the side. The kinetoplast is situated just posterior to the base of the reservoir and usually anterior to or beside the nucleus, but in occasional individuals, it occurs behind the nucleus.

The flagellum arises near the kinetoplast and passes out through the reservoir and along an undulating membrane to the anterior end, whence it continues as a free flagellum. These parasites may retard development of the host, e.g. B triatome in triatomid bugs. Flagellar cysts occur in some species. There are no intermediate hosts. Sample species: B. gerridis.  

Genus Leishmania:

These are rounded or oval parasites (1.5 to 3 µm) of invertebrates and vertebrates with a morphologically complex life cycle. Body forms include a promastigote with a free flagellum and the characteristic amastigote in which the flagellum is never fully emergent. The fine structure of the kinetoplast is like that of Trypanosoma. Skin sores requires a few weeks to a few months. The infection passes from rodent to rodent, the natural host.

Cutaneous leishmaniasis of the Old World resulting from infection with Leishmania tropica occurs in three major forms:

(1) Moist (or rural), caused by L. tropica major; a self-limited lesion begins at the site of the bite, develops rapidly, and subsides within about six months; the infection is largely transmitted out of doors;

(2) Dry (or urban), caused by L. tropica minor; the lesion grows slowly and may ulcerate, but heals with little scarring in about a year;

(3) Lupoid (or relapsing); the lesion enlarges slowly over a period of years, healing at the center while advancing at the periphery; this type occurs in the Middle East.

Leishmania mexicana occurs in some countries of Central and South America, principally Mexico and Guyana and, to a lesser extent, the Amazon region. It causes a cutaneous lesion and does not spread to mucous areas. Ear lesions are known as chiclero ulcers. In experimental animals, the infection may lead to vascularization, especially to involvement of the spleen and the liver. The vector seems to be Lutzpmyia flaviscutellata. Several species of forest rodents are found infected in nature.

Leishmania mexicana is actually a group of parasites, three of which are not readily distinguished from one another. They differ in reservoir hosts, sand-fly vector, geographic distribution, and clinical features. They are L. mexicana mexicana, L. m. amazonensis, L. m. pifanoi, and L. enriettii. The last is distinguished from the others by its unusually large amastigotes. It is found in laboratory guinea pigs.

Leishmania braziliensis is present in most parts of the tropic and subtropics regions of the new world, ranging at least from Panama to Argentina. The pathology, epidemiology, reservoir hosts, and species of sandflies involved in transmission vary considerably from one place to another.

The most severe form of this infection, called espundia, is endemic in the jungles of Brazil, Bolivia, Peru, and some other South American countries. The clinical form frequently involves the mucous membranes of mouth, nose, and pharynx and may result in complete destruction of these tissues and associated cartilage.

The lesions are resistant to treatment. In certain arid areas of western Peru, however, a benign form called uta is present. In these areas, involvement of the respiratory membranes has not been observed, and the skin lesions usually heal spontaneously. Between the espundia and uta occur all the transitional forms of cutaneous leishmaniasis in the New Worlds.

Throughout areas where Leshmania braziliensis is endemic, several mammals, both domestic and wild, have been found naturally infected. The list includes dogs, horses, wild rodents, and certain forest carnivores. The importance of such animals as reservoir hosts in relation to the disease in man is still to be determined.

Among the several species of phlebotomine sandflies that could be incriminated as vectors are Lutzomyia flaviscutellata, L. intermedius, and L. trapidoi. Other species have been found naturally infected with promastigote flagellates, but further investigations are necessary in order to determine their relation, if any, to leishmaniasis.

As with Leishmania mexicana, L. braziliensis includes several varieties. Lainson and Shaw have grouped them as follows: L. b. braziliensis, L. b. guyanensis, L. b. panamensis, and L. peruviana, which causes the lesion “uta”.

Leishmania donovanicauses visceral leishmaniasis, a killing disease. Infection occurs chiefly in the spleen and liver, secondarily in bone marrow, intestinal villi and other areas. The disease is called kala-azar and dum dum fever. It occurs in east India, Assam, and the Mediterranean area, southern Russia, North Africa, central Asia, northeast Brazil, Colombia, Argentina, Paraguay, El Salvador, Guatemala, and Mexico.

It is a rural disease with reservoirs of infection in dogs, foxes, rodents, and other mammals. The strain in children is sometimes called L. infantum. Promastigotes may be found in flies (e.g., Phlebotomus argneticpes, P. orientalis) three days after feeding. They occupy the anterior portion of the gut by the fourth or fifth day. On the seventh to ninth day after the fly has fed a second time, promastigotes are in the proboscis and becomes infective. The fly lives 14 to 15 days.

The first response to a bite is a small, nonulceated skin sore. Infection metastasizes to the viscera. Headache and weakness often accompany infection. Increase of blood volume, an increase of IgG, and a decrease of IgM may also occur. Infection of reticuloendothelial cells throughout the body is the basic factor.

The disease is characterized by, “a lengthy incubation period, an insidious onset, and a chronic course at tended by irregular fever, increasing enlargement of the spleen and of the liver, leucopenia, anemia and progressive wasting. The mortality is high; death occurs in untreated cases in 2 months to 2 years”. The most obvious physical signs are progressive enlargement of the spleen and, to a lesser extent, of the liver.

This disease occurs as three types or varieties, separated geographically. The first two types, Indian and Sudanese, are found mainly in human adults, rodents, and possibly lizards, but not in dogs. The third type, Mediterranean, is much more widespread, occurring in southern Europe, middle Asia, China, and Central and South America. In this type, dogs are important hosts, and jackals and other mammals have been found to be infected. Transmission of the disease may occur from vertebrate to vertebrate by direct contact, thus omitting the vector.

About two years after the acute stage of kala-azar occurs in the viscera, post-kala-azar leishmaniasis may appear. Manifestations range from de-pigmented areas of the skin to pronounced nodular lesions.

Dogs also show pathogenic effects of infection. Loss of hair is a characteristic manifestation of severe visceral leishmaniasis in these animals. Ulcers on the lips and eyelids, weakness, and enlargement of the liver are common symptoms. Positive diagnosis relies on discovery of the parasite in infected tissues and in peripheral blood. Stray dogs should be eliminated, and insecticides should be used to control the sandflies.

Probably many other species of Leishmania occur in animals but have not yet been reported. Those that have been described include L. caninum in dogs, L.chamaeleonis in lizards, and L. denticis in the silverfish, Dentex argyrozona. For a review of leishmania and leishmaniasis, see Bray and Manson-Bahr. For taxonomy and transmission of Leishmania, see Williams and Coelho.

Trichomonas tenax is smaller than Pentatrichomonas hominis and averages about 7µm in length. It is similar to P. hominis in general appearance, but the undulating membrane extends about two-thirds the length of the body, and there is no trailing flagellum. The parabasal body is elongate and prominent. This flagellate lives in the human mouth and is a harmless commensal. Its habitat provides the basis for the name T.buccalis, by which it is sometimes called.

Trichomonas vaginalis is the largest of the three trichomonads of man. It averages about 13 µm in length, but the range is from 10 to 20 µm. The undulating membrane usually reaches to the middle of the body, but it may be shorter. There is no trailing flagellum. The parabasal body, with a parabasal filament, is large.

The axostyle characteristically curves slightly around the nucleus. The most significant difference between this species and the other two is its habitat. It lives in the vagina, urethra, or in the prostate gland. The parasites are usually transferred from on host to another through sexual intercourse.

Trichomonas vaginalis is worldwide in distribution, and the incidence of infection in women varies from 20 to 40%, whereas in men it varies from 4 to 15%. Its incidence in husbands or consorts of infected women, however, is probably about 50%. Men, therefore, appear to be the cause of the persistence of trichomonal infection in women.

The sites of infection in the male are: renal pelvis, ureter, bladder, prostate, urethral glands, urethra, and epididymis. In women with abnormal vaginal secretion (usually a white discharge), the incidence of infection may be as high as 70%. The flagellates can be found in abundance in this leucorrhea discharge.

As with the other species, no cysts are produced. The parasite may be found in newborn babies and children. Pathogenic strains have been found within the cytoplasm of macrophages and epithelial cells. The flagellates may cause severe erosion of the vaginal mucosa. Damage may be due both to direct contact with the parasite and to its toxic products. The flagellates were found to be 80 to 100% viable after long storage at – 196°C.

Trichomonas gallinarum causes avian trichomoniasis in chickens, turkeys, and other domestic birds. It is pear-shaped, like other members of the genus, and averages about 7 × 10 µm in size.

The flagellate lives in the lower intestines of the birds and is the cause of diarrhea, loss of appetite and weight, ruffled feathers, and lesions in the intestinal wall. Cysts are not produced, and the method of transmission from bird to bird is unknown. Trichomonas galliane is a similar parasite that infects the upper intestinal tract of poultry and other birds. In young pigeons, it is commonly fatal.

Tritrichomonas foetus reaches a length of 24 pm. It possesses a long undulating membrane, which is bordered on its outer margin by a flagellum that becomes free posteriorly. The axostyle is unusually wide, and it projects a short distance from the posterior end of the animal; the parabasal body is large. The parasites lives in the perpetual cavities of bulls and are thus readily transferred to the vaginas of cows during coitus. In the vagina, the trichomonads multiply for about three weeks.

When the cow is in heat again, the parasites become reduced in numbers or disappear completely. This cycle continues for three or four months, after which time the infection is usually lost. These flagellates may invade other reproductive organs and are apparently able to carry on their metabolic activities both aerobically (ineffectively) and anaerobically.

If trichomonads enter into the uterus, as they easily do, they may cause temporary infertility or abortion. They may even infect the unborn young, appearing in the foetal membranes, the amniotic and allantoic fluids, and often in the stomach of the foetus. The parasites seem to have little effect on bulls. Some bulls apparently have a natural resistance to infection, and cows are able to develop some degree of immunity.