What is Trypanosoma? |

Definition

The numerous species of Trypanosoma cause many diseases in
vertebrates, most notably Chagas’ disease and trypanosomiasis in humans.

Natural Habitat and Features

Trypanosoma is one of several genera within the order
Kinetoplastida. All species are flagellate parasites that contain a special
structure unique to this order called the kinetoplast, found within the
kinetosome, which contains the mitochondrial DNA (deoxyribonucleic acid). Most
trypanosomes are heterozenous, living one stage of their lives in the blood and
tissues of a vertebrate host; in other stages they dwell within
the intestines of blood-sucking (hematophagous) invertebrates.

Within the Trypanosomatidae, six life cycles occur, depending upon the genus. These life cycles are the amastigote, promastigote, choanomastigote, epimastigote, opisthomastigote, and trypanomastigote. The life-cycle designations are based upon the location of the flagellum on the body surface, the body shape, and the position of the kinetoplast/kinetosome. The life cycle that defines Trypanosoma is the trypanomastigote. The morphological features of this stage include a posterior position of the kinetosome; a long, whiplike flagellum running along the surface of the organism; and a set of pellicular microtubules that provide support for the parasite when the flagellum beats.

Two broad groups, or sections, of trypanosomes designated by parasitologists are the Salivaria and the Stercoraria. These designations are based upon where the parasites settle within the invertebrate vector’s body. If the trypanosomes develop within the anterior portion of the invertebrate’s digestive tract, they belong to the Salivaria section. These parasites will be transmitted to the vertebrate host through the invertebrate’s saliva or other oral secretions. If the trypanosomes develop in the posterior portion or hind gut of the invertebrate host, they are in the Stercoraria section. Trypanosome species infect the vertebrate host through fecal material that the invertebrate vector sheds while feeding.

Pathogenicity and Clinical Significance

Within the Salivaria section are three subspecies of trypanosomes: T.
brucei brucei, T. brucei gambiense, and T. brucei
rhodesiense. These subspecies occur in parts of Africa, specifically
the area that coincides with the range of their vector, the tsetse fly
(Glossina
spp.). T. b. brucei is a parasite of the native
antelopes and other ruminant animals of this region; the parasite causes a deadly
disease called nagana in domestic livestock.

T. b. gambiense and T. b. rhodesiense are the
parasites of both East and West types of trypanosomiasis (African sleeping sickness), which are transmitted by the bite of the tsetse fly. Humans are the reservoirs for T. b. gambiense,
whereas native game animals provide the reservoirs for T. b.
rhodesiense. In both forms of sleeping sickness, pathogenesis is
similar, with the trypanosomes entering the site of the tsetse fly’s bite. A small
sore develops at the spot, and within one to two weeks a widespread parasitemia
develops in the bitten person. Initially, the trypanosomes live in the blood,
lymph nodes, and spleen, causing intermittent fever episodes. T. b.
rhodesiense rarely enters the central nervous system because the
infected person tends to die before this can occur. T. b.
gambiense does invade the central nervous system, causing increased
somnolence, tremors, paralysis, and convulsions before coma and death ensue.

T. cruzi, of the Stercoraria section of trypanosomes, causes Chagas’ disease. T. cruzi is transmitted by hemipteran insects of the family Reduviidae, which are known colloquially as kissing bugs or cone-nosed bloodsuckers. T. cruzi occurs throughout most of Central America and South America, and in some areas of the southern and southwestern United States. Dogs, cats, armadillos, opossums, wood rats, and a number of other domestic and wild animals serve as reservoirs for the parasite, which afflicts millions of people.

When a reduviid insect bites, it often deposits feces containing trypanosomes
on the skin of the human. If the bitten person then scratches the bite or
inadvertently rubs mucous membranes that contain fecal material, the trypanosomes
gain entry to the body. An acute local inflammatory reaction occurs at the site,
producing a red sore called a chagoma, or a swelling of the eyelid and conjunctiva
(Romana’s sign) if the eyelid was the infection site. The local reaction is
followed in one to two weeks by a generalized parasitemia, which affects virtually
every body tissue. Muscle and nerve cells are especially affected. If left
untreated, Chagas’ disease may cause death in three to four weeks. If the person
survives, the chronic stage of the disease generally affects the heart, destroying
the cardiac muscle. In some manifestations of Chagas’ disease, the esophagus and
colon become greatly enlarged because of the destruction of muscle and nervous
tissue.

Throughout northern Africa, Asia Minor, southern Russia, India, parts of southwestern Asia, Indonesia, the Philippines, Central America, and South America, another trypanosome, T. evansi, causes a fatal disease generally known as surra. Horses, elephants, camels, deer, and other mammals are susceptible to infection from this disease. Horseflies (Tabanus spp.) are the primary vectors of T. evansi, although in South America, vampire bats fulfill that role.

For many years, T. evansi was not known to infect humans; however, in 2005, the first case of typanosomiasis caused by this species was diagnosed in a person in India.

Drug Susceptibility

Trypanosomiasis in humans has proved challenging to treat because trypanosomes are continuously changing their surface antigens. Because the surface antigens of the parasites are being released into the blood of the bitten person almost constantly, large amounts of the host’s immunoglobulins are being produced in an attempt to counteract the trypanosomes’ attack.

In the early stage of infection by T. b. gambiense, treatment involves the use of the drug pentamidine or, alternatively, suramin. In later stages, if the central nervous system is involved, eflornithine, melarsoprol, or nifurtimax are used. For cases of T. b. rhodesiense infection, early-stage treatment is by suramin and late-stage treatment is with melarsoprol. Treatment with melarsoprol, because of its arsenical basis, may cause encephalopathy in the patient and must be used with great care.

Bibliography

Bacchi, Cyrus J. “Chemotherapy of Human African Trypanosomiasis.” Interdisciplinary Perspectives on Infectious Diseases (2009): 1-6. Provides an update on chemotherapeutic treatments for both forms of African sleeping sickness. Available at http://www.hindawi.com/journals/ipid/2009/195040.cta.html.

Jong, Elaine C., and Russell McMullen, eds. Travel and Tropical Medicine Manual. 4th ed. Philadelphia: Saunders/Elsevier, 2008. A useful reference manual with advice on preventing, evaluating, and managing diseases that can be acquired in tropical environments and countries outside the United States.

Joshi, P. P., et al. “Treatment and Follow-up of the First Case of Human Trypanosomiasis Caused by Trypanosoma evansi in India.” Transactions of the Royal Society of Tropical Medicine and Hygiene 100, no. 10 (2006): 989-991. Provides details of the medical treatment of the person in India who contracted T. evansi.

Roberts, Larry S., and John Janovy, Jr. Gerald D. Schmidt and Larry S. Roberts’ Foundations of Parasitology. 8th ed. Boston: McGraw-Hill, 2009. A classic work focusing on parasites of humans and domestic animals.

Seguraa, E. L., and S. Sosa-Estani. “Protozoan Diseases: Chagas’ Disease.” In International Encyclopedia of Public Health, edited by Stella Quah and Kris Heggenhougen. Boston: Academic Press/Elsevier, 2008.