Trypanosoma (genus)
Trypanosoma is a genus of flagellate protozoan parasites known for causing significant diseases in vertebrates, particularly in humans. Most notably, species such as Trypanosoma brucei and Trypanosoma cruzi are responsible for African sleeping sickness and Chagas' disease, respectively. These parasites typically have a complex life cycle that involves both a vertebrate host and a blood-sucking invertebrate vector, such as the tsetse fly or kissing bugs.
Trypanosomes are characterized by their unique structure known as the kinetoplast, which contains mitochondrial DNA. They can be categorized into two main sections based on their development in the vector: Salivaria, where they develop in the anterior part of the digestive tract and are transmitted through saliva, and Stercoraria, where they develop in the hindgut and are transmitted via feces.
Infection with these parasites can lead to severe health complications, with symptoms ranging from fever and lethargy to severe cardiac issues and neurological damage, especially in untreated cases. Treatment options exist but can be complex due to the parasites' ability to change their surface antigens, necessitating different therapeutic approaches depending on the infection stage and species involved. Understanding the transmission and clinical implications of Trypanosoma infections is crucial for managing and preventing these diseases, which continue to impact millions, particularly in affected regions of Africa and South America.
Trypanosoma (genus)
- TRANSMISSION ROUTE: Blood
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 in the group 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 heteroxenousliving 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 on the location of the flagellum on the body's 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), 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, colloquially known 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 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 human’s skin. If the bitten person then scratches the bite or inadvertently rubs mucous membranes containing fecal material, the trypanosomes enter 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 trypanosomiasis caused by this species was diagnosed in a person in India. Several further cases of T. evansi causing illness in humans were documented in the following decades, but the species infecting humans remained rare.
Drug Susceptibility
Trypanosomiasis in humans is 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 fexinidazole. In later stages, if the central nervous system is involved, nifurtimox eflornithine combination therapy (NECT), fexinidazole, 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, pp. 1-6, www.hindawi.com/journals/ipid/2009/195040.cta.html. Accessed 20 Oct. 2024.
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, vol. 100, no. 10, 2006, pp. 989–91, doi.org/10.1016/j.trstmh.2005.11.003. Accessed 20 Oct. 2024.
Roberts, Larry S., and John Janovy, Jr. Gerald D. Schmidt and Larry S. Roberts’ Foundations of Parasitology. 9th ed., McGraw-Hill, 2013.
Sanford, Christopher, et al. The Travel and Tropical Medicine Manual. 5th ed., Elsevier, 2017.
Seguraa, E. L., and S. Sosa-Estani. “Protozoan Diseases: Chagas’ Disease.” International Encyclopedia of Public Health, edited by Stella Quah and Kris Heggenhougen, Academic Press/Elsevier, 2008.
"Trypanosomiasis, African." Centers for Disease Control, www.cdc.gov/dpdx/trypanosomiasisafrican/index.html. Accessed 20 Oct. 2024.
"Trypanosomiasis, Human African (Sleeping Sickness)." World Health Organization, 2 May 2023, www.who.int/news-room/fact-sheets/detail/trypanosomiasis-human-african-(sleeping-sickness). Accessed 20 Oct. 2024.