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Trypanosoma gambiense – Life Cycle, Pathogenesis, Prophylaxis, Structure, Treatment

Human African trypanosomiasis, also known as sleeping sickness, is a parasitic disease transmitted by vectors and caused by Trypanosoma-genus protozoa. There are three subspecies of the parasite: Trypanosoma brucei gambiense, T. brucei rhodesiense, and T. brucei brucei. The latter subspecies is not human-pathogenic.

These subspecies are morphologically indistinguishable. T. b. gambiense is located in western and central Africa and is responsible for chronic disease, while T. b. rhodesiense is found in eastern and southern Africa and produces acute severe sickness. The distribution of their respective vectors, Glossina palpalis and Glossina morsitans, also influences the epidemiology of these parasite species. The G. palpalis inhabits the vegetation surrounding rivers or agricultural fields. G. morsitans relies primarily on savannah animals that live distant from human settlements.

The disease is spread to humans by tsetse flies, which acquire their infection from infected humans or wild animals. Certain species of Trypanosomes are nonpathogenic and harmless to people, whereas others, such as Trypanosoma gambiense, are pathogenic and cause serious sickness in humans and animals. We will explore the anatomy, life cycle, and pathology of Trypanosoma gambiense in this module. We will also examine the disease’s diagnosis and therapy.



Forms of Human African Trypanosomiasis

Human African Trypanosomiasis manifests differently depending on the parasite involved:

  • Trypanosoma brucei gambiense is endemic to west and central Africa, responsible for approximately 95% of cases of sleeping sickness, and causes a chronic illness. In this condition, the parasite-infected individual can survive without disease signs for several months or years. The patient’s central nervous system is already compromised at the onset of a symptom, indicating an advanced stage of disease.
  • Throughout eastern and southern Africa, Trypanosoma brucei rhodesiense is present. This variety accounts for 5% of all occurrences and causes an acute infection. The disease’s symptoms occur within a few months or weeks following infection. The disease rapidly spreads and infects the central nervous system.
  • Trypanosoma cruzi is prevalent in approximately twenty-one Latin American nations. This condition is known as American trypanosomiasis or Chagas disease. The pathogen is a distinct species than those responsible for the African type of the disease.
  • T. rangeli is a nonpathogenic trypanosome identified in Venezuelan and Colombian human blood.

Animal Trypanosomiasis

Several Trypanosoma species are harmful to animals and cause trypanosomiasis in both domestic and wild animals. The sickness in cattle is known as Nagana, a Zulu word that meaning “to be depressed.” Animals can also become hosts for human disease parasites, primarily T. b. rhodesiense, and play a crucial role as parasite reservoirs. T.b. gambiense can also infect animals, which serve as reservoirs. However, the precise epidemiological function of this reservoir is yet unknown. The disease in domestic animals, particularly cattle, is a severe impediment to the economic growth of rural areas afflicted by it.

What is Trypanosoma gambiense?

  • Valentine was the first to report the presence of Trypanosoma in trout blood. Gruby established the genus, and Lewis discovered it in rat blood. Evans and Bruce described Trypanosoma in horses’, camels’, and cats’ blood. Forde (1901) was the first to observe this parasite in human blood.
  • Dutton once again confirmed it (1902). This parasite was discovered by Castellani in the cerebral fluid of humans. Then, Bruce and Nabarro determined the connection between sleeping sickness and this parasite. Bruce also established that tsetse flies transmit the disease.
  • African trypanosomiasis, widely known as sleeping sickness, is caused by the parasite protozoan species Trypanosoma gambiense. It is transmitted to humans by the bites of sub-Saharan Africa’s tsetse flies.
  • Initial manifestations of the parasite include fever, headache, joint pain, and itching. When the infection advances, it can impact the central nervous system, causing symptoms such as disorientation and sleep difficulties and, if left untreated, coma and death.
  • Typically, the parasite is identified in blood or other bodily fluids in order to diagnose African trypanosomiasis, and pentamidine or suramin are frequently used to treat the disease. In advanced situations in which the parasite has passed the blood-brain barrier, it may be essential to provide drugs such as melarsoprol or eflornithine.
  • Preventing African trypanosomiasis entails wearing protective garments, applying insect repellents, and avoiding places with dense populations of tsetse flies. In addition to insecticide-treated traps and aerial spraying, the control of tsetse flies has been helpful in reducing the spread of the disease.

Morphology of Trypanosoma gambiense

  • T. gambiense are microscopic, elongated, flattened, have a fusiform body with pointy ends, and are covered by a membranous pellicle that maintains the body’s shape.
  • It ranges in size from 10 to 40 µm in length and 2.5 to 10 µm in width. Depending on the length of the parasite, a single flagellum originates from a basal body located near the posterior end and spirals around the body to form a membrane with three or four folds.
  • The undulating membrane is thought to be an adaption for blood movement. At its anterior end, the flagellum is free.
  • The nucleus is huge and oval, located in the body’s centre, and the cytoplasm contains numerous volutin granules, which are greenish granules with refractile properties.
  • These granules store primarily glycogen and phosphate as food particles. The basal granule or blepharoplast is found at the base of the flagellum, near to another granule, the parabasal body.

Characteristics of Trypanosoma Gambiense

  • Locomotion of Trypanosoma Gambiense: The undulating membrane and flagellum of Trypanosoma gambiense are responsible for its motility. They swim (in blood and lymph) in the direction of the body’s pointed end, propelled by the membrane’s undulating wave patterns.
  • Nutrition in Trypanosoma Gambiense: Nutrition is saprozoic. Trypanosoma gambiense feeds on the blood and tissue fluids of its host via osmotrophy. It digests sugars by the action of enzymes. From the blood and intercellular fluids of the tissues, the nutrients is absorbed through the general body surface.
  • Respiration in Trypanosoma Gambiense: Respiration is fundamentally anaerobic since it occurs in an oxygen-free environment. The glucose received undergoes glycolysis to release the energy required for metabolic processes.
  • Excretion in Trypanosoma Gambiense: The metabolic waste products are distributed directly into the host’s blood and lymph through the pellicle or general body surface. Due to its parasitic nature, the osmoregulatory system is ineffective in every way.
  • Reproduction in Trypanosoma Gambiense: The asexual reproduction of Trypanosoma gambiense is facilitated by longitudinal binary fission. Sexual reproduction in this species is unknown.

Transmission of Trypanosoma Gambiense

Transmission from one vertebrate host to another is facilitated by the bloodsucking fly Glossina palpaiis, which serves as an intermediary host (Tsetse fly). Transmission takes place in two ways:

1. Mechanical or direct transmission

  • When a tsetse fly (carrier fly) attacks a man infected with Trypanosome, some Trypanosomes adhere to the fly’s proboscis, and when the fly bites another man, the Trypanosomes are introduced into his circulation if the interval between bites is less than 24 hours.
  • Such transmission is referred to be mechanical or direct since the fly only serves as a mechanical carrier and the parasites undergo no modifications.

2. Cyclical transmission

  • When a fly ingests the blood of an infected man, the parasites reach the midgut of the fly, where they remain for two days and begin to grow. Parasites can only be introduced into another man’s blood after passing through a series of stages. The term for this sort of transmission is cycle transmission.

Reservoirs of Trypanosoma Gambiense

  • Trypanosomes are harmless to their natural hosts, which include wild antelopes, pigs, and buffaloes, etc. The parasite does not damage these wild antelopes and mammals; hence, they serve as reservoir hosts from which the infection is transmitted by vectors or intermediary hosts.

Structure of Trypanosoma Gambiense

Structure of Trypanosoma Gambiense
Structure of Trypanosoma GambienseStructure of Trypanosoma Gambiense

Shape and size

  • The microscopic body of Trypanosoma gambiense is slender, elongated, colourless, sickle-shaped, and flattened at both ends. The front end is sharper than the posterior end, which is rounded.
  • The length of its body ranges from 15 to 30 microns, and its breadth from 1 to 3 microns. The shape and size of its body varies depending on its form.

Pellicle and Undulating Membrane

  • A thin, elastic, and resilient pellicle covers the body. It maintains the body’s general form. The pellicle is composed of fine fibrils that run the length of the entire body. These filaments are known as microtubules. When its flagellum beats, the pellicle is drawn out into an uneven membranous fold to one side.
  • This fold is referred to as undulating membrane, which is thought to be an adaptation structure for mobility in a viscous environment (blood, lymph) in which it resides.


  • Trypanosoma has a single flagellum, i.e., it is uniflagellate. The flagellum originates from the basal granule located towards the body’s posterior end. The flagellum runs forward and remains attached along the entire length of the body, marking the boundary of a membrane that undulates.
  • When reaching the anterior end of the body, the flagellum becomes free and hangs freely. Similar to that of Euglena, the flagellum consists of an axoneme surrounded by a thin cytoplasmic sheath.


  • Immediately posterior to the basal granule is a tiny, spherical or disc-shaped parabasal body or kinetoplast that includes extra-nuclear DNA and is, therefore, a body that duplicates itself. Kinetoplasts are associated with movement.


  • It has separate ectoplasm and endoplasm within its cytoplasm. Many volutin granules, which are greenish, refractile, and deeply stained, are dispersed throughout the cytoplasm. The granules of volutin are metabolic food stores consisting primarily of glycogen and phosphates.
  • In addition to tiny vacuoles containing hydrolytic enzymes, the cytoplasm contains all other cellular components, including the Golgi apparatus, mitochondria, endoplasmic reticulum, and nucleus.


  • In the middle of its body, a solitary, oval or spherical, vesicular nucleus (trophonucleus) is visible. There is a huge endosome enclosed by chromatin in the nucleus.

Electron structure of Trypanosoma

  • With an electron microscope, Vickerman (1965) has examined the structure of Trypanosoma Gambiense. He has observed a pocket-like structure dubbed the flagellar pocket near the posterior end of the basal body.
  • It is assumed that the flagellar pocket is a reservoir similar to that of Euglena. Its flagellum has a 9 + 2 internal fibrillar configuration, similar to that of Euglena.
  • From its anterior to its posterior end, a single, elongated, enormous mitochondrion is differentiated into an anterior mitochondrion or anterior chondriome and a posterior mitochondrion or posterior chondriome.
  • Around the basal granule, it is assumed that the posterior mitochondrion with additional nuclear DNA forms kinetoplast.
  • This DNA consists of two strands. There is one Golgi apparatus between the flagellar pocket and the nucleus. The usual structure of the nucleus is a double-layered nuclear membrane with nuclear pores.
  • Either the endoplasmic reticulum is linked to the outer nuclear membrane or it is located loose in the cytoplasm. In addition to being connected to the endoplasmic reticulum, ribosomes are also present as free entities in the cytoplasm.

Life cycle of Trypanosoma gambiense

  • T. gambiense is a digenetic parasite that requires the participation of two hosts to complete its life cycle. Humans are the principal host, whereas the intermediate host is the blood-sucking Tsetse fly of the species Glossina.
  • Mammals such as pigs, antelopes, and buffaloes serve as reservoir hosts for the parasite. As the Tsetse fly draws blood from an infected human or wild mammal, it transports the trypanosomes to its midgut, where they divide asexually via longitudinal binary fission.
  • Here, the parasite alters its shape and gives rise to short, stumpy metacyclic forms. At this point, the fly is considered infectious.
  • When an infected tsetse fly bites a healthy human host, these metacyclic trypanosomes are released into the bloodstream and the life cycle is repeated.
  • Sexual reproduction in T. gambiense is unknown. It is primarily a parasite of human connective tissue, where it proliferates rapidly.
  • It consumes a considerable quantity of glucose, invades regional lymph nodes via the lymphatic system, and also invades the blood system, resulting in parasitaemia. It eventually settles in the brain. It is important to understand that African sleeping sickness is a central nervous system disorder.
Life cycle of Trypanosoma gambiense
Life cycle of Trypanosoma gambiense

Trypanosoma gambiense Life cycle in human

1. Infection

  • The healthy individual becomes infected when a tsetse fly carrying the infectious metacyclic form bites them.
  • As the fly bites, it releases trypanosomes into the bloodstream, which then evolve into long, slender forms and proliferate asexually at the site of inoculation by binary longitudinal fission.
  • They become “stupid” through “intermediate forms.” Hence, parasites enter the bloodstream, causing parasitaemia.
  • The trypomastigote forms, particularly the small, stumpy ones, are ingested by the tsetse fly along with its blood meal and undergo a series of intricate biological transformations within the insect host prior to infecting humans.

2. Multiplication

  • All human parasite stages are extracellular because they are present in the blood cells. In human blood, flagellum-less metacyclic forms develop into long, slender forms with long flagella.
  • These stages are able to swim freely due to the pounding of their flagellum and the vibratory movements of the undulating membrane.
  • They reproduce asexually through longitudinal binary fission and gain energy through anaerobic glycolysis.

3. Metamorphosis

  • When blood-produced antibodies prevent the absorption of glucose, glycolysis is inhibited. As a result, the trypanosomes cease to divide and shrink into short, stubby forms devoid of flagellum.
  • These stubby forms do not eat and will ultimately perish if not ingested by a tsetse fly coupled with a blood meal from an infected human.

4. Relapse of infection

  • However, it has been noted that some of the long and slender forms of trypanosomes do not undergo any transformation, but rather alter their antigen in blood against which the host has generated antibodies.
  • These unchanged, skinny forms continue to live and proliferate in the blood, resulting in subsequent relapses of the infection.
Trypanosoma gambiense Life cycle in human
Trypanosoma gambiense Life cycle in human

Trypanosoma gambiense Life cycle in tsetse fly

1. Transfer to tsetse fly

  • When tsetse flies feed on the blood of an infected individual, they also consume short, stumpy forms of parasites. It is the stubby forms that continue vector development.

2. Development in mid gut

  • Within the insect midgut’s peritrophic membrane, further growth of stubby forms occurs. In the middle of the intestine, the parasite transforms into a long, slender form and reproduces asexually through longitudinal binary fission.
  • The kinetoplast travels away from the body’s posterior end. The energy-producing process is related to mitochondrial pyruvic acid oxidation.

3. Development in salivary gland

  • Eventually, the long, slender forms travel into insect salivary glands via the oesophagus and mouthparts.
  • Here, they transform into crithidial forms, which have a shorter body, a decreased flagellum, and a kinetoplast in front of the nucleus. As blood glucose gradually falls, the mitochondria expand their cristae network, and the parasite respires more efficiently.
  • In the lumen of salivary glands, crithidial forms multiply and change into slender metacyclic forms. When a healthy individual is bitten by a tsetse fly, the metacyclic stage is transferred into his bloodstream, where it initiates another illness.

4. Sleeping sickness

  • The pathogen T. gambiense causes West African sleeping sickness. It differs from American sleeping sickness and encephalitis, both of which are caused by filterable viruses.
Trypanosoma gambiense Life cycle
Trypanosoma gambiense Life cycle

Reproduction in Trypanosoma Gambiense

The asexual reproduction of Trypanosoma gambiense is facilitated by longitudinal binary fission. Sexual reproduction in this species is unknown.

Longitudinal Binary Fission

In longitudinal binary fission, the basal granule (blepharoplast) initiates the division, which is then followed by the kinetoplast.

Following this, a new flagellum begins to emerge along the edge of the undulating membrane. The division of the nucleus is subsequently followed by the longitudinal division of the cytoplasm, beginning at the front end and extending backwards until the daughter cells split. By repeatedly dividing, parasites in the blood of their vertebrate host multiply until the blood is swarming with them.

Pathogenicity of Trypanosoma Gambiense

  • Local chancre at the site of inoculation and lymphadenitis – Trypomastigote multiplication at the site of inoculation results in a localised inflammatory lesion. After the formation of this chancre, organisms travel through lymphatic routes to the bloodstream, resulting in lymph node proliferation. The ensuing parasitemia is often mild and intermittent.
  • Intermittent parasitemia accompanied by antigenic changes – Replicating organisms of the dominant antigenic type manufacture surface glycoproteins continually. As a new dominant antigenic variant emerges, the trypomastigotes vanish from the blood for 3 to 8 days before reappearing.
  • During parasitemia, trypanosomes localise in the tiny blood arteries of the heart and central nervous system accompanied with local vasculitis (CNS). This localization leads in endothelial growth and the infiltration of plasma cells and lymphocytes into the perivascular space. Hemorrhage and demyelinating panencephalitis may ensue in the brain. Uncertain is the mechanism through which trypanosomes induce vasculitis.
  • High quantities of IgM contain both specific and nonspecific antibodies. The majority of IgM is shed from the parasite’s surface and functions as a T-cell–independent antigen to directly stimulate B cells to make antibodies. The antibody produced in this manner is IgM, which can bind to the organism and destroy it through lysis and opsonization.
  • Immune complexes may induce anaemia and vasculitis

The infection induces a vast, nonspecific polyclonal activation of B cells, the generation of high amounts of IgM (usually eight to sixteen times the normal limit), and the inhibition of other immune responses. The majority of this reaction consists of specialised protective antibodies that are eventually accountable for the parasitemia’s management. Some, however, consist of heterophile antibodies that are not specific, DNA antibodies, and rheumatoid factor. The elimination of trypanosomes by antibodies results in the release of invariant nuclear and cytoplasmic antigens and the formation of circulating immune complexes.


The trypanosomal chancre emerges as a raised, ruddy nodule on one of the exposed body surfaces two to three days following the bite of the tsetse fly. Two to three weeks after the commencement of parasitemia, the patient gets recurring fever, lymphadenopathy, skin rash, headache, and mental impairment. Between four to six weeks, myocarditis and Brain involvement manifest in the Rhodesian type of the disease. In 6 to 9 months, heart failure, convulsions, coma, and death will ensue. Typically, sleeping sickness in the Gambia progresses more slowly. Frequent bouts of fever occur for years prior to the progressive appearance of Neurological symptoms. In the ultimate phase, the patient gets a fatal intercurrent infection or falls into a coma.

Polymorphic Forms of Trypanosoma Gambiense

The form of Trypanosoma Gambiense is polymorphic. Hoare (1966) identified as many as six morphologic stages in the life cycle of various Trypanosoma species. These classifications are mostly based on the configuration of the flagellum, its origin, and its path through the body. Yet, two or more of these forms exist in either one or both hosts during the life cycle of the various Trypanosoma species. Some polymorphic forms include the following:

  1. Leishmanial (amastigote): It has a nucleus and a tiny, oval or spherical body. The basal granule and kinetoplast appear as decreased spots in front of the nucleus. The flagellum is diminished and embedded within the cytoplasm; an external flagellum is absent.
  2. Leptomonad (promastigote): It has an elongated body with a central nucleus. In the anterior end are located the basal granule and kinetoplast. The basal granule gives rise to a free flagellum, and no undulating membrane is produced.
  3. Crithidial (epimastigote): It has a short, elongated, yet stumpy body. The basal granule and kinetoplast are positioned in front of the central nucleus. A lengthy flagellum emerges from the basal granule and becomes independent anteriorly. Undeveloped membrane with undulations.
  4. Trypanosome (trypomastigote): It has an elongated and thin body. The basal granule and kinetoplast are located at the body’s posterior end. Large flagellum that becomes free anteriorly. The membrane’s undulations are fully developed.

Disease Caused by Trypanosoma Gambiense

  • Trypanosoma gambiense is the causative agent of trypanosomiasis, also known as sleeping sickness, which ultimately results in the patient’s demise.
  • In fact, Trypanosome causes two diseases with symptoms that are practically identical. This is Gambia sleeping sickness and Rhodesian sleeping sickness.
  • The vector of the Gambian sleeping sickness is Glossina palpalis, while the vector of the Rhodesian sleeping sickness is Glossina morsitans. The Gambian sleeping sickness occurs in the western portion of Africa, while the Rhodesian sleeping sickness occurs throughout the remainder of Africa.
  • The sole distinction between the two is that the latter is more lethal, causing death within three to four months after infection.


  • Examining lymph node aspirates, blood, or cerebrospinal fluid for the presence of trypomastigotes using a microscope.
  • Actively motile organisms are frequently visible in a simple wet mount preparation smear during the onset of an illness.
  • Patients can be examined for high levels of IgM in the blood and spinal fluid, as well as particular trypanosomal antibodies, utilising a variety of methods.
  • A card agglutination test for trypanosomiasis (CATT) done on blood drawn from a fingerstick can provide serologic confirmation within minutes.
  • Subspecies-specific DNA probes could be beneficial for identifying organisms in clinical specimens.


  • If the material displays signs of CNS involvement, agents that can cross the blood–brain barrier are required.
  • Melarsoprol, a highly poisonous arsenical, is the most effective anti-tuberculosis medication (Mel B). Although this medication rarely causes fatal hemorrhagic encephalopathy, the deadly consequence of untreated CNS illness necessitates its usage.
  • When taken alone or in conjunction with suramin, the ornithine decarboxylase inhibitor eflornithine (DFMO) appears capable of treating CNS illness caused by T brucei gambiense without the severe adverse effects associated with melarsoprol. Unfortunately, it is somewhat costly.
  • If the central nervous system (CNS) is not involved, less toxic drugs such as suramin, pentamidine, and eflornithine can be employed. In such instances, the rate of recovery is high and complete.

Prevention (Prophylaxis)

  • There have been numerous attempts to suppress tsetse flies, including the use of insecticides, deforestation, and the introduction of sterile males into the population.
  • Nevertheless, none of these methods have proven entirely effective. The tsetse fly is larviparous and carries a developing larva until it is ready to pupate. This improves the chances of survival for flies.
  • Moreover, adults are capable fliers. There has been minimal success in eradicating disease reservoirs through early detection and treatment of human infections and the elimination of wildlife.
  • Efficacious vaccine development is under underway, but is hindered by the antigenic diversity of trypanosomes.
  • With bug repellents and protective clothes, one can accomplish personal safety. Notwithstanding the fact that pentamidine was formerly advised for preventative usage,


What is Trypanosoma gambiense?

Trypanosoma gambiense is a species of parasitic protozoa that causes African trypanosomiasis, also known as sleeping sickness.

How is Trypanosoma gambiense transmitted to humans?

Trypanosoma gambiense is transmitted to humans through the bite of infected tsetse flies, which are found in sub-Saharan Africa.

What are the symptoms of African trypanosomiasis?

Symptoms of African trypanosomiasis can include fever, headache, joint pain, itching, confusion, sleep disturbances, and ultimately, coma and death if left untreated.

How is African trypanosomiasis diagnosed?

Diagnosis of African trypanosomiasis typically involves identifying the parasite in blood or other bodily fluids.

How is African trypanosomiasis treated?

Treatment for African trypanosomiasis often involves medications such as pentamidine or suramin, but advanced cases may require medications such as melarsoprol or eflornithine.

How can African trypanosomiasis be prevented?

Prevention measures for African trypanosomiasis include wearing protective clothing, using insect repellents, and avoiding areas with high tsetse fly populations.

Where is Trypanosoma gambiense found?

Trypanosoma gambiense is found in sub-Saharan Africa, primarily in rural areas where tsetse flies are present.

Can animals be affected by Trypanosoma gambiense?

Yes, animals such as cattle and wild game can also be affected by Trypanosoma gambiense.

How is the spread of Trypanosoma gambiense controlled?

Control of tsetse flies through techniques such as insecticide-treated traps and aerial spraying has been effective in reducing the spread of Trypanosoma gambiense.

How many people are affected by Trypanosoma gambiense?

The World Health Organization estimates that approximately 10,000 cases of Trypanosoma gambiense occur annually, although the true number of cases may be higher due to underreporting in remote areas.



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