African Sleeping Sickness - Tsetse Fly

Life Cycle of Trypanosoma Gambiense

African Sleeping Sickness is caused by Trypanosoma gambiense. Trypanosoma gambiense as a human parasite was first observed by Forde in 1901. David Bruce in 1895 brought it forward that sleeping sickness is transmitted by the tsetse fly. Trypanosoma gambiense is distributed mainly in Central and West Africa particularly in Nigeria and Congo therefore it is called African Sleeping Sickness and occurs mostly in these regions. Areas near the rivers and lakes have the greatest incidence of infection since tsetse fly lives there in low and thick vegetation.

African Sleeping Sickness - Trypanosoma Gambiense

Taxonomy of Trypanosoma Gambiense: -

Phylum - Protozoa

Subphylum - Sarcomastigophora

Superclass - Mastigophora

Class - Zoomastigophora

Order - Kinetoplastida

Genus - Trypanosoma

Species - Gambiense

Tsetse Fly

It is the vector that transmits T.Gambiense from man to man and therefore spreads African Sleeping Sickness.

Trypanosoma Gambiense Habitat

Trypanosoma lives in the bloodstream and in the lymph gland of infected persons in the early stages of the disease. After that, it invades the cerebrospinal fluid (CSF) of the central nervous system causing fever, anemia, and death. The tsetse fly (Glossonia Palpalis) and Glossonia tachinoides are the chief vectors that transmit trypanosomes from man to man causing African Sleeping Sickness.

The Trypanosomes utilize domestic and wild mammals such as monkeys, dogs, buffaloes, pigs and red bucks as Reservoir hosts. In these hosts, it does not undergo any developmental cycle but it waits for its introduction into the human organisms. Entry into and exit from Reservoir host occurs always through the bite of tsetse fly which feeds upon the blood of man as well as the Reservoir hosts and causes African Sleeping Sickness.

Structure of Trypanosoma Gambiense

The structure of Trypanosoma gambiense can be studied under the following heads.

Shape and Size

It is a unicellular and microscopic organism having an elongated and fusiform body. It measures 10 to 40 micron in length and 2.5 to 10 micron in width. The anterior end is pointed and the posterior is blunt. T. gambiense is a polymorphic species that occurs in two developmental forms, the trypanosome form, and the crithidial form. In humans, the trypanosome form may be slender or short stumpy. Whereas, In tsetse fly its form is long and Slender in the midgut and short and stumpy in salivary glands. In Contrast, Crithidial form occurs only in the salivary gland of the tsetse fly.


The whole body is enclosed in a thin, tough and elastic pellicle. It is supported by fine fibrils called microtubules. These run along the whole length of the body. Microtubules help in maintaining the shape of the body.


Trypanosomes bear a single flagellum. It arises from the basal body or blepharoplast (kinetosome) situated near the posterior end of the body. It runs forward, attached along the entire length of the body, and becomes free at the anterior end. However, If the TS of the flagellum is seen under the electron microscope it shows the usual 9 + 2 internal fibril arrangement. It also bears unilateral hair. When trypanosome moves in blood, the undulating waves pass from tip to base of the flagellum.

 Undulating membrane

When the flagellum beats, the pellicle pulls up into a membranous fold known as the undulating membrane. This helps in locomotion in viscous.


The cytoplasm encloses within the Pellicle. The cytoplasm is not differentiated into ectoplasm and endoplasm. Electron microscopic studies show that there is a Reservoir at the posterior end of the body. The basal body or of the flagellum is located at the base of the reservoir. Moreover, An elongated and uneven mitochondrion with tubular cristae is present in the cytoplasm from one end of the body to the other. Just near blepharoplast, the mitochondria form the disk-like parabasal body or kinetoplast. Additionally, the Golgi apparatus is present between the Reservoir and nucleus. The endoplasmic reticulum is present throughout the cytoplasm. Ribosomes are found attached to the endoplasmic reticulum as well as scattered freely in the cytoplasm.

The cytoplasm also contains several greenish refractile granules, called the volutin granules. These are stored food granules and contain glycogen and phosphates. The cytoplasm also contains many small vacuoles with hydrolytic enzymes.


Within the Cytoplasm a large, oval and vesicular nucleus in the center of the body. A double unit membrane surrounds the nucleus and bears pores. Whereas, The nucleolus lies centrally within the nucleus.


In trypanosome gambiense sexual reproduction is absent. Asexual reproduction takes place by longitudinal binary fission. In this process first, the kinetoplast and the blepharoplast divide to become paired. The old flagellum remains attached to one of the blepharoplast, while a new one begins to grow out from the other blepharoplast. The nucleus divides mitotically into two daughter nuclei. Finally, the body splits mid- longitudinally, from the anterior end backward, forming two daughter trypanosomes.

Life Cycle of Trypanosoma Gambiense

The life history of T.gambiense is digenetic and occurs in two hosts. The primary host is the man and the intermediate host is a blood-sucking insect called tsetse fly. Mammals like pigs, monkeys, buffaloes, antelopes act as reservoir hosts.

Life Cycle in man


T.Gambiense is introduced into the bloodstream of Man by the bite of the tsetse fly, which harbors the infective metacyclic forms in the lumen of its salivary glands. When tsetse fly feeds upon man's blood, it releases the trypanosomes into his bloodstream.


That is to say, All the stages of trypanosomes in man are extracellular. Therefore, they are present in the blood plasma. In human blood, the metacyclic forms transform into long slender forms. These swim by the beating of their flagellum and the vibratile movement of the undulating membrane. These multiply by longitudinal binary fission. The multiplying trypanosomes obtain energy by anaerobic glycolysis.


When the absorption of glucose ceases due to antibodies produced in the blood, trypanosomes stop multiplying. As a result, They now shrink and form short stumpy forms. They have no flagellum. During the transformation from long Slender forms to short stumpy forms the intermediate forms with a somewhat shortened body and a free flagellum also appear. The stumpy forms do not feed and die if not sucked by the tsetse fly along with the blood meal.

Relapse of infection

However, Some of the long and Slender forms do not undergo a transformation, survive and continue to multiply in the blood leading to future relapses of the infection (African Sleeping Sickness).

 Life cycle in the tsetse fly 

The life cycle of T.Gambiense continues in the Tsetse fly by following ways -

Transfer to the tsetse fly

When a tsetse fly sucks the blood of an infected person, it also takes in the short stumpy forms along with the sucked blood.

Development in midgut

The short stumpy forms develop in the insect's midgut into long slender form. And multiply by longitudinal binary fission. Meanwhile, from the posterior end of the body, the kinetoplast moves father.

Development in salivary glands

The long and slender forms make their way into the salivary gland via the esophagus and mouthparts of the insect. Here they metamorphose into crithidial forms. These multiply in the lumen of the salivary gland and transform into Slender metacyclic forms. When the tsetse fly bites a healthy person, it transfers the metacyclic forms, along with saliva into his blood where they initiate another infection.

 African Sleeping Sickness caused by

African Sleeping Sickness is caused by Trypanosoma Gambiense. It is a fatal disease and thus results in the death of the patient. It is widespread in tropical and sub-tropical areas of South-Africa and is, therefore, known as African Sleeping Sickness.

Transmission of Disease

When tsetse fly (Glossonia Palpalis) sucks the blood of an infected man, it also takes in the short stumpy trypanosomes along with the sucked blood. The stumpy forms continue development in the vector. When this infected fly, bites a healthy man, the parasites reach the blood and cause African Sleeping Sickness. Thus the infection is transmitted by tsetse fly from man to man.

Symptoms and Pathogenesis of African Sleeping Sickness

The bite of tsetse fly causes local irritation which subsides after a few days. The inoculation of trypanosomes into the human bloodstream causes the Infection. Besides undergoing development in blood plasma, they also invade the lymphatic glands and the central nervous system. The invasion of lymphatic glands results in the swelling of these glands. When the parasites invade the cerebrospinal fluid (CSF), it causes the disease sleeping sickness. However, the first symptom of the disease is the irregular recurrent fever. Whereas, Other symptoms that follow the infection are weakness, loss of weight, anemia, an increase in pulse rate and severe headache. After some time, the patient falls asleep, first at irregular intervals and then lies in a coma. Death is always the ultimate fate.

Diagnosis of African Sleeping Sickness

In the laboratory, trypanosomes may be available in fresh or stained blood films, or in the extract of enlarged lymph glands. However, In the sleeping sickness stage, the examination of cerebrospinal fluid becomes necessary. 

African Sleeping Sickness Treatment

That is to say, the treatment of Gambient fever or African trypanosomiasis is possible in its early stages. But it is difficult to control when the parasites have entered CSF.

Drugs like Suramin sodium, Bayer 205, Atoxyl and Tryparsamide have been found useful in the early stages of African Sleeping Sickness. Persenophenyl Butyric Acid, Germanin, and Pentamidine are also effective in the early stages.Orsamine and Mealrsen oxide are fairly effective when it involves the central nervous.

Prevention and Control

  1. Prevention and control of African sleeping sickness depend upon the eradication of the tsetse fly. The flies can be eradicated by clearing out bushes and low trees along rivers in the endemic areas.
  2. Spraying of DDT over bushy areas in the vicinity of villages is effective in controlling the tsetse flies.
  3. Wild game animals act as a reservoir of Trypanosoma. Though its unfortunate to kill these reservoir hosts on a large scale, it becomes essential for the eradication of this disease.
  4. Injections of pentamidine or naphuride or antrypol should be given to people living in endemic areas. These infections remain effective for 3-6 months and prevent the chances of African Sleeping Sickness.
So after reading this article, we came to know that African Sleeping Sickness is because of Trypanosoma Gambiense. Its vector is Tsetse fly (Glossonia Palpalis). Moreover, the article told us about the habitat, life cycle, structure and various other information about the tsetse fly.

Certainly, You can share your views with us by sending an email and to know more about the science, nature and life processes stay connected to 

Other Articles - 
What is Sericulture








Post a Comment