2. References:
• Murray, P.R., K.S. Rosenthal, G.S. Kobayashi and M.A. Pfaller. 2000.
Chapter 76: Blood and Tissue Protozoa. Medical Microbiology. 4th
edition. Mosby Publishing. St. Louis
Centers for Disease Control and Prevention. 2015. Parasites - African
Trypanosomiasis (also known as Sleeping Sickness). 1600 Clifton Rd.
Atlanta, GA 30329-4027, USA. Retrieved from:
http://www.cdc.gov/parasites/sleepingsickness/biology.html
Odero, R. 2015. African trypanosomiasis. Medscape. Retrieved from:
http://emedicine.medscape.com/article/228613-overview#a5
3. The Culprit!
Trypanosoma brucei gambiense
Kingdom: Protista
Phylum: Sarcomastigophora
Class: Zoomastigophora
Order: Kinetplastida
Family: Trypanosomatidae
Genus: Trypanosoma
Species: T. brucei
Subspecies: T. b. gambiense
6. Brief Description:
The African trypanosomiasis is a
deadly disease caused by the
Trypanosoma brucei gambiense and
trasnsmitted by the tsetse fly.
7. Causes
• A bite from an infected tsetse fly causes African
trypanosomiasis .
• Blood transfusions are a rare cause of parasitic
transmission.
• In rare cases, accidental transmission in the laboratory has
been implicated.
9. Symptoms
Short term symptoms Long term symptoms
1. Occasional Ulcer 1. Lethargy
2. Fever 2. Tremors
3. Myalgia 3.Meningoencephalitis
4. Athralgia 4.Mental retardation
5. Lymph Node Enlargement 5. General Deterioration
Final Stages of the Disease
1. Convulsions
2. Hemiplegia
3. Comatose State
4. DEATH
10. Laboratory Diagnosis
• Thin and thick blood smears
• Centrifugation of heparized
samples and anion-exchange
chromatography
• Serologic test
• Immunofluorescence
• ELISA
• agglulation
11. Treatment, Prevention and Control
Acute stages:
1. Suramin
2. Pentamidine
3. Difluoromethylorithine
Chronic Stages:
1. Melarsoprol
2. Tryparsamide with suramin
3. Difluoromethylorithine
12. Treatment, Prevention and Control
1. Control Breeding Sites
2. Insecticides
3. Treatment of Human Cases
Editor's Notes
For further reading:
Hemoflagellates- any parasitic flagelatte protozoan that lies in the bloodstream
The infective stage of the organism is the trypomastigote which is present in the salivary glands of transmitting tsetse fly
The organism at this stage has a free flagellum and an undulating membrane running the full length of the body
The trypomastigotes enter the wound created by the fly and find their way in blood and lymph eventually invading cells.
Reproduction of the trypomastigotes in blood is by binary or longitudinal fission
These trypomastigotes in blood are then infective for biting tsetse flies in the midgut of which further reproduction occurs
The organisms then migrate to the salivary glands where an epimastigote form (with a free flagellum but only a partial undulating membrane) continues reproduction to the infective trypomastigote stage
Tsetse flies became infective 4 to 6 weeks after feeding on blood from a diseased patient.
Life cycle:
1. Tsetse fly takes a blood meal (injects metacyclic trypomastigote)
during a blood meal of the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into bloodstream
2. Injected metacyclic trypomastigotes transform into bloodstream trypomastigotes are carried to the other sites
inside the host, they transform into bloodstream trypomastigotes are carried to the other sites throughout the body reach other blood fluids (e.g. lymph, spinal fluid) and continue the replication by binary fission.
3. Trypomastigotes multiply by binary fission in various body fluids eg. Blood lymph and spinal fluid
the entire life cycle of African trypanosome is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host.
Trypomastigotes in blood
Testse fly takes a blood meal (bloodstream trypomastigotes are ingected)
in the fly’s midgut, the parasite transform procyclic trypomastigotes mulitiply by binary fission
6. Bloodstream trypomastigotes transform into procyclic trypomastigotes in tsetse fky’s midgut. Procyclic trypomastigotes multiply by binary fission
leaves the midgut and transform into epimastigote
7. Procyclic trpomastigotes will transform into epimastigotes
the epimastigotes reach the fly’s salivary gland and continue multiplication by binary fission
8. Epimastigotes will transform into metacyclic trypomastigotes
the cycle in the fly take appox. 3-4 weeks. Humans are main reservoirs of T.b. gambiense
Sometimes spelled tzetze and also known as tik-tik flies
Are large biting flies that inhabit much of Mid-continental Africa between the Sahara and the Kalahari deserts
That live by feeding on the blood of vertebrate animals and are the primary African biological vectors of trypanosomes which cause human sleeping sickness and animal trypanosomiasis also known as nagana
Tsetse have been exclusively studied because of their disease transmission. These flies are multivoltine, typoically producing about four generations yearly and upo to 31 generations total over their entire lifespan
They are different fro housefly but can be distinguished by various characteristics of their anatomy.
Tsetse fold their wings completely when they are resting so that one wing rests directly on top of the other over the abdomen
Have long proboscis which extends directly forward and is attached by a distinct bulb to the bottom of their head
Also known as Sleeping disease
is found in 24 countries in west and central Africa. This form currently accounts for over 98% of reported cases of sleeping sickness and causes a chronic infection
A person can be infected for months or even years without major signs of the disease. When more evident symptoms emerge, the patient is often already in an advanced disease stage where the CNS is affected
Is limited to tropical west and central Africa, correlating with the range of the tsetse fly vector