Sleeping Sickness
Sleeping Sickness
Definition
Sleeping sickness (also called trypanosomiasis) is an infection caused by Trypanosoma protozoa; it is passed to humans through the bite of the tsetse fly. If left untreated, the infection progresses to death within months or years.
Description
Protozoa are single-celled organisms considered to be the simplest life form in the animal kingdom. The protozoa responsible for sleeping sickness are a variety that bear numerous flagella (hair-like projections from the cell that help the cell to move). These protozoa exist only on the continent of Africa. The type of protozoa causing sleeping sickness in humans is referred to as the Trypanasoma brucei complex, which can be divided further into Rhodesian (Central and East African) and Gambian (Central and West African) subspecies.
The Rhodesian variety live within antelopes in savanna and woodland areas, and they cause no problems with the antelope's health. The protozoa are then acquired by tsetse flies when they bite and suck the blood of an infected antelope or cow.
DAVID BRUCE (1855–1931)
David Bruce was born in Melbourne, Australia, on May 29, 1855, to Scottish immigrants. Bruce's family moved back to Scotland when he was five years old. Bruce attended the University of Edinburgh where he studied natural history and medicine. Following his graduation, he accepted a position working with a doctor. In 1883, Bruce married Mary Elizabeth Steele who would help him with his work throughout his life.
In 1884, Bruce began to study the disease "Malta, Mediterranean" when he and Mary were stationed in Malta with the Army Medical Service. Using a microscope, Bruce discovered that the disease was caused by a "microccus" that grew in the individual's spleen. The organism responsible for this disease was ultimately isolated by Bernhard L. F. Bang. In 1905, Bruce led a scientific team that discovered that the soldiers who contracted the disease had ingested the milk of infected goats. The disease disappeared when the soldiers quit drinking goat's milk. Many physicians began calling the disease "brucellosis" in honor of Bruce's discoveries. Bruce also conducted research in Africa where he found that the tsetse fly could infect humans, as well as animals, with the "nagana" disease. Ultimately, his work would prove that sleeping sickness was caused by the tsetse fly.
In 1903, Bruce became the director of the Royal Society's Sleeping Sickness Commission and, in 1908, he was knighted. He served as commandant of the Royal Army Medical College after he and his wife returned to England. Bruce died on November 20, 1931.
Within the tsetse fly, the protozoa cycle through several different life forms; ultimately they migrate to the salivary glands of the tsetse fly. Once the protozoa are harbored in the salivary glands, they are ready to be deposited into the bloodstream of the fly's next source of a blood meal.
Humans most likely to become infected by Rhodesian trypanosomes are people such as game wardens and visitors to game parks in East Africa, who may be bitten by a tsetse fly that has fed on game (antelope) carrying the protozoa. The Rhodesian variety of sleeping sickness causes a much more severe illness, with even greater likelihood of eventual death than the Gambian form.
The Gambian variety of Trypanosoma thrives in tropical rain forests throughout Central and West Africa; it does not infect game or cattle, and is primarily a threat to people dwelling in such areas, rarely infecting visitors.
Causes and symptoms
The first sign of infection with the trypanosome may be a sore appearing at the site of the tsetse fly bite about two to tree days after having been bitten. Redness, pain, and swelling occur, but are often ignored by the patient.
Stage I illness
Two to three weeks later, Stage I disease develops as a result of the protozoa being carried through the blood and lymph circulation of the host. This systemic (meaning that symptoms affect the whole body) phase of the illness is characterized by a fever that rises quite high, then falls to normal, then respikes (rises rapidly). A rash with intense itching may be present, and headache and mental confusion may occur. The Gambian form, in particular, includes extreme swelling of lymph tissue, with enlargement of both the spleen and liver, and greatly swollen lymph nodes. "Winterbottom's sign" is classic of Gambian sleeping sickness, and consists of a visibly swollen area of lymph nodes located behind the ear and just above the base of the neck. During this stage, the heart may be affected by a severe inflammatory reaction, particularly when the infection is caused by the Rhodesian variety of trypanosomiasis.
Many of the symptoms of sleeping sickness are actually the result of attempts by the patient's immune system to get rid of the invading organism. The heightened activity of the cells of the immune system result in damage to the patient's own organs, anemia, and leaky blood vessels. These leaks in the blood vessels end up helping to further spread the protozoa throughout the afflicted person's body.
One reason for the intense reaction of the immune system to the presence of the trypanosomes is also the reason why the trypanosomes survive so well despite the efforts of the immune system to eradicate them. The protozoa causing sleeping sickness are able to rapidly change specific markers (unique proteins) on their outer coats. These kinds of markers usually serve to stimulate the host's immune system to produce immune cells that will specifically target the marker, allowing quick destruction of those cells bearing the markers. Trypanosomes, however, are able to express new markers at such a high rate of change that the host's immune system is constantly trying to catch up.
Stage II illness
Stage II sleeping sickness involves the nervous system. Gambian sleeping sickness, in particular, has a clearly delineated phase in which the predominant symptoms involve the brain. The patient's speech becomes slurred, mental processes slow, and the patient sits and stares for long periods of time, or sleeps. Other symptoms resemble Parkinson's disease, including imbalance when walking, slow and shuffling gait, trembling of the limbs, involuntary movements, muscle tightness, and increasing mental confusion. Untreated, these symptoms eventually lead to coma and then to death.
Diagnosis
Diagnosis of sleeping sickness can be made by microscopic examination of fluid from the original sore at the site of the tsetse fly bite. Trypanosomes will be present in the fluid for a short period of time following the bite. If the sore has already resolved, fluid can be obtained from swollen lymph nodes for examination. Other methods of trypanosome diagnosis involve culturing blood, lymph node fluid, bone marrow, or spinal fluid. These cultures are then injected into rats, which develop blood-borne protozoa infection that can be detected in blood smears within one to two weeks. However, this last method is effective only for the Rhodesian variety of sleeping sickness.
Treatment
Without treatment, sleeping sickness will lead to death. Unfortunately, however, those medications effective against the Trypanosoma brucei complex protozoa all have significant potential side effects for the patient. Suramin, eflornithine, pentamidine, and several drugs that contain arsenic (a chemical which in higher doses is highly poisonous to humans), are all effective anti-trypanosomal agents. Each of these drugs, however, requires careful monitoring to ensure that the drugs themselves do not cause serious complications such as fatal hypersensitivity (allergic) reaction, kidney or liver damage, or inflammation of the brain.
Prevention
Prevention of sleeping sickness requires avoiding contact with the tsetse fly. Insect repellents and clothing that covers the limbs to the wrists and ankles are advisable. Public health measures have included drug treatment of humans who are infected with one of the Trypanosoma brucei complex. There are currently no immunizations available to prevent the acquisition of sleeping sickness.
Resources
ORGANIZATIONS
Centers for Disease Control and Prevention. 1600 Clifton Rd., NE, Atlanta, GA 30333. (800) 311-3435, (404) 639-3311. 〈http://www.cdc.gov〉.
KEY TERMS
Immune system— That network of tissues and cells throughout the body that is responsible for ridding the body of any invaders, such as viruses, bacteria, protozoa, etc.
Protozoa— Single-celled organisms considered to be the simplest life form in the animal kingdom.
Sleeping Sickness
Sleeping Sickness
Causes of sleeping sickness, and geographical distribution of the disease
Symptoms and progression of sleeping sickness
Sleeping sickness, also known as trypanosomiasis, is a protozoan infection passed to humans through the bite of the tsetse fly. If left untreated, it can progress to death within months or years.
Causes of sleeping sickness, and geographical distribution of the disease
Protozoa are single-celled organisms considered to be among the simplest animal life forms. The protozoa responsible for sleeping sickness are a flagellated variety (flagella are hair like projections from the cell which aid in mobility) that exist only in Africa. The type of protozoa causing sleeping sickness in humans is referred to as the Trypanosoma brucei complex. It is divided further into Rhodesian (affecting Central and East African countries) and Gambian (affecting Central and West African countries) subspecies.
The Rhodesian variety live within antelopes in savanna and woodland areas, causing no disruption to the antelope’s health. (While the protozoa cause no illness in antelopes, they are lethal to cattle that may become infected.) The protozoa are acquired by tsetse flies who bite and suck the blood of an infected antelope or cow.
Within the tsetse fly, the protozoa cycle through several different life forms, ultimately migrating to the salivary glands of the tsetse fly. Once the protozoa are harbored in the salivary glands they can be deposited into the bloodstream of the fly’s next blood meal.
Humans most likely to become infected by Rhodesian trypanosomes are game wardens or visitors to game parks in East Africa. The Rhodesian variety of sleeping sickness causes a much more severe illness with a greater likelihood of eventual death.
The Gambian variety of Trypanosoma thrives in tropical rain forests throughout Central and West Africa, does not infect game or cattle, and is primarily a threat to people dwelling in such areas. It rarely infects visitors.
Symptoms and progression of sleeping sickness
The first sign of sleeping sickness may be a sore appearing at the tsetse fly bite site about two to three days after having been bitten. Redness, pain, and swelling occur.
Two to three weeks later Stage I disease develops as a result of the protozoa being carried through the blood and lymphatic circulations. This systemic (meaning that symptoms affect the whole body) phase of the illness is characterized by a high fever that falls to normal then respikes. A rash with intense itching may be present, and headache and mental confusion may occur. The Gambian form includes extreme swelling of lymph tissue, enlargement of the spleen and liver, and greatly swollen lymph nodes. Winterbottom’s sign is classic of Gambian sleeping sickness; it consists of a visibly swollen area of lymph nodes located behind the ear and just above the base of the neck. During this stage the heart may be affected by a severe inflammatory reaction, particularly when the infection is caused by the Rhodesian form of the parasite.
Many of the symptoms of sleeping sickness are actually the result of attempts by the patient’s immune system to get rid of the invading organism. The overly exuberant cells of the immune system damage the patient’s organs, resulting in anemia, and leaky minute blood vessels. These leaky blood vessels help to spread the protozoa throughout the patient’s body.
One reason for the immune body’s intense reaction to the Trypanosomes is also the reason why the Trypanosomes survive so effectively. The protozoa are able to change rapidly specific markers on their outer coats. These kinds of markers usually stimulate the host’s immune system to produce immune cells specifically to target the markers and allow quick destruction of these invading cells. Trypanosomes are able to express new markers at such a high rate of change that the host’s immune system cannot catch up.
Stage II sleeping sickness involves the nervous system. The Gambian strain has a clearly delineated phase in which the predominant symptomatology involves the brain. The patient’s speech becomes slurred, mental processes slow, and he or she sits and stares or sleeps for long periods of time. Other symptoms resemble Parkinson disease: imbalance when walking, slow and shuffling gait, trembling of the limbs, involuntary movement, muscle tightness, and increasing mental confusion. These symptoms culminate in coma, then death.
Diagnosis
Diagnosis of sleeping sickness can be made by microscopic examination of fluid from the site of the tsetse fly bite or swollen lymph nodes for examination. A method to diagnose Rhodesian trypanosome involves culturing blood, bone marrow, or spinal fluid. These cultures are injected into rats to promote the development of blood-borne protozoan infection. This infection can be detected in blood smears within one to two weeks.
Treatment
Medications effective against the Trypanosoma brucei complex protozoa have significant potential for side effects. Suramin, eflornithine, pentamidine, and several drugs that contain arsenic (a chemical which is potentially poisonous) are effective anti-trypanosomal agents. Each of these drugs requires careful monitoring
KEY TERMS
Immune system —That network of tissues and cells throughout the body which is responsible for ridding the body of invaders such as viruses, bacteria, protozoa, etc.
Protozoa —Single-celled organisms considered to be the simplest life form in the animal kingdom.
to ensure that they do not cause serious complications such as a fatal hypersensitivity reaction, kidney or liver damage, or inflammation of the brain.
Prevention
Prevention of sleeping sickness requires avoiding contact with the tsetse fly; insect repellents and clothing which covers the limbs to the wrists and ankles are mainstays. There are currently no immunizations available to prevent sleeping sickness.
Resources
BOOKS
Cormican, M.G., and M.A. Pfaller. “Molecular Pathology of Infectious Diseases,” in Clinical Diagnosis and Management by Laboratory Methods. 20th ed. Philadelphia: W. B. Saunders, 2001.
Isselbacher, Kurt J., et al. Harrison’s Principles of Internal Medicine. 16th ed. New York: McGraw Hill, 2004.
Kobayashi, G., Patrick R. Murray, Ken Rosenthal, and Michael Pfaller. Medical Microbiology. St. Louis, MO: Mosby, 2003.
Mandell, Douglas, et al. Principles and Practice of Infectious Diseases. New York: Churchill Livingstone Inc., 2004.
OTHER
Centers for Disease Control and Prevention. “African Trypanosomiasis.” <http://www2.ncid.cdc.gov/travel/yb/utils/ybGet.asp?section=dis&obj=aftrypano.htm&cssNav=browseoyb> (accessed November 26, 2006).
Rosalyn Carson-DeWitt
Sleeping Sickness
Sleeping sickness
Sleeping sickness is a protozoan infection passed to humans through the bite of the tsetse fly. It progresses to death within months or years if left untreated.
Causes of sleeping sickness, and geographical distribution of the disease
Protozoa are single-celled organisms considered to be the simplest animal life form. The protozoa responsible for sleeping sickness are a flagellated variety (flagella are hair-like projections from the cell which aid in mobility) which exist only in Africa . The type of protozoa causing sleeping sickness in humans is referred to as the Trypanosoma brucei complex. It is divided further into Rhodesian (Central and East Africa) and Gambian (Central and West Africa) subspecies.
The Rhodesian variety live within antelopes in savanna and woodland areas, causing no disruption to the antelope's health. (While the protozoa cause no illness in antelopes they are lethal to cattle who may become infected.) The protozoa are acquired by tsetse flies who bite and suck the blood of an infected antelope or cow.
Within the tsetse fly, the protozoa cycle through several different life forms, ultimately migrating to the salivary glands of the tsetse fly. Once the protozoa are harbored in the salivary glands they can be deposited into the bloodstream of the fly's next blood meal.
Humans most likely to become infected by Rhodesian trypanosomes are game wardens or visitors to game parks in East Africa. The Rhodesian variety of sleeping sickness causes a much more severe illness with a greater likelihood of eventual death.
The Gambian variety of Trypanosoma thrives in tropical rain forests throughout Central and West Africa, does not infect game or cattle, and is primarily a threat to people dwelling in such areas. It rarely infects visitors.
Symptoms and progression of sleeping sickness
The first sign of sleeping sickness may be a sore appearing at the tsetse fly bite site about two to three days after having been bitten. Redness, pain , and swelling occur.
Two to three weeks later Stage I disease develops as a result of the protozoa being carried through the blood and lymphatic circulations. This systemic (meaning that symptoms affect the whole body) phase of the illness is characterized by a high fever that falls to normal then respikes. A rash with intense itching may be present, and headache and mental confusion may occur. The Gambian form includes extreme swelling of lymph tissue , enlargement of the spleen and liver, and greatly swollen lymph nodes. Winterbottom's sign is classic of Gambian sleeping sickness; it consists of a visibly swollen area of lymph nodes located behind the ear and just above the base of the neck. During this stage the heart may be affected by a severe inflammatory reaction particularly when the infection is caused by the Rhodesian form.
Many of the symptoms of sleeping sickness are actually the result of attempts by the patient's immune system to get rid of the invading organism . The overly exuberant cells of the immune system damage the patient's organs, anemia , and leaky blood vessels. These leaky blood vessels help to spread the protozoa throughout the patient's body.
One reason for the immune system's intense reaction to the Trypanosomes is also the reason why the Trypanosomes survive so effectively. The protozoa are able to change rapidly specific markers on their outer coats. These kinds of markers usually stimulate the host's immune system to produce immune cells specifically to target the markers and allow quick destruction of these invading cells. Trypanosomes are able to express new markers at such a high rate of change that the host's immune system cannot catch up.
Stage II sleeping sickness involves the nervous system . The Gambian strain has a clearly delineated phase in which the predominant symptomatology involves the brain . The patient's speech becomes slurred, mental processes slow, and he or she sits and stares or sleeps for long periods of time. Other symptoms resemble Parkinson's disease: imbalance when walking, slow and shuffling gait, trembling of the limbs, involuntary movement, muscle tightness, and increasing mental confusion. These symptoms culminate in coma , then death.
Diagnosis
Diagnosis of sleeping sickness can be made by microscopic examination of fluid from the site of the tsetse fly bite or swollen lymph nodes for examination. A method to diagnose Rhodesian trypanosome involves culturing blood, bone marrow, or spinal fluid. These cultures are injected into rats to promote the development of blood-borne protozoan infection. This infection can be detected in blood smears within one to two weeks.
Treatment
Medications effective against the Trypanosoma brucei complex protozoa have significant potential for side effects. Suramin, eflornithine, pentamidine, and several drugs which contain arsenic (a chemical which is potentially poisonous) are effective anti-trypanosomal agents. Each of these drugs requires careful monitoring to ensure that they do not cause serious complications such as a fatal hypersensitivity reaction, kidney or liver damage, or inflammation of the brain.
Prevention
Prevention of sleeping sickness requires avoiding contact with the tsetse fly; insect repellents and clothing which covers the limbs to the wrists and ankles are mainstays. There are currently no immunizations available to prevent sleeping sickness.
Resources
books
Andreoli, Thomas E., et al. Cecil Essentials of Medicine. Philadelphia: W.B. Saunders Company, 1993.
Berkow, Robert, and Andrew J. Fletcher. The Merck Manual of Diagnosis and Therapy. Rahway: Merck Research Laboratories, 1992.
Cormican, M.G., and M.A. Pfaller. "Molecular Pathology of Infectious Diseases," in Clinical Diagnosis and Management by Laboratory Methods. 20th ed. Philadelphia: W. B. Saunders, 2001.
Isselbacher, Kurt J., et al. Harrison's Principles of Internal Medicine. New York: McGraw Hill, 1994.
Kobayashi, G., Patrick R. Murray, Ken Rosenthal, and Michael Pfaller. Medical Microbiology. St. Louis, MO: Mosby, 2003.
Mandell, Douglas, et al. Principles and Practice of Infectious Diseases. New York: Churchill Livingstone Inc., 1995.
Rosalyn Carson-DeWitt
KEY TERMS
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .- Immune system
—That network of tissues and cells throughout the body which is responsible for ridding the body of invaders such as viruses, bacteria, protozoa, etc.
- Protozoa
—Single-celled organisms considered to be the simplest life form in the animal kingdom.
Sleeping Sickness
Sleeping sickness
Sleeping sickness (trypanosomiasis) is a protozoan infection passed to humans through the bite of the tsetse fly. It progresses to death within months or years if left untreated. Near-control of trypanosomiasis was achieved in the 1960s, but the disease has since re-emerged in Sub-Saharan Africa, where political instability and war have hampered public health efforts. As of 2002, the World Health Organization , in conjunction with Médicines Sans Frontièrs (Doctors Without Borders) and major pharmaceutical companies were in the midst of a five-year major effort to halt the spread of trypanosomiasis and treat its victims.
Protozoa are single-celled organisms considered to be the simplest animal life form. The protozoa responsible for sleeping sickness are a flagellated variety (flagella are hair-like projections from the cell which aid in mobility) which exist only in Africa. The type of protozoa causing sleeping sickness in humans is referred to as the Trypanosoma brucei complex. It is divided further into Rhodesian (Central and East Africa) and Gambian (Central and West Africa) subspecies.
The Rhodesian variety live within antelopes in savanna and woodland areas, causing no disruption to the antelope's health. (While the protozoa cause no illness in antelopes, they are lethal to cattle who may become infected.) The protozoa are acquired by tsetse flies who bite and suck the blood of an infected antelope or cow. Within the tsetse fly, the protozoa cycle through several different life forms, ultimately migrating to the salivary glands of the tsetse fly. Once the protozoa are harbored in the salivary glands, they can be deposited into the bloodstream of the fly's next blood meal.
Humans most likely to become infected by Rhodesian trypanosomes are game wardens or visitors to game parks in East Africa. The Rhodesian variety of sleeping sickness causes a much more severe illness with a greater likelihood of eventual death. The Gambian variety of Trypanosoma thrives in tropical rain forests throughout Central and West Africa, does not infect game or cattle, and is primarily a threat to people dwelling in such areas. It rarely infects visitors.
The first sign of sleeping sickness may be a sore appearing at the tsetse fly bite spot about two to three days after having been bitten. Redness, pain, and swelling occur. Two to three weeks later, Stage I disease develops as a result of the protozoa being carried through the blood and lymphatic circulations. This systemic (meaning that symptoms affect the whole body) phase of the illness is characterized by a high fever that falls to normal then re-spikes. A rash with intense itching may be present, and headache and mental confusion may occur. The Gambian form includes extreme swelling of lymph tissue, enlargement of the spleen and liver, and swollen lymph nodes. Winterbottom's sign is classic of Gambian sleeping sickness; it consists of a visibly swollen area of lymph nodes located behind the ear and just above the base of the neck. During this stage, the heart may be affected by a severe inflammatory reaction, particularly when the infection is caused by the Rhodesian form.
Many of the symptoms of sleeping sickness are actually the result of attempts by the patient's immune system to get rid of the invading organism. The overly exuberant cells of the immune system damage the patient's organs, causing anemia and leaky blood vessels. These leaky blood vessels help to spread the protozoa throughout the patient's body.
One reason for the immune system's intense reaction to the Trypanosomes is also the reason why the Trypanosomes survive so effectively. The protozoa are able to change rapidly specific markers on their outer coats. These kinds of markers usually stimulate the host's immune system to produce immune cells specifically to target the markers and allow quick destruction of these invading cells. Trypanosomes are able to express new markers at such a high rate of change that the host's immune system cannot catch up.
Stage II sleeping sickness involves the nervous system. The Gambian strain has a clearly delineated phase in which the predominant symptomatology involves the brain. The patient's speech becomes slurred, mental processes slow, and he or she sits and stares or sleeps for long periods of time. Other symptoms resemble Parkinson's disease: imbalance when walking, slow and shuffling gait, trembling of the limbs, involuntary movement, muscle tightness, and increasing mental confusion. These symptoms culminate in coma, then death.
Diagnosis of sleeping sickness can be made by microscopic examination of fluid from the site of the tsetse fly bite or swollen lymph nodes for examination. A method to diagnose Rhodesian trypanosome involves culturing blood, bone marrow, or spinal fluid. These cultures are injected into rats to promote the development of blood-borne protozoan infection. This infection can be detected in blood smears within one to two weeks.
Medications effective against the Trypanosoma brucei complex protozoa have significant potential for side effects. Suramin, eflornithine, pentamidine, and several drugs which contain arsenic (a chemical which is potentially poisonous) are effective anti-trypanosomal agents. Each of these drugs requires careful monitoring to ensure that they do not cause serious complications such as a fatal hypersensitivity reaction, kidney or liver damage, or inflammation of the brain. Trials are underway to monitor the effectiveness of new medications for treatment of trypanosomiasis.
Prevention of sleeping sickness requires avoiding contact with the tsetse fly; insect repellents , mosquito netting, and clothing that covers the limbs to the wrists and ankles are mainstays. There are currently no immunizations available to prevent sleeping sickness.
See also Protists
sleeping sickness
sleep·ing sick·ness • n. 1. a tropical disease caused by a parasitic protozoan (trypanosome) that is transmitted by the bite of the tsetse fly. It causes fever, chills, pain in the limbs, and anemia, and eventually affects the nervous system causing extreme lethargy and death. See also trypanosomiasis.2. another term for encephalitis lethargica.