African trypanosomiasis

African trypanosomiasis

Human African trypanosomiasis, sleeping sickness[1], African lethargy[1], or Congo trypanosomiasis[1] is a parasitic disease of people and animals, caused by protozoa of the species Trypanosoma brucei and transmitted by the tsetse fly.[2] The disease is endemic in some regions of Sub-Saharan Africa, covering about 36 countries and 60 million people. It is estimated that 50,000 to 70,000 people are currently infected, the number having declined somewhat in recent years.[3] Three major epidemics have occurred in recent history, one lasting from 1896–1906 and the other two in 1920 and 1970. In 2008 there was an epidemic in Uganda.[4]

Symptoms and clinical features

Symptoms begin with fever, headaches, and joint pains. As the parasites enter through both the blood and lymph systems, lymph nodes often swell up to tremendous sizes. Winterbottom's sign, the tell-tale swollen lymph nodes along the back of the neck, may appear. If untreated, the disease slowly overcomes the defenses of the infected person, and symptoms spread to include anemia, endocrine, cardiac, and kidney diseases and disorders. The disease then enters a neurological phase when the parasite passes through the blood-brain barrier. The symptoms of the second phase give the disease its name; besides confusion and reduced coordination, the sleep cycle is disturbed with bouts of fatigue punctuated with manic periods progressing to daytime slumber and night-time insomnia. Without treatment, the disease is invariably fatal, with progressive mental deterioration leading to coma and death. Damage caused in the neurological phase can be irreversible.[4]

In addition to the bite of the tsetse fly, the disease is contractible in the following ways:

Mother to child infection: the trypanosome can sometimes cross the placenta and infect the fetus.[5]
Laboratories: accidental infections, for example, through the handling of blood of an infected person and organ transplantation, although this is uncommon.
Blood transfusion
Sexual contact (might be possible, but happens rarely)[6]

Life cycle: The tsetse fly is large, brown and stealthy. While taking blood from a mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream

Inside the host, they transform into bloodstream trypomastigotes
are carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission
The entire life cycle of African Trypanosomes is represented by extracellular stages. A tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host
In the fly's midgut, the parasites transform into procyclic trypomastigotes,
multiply by binary fission,
leave the midgut, and
transform into epimastigotes
The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission.

The cycle in the fly takes approximately 3 weeks to progress.

Laboratory diagnosis: The diagnosis rests upon demonstrating trypanosomes by microscopic examination of chancre fluid, lymph node aspirates, blood, bone marrow, or, in the late stages of infection, cerebrospinal fluid. A wet preparation should be examined for the motile trypanosomes, and in addition a smear should be fixed, stained with Giemsa (or Field), and examined. Concentration techniques can be used prior to microscopic examination. For blood samples, these include centrifugation followed by examination of the buffy coat; mini anion-exchange/centrifugation; and the Quantitative Buffy Coat (QBC) technique. For other samples such as spinal fluid, concentration techniques include centrifugation followed by examination of the sediment. Isolation of the parasite by inoculation of rats or mice is a sensitive method, but its use is limited to T. b. rhodesiense. Antibody detection has sensitivity and specificity that are too variable for clinical decisions. In addition, in infections with T. b. rhodesiense, seroconversion occurs after the onset of clinical symptoms and thus is of limited use.

Three similar serological tests are available for detection of the parasite; the micro-CATT, wb-CATT, and wb-LATEX. The first uses dried blood while the other two use whole blood samples. A 2002 study found the wb-CATT to be the most efficient for diagnosis, while the wb-LATEX is a better exam for situations where greater sensitivity is required.[12]

Treatment:

First line, first stage: The current standard treatment for first stage disease is:
Intravenous pentamidine (for T.b. gambiense); or
Intravenous suramin (for T.b. rhodesiense)

The drug Eflornithine — previously used only as an alternative treatment for sleeping sickness due to its labour-intensive administration — was found to be safe and effective as a first-line treatment for the disease in 2008, according to the Science and Development Network's Sub-Saharan Africa news updates. [1]. Researchers tracked over 1,000 adults and children at a centre in Ibba, Southern Sudan—the first use of eflornithine on a large scale— and it was highly effective in treating the issue.

According to a treatment study of Trypanosoma gambiense caused human African trypanosomiasis, use of eflornithine (DMFO) resulted in fewer adverse events than treatment with melarsoprol. [13]

All patients should be followed up for two years with lumbar punctures every six months to look for relapse.

First line, second stage: The current standard treatment for second stage (later stage) disease is:
Intravenous melarsoprol 2.2 mg/kg daily for 10 consecutive days.[14]

Alternative first line therapies include:

Intravenous melarsoprol 0.6 mg/kg on day 1, 1.2 mg/kg IV melarsoprol on day 2, and 1.2 mg/kg/day IV melarsoprol combined with oral 7.5 mg/kg nifurtimox twice a day on days 3 to 10;[15] or
Intravenous eflornithine 50 mg/kg every six hours for 14 days.[16]

Combination therapy with eflornithine and nifurtimox is safer and easier than treatment with eflornithine alone, and appears to be equally or more effective. It has been recommended as first-line treatment for second stage T. b. gambiensis disease.[17]

Resistant disease: In areas with melarsoprol resistance or in patients who have relapsed after melarsoprol monotherapy, the treatment should be:
melarsoprol and nifurtimox, or
eflornithine

Prevention and control: For in depth information on prevention of the disease via tsetse fly control see Tsetse fly control.

Prevention and control focus on, where it is possible, the eradication of the parasitic host, the tsetse fly. Two alternative strategies have been used in the attempts to reduce the African trypanosomiases. One tactic is primarily medical or veterinary and targets the disease directly using monitoring, prophylaxis, treatment, and surveillance to reduce the number of organisms which carry the disease. The second strategy is generally entomological and intends to disrupt the cycle of transmission by reducing the number of flies. Instances of sleeping sickness are being reduced by the use of the sterile insect technique.

Regular active surveillance, involving case detection and treatment, in addition to tsetse fly control, is the backbone of the strategy for control of sleeping sickness. Systematic screening of communities in identified foci is the best approach as case-by-case screening is not practically possible in highly endemic regions. Systematic screening may be in the form of mobile clinics or fixed screening centres where teams travel daily to the foci. The nature of gambiense disease is such that patients do not seek treatment early enough because the symptoms at that stage are not evident or serious enough to warrant seeking medical attention, considering the remoteness of some affected areas. Also, diagnosis of the disease is difficult and most health workers may not be able to detect it. Systematic screening allows early-stage disease to be detected and treated before the disease progresses, and removes the potential human reservoir.[24] There is a single case report of sexual transmission of West African sleeping sickness,[25] but this is not believed to be an important route of transmission.

African trypanosomiasis
Norovirus Marfan syndrome Nasal Cancer Marburg Hemorrhagic Fever Malignant Hyperthermia Male Breast Cancer Lyme disease Lung cancer Legionellosis Latex Allergy Lassa Fever Jaundice / Kernicterus Hypothyroidism Kawasaki disease Genetic-Brain-Disorders Gallbladder-Diseases Fetal alcohol syndrome Diabetes Crimean-Congo Hemorrhagic Fever Dengue-and-Dengue-Hemorrhagic-Fever Chikungunya-Fever Cat Scratch Disease Cancer Larynx Cancer Among Children Borderline Personality Disorder Bladder cancer Baylisascaris Infection Benign tumor Skin Cancer African trypanosomiasis Coming Soon	African trypanosomiasis Human African trypanosomiasis, sleeping sickness[1], African lethargy[1], or Congo trypanosomiasis[1] is a parasitic disease of people and animals, caused by protozoa of the species Trypanosoma brucei and transmitted by the tsetse fly.[2] The disease is endemic in some regions of Sub-Saharan Africa, covering about 36 countries and 60 million people. It is estimated that 50,000 to 70,000 people are currently infected, the number having declined somewhat in recent years.[3] Three major epidemics have occurred in recent history, one lasting from 1896–1906 and the other two in 1920 and 1970. In 2008 there was an epidemic in Uganda.[4] Symptoms and clinical features Symptoms begin with fever, headaches, and joint pains. As the parasites enter through both the blood and lymph systems, lymph nodes often swell up to tremendous sizes. Winterbottom's sign, the tell-tale swollen lymph nodes along the back of the neck, may appear. If untreated, the disease slowly overcomes the defenses of the infected person, and symptoms spread to include anemia, endocrine, cardiac, and kidney diseases and disorders. The disease then enters a neurological phase when the parasite passes through the blood-brain barrier. The symptoms of the second phase give the disease its name; besides confusion and reduced coordination, the sleep cycle is disturbed with bouts of fatigue punctuated with manic periods progressing to daytime slumber and night-time insomnia. Without treatment, the disease is invariably fatal, with progressive mental deterioration leading to coma and death. Damage caused in the neurological phase can be irreversible.[4] In addition to the bite of the tsetse fly, the disease is contractible in the following ways: Mother to child infection: the trypanosome can sometimes cross the placenta and infect the fetus.[5] Laboratories: accidental infections, for example, through the handling of blood of an infected person and organ transplantation, although this is uncommon. Blood transfusion Sexual contact (might be possible, but happens rarely)[6] Life cycle: The tsetse fly is large, brown and stealthy. While taking blood from a mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream Inside the host, they transform into bloodstream trypomastigotes are carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission The entire life cycle of African Trypanosomes is represented by extracellular stages. A tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission, leave the midgut, and transform into epimastigotes The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission. The cycle in the fly takes approximately 3 weeks to progress. Laboratory diagnosis: The diagnosis rests upon demonstrating trypanosomes by microscopic examination of chancre fluid, lymph node aspirates, blood, bone marrow, or, in the late stages of infection, cerebrospinal fluid. A wet preparation should be examined for the motile trypanosomes, and in addition a smear should be fixed, stained with Giemsa (or Field), and examined. Concentration techniques can be used prior to microscopic examination. For blood samples, these include centrifugation followed by examination of the buffy coat; mini anion-exchange/centrifugation; and the Quantitative Buffy Coat (QBC) technique. For other samples such as spinal fluid, concentration techniques include centrifugation followed by examination of the sediment. Isolation of the parasite by inoculation of rats or mice is a sensitive method, but its use is limited to T. b. rhodesiense. Antibody detection has sensitivity and specificity that are too variable for clinical decisions. In addition, in infections with T. b. rhodesiense, seroconversion occurs after the onset of clinical symptoms and thus is of limited use. Three similar serological tests are available for detection of the parasite; the micro-CATT, wb-CATT, and wb-LATEX. The first uses dried blood while the other two use whole blood samples. A 2002 study found the wb-CATT to be the most efficient for diagnosis, while the wb-LATEX is a better exam for situations where greater sensitivity is required.[12] Treatment: First line, first stage: The current standard treatment for first stage disease is: Intravenous pentamidine (for T.b. gambiense); or Intravenous suramin (for T.b. rhodesiense) The drug Eflornithine — previously used only as an alternative treatment for sleeping sickness due to its labour-intensive administration — was found to be safe and effective as a first-line treatment for the disease in 2008, according to the Science and Development Network's Sub-Saharan Africa news updates. [1]. Researchers tracked over 1,000 adults and children at a centre in Ibba, Southern Sudan—the first use of eflornithine on a large scale— and it was highly effective in treating the issue. According to a treatment study of Trypanosoma gambiense caused human African trypanosomiasis, use of eflornithine (DMFO) resulted in fewer adverse events than treatment with melarsoprol. [13] All patients should be followed up for two years with lumbar punctures every six months to look for relapse. First line, second stage: The current standard treatment for second stage (later stage) disease is: Intravenous melarsoprol 2.2 mg/kg daily for 10 consecutive days.[14] Alternative first line therapies include: Intravenous melarsoprol 0.6 mg/kg on day 1, 1.2 mg/kg IV melarsoprol on day 2, and 1.2 mg/kg/day IV melarsoprol combined with oral 7.5 mg/kg nifurtimox twice a day on days 3 to 10;[15] or Intravenous eflornithine 50 mg/kg every six hours for 14 days.[16] Combination therapy with eflornithine and nifurtimox is safer and easier than treatment with eflornithine alone, and appears to be equally or more effective. It has been recommended as first-line treatment for second stage T. b. gambiensis disease.[17] Resistant disease: In areas with melarsoprol resistance or in patients who have relapsed after melarsoprol monotherapy, the treatment should be: melarsoprol and nifurtimox, or eflornithine Prevention and control: For in depth information on prevention of the disease via tsetse fly control see Tsetse fly control. Prevention and control focus on, where it is possible, the eradication of the parasitic host, the tsetse fly. Two alternative strategies have been used in the attempts to reduce the African trypanosomiases. One tactic is primarily medical or veterinary and targets the disease directly using monitoring, prophylaxis, treatment, and surveillance to reduce the number of organisms which carry the disease. The second strategy is generally entomological and intends to disrupt the cycle of transmission by reducing the number of flies. Instances of sleeping sickness are being reduced by the use of the sterile insect technique. Regular active surveillance, involving case detection and treatment, in addition to tsetse fly control, is the backbone of the strategy for control of sleeping sickness. Systematic screening of communities in identified foci is the best approach as case-by-case screening is not practically possible in highly endemic regions. Systematic screening may be in the form of mobile clinics or fixed screening centres where teams travel daily to the foci. The nature of gambiense disease is such that patients do not seek treatment early enough because the symptoms at that stage are not evident or serious enough to warrant seeking medical attention, considering the remoteness of some affected areas. Also, diagnosis of the disease is difficult and most health workers may not be able to detect it. Systematic screening allows early-stage disease to be detected and treated before the disease progresses, and removes the potential human reservoir.[24] There is a single case report of sexual transmission of West African sleeping sickness,[25] but this is not believed to be an important route of transmission.
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