Tag Archives: sub-Saharan Africa

Impatiens walleriana

Botanical Name : Impatiens walleriana
Family: Balsaminaceae
Genus: Impatiens
Species:I. wallerana
Kingdom:Plantae
Order: Ericales

Synonyms:
*Impatiens giorgii De Wild.
*Impatiens holstii Engl. & Warb.
*Impatiens lujai De Wild.
*Impatiens sultani Hook.f.

Common Names: Busy Lizzie (United Kingdom), Balsam, Sultana, or Simply impatiens

Habitat :Impatiens walleriana is native to eastern Africa from Kenya to Mozambique.

Description:
Impatiens walleriana is a herbaceous perennial flowering plant growing to 15–60 cm (6–24 in) tall, with broad lanceolate leaves 3–12 cm long and 2–5 cm broad. Leaves are mostly alternate, although they may be opposite near the top of the plant. The flowers are profusely borne, 2–5 cm diameter, with five petals and a 1 cm spur. The seedpod explodes when ripe in the same manner as other Impatiens species, an evolutionary adaptation for seed dispersal. The stems are semi-succulent, and all parts of the plant (leaves, stems, flowers, roots) are soft and easily damaged.

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Edible Uses:
Root – cooked. It is a source of ’salep’, a fine white to yellowish-white powder that is obtained by drying the tuber and grinding it into a powder. Salep is a starch-like substance with a sweetish taste and a faint somewhat unpleasant smell. It is said to be very nutritious and is made into a drink or can be added to cereals and used in making bread etc. One ounce of salep is said to be enough to sustain a person for a day.

Medicinal Uses:
Salep is very nutritive and demulcent. It has been used as a diet of special value for children and convalescents, being boiled with water, flavored and prepared in the same way as arrowroot. Rich in mucilage, it forms a soothing and demulcent jelly that is used in the treatment of irritations of the gastro-intestinal canal. One part of salep to fifty parts of water is sufficient to make a jelly.

This essence of the remedy addresses mental stresses and tensions. It calms feelings of impatience and irritability. It slows the tendency to move too quickly without care or forethought. Calming. Allows one to deepen his/her life experience without experiencing burnout.

Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider.
Resources:
https://en.wikipedia.org/wiki/Impatiens_walleriana
http://healthyhomegardening.com/Plant.php?pid=2173

Prunus africana

Botanical Name :Prunus africanum
Family: Rosaceae
Genus: Prunus
Subgenus: Cerasus
Section: Laurocerasus
Species: P. africana
Order: Rosales

Syn. : P. africana

Common Names:  Pygeum, Iron wood, (Red) Stinkwood, African Plum, African Prune, African Cherry, and Bitter Almond. In other languages where it grows it is known as; in Amharic tikur inchet, in Chagga Mkonde-konde, in Kikuyu muiri, in Ganda entasesa or ngwabuzito, in Xhosa uMkakase, in Zulu inyazangoma-elimnyama or Umdumezulu, and in Afrikaans Rooi-Stinkhout.

Habitat :Prunus africanum is native to the montane regions of Sub-Saharan Africa and the Islands of Madagascar, Sao Tome, Fernando Po and Grande Comore at about 900–3400 m. of altitude. The mature tree is 10–25 m. high, open-branched and often pendulous in forest, shorter and with a round crown of 10–20 m. diameter in grassland. It requires a moist climate, 900–3400 mm annual rainfall, and is moderately frost-tolerant.

Description:
Prunus africanum  is an evergreen tree, growing up to 150 feet in height.The bark is black to brown, corrugated or fissured and scaly, fissuring in a characteristic rectangular pattern. The leaves are alternate, simple, long (8–20 cm.), elliptic, bluntly or acutely pointed, glabrous and dark green above, pale green below, with mildly serrate margins. A central vein is depressed on top, prominent on the bottom. The 2-cm petiole is pink or red. The flowers are androgynous, 10-20 stamens, insect-pollinated, 3–8 cm., greenish white or buff, and are distributed in 70-mm axillary racemes. The plant flowers October through May. The fruit is red to brown, 7–13 mm., wider than long, two-lobed with a seed in each lobe. It grows in bunches ripening September through November, several months after pollination.

click to see the pictures…..>……(01)....….(1)..……(2)..…...(3)….

Chemical Constituents:
The primary active components in pygeum bark are fat-soluble compounds, which include terpenes, sterols (including beta-sitosterol), and ferulic acid esters. Pygeum extracts are commonly standardized to 13% sterol concentration for consistent potency.

Medicinal Uses:
Traditionally used for fevers, malaria, wound dressing, arrow poison, stomach pain, purgative, kidney disease, appetite stimulant
An extract, pygeum, an herbal remedy prepared from the bark of Prunus africana, is used as an alternative medicine in patients with benign prostatic hyperplasia (BPH) though clinical trials have not yet been conducted. It has shown positive results in in vitro studies and mouse models of prostate cancer.

The collection of mature bark for this purpose and for other medical uses has resulted in the species becoming endangered. Prunus africana continues to be taken from the wild. Plantecam Medicam deserves credit for attempting sustainable bark harvesting by removing opposing quarters of trunk bark rather than girdling the trees. However, quotas have been awarded by the Forestry Department without adequate forest inventories due to some harvesters, spurred on by the high price per kilogram of bark, removing too much of the bark in an unsustainable manner. In the 1990s it was estimated that 35,000 debarked trees were being processed annually. The growing demand for the bark has led to the cultivation of the tree for its medicinal uses.

The terpenes in pygeum have an anti-swelling effect. Terpenes are present in many plants that produce fragrant essential oils. Prostaglandins are inflammatory hormones that tend to accumulate in the prostates of men with BPH. Research indicates that the phytosterols in pygeum interfere with the formation of these prostaglandins, helping to reduce inflammation and swelling of the prostate. When taken correctly, pygeum is considered one of the safest herbs used for male health, and often is combined with saw palmetto for maximum results.

Other Uses:
The timber is a hardwood employed in the manufacture of axe and hoe handles, utensils, wagons, floors, chopping blocks, carving, bridge decks and furniture. The wood is tough, heavy, straight-grained and pink, with a pungent bitter-almond smell when first cut, turning mahogony and odorless later

Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider

Resources:
http://www.anniesremedy.com/herb_detail296.php
http://en.wikipedia.org/wiki/Prunus_africana
http://www.swansonvitamins.com/health-library/encyclopedia/herbs/pygeum.html

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Acacia senegal

Botanical Name :Acacia senegal
Family: Fabaceae
Genus: Acacia
Species: A. senegal
Kingdom: Plantae
Division: Magnoliophyta
Class: Magnoliopsida
Order: Fabales
Commo Names:Swet khadira, khair swet, Catechu tree, Goradiobabul, Rfaudraksha, Gum Acacia, Gum Arabic Tree, or Gum Senegal Tree.  Svetakhadira.

Habitat : It is native to semi-desert regions of Sub-Saharan Africa, as well as Oman, Pakistan, and northwestern India. It grows to a height of 5-12m, with a trunk up to 30 ft in diameter.

Description:
Bush or small tree, usually 2 -6 m high, occasionally reaching 10 m under optimal conditions, frequently forming thickets. It has a short stem, is usually low branched with many upright twigs, the crown eventually flattened, umbrella-shaped. Bark pale brown to pale grey, smooth in young individuals, brown scaly on the older parts, slash mottled red and white, prickles up to 0.5 cm long, the centre one sharply curved, the other two more or less straight and directed forward. Leaves bipinnate, small, greenish-grey, with 3-6 pairs of pinnulae having 10-20 pairs of leaflets each. Leaflets grey-green, 3-8 x 1-2 mm. Flowers very fragrant, creamy white (red in bud), usually appearing before the leaves in pedunculate spikes 3-10 cm long either solitary or two to three together. Pods 7-10 cm long x 2 cm wide, flat and thin, papery, attenuated at both ends, containing 3-6 flat, round, light-brown to brown-greenish seeds. Both tap roots and lateral roots are very developed ; the latter may spread many metres from the tree, particularly in sandy terrain. The tree is deciduous, drooping its leaves in November in the Sudan.

You may click to see the pictures of Acacia senegal

 

The senegal gum acacia is a small to average sized thorn tree of the African grassland savanna. It can grow up to 20 meters tall. It has many branches that spread out into a flat and rounded top. These branches have many thorns that come in pairs. The leaves are a grey-green color. The flowers are yellow or cream colored and grow on spikes just above the thorns. These flowers turn into seed pods about 8 inches long and 2-3 inches wide. They look like giant dried up pea pods, and are yellowish to brown in color, and flat.

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The acacia can live through long periods of drought. They tend to grow in sandy places where there is only between 12 to 15 inches of rain a year. Periods without rain can last from 5 to 11 months a year.

Cultivation:
A. senegal is sensitive to frost but is very heat tolerant.

Water:  Occurring between the 100 and 800 mm of MAR, mainly between 200 and 600 mm. It is extremely drought resistant as it occurs close to the very border of the Sahara and West Asian Deserts.

Soil :  A. senegal is sensitive to water logging. In the drier parts of its area of distribution it tends to be restricted to sandy habitats and dry river beds, but to fine textured soils under the higher rainfalls of the South Sahelian and North Sudanian ecozones., it may also occur on shallow soils and duripan lithosols. The tolerance to pH is quite broad : 5-8 .

Propagation :
Propagation is made either from direct seeding of treated seeds (8,000-18,000 per kg) or via nursery-grown seedlings in various kinds of containers ; naturally the former is much cheaper and used to be a part of the traditional management of the Acacia bush-fallow production system of Kordofan (Seif el Din; 1965 ; Seif el Din & Mubarak, 1971).

Food Uses:It is also used as flavoring in certain soda (pop).

Gum arabic
It produces gum arabic, which is used as a food additive, in crafts, and as a cosmetic. The gum is drained from cuts in the bark, and an individual tree will yield 200 to 300 grams. Seventy percent of the world’s gum arabic is produced in Sudan.


Medicinal Uses:

Gum Arabic is used in making medicine. It is used to make a cream for skin inflammations and ailments of the respiratory and urinary tracts. Its also used for coughs, sore throats, eyewash, diarrhea, and dysentery. It is also used as flavoring in certain soda (pop).

The gum is used for soothing mucous membranes of the intestine . It is also reportedly used as for its astringent properties, to treat bleeding, bronchitis, diarrhea, gonorrhea, leprosy, typhoid fever and upper respiratory tract infections.


Other Uses:

Rope :Roots near the surface of the ground are quite useful in making all kinds of very strong ropes and cords. The tree bark is also used to make rope.

Wood : Handles for tools, parts for weaving looms.

The acacia provides shade and shelter for the animals of the savanna. Giraffes, antelopes and elephants eat its leaves, and birds make their nests in its branches and use them as perches to look out over the flat grasslands.

Acacia was considered sacred by the ancient Hebrew. It is said that Moses used acacia wood to build the Ark of the Covenant and the sacred Tabernacle (Exodus, chapters 25-40). Legend also has it that the thorns of the acacia were used for Christ’s crown of thorns.

Click to see Other Botanical variations
Acacia senegal var. leiorhachis Brenan  :
Acacia senegal var. rostrata Brenan   :
Acacia senegal var. senegal :

Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider.

Resources:
http://en.wikipedia.org/wiki/Acacia_senegal
http://www.blueplanetbiomes.org/acacia_senegal.htm
http://www.fao.org/ag/AGP/agpc/doc/gbase/DATA/Pf000131.htm

http://www.whack.org/~xanthia/herbs/az/acacia.html

Sleeping Sickness (African trypanosomiasis)

Other Names:- Human African trypanosomiasis, sleeping sickness, African lethargy, or Congo trypanosomiasis.

Defenition:
African trypanosomiasis or Sleeping sickness is infection with organisms carried by certain flies. It results in swelling of the brain. It is a parasitic disease of people and animals, caused by protozoa of the species Trypanosoma brucei and transmitted by the tsetse fly.

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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.  Four 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.

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History
The condition has been present in Africa since at least the 14th century, and probably for thousands of years before that. The causative agent and vector were identified in 1902–1903 by Sir David Bruce, and the differentiation between the subspecies of the protozoa made in 1910. The first effective treatment, Atoxyl, an arsenic-based drug developed by Paul Ehrlich and Kiyoshi Shiga, was introduced in 1910 but blindness was a serious side effect. Numerous drugs designed to treat the disease have been introduced since then.

Symptoms and clinical features:-
Gambienseinfections lead to drowsiness during the day, but insomnia at night. Sleep becomes uncontrollable as the disease gets worse, and eventually leads to coma.

General symptoms include:

*Anxiety
*Drowsiness
*Fever
*Headache
*Increased sleepiness
*Insomnia at night
*Mood changes
*Sweating
*Swollen lymph nodes all over the body
*Swollen, red, painful nodule at site of fly bite
*Uncontrollable urge to sleep

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.

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.
*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)

Causes:
Sleeping sickness is caused by two organisms, Trypanosoma brucei rhodesiense and Trypanosomoa brucei gambiense. The more severe form of the illness is caused by rhodesiense.

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Trypanosoma forms in a blood smear.

Tsetse flies carry the infection. When an infected fly bites you, painful, red swelling occurs at the site of the bite. The infection then spreads through your blood, causing episodes of fever, headache, sweating, and swelling of the lymph nodes.

The flagellate reproduces in the bloodstream, and the symptoms develop gradually as the burden of parasites and their harmful effects increases. It also migrates into the central nervous system, producing the characteristic symptoms.

T. brucei gambiense is the cause of a persistent infection that lasts several years until it finally develops into a coma, from which the patient cannot be woken. Hence the name ‘sleeping sickness’.

If the central nervous system is sufficiently affected, the patient can no longer be cured, and eventually dies, possibly from other infections that may be superimposed on the primary disease.

When the infection spreads to the central nervous system, it causes the symptoms typical of sleeping sickness . When it reaches the brain, behavioral changes such as fear and mood swings occur, followed by headache, fever, and weakness. Inflammation of the heart ( myocarditis) may develop.

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

1.Inside the host, they transform into bloodstream trypomastigotes

2.are carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission

3.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

4.In the fly’s midgut, the parasites transform into procyclic trypomastigotes,

5.multiply by binary fission,

6.leave the midgut, and

7.transform into epimastigotes

8.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.

Diagnosis:
A physical examination may show signs of meningoencephalitis (inflammation of the brain and its covering, the meninges).

Tests include the following:

*Albumin levels
*Blood smear
*Cerebrospinal fluid tests
*Complete blood count (CBC)
*Globulin levels
*Lymph node aspiration

Most antibody and antigen test are not very helpful because they can’t distinguish between current and previous infection. Specific IgM levels in the cerebrospinal fluid may be helpful, however.

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.

Possible Complications:-
Complications include injury related to falling asleep while driving or performing other activities, and progressive damage to the nervous system.

Treatment:-
First line, first stage
The current standard treatment for first stage disease is:

*Intravenous or intramuscular 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. 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.

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.
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; or
Intravenous eflornithine 50 mg/kg every six hours for 14 days.
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.

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

Outdated protocols
The following traditional regimens should no longer be used:

*(old “standard” 26-day melarsoprol therapy) Intravenous melarsoprol therapy (3 series of 3.6 mg/kg/day intravenously for 3 days, with 7-day breaks between the series) (this regimen is less convenient and patients are less likely to complete therapy);

*(incremental melarsoprol therapy) 10-day incremental-dose melarsoprol therapy (0.6 mg/kg iv on day 1, 1.2 mg/kg iv on day 2, and 1.8 mg/kg iv on days 3–10) (previously thought to reduce the risk of treatment-induced encephalopathy, but now known to be associated with an increased risk of relapse and a higher incidence of encephalopathy)

History and research:-
Suramin was introduced in 1920 to treat the first stage of the disease. By 1922, Suramin was generally combined with Tryparsamide (another pentavalent organo-arsenic drug) in the treatment of the second stage of the gambiense form. It was used during the grand epidemic in West and Central Africa in millions of people and was the mainstay of therapy until 1969.

Pentamidine, a highly effective drug for the first stage of the disease, has been used since 1939. During the fifties, it was widely used as a prophylactic agent in Western Africa, leading to a sharp decline in infection rates. At the time, it was thought that eradication of the disease was at hand.

The organo-arsenical melarsoprol (Arsobal) was developed in the 1940s, and is effective for patients with second stage sleeping sickness. However, 3 – 10% of those injected have reactive encephalopathy (convulsions, progressive coma, or psychotic reactions), and 10 – 70% of such cases result in death; it can cause brain damage in those who survive the encephalopathy. However, due to its effectiveness, melarsoprol is still used today. Resistance to melarsoprol is increasing, and combination therapy with nifurtimox is currently under research.

Eflornithine (difluoromethylornithine or DFMO), the most modern treatment, was developed in the 1970s by Albert Sjoerdsmanot and underwent clinical trials in the 1980s. The drug was approved by the United States Food and Drug Administration in 1990, but Aventis, the company responsible for its manufacture, halted production in 1999. In 2001, however, Aventis, in association with Médecins Sans Frontières and the World Health Organization, signed a long-term agreement to manufacture and donate the drug.

An international research team working in the Democratic Republic of the Congo, Southern Sudan and Angola involving Immtech International and University of North Carolina at Chapel Hill have completed a Phase IIb clinical trial and commenced a Phase III trial in 2005 testing the efficacy of the first oral treatment for Sleeping Sickness, known at this point as “DB289”.

Trypanosomiasis vaccines are undergoing research.

Drug targets and drug discovery:-
The genome of the parasite has been decoded and several proteins have been identified as potential targets for drug treatment. The decoded DNA also revealed the reason why generating a vaccine for this disease has been so difficult. T. brucei has over 800 genes that manufacture proteins that the organism mixes and matches to evade immune system detection.

Recent findings indicate that the parasite is unable to survive in the bloodstream without its flagellum. This insight gives researchers a new angle with which to attack the parasite.

A new treatment based on a truncated version of the apolipoprotein L-1 of high density lipoprotein and a single domain antibody has recently been found to work in mice, but has not been tested in humans.

The cover story of the August 25, 2006 issue of Cell journal describes an advance; Dr. Lee Soo Hee and colleagues, working at Johns Hopkins, have investigated the pathway by which the organism makes myristate, a 14-carbon length fatty acid. Myristate is a component of the variant surface glycoprotein (VSG), the molecule that makes up the trypanosome’s outer layer. This outer surface coat of VSG is vital to the trypanosome’s avoidance of immunological capture. Dr. Lee and colleagues discovered trypanosomes use a novel fatty acid synthesis pathway involving fatty acid elongases to make myristate and other fatty acids.

Prognosis:
Without treatment, death may occur within 6 months from cardiac failure or from rhodesiense infection itself. Gambiense infection causes the classic “sleeping sickness” disease and gets worse more quickly, often over a few weeks. Both diseases should be treated immediately.

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

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. There is a single case report of sexual transmission of West African sleeping sickness, but this is not believed to be an important route of transmission.

Other animals:
Trypanosoma of both the rhodesiense and gambiense types can affect other animals such as cattle and wild animals. In animals it is known as nagana (animal African trypanosomiasis)

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.


Resources:

http://en.wikipedia.org/wiki/African_trypanosomiasis
http://www.netdoctor.co.uk/travel/diseases/sleeping_sickness.htm
http://www.nlm.nih.gov/medlineplus/ency/article/001362.htm

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Malaria Vaccine May be Available in 2012

RTS,S more than halved malaria cases in field trials and could be safely given with other childhood inoculations, two studies have reported.

A vaccine against the parasitic disease malaria cut illnesses by more than half in field trials and could be safely given with other childhood inoculations, two studies have reported. The vaccine, which will begin a third and final phase of clinical trials early next year, could become the first to protect children from malaria, which kills nearly 1 million people worldwide every year.


FOR THE RECORD:
An article in Section A on Tuesday about an experimental malaria vaccine omitted the full name of a scientist who predicted that the vaccine, RTS,S, could be available as early as 2012. He is Joe Cohen, vice president for vaccines for emerging diseases at GlaxoSmithKline, who has worked on RTS,S since its inception 22 years ago

The studies, published online Monday in the New England Journal of Medicine, were reported at a New Orleans meeting of tropical medicine researchers and were hailed as a significant breakthroughin the fight against one of the most intractable and deadly infectious diseases.

If the phase three trials are successful, it would be “an extraordinary scientific triumph,” said Dr. W. Ripley Ballou, deputy director for vaccines and infectious diseases for the Bill and Melinda Gates Foundation, which helped fund the research.

“But more importantly,” Ballou added, “it could save millions of children’s lives.”

Malaria kills nearly 1 million people each year and sickens about 2 million others, according to estimates from the World Health Organization. Most of the deaths are among children younger than 5 in sub-Saharan Africa, the population that the vaccine targets.

The vaccine RTS,S was developed by Belgium-basedGlaxoSmithKline Biologicals with support from the PATH Malaria Vaccine Initiative, a global nonprofit consortium that works with pharmaceutical companies.

In the first study, conducted in Kenya and Tanzania, 894 children ages 5 months to 17 months were inoculated either with the three-dose experimental malaria vaccine or a rabies vaccine as a control group. In the eight-month follow-up period, researchers found that children receiving RTS,S had 53% fewer diagnosed cases of malaria — 38 episodes compared with 86 among recipients of the control rabies vaccine.

In the other study, conducted in Tanzania, the vaccine was given to 340 infants at 8, 12 and 16 weeks old, along with vaccines against polio, diphtheria, tetanus, pertussis (whooping cough) and Haemophilus influenzae B without lessening the safety or effectiveness of the vaccines. The ability to administer the vaccine as part of already established immunization programs is important for countries where health workers, clinics and roads are in such shortage that delivering a drug can be almost as challenging as developing one, researchers say.

Again, the trial was randomized and double-blinded — considered the scientific gold standard — with half the infants receiving the malaria vaccine and the other half receiving a hepatitis B vaccine as a control. Although it was not the main object of the study, the researchers found that infants who received the malaria vaccine had 65% fewer infections, as measured by the presence of parasite in the bloodstream, over a six-month period than those who did not, confirming the findings from an earlier, smaller study.

Although half the world’s population lives in areas where malaria is transmitted, the disease received little public attention for about 50 years after being eradicated in the United States and Europe. About a decade ago, world leaders called for a renewed effort to fight the mosquito-borne disease caused by parasitic organisms, most seriously Plasmodium falciparum.

In the last few years, widespread distribution of insecticide-treated bed nets and a new combination of medicines have reduced malaria deaths in Ethiopia, Rwanda and Zambia by 50% and more. But because of the threat that Plasmodium falciparum could develop resistance to medications or insecticides, health workers consider a vaccine to be a vital tool. Developing such a vaccine has proven a challenge because the parasite is adept at evading the immune system.

Dr. Carlos C. “Kent” Campbell, who led the malaria program at the national Centers for Disease Control and Prevention for almost 20 years and was not involved in the research, said the findings were impressive.

Larger, clinical trials will continue to test the vaccine on 16,000 infants at 11 sites in Africa. If all goes as planned, the vaccine could be ready for licensure in 2011 and available for use by 2012, Cohen said.

Sources: Los Angles Times

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