African Sleeping Sickness Research Paper

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Introduction

As early as the 14th century an Arab writer described symptoms resembling those of African sleeping sickness. But it was only after the success of European colonization that the disease became well known in the Western world. This medical phenomenon is a vector-borne parasitic disease. The causative agent is a parasite belonging to the Trypanosoma Genus and this is transmitted to humans by tsetse fly bites, which acquired their infection from human beings or from animals who are carriers of the said parasites (WHO, 2009). The African sleeping sickness is the main reason why there is negative socio-economic development in East and West Africa. The World Health Organization, concerned citizens as well as a few pharmaceutical companies are working hand-in-hand to prevent another outbreak and to significantly reduce the number of infections.

Causative Agent

The causative agent is a parasite called trypanosomes. The said parasite is not airborne or waterborne; they are vector-borne using the Tsetse flies to infect humans and animals alike (CDC, 2009). Both male and female tsetse flies feed on blood and bite during the day (Goddard, 2008). When it infects humans it is called African sleeping sickness and when it infects animals the correct term is Nagana (Krinsky, 2002). There are two forms of African sleeping sickness and are named according to their geographic distribution (Krinsky, 2002). The first type is called the West African trypanosome and named Trypanosoma gambiense (T. b. gambiense) for Gambia (Krinsky, 2002).

The second type is called the East African trypanosome and named Trypanosoma rhodesiense (T.b. rhodesiense) for Rhodesia, now Zimbabwe (Krinsky, 2002). Tsetse flies are only found in Sub-Saharan Africa. There are six species of Tsetse flies that are of primary importance to healthcare and disease prevention in Africa. This is because these are vectors of human trypanosomiasis. In the case of T. b. gambiense, the chief vectors are a) Glossina palpalis; b) Glossina fuscipes; and c) Glossina tachinoides (CDC, 2008). The primary vectors of T. b. rhodesiense on the other hand are a) Glossina morsitans; b) Glossina swynnertoni; c) Glossina pallidipes (CDC, 2008). Glossina morsitans can be readily found in wooded areas and brush country in eastern Africa while the Glossina palpalis group can be easily found in banks of streams, rivers, and lakes of western and central Africa (Goddard, 2008).

Disease History

Although the disease was known to Arab scholars as early as the 14th century it was a surgeon named John Atkins – who was on board a slave-trading ship traveling from West Africa to the West Indies – who first provided a more scientific description of the disease (Krinsky, 2002). Atkins was correct in most of his observations regarding the symptoms but he was greatly mistaken when he made assumptions as to the causative agent of the said disease. He reasoned that it was due to the inherent weakness of the African mind, which he labeled as “Negro lethargy” and Atkins attributed to causing of the disease to the “…natural weakness of the brain … brought about by lack of use” (Krinsky, 2002).

Later on, an unbiased scientific study of sleeping sickness revealed that it was trypanosomes and tsetse flies that are the main culprit in the outbreak within Sub-Saharan Africa. In 1903 a team was sent by the British Tsetse Fly commission to investigate outbreaks among the British colony (Krinsky, 2002). The team was led by David Bruce, David Nabarro, and Aldo Castellani (Krinsky, 2002). The team was able to provide more scientific information regarding the disease, especially the link between tsetse fly and the causative agent.

The first major outbreak was recorded in the 19th century. The spread of the disease was linked to the rapid success of the European colonizers. The movement of Europeans in their exploration and conquest of Africa led to the significant dispersal of the disease (Krinsky, 2002). As a result more than 750, 000 people died from African sleeping sickness in the period between 1896 and 1906 (Krinsky, 2002). It is estimated that there are 50 million Africans in 38 countries that are at risk of infection (Krinsky, 2002). There are more than 25,000 individuals that will be infected annually (Krinsky, 2002). The only good thing about this dreadful disease is that it is limited to Africa and the rare cases of infections in the United States are linked to tourists who visited Africa (Krinsky, 2002).

Disease Epidemiology

The term African sleeping sickness refers to the abnormally drowsy demeanor of ill patients (Krinsky, 2002). But the feeling of drowsiness is just the prelude because in many cases there is a steady progression of meningoencephalitis, with an increase of apathy and somnolence (Goddard, 2008). The sleepiness, as well as the increasing time, spent sleeping will gradually lead to the patient becoming more difficult to arouse and if left untreated the patient will become comatose (Goddard, 2008). T. b. gambiense is less severe compared to T. b. rhodesiense (WHO, 2009). When infected with T. b. gambiense the initial symptoms of African sleeping sickness can be characterized by fever, malaise, headache, and anorexia (Goddard, 2008). The fever is not regular and can be initiated by rigor (Goddard, 2008). The sickness is also characterized by enlarged cervical lymph nodes, a condition known as Winterbottom’s sign (Goddard, 2008). If left untreated the parasite will invade the central nervous system.

T. b. gambiense is less severe and more of a chronic illness involving mental deterioration and progressive weakening over a long period of time. But with T. b. rhodesiense the effect is acute and rapidly fatal. Accurate diagnosis is done by demonstrating the presence of trypanosomes in the blood, cerebrospinal fluid, or lymph (Goddard, 2008). Another method of diagnosis is the detection of antibodies specific to T. b. gambiense and T.b. rhodesiense (Goddard, 2008). Using the various forms of detection and diagnosis it was discovered that African sleeping sickness is a major problem in Sub-Saharan Africa.

The following data collated by the World Health Organization provides an overview of the challenges faced by Africans living in Western and Eastern Africa:

In recent epidemic periods, in several villages in the Democratic Republic of Congo, Angola, and Southern Sudan prevalence is as high as 50 percent. Health experts even highlighted the fact that sleeping sickness is the first or second greatest cause of mortality that sometimes overtakes HIV/AIDS (WHO, 2009).

This prompted the World Health Organization to establish a public-private partnership with Aventis Pharma (now Sanofi-Aventis) and this partnership resulted in the creation of a surveillance team that provides support to endemic countries (WHO, 2009). The partnership also made it possible to educate people in practicing control activities it also supplied drugs free of charge (WHO, 2009).

There are two stages in the progression of the disease. During the first stage which often is the case with the less virulent type of sleeping sickness the drugs used are less toxic and easier to administer (WHO, 2009). It is also more effective as it requires less training for health workers who will administer the drug as well as the damage of the parasite is not yet life-threatening (WHO, 2009). But when the disease progressed to stage two, which is often the case with the more virulent type, treatment involves more toxic medications that are also more complicated to administer (WHO, 2009).

There are four drugs that are being used to treat sleeping sickness and these are listed as follows:

  • Pentamidine
  • Suramin
  • Melarsoprol
  • Eflornithine

Pentamidine was first discovered in 1941 and is the drug of choice for stage one (WHO, 2009). There are side effects but they can be easily tolerated by patients. Suramin was discovered in 1921 and also used in stage one of the disease. The side effects are in the urinary tract (WHO, 2009). Melarsoprol was discovered in 1949 and used in both stage one and stage two. According to experts, the general mode of treatment uses Suramin and/or Melarsoprol but there are reports that Melarsoprol is fatal in 3-10% of patients treated with the said medication (Goddard, 2008). Eflornithine is less toxic was made available in 1990 only. But it is only effective against T. b. gambiense (WHO, 2009).

Aside from providing prompt treatments, especially those who live in isolated places – there is also a need to look into preventive measures to reduce the number of infections. This includes bush clearing along streams to control breeding sites; aerial spraying of insecticides, surveillance; and case detection (Goddard, ). There is also a need to look into more novel approaches such as fly trapping techniques as well as the releasing of sterile males into the environment (Goddard, 2008).

Conclusion

With the use of modern medicine as well as the expert use of insecticides the disease was significantly reduced in the middle part of the 1960s (Goddard, 2008). But complacency and the difficulty of providing the necessary tools of prevention in more isolated resulted in the re-emergence of the disease in many parts of Africa (Goddard, 2008). There is a need for a more concerted effort to reduce the number of infections. The World Health Organization must take the lead in this endeavor.

The public-private partnership initiated by WHO is doing wonders for the people in Sub-Saharan Africa, especially those who are already infected with the said disease. It is important for those who suffer from stage one of sleeping sickness to be diagnosed immediately. If left untreated all forms of trypanosomiasis are lethal; therefore there is a need to send more teams and more health workers to reach these people in time.

References

  1. Centers for Disease Control. (2008). East African Trypanosomiasis.
  2. Centers for Disease Control. (2008). West African Trypanosomiasis Infection.
  3. Goddard, J. (2008). Infectious Diseases and Arthropods. New York: Springer.
  4. Krinsky, W. (2002). Tsetse Flies (Glossinidae). In G. Mullen & L. Durden. (Eds.), Medical and Veterinary Entomology (pp. 303-312). CA: Academic
  5. World Health Organization. (2009). Web.
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