
Key points
African sleeping sickness is a debilitating and fatal neurological disease that is widespread in sub Saharan Africa (CDC. 2002 African Trypanosomiaisis). In 1998, there were roughly 40,000 reported cases; however this did not accurately depict the actual number of cases. Considering the economical instabilities of the individuals in the endemic regions, proper screening and diagnosis is improbable. It is estimated that between 300,000 and 500,000 people are undiagnosed and therefore untreated (Smith et al. 1998). This fact is astonishing, bearing in mind that the mortality rate for untreated individuals is 100 %.
It may seem that 40,000 reported cases a year it a relatively insignificant number compared to other diseases such as malaria which has 1.5 million reported deaths a year, however it was not all too long ago that reported cases were in the hundreds of thousands. Within the past century there have been three notable epidemics that have occurred throughout Africa, with high incidence in the Busoga region located in Uganda, resulting in cataclysmic statistics (Hide, 1999). The more notable of the two was the 1920 epidemic, in which more than 250,000 people died and countless others infected (Coleman, 2004). The more recent epidemic occurred between 1976 and 1983 in sub Saharan Africa, also with a high frequency rate in the Busoga region. In the Busoga region alone this epidemic produced 10,414 infected males and 9,560 infected females (Hide, 1999). These numbers are likely inaccurate, the actual numbers are undoubtedly higher, considering Ugandans have a relatively high amount of economically deprived individuals that are unable to seek medical attention, resulting in those people being undiagnosed and consequently not recorded.
The disease is caused by a vector borne parasite called trypanosome (part of the Trypanosoma genus). Once within the hosts Trypanosomes invade the lymphatic system leading to a characteristic swelling of the lymph nodes known as Winterbottoms’s sign (Robays et al. 2004). The infection progresses into the blood stream and eventually crosses the blood brain barrier in the CNS resulting in severe neurological complications, and eventually death. (Hofer et al. 2001). The early first stage of the disease is most often asymptomatic, making the disease extremely hard to detect. In the late second stage after the pathogen has crossed into the CNS the individuals become exteremely lethargic and unable to stay awake, hence the term "sleeping sickness".
This pathogen is subdivided into two classes Trypanosoma brucei gambiense (Tbg) and Trypanosoma brucei rhodesiense (Tbr) (CDC, 2002). Tbg is known as the more chronic form and is found in west and central African representing more than 90% of reported causes. Tbg has an incubation period of months to years with the ultimate result being death if untreated. After the asymptomatic stage and symptoms arise it is often already in its advanced stage, and the central nervous system is permanently damaged (CDC, 2002 & Robays et al. 2004). Tbr is found in eastern and southern Africa and represents less than 10% of the reported cases and has an incubation period of weeks to a few months (CDC 2002). Tbr tends to be more virulent because it has a lower incubation period and an acute onset that rapidly invades the central nervous system (Robays et al, 2004). The epidemics in Uganda that were mentioned in the previous texts were once thought as to be caused by Tbg, however with recent studies; it has now been linked to Tbr (Coleman, 2004).
The primary mode of transmission for the trypanosome parasite is the tsetse fly. Much like the mosquito for malaria the tsetse fly infects the individuals via salivary excretion. Unlike the Anopheles mosquito, the tsetse flies are primarily active during the day. Therefore, mosquito nets would be irrelevant in the fight against the pathogens transmission, however mosquito proofing ones house would be advantageous. The bites of the tsetse flies are also painful; this is in opposition to the Anopheles which can infect one without pain. The pathogen is occasionally transmitted within humans via vertical transmission and infected blood contamination.
Sleeping sickness is a continued public health concern since its identification in 1898 (Odiit, 2003). Recently the neglected disease is becoming a growing concern as a result of an increase in case numbers (Smith et al. 1998). With increasing numbers and the range of the pathogen reaching up to 60 million humans within 36 countries being at risk, it is likely that the endemic numbers will resurface (Ripamonti et al. 2001). As we have seen in the recent century, epidemics have the potential to devastate large amounts of people. We as a society cannot wait any longer for the epidemics to arise until we start taking appropriate actions. Too many people die that can be spared, we need to take the initiative now before another epidemic ravages the African people.
Discussion of Issues
What do we propose to do?
We propose to implement a plan using 5 million dollars to hopefully reduce the occurrence of the disease. Considering the relatively insignificant amount of 5 million dollars that we have, we will focus on a specific region (Busoga, Uganda). The study will occur over a two year period, with initial and post incidence statistics. The objective for the study is for the frequency of infected individuals to be significantly reduced after the two year period. If the study is effective we will use the data in order to attract more significant donations from other donating organizations. When adequate donations are collected, we may be able to apply the techniques used in Busoga and utilize them for the rest of Africa, which would optimistically eradicate the disease entirely.
Why Busoga, Uganda?
Most of the experiment will take place in the region of Busoga located near Lake Victoria. The shores of Lake Victoria are a suitable environment for the tsetse flies, which increase the probability for incidence to occur (Leak, 1999). Considering that epidemics have occurred in this region in the past and killed nearly 27,832 in the region, this proves as an ideal location for the study to take place. Currently today there are roughly 1,000 reported cases in Busoga, however these numbers are unquestionably skewed for the reason that most of the people in the region due to their financial inabilities are unable to seek medical attention. The more likely number of infected individuals in the region is roughly 10,000. One can compare this to the total population of the region which is 3 million. The 1 to 3000 infected persons to uninfected persons may seem low, but it may not be long before another epidemic occurs and another 27,832 people are infected which would make the incidence one in 100 people for being infected.
Why hasn’t there been appropriate actions taken to prevent the disease? Why do we wait until it happens to do something about it?
Appropriate actions have not been taken because the disease is classified as a comparatively low risk disease. Consequently, funds for disease control are diverted to ones that have a higher frequency such as Malaria and AIDS. This would appear to make sense; however it doesn’t take into consideration that this disease can completely be wiped out and the fact that epidemic numbers are more than likely going to resurface. During epidemics (that were more than likely caused by an increase in transmission rate) in the past century the incidence of infected individuals grew drastically. The government would than take drastic measures in order to reduce transmission rates of the disease. An example of this is the government in Uganda responding to the 1920 epidemic by creating a massive evacuation campaign of up to 24 km from the shore of Lake Victoria (Leak, 1999). Immediately preceding these drastic measures the incidence of infected individuals decreased. Therefore if we were to take appropriate measures now, which would be not as drastic as the ones that preceded the epidemics, we would possibly be able to completely reduce the incidence. Hence, in order to save more money and lives in the long run, preventative measures to control this widespread disease should be taken now and not after epidemics occur.
Why would a lower in transmission lead to a reduction in virulence?
The entire goal of the project is to reduce transmission rates. Different types of methods will be used but they all will be geared in the reduction of transmission. Implementing Paul Ewald’s transmission rate hypothesis, the reduction of transmission will also lead to less virulent strains of the pathogen. The plan will act as a two fold plan which addresses short and long term goals. The immediate short term goal will be less people getting the disease and the long term goal will be an eventual reduction of the virulence of the pathogen. Therefore if the pathogen is still present in our society, only less virulent strains that are begin will be able to thrive, because these strains will be the only strains that will be able to transmit (Ewald, 1994).
CALL OF ACTION:
Our proposal to help alleviate the sleeping sickness crisis in Busoga is based on four factors. The primary factor which the proposal is based on is education. The next important factor is properly identifying those in stage two and consequently treating them, and research in more effective drug therapies. The development for improved screening methods so latent stage individuals can be identified will also be a factor in our proposal. The next factor includes research for a vaccine.
An educational infrastructure that we plan to implement is the foundation for the entire project. As such, a majority of the funds will be used for this educational infrastructure. The primary reason that this disease is such a problem is that most of the people do not have proper education of the disease. Effective pathogen screening, treatment, and preventive measures are useless, unless the people are aware of their existence and their importance. A majority of the people that live in the endemic areas (rural farmlands) due to their social statuses do not have access to proper schooling for sleeping sickness or for that matter school in general. With the relatively small amount of money we have, it would only be logical to focus on educating, because effectively screening and treating, would be too costly and therefore improbable.
Currently the treatment for both West and East African sleeping sickness is not as advanced as it could be. There are two types of drugs that currently treat the disease. The first type treats the disease in its first stage and is extremely effective. The second type treats the disease in its second stage after it has crossed the blood brain barrier. Many of the drugs that treat African sleeping sickness in the second stage are almost as detrimental as they are beneficial. The drugs that treat the disease like Eflornithine are expensive; it costs roughly 300 US dollars to treat a single patient infected with African sleeping sickness (Smith et al. 1998). This price is totally out of reach for most infected individuals within the endemic regions and the price will keep them from surviving. Therefore research is needed in order to better treat the disease, and to make it less expensive.
Screening is an effective way of identifying the pathogen. If the pathogen is identified early on, it may lead to a more effective and less invasive treatment plan. Screening can also lead to a reduction in transmission; most of those who have the disease are in their latent stage with no clinical symptoms. Those that are in the latent stage can still transmit the disease. Therefore if we could identify the patients in the latent stage, preventative measures could be taken to stop the carriers from unconsciously spreading the pathogen. Although screening is a great tool, it is very costly. The next logical step is then to offset the screening cost by researching new less costly ways to diagnose, research a way to have generic forms of present screening methods that are less costly, and to possibly ask for the pharmaceutical companies to donate or reduce the price of diagnostic test. Screening has also been proven ineffective because people do not show up to the test. This problem relates back to the educational deficiencies. If the people were properly educated of the dangers, attendance rates would more than likely skyrocket. In an ideal world, with more funds, screening would be implemented in conjunction with the educational infrastructure. Therefore it is only probable to give money to screening research oppose to actually screening three million people.
If a vaccine is created, it will help eradicate the disease all together. Although this may take awhile, in the long run if the disease is completely eradicated, it will create less of a problem. Due to the fact of the relatively low funds, allocation to this factor will be significantly lower than the primary two. Hypothetically if we were to donate the entire amount in finding a vaccine, it would more than likely not lead to an adequate vaccine. This is a result of the tremendous amount of research and funds it takes to properly cultivate a vaccine. Research for a vaccine is still extremely important and if more funds were available the ratio of funds deferred to vaccine research would increase tremendously.
BUDGET:
2 YEAR PLAN OF ACTION
EDUCATION: $2,342,400.00 Million
Treatment = $1,300,000.00
Screening = $1,157,600.00
Vaccine= $200,000
References:
Berrang-Ford, L., Odiit, M., Maiso, F., Waltner-McDermott, D., 2006. Sleeping Sickness in Uganda: revisiting current and historical distributions. African Health Science 6(4):223-231.
CDC. 2002. African Trypanosomiasis
Coleman, P., Ferve E., Odiit, M., Magona, J., Welburn, S., Woolhouse, M., 2001. The origins of a new Trypanosoma brucei rhodesiense sleeping sickness outbreak in eastern Uganda. The Lancet. 358: 625-628.
Ewald, P. Evolution of Infectious Disease. Oxford Press. New York, New York. 1994.
FDA News. 2007. Immtech receives $5.1 million for African sleeping sickness trials. Daily International Pharma Alert. 4:218
Hide, G., 1999. History of sleeping sickness in east Africa. Clinical microbiology reviews. 12(1):112-125.
Hofer, A., Steverding, D., Chabes, A., Brun, R., Thelander, L., 2001. Trypanosoma brucei ctp synthetase: a target for treatment of African sleeping sickness. Proceedings of the National Academy of Sciences of the United States of America. 98: 6412-6416.
Leak, SGA. Tsetse Biology and Ecology: Their Role in the Epidemiology and Control of Trypanosomosis. Wallingford, UK: CABI Publishing in association with the International Livestock Research Institute, Nairobi, Kenya; 1999.
Ripamonti, D., Massari, M., Arici, C., Gabbi, E., Farina, C., Brini, M., Capatti, C., Suter, F., 2001. African sleeping sickness in tourist returning from Tanzania: the first 2 italian cases from a small outbreak among eurpoean travelers. Clinical Infectious Diseases. 34: 18-22.
Robays, J., Eilengue, M., Vanderstuyft, P., Boelaert, M., 2004. The effectiveness or active population screening and treatment for sleeping sickness control in democratic republic of Congo. Tropical Medicine and Internal Health. 9:542-550.
Smith, D., Pepin, J., Stich, A., 1998. Human African trypanosomiasis: an emerging public health crisis. British Medical Bulletin. 54:341-355.
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