Introduction
African trypanosomiasis or simply sleeping sickness is a vector-borne parasitic disease. It is also abbreviated as HAT, which stands for Human African trypanosomiasis. Sleeping sickness has two forms, depending on the type of the parasite that caused the infection (WHO, 2014).
The first type is Trypanosoma brucei gambiense. It is found in 24 countries in west and central Africa. It accounts for over 98% of the reported cases. It is possible for someone to be infected with this type of the sleeping sickness for long durations without major signs or symptoms. When major symptoms do emerge, the patient would often already be in an advanced stage where the disease already affects the central nervous system (WHO, 2014).
The second type is Trypanosoma brucei rhodesiense. It is found in 13 countries in eastern and southern Africa. There are only under 2% of reported cases. Its signs and symptoms appear during the first few weeks or months upon being infected and it develops rapidly to the central nervous system (WHO, 2014).
Etiology
African trypanosomiasis is caused by infection with the protozoan parasites that belong to the genus Trypanosoma. The parasites are transmitted through the bites of Tsetse flies, which breed in warm and humid areas. The infection comes from human beings, although domestic and wild animals can also host the human pathogen parasites. In this regard, the flies become a parasite reservoir and a source of infection. Tsetse flies are found in 36 countries of sub-Saharan Africa (MSF, 2013).
It should be noted, though, that only certain species of the Tsetse fly transmit the disease. There are many regions where the flies exist but where sleeping sickness does not occur. Most of the transmissions occur in rural populations, which depend on agriculture, fishing, and hunting. The disease may spread from a single village to an entire region. The intensity of the disease can vary from one village to the next (MSF, 2013; WHO, 2014).
While the disease is commonly spread through Tsetse bites, there are other ways that a person is infected. Infection from mother to child is an example. The disease can transfer to the womb and infect the fetus. Other blood-sucking insects may also be transmitters. As well, accidental transmissions can happen. More specifically, researchers can be pricked with contaminated needles during laboratory tests (WHO, 2014).
Distribution
Around 40 000 cases were reported. However, an estimated 300,000 cases were undiagnosed and left untreated in 1998. Prevalence reached 50% during the epidemic periods of 1896-1906, 1920, and 1970-1990 in Angola, Congo, and Sudan. Through the continued control efforts in 2009, the number of cases reported dropped to less than 10, 000 for the first time in 50 years. The decline continued in 2012 with 7216 cases. Despite this, however, around 70 million people are still at risk. Also, there are still an estimated 20, 000 actual cases left (WHO, 2014).
Natural history of the disease
The disease progresses in two stages. The first stage is called hemolymphatic. In this early stage of the disease, parasites rapidly increase in the blood and lymphatic system. The patient experiences fever, headaches, joint pains, and itching. The second stage is called neurological or meningoencephalitic. In this late stage of the disease, parasites invade the blood brain barrier. They persist and multiply in the central nervous system and causes an encephalitic reaction. More obvious signs and symptoms of the disease appear such as changes in behavior, confusion, sensory disturbances, poor coordination, and most distinctly, disturbance in the sleep cycle. It may lead to death if left untreated (MacLean, Reiber, Kennedy & Sternberg, 2012; WHO, 2014).
Treatment of the disease
Patients with early-stage disease are treated with suramin for T. brucei rhodesiense and pentamidine for T. brucei gambiense while melarsorpol is used for late-stage T. brucei rhodesiense sleeping sickness. Patients with late-stage gambiense trypanosomiasis can be treated with melarsoprol. Eflornithine can also be used. This is available from the World Health Organization or WHO. These have instructions and various detailed regimens given elsewhere (Pepin, 2007; WHO, 2014).
After treatment, patients need to be followed up with Lumbar Puncture every 6 months for 2 years in order to identify relapses that need to be addressed. Although quite toxic, melarsoprol remains to be an effective drug against trypanosomes. 5 to 10% of patients also develop a reactive encephalopathy, most probably because of the rapid destruction of trypanosomes, which induces autoimmune central nervous system vasculitis.
Eflornithine, the latest trypanocidal drug developed in the last 60 years, is as effective as melarsoprol (Pepin, 2007). However, it’s better tolerated, possibly because of the slow manner by which it kills parasites. Its major drawback is the need for intravenous administration every 6 hours for 14 days. This is problematic in the rural hospitals of Congo or Sudan. Also, as with the drugs used for the treatment of other infectious diseases, a patient’s eventual resistance to trypanocidal drugs is a cause for concern, especially with the frequent treatment failures that have been reported for melarsoprol in Sudan, Uganda, and Angola, and for eflornithine in Uganda. Thus, it is important for novel treatments to be developed, as they can serve as second-line options for patients who undergo a relapse (Pepin, 2007).
Prevention
In epidemics such as this, people could have simply left the area. However, many depend on the animal livelihood. Moving out would also harm their lives just as much. As such, the least that people can do is to regularly visit the doctor. This ensures that one’s health condition is regularly checked; hence, enabling the signs and symptoms of the disease to be spotted before it gets worse. The diagnosis has three steps. The first step is screening for potential infection. The second is observing if the parasite is present, and the third is examining the cerebrospinal fluid to determine the disease’s progression (WHO, 2014).
Based on the findings, the reason that the death rates are up is because cases were undiagnosed. Thus, victims were not given proper and adequate medical attention. Had the victims monitored their health, they would have not succumbed to the disease. Nevertheless, victims may not have the chance to visit the doctor or even use health facilities due to their distance from the rural areas. In this regard, with the help of the governments and health organizations from the affected countries of Africa, a continuous and far-reaching effort must be extended to these areas. Through the epidemiologic triad, let us determine the potential interventions to reduce and eventually eliminate the sleeping sickness disease.
Application of the Epidemiologic Triad
The epidemiologic triad consists of the host, vector, agent, and the environment. In this particular disease, the host is the humans and the animals. The vector is the Tsetse flies. The agent is the trypanosomiasis parasite. The environment is the African region and the institutions that relate with Africa, such as the different governments of Africa, businesses, health organizations, and foundations.
Based on the findings, the disease is vector-borne parasitic. This means that the agent travels through the vector to suck the life out of the host. The more the agent hops into a vector, the more that the host would be infected and die. The environment is the receiver of the mortality effects caused by this agent-vector combination.
When the agent has infected all the possible hosts, there would be nothing left for them to grow in. Eventually, the agent would likely die. However, this would also mean the end for the human and animal host. As such, this is clearly not a viable scenario.
Through interventions on the vector through the environment, the agent would cease infecting the host while the host continues to observe preventive measures and continuously seek treatment. Based on the findings, not all Tsetse flies (i.e. the vector) guarantee transmission of the disease. However, there’s no adequate data on how to determine which flies do infect.
In this regard, it would be best to consider all Tsetse flies as an active disease transmitter. With this, the disruption may consist of coming up with an insecticide or repellant against these flies. Products may adapt the range of lines produced to fight houseflies and mosquitoes. Health companies may also manufacture lamps and coils.
In a more far-reaching scale, institutions must collaborate in programs and projects for the implementation of continuous efforts and the advancement of tools and medications to fight the disease. For the past two decades, the World Health Organization led assemblies that focused on one goal, which is the elimination of the disease. It’s important to address the disease as a public health concern and for institutions to acknowledge the seriousness of the problem.
WHO established the HAT Surveillance and Control Programme against African Trypanosomiasis or PAAT, with support from public and private institutions such as Sanofi-Aventis, Bayer HealthCare, the Bill & Melinda Gates Foundation, and the Belgium and French Cooperation. In 2000, the African Union also collectively embarked on the Pan African Tsetse and Trypanosomosis Eradication Campaign or PATTEC (Simarro, Jannin, & Cattand, 2008).
The heads of governments agreed that developing a solution for the problem with the Tsetse fly would contribute greatly to Africa’s development. Yet, this couldn’t be achieved when a country acts alone. In 2006, 20 out of 36 affected countries achieved or were close to achieving the target of reporting no new cases, and 8 countries reported less than one hundred new cases each year. With these milestones, elimination has become a feasible objective (Simarro, Jannin, & Cattand, 2008).
Future outlook of the disease
Effective surveillance with good reporting will also be crucial. In addition, advocacy in the affected countries must be maintained in the face of the decreasing number of cases reported. Health policy makers and planners should retain the high priority accorded to sleeping sickness. As well, research must be encouraged to resolve issues that hinder the development of new approaches to the disease’s control and surveillance (Simarro, Jannin, & Cattand, 2008).
Since elimination is considered feasible, the World Health Organization will be adopting the perspective of other countries. In particular, these countries have demonstrated 3 views. The first is that the existing health systems play a major role in ensuring surveillance and control sustainability. Second, it is important to continuously develop new diagnostic tools and drugs in order to guarantee the effective participation of existing health structures. Lastly, it is important to maintain a specialized central structure at the national level in order to ensure effective coordination within the health system, as well as to ensure that the healthcare institutions are provided with the technical assistance that they need. With this, WHO is ready to take up the challenge and continue to lead countries – coordinating with them and providing them with the support that they need (Simarro, Jannin, & Cattand, 2008).
Summary
African trypanosomiasis or simply sleeping sickness is a vector-borne parasitic disease caused by being infected with protozoan parasites that belong to the genus Trypanosoma. The parasites are transmitted to humans through the bites of Tsetse flies. However, animals can also carry the parasites. The disease undergoes two stages. The early stage is hemolymphatic while the late stage is the fatal meningoencephalitic. It affects the central nervous system and its most distinct symptom is the disruption of sleep cycle.
It has two types of parasites, namely the Trypanosoma brucei gambiense and the Trypanosoma brucei rhodesiense. Each of the two is treated differently. Pentamidine is for T. brucei gambiense while suramin is for T. brucei rhodesiense. As the years passed, other drugs were developed and introduced, such as Melarsoprol and Eflornithine. Melarsoprol is considered effective for the late stage of rhodesiense parasite. However, it is toxic. In this regard, eflornithine is the alternative. On the other hand, people are encouraged to wear clothes that cover their skin and that are thick enough in order to avoid being bitten by Tsetse flies. It is also suggested that they use DEET repellants.
Through the epidemiologic triad, other preventive measures are explored. It is found that intervention on the vector through the environment would cease infection of the host from the agent. The World Health Organization -- one of the institutions that comprise the environment -- has launched programs in the past two decades to control the Tsetse flies, which is the vector. This institution also formed ties with the African Union, Sanofi-Aventis, Bayer HealthCare, the Bill & Melinda Gates Foundation, and the Belgium and French Cooperation.
The disease has spread in 36 African countries, with 40, 000 reported cases and 300, 000 undiagnosed. This number has declined through 2012. 20 out of 36 affected countries have also achieved or are at least close to achieving the elimination campaign goal. This is due to the continuous efforts of the various public, private, government, and non-government institutions.
However, despite the notable improvements and the move towards medical advancements, threats are still projected in the future. The declining numbers may mean the disease being given less priority by the participating institutions. This may result in the decreased support for the disease and a shift of focus to other concerns. However, it is important to note that continuous effort is necessary to truly achieve the goal of entirely eliminating the disease.
References
MacLean, L., Reiber, H., Kennedy, P. G. E., &Sternberg, J. M. (2012). “Stage Progression and Neurological Symptoms in Trypanosoma brucei rhodesiense Sleeping Sickness: Role of the CNS Inflammatory Response.”PLOS Neglected Tropical Diseases 6(10): 1-8. Doi:10.1371/journal.pntd.0001857
Medicin Sans Frontieres (MSF). (2013). “Sleeping sickness.” Retrieved from http://www.doctorswithoutborders.org/our-work/medical-issues/sleeping-sickness
Moore, A. (2013). “Trypanosomiasis African sleeping sickess.”Infectious Diseases Related to Travel. Atlanta, Georgia: Centers for Disease Control and Prevention.
Pepin, J. (2007). “Combination Therapy for sleeping sickness: A wake-up call.”The Journal of Infectious Diseases 195(3): 311-313. Doi: 10.1086/510540
Simarro, P. P., Jannin, J., & Cattand, P. (2008). “Eliminating human African trypanosomiasis: Where do we stand and what comes next.”PLoS Medicine 5(2): 0174-0180. Doi:10.1371/journal.pmed.0050055
World Health Organization (WHO). (2014). Trypanosomiasis human African sleeping sickness. Retrieved from http://www.who.int/mediacentre/factsheets/fs259/en/
