African Sleeping Sickness

AFRICAN SLEEPING SICKNESS By Sarah Womer

What is African Sleeping Sickness?

The medical term for African Sleeping Sickness is Human African Trypanosomiasis  (trupăn"usōmī'usis) trup­ an­oo­soh­my­oo­sis

African sleeping sickness is found only in Sub-Saharan Africa

It is a “vector-borne parasitic disease” A vector is the disease-carrying body or animal; the “host”

The “host” is usually a human or domestic animal but can be wild animals as well.

The parasites are spread by “arthropod transmission” or “bug bites” But not just any bugs: tsetse flies (Glossina genus).

The parasites can also be spread from mother to child in utero (“vertical transmission” And by what is called “mechanical transmission.”

This means through filth and poor sanitation.

These parasites are known as Trypanosoma They are protozoa (single-celled organisms) which survive by feeding off of human or nonhuman animals

There are two strains of H.A.T. The first strain is known as trypanosoma brucei gambiense also called “West African Sleeping Sickness a/o West African Trypanosomiasis” This strain is commonly found in Democratic Republic of Congo, Angola, Sudan, Central African Republic, Republic of Congo, Chad, and northern Uganda

Trypanosoma brucei gambiense is a chronic infection An infection can occur for months or  years without any major signs or  symptoms.   When the disease finally emerges or is  diagnosed, the central nervous system has  been affected, the victim is generally in the advanced  stages.

The second strain is known as trypanosoma brucei rhodesiense Also called East African Sleeping Sickness and/ or East African Trypanosomiasis East African Sleeping Sickness is commonly found in Uganda, Kenya, Tanzania, Malawi, Ethiopia, Zaire, Zimbabwe, and Botswana

Trypanosoma brucei rhodesiense is an acute infection Noticeable signs and symptoms of the infection appear within weeks or months instead of years. The progression is the same as gambiense strain: “trademark” sleeping sickness signs indicate central nervous system infection.

West African trypanosomiasis accounts for 90 % of all reported cases of H.A.T. (Human African Trypanosomiasis)

The 10 % of remaining cases are East African trypanosomiasis in origin.

Human African Trypanosoma (H.A.T. for short) has a long history…

The first reports of the disease Ibn Khaldoun wrote about the disease while recording histories of North Africa (upper Niger) in the 14th century

The next report of the disease came from Guinea in 1734.

Enter Winterbottom… • In West Africa in 1803, visibly swollen lymph glands became known as Winterbottom's Sign after the description of this disease symptom by parasitologist Chris Winterbottom.

Such diagnosis was welcomed by slave traders who refused trading and buying of slaves possessing such symptoms.

Finding the disease itself • The earliest detection of trypanosomes in human blood was in 1902

• Similar discoveries of filiaria-like organisms in the blood were made by J.H. Cook in East Africa, • J.E. Dutton during a visit to Gambia, first correctly identified the parasite as a trypanosome and subsequently named it Trypanosoma gambiense

And finally… In 1903 Sir David Bruce put it together that: 1. trypanosomes were the causative 2. The disease was agents of sleeping transmitted to sickness humans by tsetse flies, and

3. trypanosome fever and sleeping sickness were the same terrible disease!

Since then, the epidemic has continued… With notable outbreaks recorded: 1896­1906 in Uganda and the Congo Basin  1920 in vast sub­Saharan areas in Africa 1960 saw near disappearance of disease. 1970 resurgence of disease that continues today.

So what exactly is a trypanosome?

A trypanosome is a protozoa Protozoa: noun, singular; a single-celled Eukaryotic organism, most of them motile and heterotrophic •Greek- protohi first + zoa animals … and the rest of that means: Eukaryote: noun, plural; Any of the single or multi-cellular organisms whose cell contains a distinct, membrane-bound nucleus. Motile: Actively moving and self-propelled. Heterotrophic: adjective; the utilization of organic compounds as a source of carbon. (Examples of such organisms are animals, which are not capable of manufacturing food by inorganic sources, hence, must consume organic substrates for sustenance). Greek- heterone (an) other + trophe nutrition •From http://www.biology­online.org/dictionary/

What does that even mean? that means that a trypanosome is a very simple life-form (single celled). & its source of nutrition is the body of the host human or non-human animal. Or… It is a parasite that eats human blood until death do them part.

The trypanosomes grow through a 2­host life  cycle: human or non­human mammal  and tse­tse fly. When the trypanosomes are ingested  during a blood meal by the tsetse fly from an infected  human or non­human  animal vector,  the lifecycle begins.

Inside the fly’s “mid­gut” the  parasite, trypanosome,  multiplies.

At 2­3 weeks, the trypanosome  migrates to the tse tse fly’s salivary  gland to transfer to a new animal  vector.

The tse­tse fly bites a human or  non­human animal infecting the  animal.  

This is very similar to how malaria is transmitted.

Sleeping sickness Disease Progression Warning: there is a really gross picture about to be displayed on the screen

Or… the “infected vector”

A man in the late, and fatal, stage of H.A.T.

First you are bitten… Or as they say in the professional field, the tsetse fly has a “blood meal,” where it will transmit the parasites via the salivary glands.

mmm blood meal…

Once you are the dinner of a tsetse fly…

The infected area will appear as a “chancre” or the incredibly disgusting looking lesion-like thing you see above.

the trypanosomes begin to grow… the protozoa multiply in the subcutaneous tissues, blood, and lymph nodes. 

Left untreated… eventually the blood­ brain barrier is  crossed by the  parasites and the central nervous  system becomes  infected. Once that happens,  death is likely.

Stages, Signs and Symptoms

There are two official stages of Human African Trypanosomiasis regardless of whether it is West or East African Sleeping Sickness

Stage One: haemolymphatic phase Stage Two: neurological phase

Stage One This is when the initial bite occurs and the  body is trying to fight off the parasites.   Symptoms begin 1­4 weeks after the first  bite!! Symptoms include “bouts of fever”,  headaches, joint pains, and itching!

Stage Two Stage two is when the “trademark” African Sleeping Sickness symptoms appear. When these symptoms manifest, that means the blood-brain barrier has been crossed.

Symptoms of stage two include: • confusion  •  poor coordination •  sensory disturbances (like hyper­ sensitivity to touch) •  and sleep cycle disturbance (hence  sleeping sickness)

How is H.A.T. treated? "The earlier the identification of the  disease, the better the prospect of a  cure." ­­ World Health Organization

Disease Treatment • Treatment varies on the progression of  the disease (stage one or two).   •  First stage disease treatments are "less  toxic" with easy administration and high  effective rates.  •  Second stage disease treatments  kill 5% of all recipients just by  administration alone 

Once the disease has crossed the blood­ brain barrier, treatment must use a drug  that can do the same thing.   Many of these drugs are incredibly toxic  and require complicated administration. 

The Drugs Needed

First Stage Drug Treatments Pentamidine Discovered in 1941 Used for first stage trypanosomiasis brucei gambiense strain sickness. Minimal side effects; generally welltolerated by patients

First Stage Drug Treatments Suramin

discovered in 1921 used for the treatment of the first stage of T.b. rhodesiense. Causes “undesirable” side effects in the urinary tract and allergic reactions in some patients

Second Stage Drug Treatments Melarsoprol

discovered in 1949 it is used in both forms of infection. It derives from arsenic and has many side effects. The most dramatic is a reactive encephalopathy (encephalopathic syndrome) which can be fatal (3% to 10%). An increase of resistance to the drug has been observed in several foci particularly in central Africa.

Second stage Drug Treatments Eflornithine

Discovered in 1980 It is only effective against T.b. gambiense Considered the best treatment available The regimen is strict and difficult to apply

Other Drugs • Nifurtimox An oral drug that kills protozoa • Fexinidazole An experimental oral that can cure late-stage sleeping sickness (in the brain) in 2 weeks

Problems with treatment Many areas lack the necessary infrastructure to deal with this disease properly or effectively There are not enough trained professionals to administer the drug regimens (if any doctors at all) There are no hospitals to administer the regimens in Drug regimens are very expensive and therefore inaccessible to most infected individuals or even hospitals.

More problems with treatment Drug regimens are extremely toxic and require long stays in the hospital Many infected persons can’t afford treatment Many hospitals can’t provide extended-stay environments Though regular check-ups for “relapse” are necessary, that is difficult for reasons including accessibility to hospitals or clinics, finances, and the existence of doctors or clinics at all

Isn’t there a way to prevent this though? No.

There is no available vaccine. trypanosomes are able to switch at random to over 1,000 different antigens making it difficult for the body to create the appropriate antibodies

Preventive measures can help Wear thick protective clothing This deters bites but doesn’t stop them as the tsetse fly can bite through fabrics.

Wear neutral colored clothing Tsetse flies are attracted to bright and dark contrasting colors This is not a good outfit to wear to prevent tsetse fly bites.

More preventive measures Use Bednets while sleeping. Inspect your vehicles before entering in tsetse prone areas. Avoid open seating in vehicles Tsetse flies are attracted to dust by moving vehicles or animals. Avoid bushes where tsetse flies rest during the day

As far as the tsetse fly is concerned: • There are 30 different kinds of tsetse flies (genus Glossina) • Only 3 species feed on humans: G. tachinoides G. palpalis G. fuscipes

Out of the 3 species of tsetse flies who feast on primate blood: • the percentage of feeds may be between 8 and 40% • Feed opportunity depends on “local conditions” (like obtaining water; living near rivers) • Anywhere from 18% to less than 5% of all tsetse fly meals are taken from primates altogether

The rate of infection amongst tsetse flies • Infected tsetse flies number less than 10% of the 3 species of tsetse flies posing a risk for primates

And just in case you’re curious… • All tsetse flies carry various strains of trypanosomes • There are 8 different strains of trypanosomiasis • Only two of the 8 strains are lethal to humans

Who is at risk of contraction?

People most likely to contract African Sleeping sickness are: Rural villagers -- especially villagers who care for livestock Hunters Workers in game reserves or parks Tourists who spend an extended time in rural areas or game reserves

Why those groups of people? only certain species of the tsetse flies transmit  the disease and not all tsetse flies are infected.    Different species are located in different habitats  with the majority of tsetse flies found in: thick vegetation by rivers and lakes,  in "gallery-forests" and "vast stretches of wooded savannah”

Extraordinary at risk groups There are some people who become “at­ risk” for infection due to extra­ordinary  circumstances Generally speaking, these populations probably would not suffer epidemics otherwise.

Extra-ordinary circumstances: • Rural villagers living in areas with a lack of infrastructure (running water, electricity) • Villagers living in extreme poverty • Displaced peoples and refugees

From the World Health Organization: "Sleeping sickness generally occurs in remote rural areas where health systems are weak or non-existent. The disease spreads in poor settings. Displacement of populations, war and poverty are important factors leading to increased transmission."

Why? “mechanical transmission” from unsanitary conditions is heightened Increased exposure to tsetse fly prone areas (like dense vegetation) from “being driven into the bush” Poverty (lack of necessary infrastructure) for health systems or alternatives to poverty

At risk population information 70 million people at risk 17,616 reported cases for the year 50­70,000 cases currently estimated. prevalence is up to 50% in villages in DRC, Angola, and Southern Sudan  ahead of HIV/AIDS still health concern in: Central African Republic, Chad, Congo, Cote  d'Ivoire, Guinea, Malawi, Uganda, and United Republic of Tanzania. 50 or less reported cases per year: Burkina Faso, Cameroon, Equatorial  Guinea, Gabon, Kenya, Mozambique, Nigeria, Rwanda, Zambia,  Zimbabwe. no new cases for decades: Benin, Botswana, Burundi, Ethiopia, Gambia,  Ghana, Guinea Bissau, Liberia, Mali, Namibia, Niger, Senegal, Sierra  Leone, Swaziland, Togo. assessment of the true situation is difficult with a lack of surveillance and  diagnostic expertise. From 2005 World Health Organization information.

Sleeping Sickness in animals • In animals, the disease is called nagana which is a  Zulu word meaning “to be depressed.” • it is also problematic and fatal for animals as well.   This includes wild and domestic animal species.  • T.b.r. (trypanosoma brucei rhodesiense: 10% of  reported cases of H.A.T.) is  the predominant strain  found in non­human animals.   • T.b.g. (trypanosoma brucei gambiense: 90% of  reported cases) can also be found in non­human  animals with the "epidemiological role" undetermined  as of yet.

Implications of animal sleeping sickness As the gambiense strain can easily be passed from animal to human, effective “vector control” is imperative.

Great economic tolls are felt by rural populations that rely on animals for sustenance and income

Implications of African Sleeping Sickness for the rest of the world or why you should care

or the POLITICS behind it all

Commonalities in disease dispersion

African Sleeping Sickness

Malaria

Disease in comparison to Livestock Distribution

African sleeping sickness

Livestock and Cattle Distribution

Disease in comparison to war and civil unrest

Distribution of sleeping sickness

Distribution of War and Civil Unrest

Our activities contribute too! • Our lack of concern and action in civil disputes like Darfur, Sudan, Rwanda in the 1990’s, and even present day Democratic Republic of Congo further degrade villagers’ lives They are forced “into the bush” exposed to diseases of which African sleeping sickness is only one of many They are forced into filthy refugee camps where unsanitary conditions are a fact of life resulting in rampant disease Malnutrition and starvation further weaken the bodies as food is scarce or non-existent Their livelihoods are corrupted and they must rely on hand-outs or try to find work doing things that may not be well-suited to their environment

Our corporate institutions and government Have been known to exploit rivalries between ethnic groups for cheap labor or inexpensive raw materials Have not used discretion in purchasing raw materials from nations engaged in war Have not provided assistance to people affected by war By sending troops to stop the wars Or by sending troops to set up refugee camps Or by providing avenues for immigration

Coltan as an example Coltan is used in production of electronics like cell phones, game consoles, and computers Coltan comes from the Democratic Republic of Congo Profits from the coltan mines go to fund rebel armies and the wars they are causing Even though this is known by much of the industry, no sanctions have been imposed and no boycotts have ensued.

In areas like the D.R.C. sleeping sickness incidents are over 50% of all fatalities! Even surpassing HIV/AIDS as a cause of death Our actions or inactions do have causes and effects ESPECIALLY in the increasingly global society we live in.