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 non-
human 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 well-

tolerated 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.