Definition of the disease

Human African trypanosomiasis, also known as sleeping sickness, is a vector-borne parasitic disease.
It is caused by infection with protozoan parasites belonging to the genus Trypanosoma.
They are transmitted to humans by tsetse fly (Glossina genus) bites which have acquired their
infection from human beings or from animals harbouring human pathogenic parasites.

Tsetse flies are found just in sub-Saharan Africa though only certain species transmit the disease. The
disease develops in areas ranging from a single village to an entire region. Within an infected area, the
intensity of the disease can vary from one village to the next.

Infection and symptoms

The disease is mostly transmitted through the bite of an infected tsetse fly but there are
other ways in which people are infected:
 Mother-to-child infection: the trypanosome can cross the placenta and infect the fetus.
 Mechanical transmission through other blood-sucking insects is possible, however, it is
difficult to assess its epidemiological impact.
 Accidental infections have occurred in laboratories due to pricks with contaminated needles.
 Transmission of the parasite through sexual contact has been documented.

Infection path

In the first stage, the trypanosomes multiply in subcutaneous tissues, blood and lymph. This
is also called haemo-lymphatic stage, which entails bouts of fever, headaches, joint pains and
itching
In the second stage the parasites cross the blood-brain barrier to infect the central nervous
system. This is known as the neurological or meningo-encephalic stage. In general this is
when more obvious signs and symptoms of the disease appear: changes of behaviour,
confusion, sensory disturbances and poor coordination. Disturbance of the sleep cycle, which
gives the disease its name, is an important feature. Without treatment, sleeping sickness is
considered fatal although cases of healthy carriers have been reported.

Trypanosomiasis; Immune evasion

- African trypanosomes modify surface membranes to evade the host systems
o This is known as antigenic variation
o Multiplying rate also evades the immune system
- Rapid membrane protein variation and replicate faster than the immune system being able
to build a defense so immune system cannot detect before the protein compositions are
altered
- The surface contains invariant antigens ones that don’t change are shielded by
impenetrable coat of 107 copies of a single variant surface glycoprotein that the parasite can
replace the immune system mounts antibodies
- Currently 806 (VSG) which they can recombine and produce mosaic genes.
o So dysfunctional genes can be recombined with trypanosome cell to create a
functional gene that express different genotypes
o So, they produce 100s of VSG variants that are so unique that the host antibodies
are not effective against all 807 forms and this can be done rapidly as every
trypanosome contains genes for every VSG
 Distribution and current

In the last 10 years, over 70% of reported cases occurred in the Democratic Republic of the
Congo (DRC).
 The DRC is the only country that currently reports more than 1000 new cases annually and
accounts for 84% of the cases reported in 2015.
 Central African Republic is the only country that declared between 100 and 200 new cases in
2015.
 Countries such as Angola, Burkina Faso, Cameroon, Chad, Congo, Côte d'Ivoire, Equatorial
Guinea, Gabon, Gjana, Guinea, Malawi, Nigeria, South Sudan, Uganda, United Republic of
Tanzania, Zambia and Zimbabwe are reporting fewer than 100 new cases per year.

Major human epidemics

There have been several epidemics in Africa over the last century:
 one between 1896 and 1906, mostly in Uganda and the Congo Basin;
 one in 1920 in a number of African countries; and
 the most recent epidemic started in 1970 and lasted until the late 1990s.