Trypanosoma are unicellular parasitic protozoa that cause serious diseases like African sleeping sickness in humans. They are transmitted primarily by tsetse fly bites. There are three main subspecies that cause human disease: T. brucei gambiense which causes a chronic form in West and Central Africa, T. brucei rhodesiense which causes an acute form in East and Southern Africa, and T. brucei brucei which infects animals. The parasites evade the human immune system through antigenic variation of surface proteins, eventually overwhelming the immune response if left untreated. Symptoms occur in two stages - an initial hemolymphatic phase with intermittent fever and joint pain, followed by
2. • Trypanosoma is a genus of kinetoplastids (class
Kinetoplastida), a monophyletic[1]
group of unicellular
parasitic flagellate protozoa. The name is derived from
the Greek trypano- (borer) and soma (body) because of
their corkscrew-like motion
• All trypanosomes are heteroxenous (requiring more than
one obligatory host to complete life cycle) and most are
transmitted via a vector. The majority of species are
transmitted by blood-feeding invertebrates, but there are
different mechanisms among the varying species
7. African trypanosomiasis
• African trypanosomiasis or sleeping
sickness[1]
is a parasitic disease of
humans and other animals. It is caused by
protozoa of the species
Trypanosoma brucei
• Vector
The tsetse fly (genus Glossina) is a large,
brown, biting fly that serves as both a host
and vector for the
trypanosome parasites
8. •There are two subspecies of the parasite that are
responsible for initiating the disease in humans.
Trypanosoma brucei gambiense causes the diseases in
west and central Africa whereas,
•, Trypanosoma brucei rhodesiense has a limited
geographical range and is responsible for causing the
disease in east and southern Africa
•In addition, a third subspecies of the parasite known as
Trypanosoma brucei brucei is responsible for affecting
animals but not humans
9. •These parasites primarily infect individuals in sub-
Saharan Africa because that is where the vector (tsetse
fly) is located
•T. b. gambiense causes a chronic condition that can
remain in a passive phase for months or years before
symptoms emerge and the infection can last about 3
years before death occurs.
•T. b. rhodesiense is the acute form of the disease and
death can occur within months since the symptoms
emerge within weeks and it is more virulent and faster
developing than T. b. gambiense
10. Furthermore
trypanosomes are surrounded by a coat that is composed of
variant surface glycoproteins (VSG). These proteins act to protect
the parasite from any lytic factors that are present in human
plasma. The host’s immune system recognizes the glycoproteins
present on the coat of the parasite leading to the production of
different antibodies (IgM and IgG). These antibodies will then act
to destroy the parasites that circulate around the blood. However,
from the several parasites present in the plasma, a small number
of them will experience changes in their surface coats resulting in
the formation of new VSGs. Thus, the antibodies produced by the
immune system will no longer recognize the parasite leading to
proliferation until new antibodies are created to combat the novel
VSGs. Eventually the immune system will no longer be able to
fight off the parasite due to the constant changes in VSGs and
infection will arise
11.
12. Signs and symptoms
African trypanosomiasis symptoms occur in two stages :
1.haemolymphatic phase, is characterized by fever, headaches,
joint pains, and itching Fever is intermittent, with attacks lasting from a
day to a week, separated by intervals of a few days to a month or
longer.
2.the neurological phase ; In this stage the parasites cross the
blood-brain barrier to infect the central nervous system 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
of the second stage of the disease.
17. Treatment
•First stage
The current treatment for first-stage disease is
intravenous or intramuscular pentamidine for T. b.
gambiense or intravenous suramin for T. b.
rhodesiense.
•Second stage
For T. b. gambiense intravenous eflornithine or the combination of nifurtimox
and eflornithine appear to be more effective and easier to give.[19]
These
treatments may replace melarsoprol when available[19]
with the combination
being first line.[3]
Intravenous melarsoprol was previously the standard
treatment for second-stage (neurological phase) disease and is effective for
both types.[3]
It is the only treatment for second stage T. b. rhodesiense
however causes death in 5% of people who take it.[3]
Resistance to
melarsoprol can occur.[3]