This document discusses several protozoan diseases that affect the whole body, including malaria, leishmaniasis, and trypanosomiasis. It provides details on the causative agents, transmission, symptoms, diagnosis, treatment and prevention of each disease. For malaria, it describes the five plasmodium species that infect humans and their life cycles. The transmission through mosquitos and clinical presentation depending on species is outlined. Diagnosis is through blood film examination and treatment depends on disease severity. Trypanosomiasis is conveyed by tsetse flies and exists in African and American forms caused by different trypanosome species. Details are given on transmission, stages of disease, diagnosis and treatment approaches depending on CNS

1. Presentation10

2. These are protozoan diseases that affect the whole
body. Some of these diseases include the following:
 Malaria
 Leishmaniasis
 Trypanosomiasis

3. Malaria is an acute infectious illness caused by
protozoa of genus Plasmodium. Five species of the
plasmodium parasite can infect humans.
 Plasmodium falciparum (or P. falciparum)
 Plasmodium malariae (or P. malariae)
 Plasmodium vivax (or P. vivax)
 Plasmodium ovale (or P. oval
 Plasmodium knowlesi (or P. knowlesis)

4.  The disease is spread through the bite of an
infected female anopheles mosquito. The most
serious forms of the disease are caused by
plasmodium falciparum.
 Malaria caused by plasmodium vivax, plasmodium
ovale and plasmodium malariae causes milder
disease in humans that is not generally fatal
(Norburg, 1999).

5.  The female anopheles mosquito becomes infected
when it feeds on human blood containing
gametocytes. Once ingested the parasite
gametocytes taken up in the blood further
differentiate into male or female gametes and then
fuse in the mosquito gut.

6. Development in the mosquito takes seven to 20
days. This produces an ookinete that penetrates
the gut lining and produces an oocyst in the gut
wall. When the oocyst ruptures, it releases
sporozoites that migrate through the mosquito's
body to the salivary glands, where they are then
ready to infect a new human host.

7.  The sporozoites are injected into the skin, alongside
saliva, when the mosquito takes a subsequent blood
meal. They disappear from human blood within half an
hour and enter the liver and change into merozoites.
 After some days merozoites leave the liver and invade
the red blood cells and mature into male and female
gametacytes. These are then ingested by a mosquito
during a bite.

8. The symptoms vary depending on the species of
malaria parasite.

9.  The onset of malaria caused by Plasmodium
falciparum is insidious with a recent history of
fever (can be intermittent), headaches, sweats or
chills (cold shaking feeling) and body pains.
Cerebral malaria is the most serious complication
of malaria caused by Plasmodium falciparum. It
presents with confusion or coma and death follows
if treatment is not given.

10. The illness cased bt Plasmodium vivax and ovale
starts within a period of several days and the
patient gets fever on alternate days. The patient
feel cold then temperature rises to about 40°C. The
spleen and liver enlarge gradually and anaemia
develops.

11.  Ilness caused by Plasmodium malariae is associated
with bouts of mild symptoms and bouts of fever
every third day. Parasiteamia may persist for many
years without clinical symptoms. This type of
diseases may cause glomerulo-nephites and
nephritic syndrome (Todd, 2002).

12.  Microscopic examination of blood films (tick and
tin blood films). Thin films identify the species of
parasite while thick films show when a patient has
low level of parasitemia. Immunochromatographic
tests for P. falciparum (Todd, 2002).

14. The treatment of malaria is divided into uncomplicated malaria
and severe malaria.
 Uncomplicated malaria is defined as symptomatic malaria
without sign of severity or evidence of organ failure. Usually
combination therapy is recommended for the treatment of
these patients. It includes the following:
 Artemether +lumefantrine
 Artesunate + amodiaquine
 Artesunate+ mefloquine
 Artesunate + sulfodoxine-pyrimethanmine

15. If the patient does not recover after 14 days and has
evidence of parasitaemia, then the following
treatment can be given:
 Artesunate + tetracycline or clindamycin
 Quinine + tetracycline or clindamycin

16. Recommended treatment for patients with severe
malaria includes the following:
 Artesunate or Artemisinin per rectol.
 Artesunate or Artemisinin im.
 Quinine im or iv: Intravenous quinine
dihydrochloride in 5% dextrose 20mg/kg loding
dose then 10mg/kg 8-12 hourly for five days.

17.  Intramuscular quinine 20mg/kg loding dose then
10mg/kg 8-12 hourly for five days.
 Or short-course IM quinine for threee days plus
single dose pyimethamine (Olumesa, 2006).

18. The methods used to prevent the spread of malaria
or to protect individuals in areas where malaria is
endemic, include the following:
 Chemoprophylaxis
 Vector avoidance
 Treatment
 Case finding

19.  Trypanosomiasis is a disease in vertebrates caused
by parasitic protozoan trypanosomes of the genus
trypanosome. It is conveyed to human through the
bite of the tsetse fly.
 There are two types of trypanosomiasis, the African
trypanosomiasis and the Chaga’s disease which is
mainly found in Latin America (Paniker 2002).

20.  This disease is found in two forms, depending on
the parasite, either trypanosoma brucei gambiense
or trypanosoma brucei rhodesiense.
 T.b. gambiense is found in central and western
Africa. It causes a chronic condition that can
extend in a passive phase for months or years
before symptoms emerge.

21.  T.b. rhodesiense is the acute form of the disease
but has a much more limited range. It is found in
southern and Eastern Africa. Its infection emerges
in a few weeks and is more virulent and develops
very fast.

22.  Humans are the main reservoir for trypanosoma
brucei gambiense, but this species can also be
found in pigs and other animals. Wild game
animals and cattle are the main reservoir of T. b.
rhodesiense.

23. Transmission of the disease takes place through the following ways:
 The bite of the tsetse fly.
 Mother to child infection: The trypanosome can sometimes cross the
placenta and infect the foetus.
 Laboratories accidental infections, for example, through the
handling of blood of an infected person and organ transplantation,
although this is uncommon.
 Blood transfusion.
 Sexual contact (might be possible, but happens rarely) (Norburg,
1999).

24.  The tsetse fly is large, brown and stealthy. While
taking blood from a mammalian host, an infected
tsetse fly (genus glossina) injects metacyclic
trypomastigotes into the skin tissue. The parasites
enter the lymphatic system and pass into the
bloodstream.

25.  Inside the host, they transform into bloodstream
trypomastigotes and are then carried to other sites
throughout the body where they reach other body
fluids such as lymph and spinal fluid, and continue
the replication by binary fission.

26.  The entire life cycle of African trypanosomes is
represented by extra cellular stages. A tsetse fly
becomes infected with bloodstream trypomastigotes
when taking a blood meal on an infected mammalian
host.
 In the fly's mid gut, the parasites transform into
procyclic trypomastigotes and multiply by binary
fission. They then leave the mid gut, and transform into
epimastigotes.

27.  The epimastigotes reach the fly's salivary glands
and continue multiplication by binary fission.
 The cycle in the fly takes approximately three
weeks to progress (Paniker 2002).

29.  This disease present in three stages, that is,
primary, systemic or blood and cerebral or
sleeping-sickness stage.

30.  Primary stage or chancre stage is seen more in T.b.
rhodesiense. Where there are painful erythematous
induration nodules at the site of bite. The chancre
resolves within one to two weeks.

31.  In systemic illness or blood stage, the disease is
disseminated through the blood and lymphatic
system. There may be fever on and off. The patient
may have debilitation, anaemia general weakness,
enlargement of the spleen and lymphnodes
(Winterbottom's sign-swollen lymph nodes along
the back of the neck).

33. Cerebral or sleeping stage is when the disease
invades the brain. In T.b. rhodesiense the stage
appears two years after the initial infection. The
patient presents with mental deterioration,
confusion and reduced coordination. If not treated,
the sleep cycle is disturbed with bouts of fatigue,
coma and eventually death (Norburg, 1999).

34.  This disease should be considered in all febrile patients
from an endemic area. In T.b. rhodesiense infection, a
stained thick and thin blood films will reveal
trypanosomes. T. b gambiense may be seen in blood in
early stages of the disease, but can be demonstrated
easily in lymph node aspirates. If CNS is involved then
the cell count and protein content of the CSF increases
and glucose is diminished. Very high serum levels of
IgM or the presence Igm in CSF are suggestive of
tyrpanosomiasis (Todd 2002)

35. The treatment of trypanosomiasis is done in reference to
whether there is CNS involvement or not and depends
on the type of infection.
 T.b rhodensiense infection is treated as follows:
 If the CSF is normal, give a course suramin.
 If the CSF is altered melarsoprol should be given.
 All patients should be followed up for two years with
lumbar punctures performed every six months to look
for relapse.

36. T.b. gambiensis infection is treated as follows:
 If the CSF is normal, give a course of suramin or a
course of pentamidine.
 If the CSF is altered, give a course of melarsoprol,
preferably preceded by two or three injections of
suramin or one injection of pentamidine or triparsamide
suramin.
 Eflornithine is also effective for treatment during both
stages (Norburg, 1999).

37.  The prevention and control of trypanosomiasis
focuses on the eradication of the parasitic host, the
tsetse fly. Early treatment of the affected patients is
very important.