Malaria

• Is an acute and chronic protozoan illness

characterized by paroxysms of

fever, chills, sweats, fatigue, anemia and

Splenomegally.
 Etiology
• Caused by intracellullar plasmodium
protozoa transmitted to humans by female
anopheles mosquito.
• Four spp: P. falciparum, P. ovale, P. vivax, P
malaria.
• Plasmodium ssp is able to survive in two
different cellular environments.
• In the human host(asexual form) and the
mosquito(sexual form).
 Life cycle.
- Begins after mosquito inoculates sporozoites into
the human blood stream.
- within minutes they enter hepatocytes of the liver
where they develop and multiply( exoerythrocytic
phase)
- The parasite referred to as schizont at this stage.
- After 1-2 weeks the hepatocytes rupture releasing
thousands of merozoites into the circulation.
• The tissue schizonts of P. falciparum and
malaria rupture once.
• For P. ovale and vivax they have 2 types: 1.
Primary and secondary.
• The merozoites penetrate RBC where they
transform into ring forms.
• These enlarge to become trophozoites.
• The later 2 can be identified on Giemsa stain.
-The trophozoites multiplies to form asexually to
produce many small erythrocytic merozoites.
- These are released into the blood stream
when RBC rupture.
- This process is associated with fever.
- They penetrate other RBC but others over
time develop into gametocytes(Male
&Female).
• This completes the life cycle once the
gametocytes are ingested by the mosquito.
• The female and male gametocytes fuse in the
stomach of the mosquito.
• After a series of transformations sporozoites
enter the salivary glands.
• At this point if mosquito bites another human
the sporozoites will be inoculated into that
person.
 Pathogenesis
• Four pathological processes have been
identified:
• 1. Fever which occurs when RBC rupture
and release merozoites.
• 2. Aneamia caused by hemolysis,
sequestration of RBC in spleen and other
organs and suppression of RBC production
in the bone marrow.
• 3. Immunopathological events result into
hypergammaglobulinemia, formation of
immune complexes, immunosuppression,
and release of tumour necrosis factor.
• 4. Cytoadherence of infected RBC to vascular
endothelium may lead to obstruction of blood
flow and capillary damage.
• This may result into vascular leakage of
protein and fluid, oedema and tissue anoxia
in the brain, heart, lungs, intestines and
kidneys.
 Immunity acquired is not complete
• Subsequent infection is averted but not
completely eradicated.
• RBCS containing hemoglobin S resist
malarial parasite growth.
• Also those containing Fetal Hb and
ovalocytes are resistant to P.
falciparum.
• Therefore newborns rarely become ill with
malaria because of fetal Hb and passive
immunity from the mother.
• In general, extracellular organism are targeted
by Ab, and intacellular by cellular defences such
as T lymphocytes, macrophages,
polymorphonuclear leukocytes and spleen.
•
 Clinical Features
• Incubation period is 9- 14 days.
• A prodrome lasting 2-3 days is noted in
some patients before parasites are
detected in blood .
• It consists of headache fatigue,
anorexia, myalgia, slight fever,and pain
in the chest, abdomen and joints.
• Classic presentation:
• Fever, rigors, sweats, nausea, vomiting,
diarrhoea, headache, convulsions,body
pains, pallor, jaundice.
• Fever coincides with hemolysis of RBC.
• Every 48 hours for vivax and ovale. 72 hours
for malaria.
 Complications
• Cerebral malaria
• Renal failure.( Black water fever)
• Pulmonary oedema,
• Hypoglycermia
• Thrombocytopnia
• Splenic rupture.
• Algid malaria
 Diagnosis
• MPS.
• PF
 Prevention
• Spraying homes for vector control.
• Use of repellants.
• Use of mosquito nets.
 Treatment
• Coartem
• Fansidar
• Quinine