2.1.2.1 Life cycle of malaria
Malaria parasites are obligate
intracellular parasites with a complex life cycle involving both a
vertebrate (e.g. man) and an invertebrate host (mosquito vector), where
they undergo different developmental stages (Ekpenyong and Eyo, 2006).
Generally, the life cycle of Plasmodium can be divided into three
phases; the exoerythrocytic or pre-erythrocytic phase which occurs in
the liver, the erythrocytic phase which occurs in the erythrocyte and
the sexual phase which occurs in the mosquito (Ekpenyong and Eyo, 2006).
The life cycle of P. falciparum (and other plasmodia) commences when
Plasmodium sporozoites enter the mammalian host through the bite of an
infected female Anopheles mosquito (Prudencio et al., 2006). Sporozoites
enter the blood vessel at the site of the bite and travel through the
blood stream to the liver where they develop into merozoites (Prescott
et al., 2005). For two of the five human species (P. vivax, P. ovale),
dormant hypnozoite forms can develop in the liver leading to delayed
clinical attacks months or years later, but for P. falciparum, there are
no dormant forms (Prescott et al., 2005). In the liver, merozoites
replicate within the hepatocytes and several thousands of merozoites are
released into the circulation (Ezeigbo, 2005). Merozoite will invade
erythrocytes, initiating a replication cycle of 48 hours, during which a
single invaded merozoite develops into “ring†trophozoite, mature
trophozoite, and finally a schizont (Sargeant et al., 2006).
Each
erythrocytic schizont, depending on the species, releases approximately 6
to 32 merozoites, which then in turn initiate a new asexual cycle by
infecting other RBCs (Ekpenyong and Eyo, 2008). This phase of the life
cycle constitutes the erythrocytic cycle, and it is the phase of the
parasite’s life cycle that gives rise to all of the clinical symptoms
and mortality due to malaria (Ekpenyong and Eyo, 2008). At this stage,
the parasite is known to cause a number of changes on the red cell
membrane including the insertion or binding of parasite-encoded
molecules to the red cell surface, which are important in host parasite
interactions (Kirk 2001). At about this time, parasitized RBCs are
detectable microscopically, and symptoms of disease occur, which are
characterized by fever, chills, headache, lassitude, and
gastro-intestinal symptoms (Sargeant et al., 2006). The Plasmodium life
cycle continues when some merozoites develop into the sexual parasite
stages, the male and female gametocytes, which can be taken up by
mosquitoes during subsequent blood meals (Good et al., 2005). The
gametocytes undergo fertilization and maturation in the mosquito midgut,
forming an infective ookinete form, which migrates through the mosquito
midgut into the hemocele, developing into an oocyst in which
sporozoites are formed (Good et al., 2005). When fully matured, the
oocysts burst and release sporozoites, which migrate into the mosquito's
salivary glands, ready for the next transmission step (Kirk 2001;
Prudencio et al., 2006).
