Biology Reference
In-Depth Information
Figure 2.9
Proposed mechanism of
Plasmodium vivax
relapse activation in a malaria
endemic area (
White, 2011
). In this example, at the time of infection (sporozoite inocula-
tion) the individual already has hypnozoites of two different genotypes acquired from
two previous inoculations, which are latent in the liver. The different genotypes are
denoted by different colours (red and white). Half the newly acquired infection spo-
rozoites (blue) develop into pre-erythrocytic schizonts and half become dormant as
hypnozoites (the estimated proportions for tropical 'strains'). Illness associated with the
blood-stage infection activates a small fraction of the hypnozoites (inset shows a 'classic'
P. vivax
fever pattern in relation to asexual parasite development). In this example, one
hypnozoite of each genotype is activated by the illness and develops into pre-erythro-
cytic schizonts. By chance, the progeny of one of the pre-existing latent hypnozoites
reach pyrogenic densities before the progeny of the recently inoculated hypnozoite
(inset shows the logarithmic growth of the three genotypically different infections; ver-
tical axis shows the number of parasites in the body). The consequent febrile illness
then suppresses further multiplication of the blood-stage infection, so that the prog-
eny of the other two pre-erythrocytic schizonts may not reach transmissible densities.
The ensuing illness activates some of the remaining hypnozoites (the same fraction as
were activated initially) and relapses continue until either the number of hypnozoites
is exhausted or some fail to be activated. If there are some hypnozoites which fail to be
activated, these may be activated at a later date by a subsequent malaria infection. For
interpretation of the references to colour in this figure legend, the reader is referred to
the online version of this topic.
