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growth of the progeny of the activated latent hypnozoite(s). In one-third
of the patients in whom the relapse is homologous or highly related with
the primary infection, either there were no latent hypnozoites (as in vol-
unteer studies) or the homologous infection's hypnozoites' progeny won
the race to patency against the heterologous hypnozoites' progeny. It is evi-
dent then that close 'races' between different genotypes to reach patency
commonly result in gametocyte genotype mixtures in relapses (which may
then recombine in the mosquito, providing genetic diversity despite very
low levels of transmission). Strong support for the ALH hypothesis comes
from observations in mothers and their infants living in a malaria endemic
area on the north-west border of Thailand (
Fig. 2.9
). The relapses of vivax
malaria in the babies' mothers were usually genetically different to those
which caused the primary infection, as in other patients studied in this area,
whereas the relapses which followed the first
P. vivax
infection of life in their
babies were usually of the
same
genotypes as those which caused the initial
infection (
Imwong et al., 2012
). Obviously, the infants could not have any
previously acquired latent hypnozoites in their livers to be activated by the
illness.
3.
Natural versus artificial infection relapse rates
Higher rates of vivax relapse in indigenous compared with artificial infec-
tion (
Swellengrebel & De Buck 1938
) would also be explained by the ALH
hypothesis. The incidence and number of relapses depends on the num-
ber of sporozoites inoculated. If all relapses derived from the inoculated
infection, then artificial infections which follow inoculations with 5-10
times more sporozoites should have much higher, not lower, rates of relapse.
Relapse rates were particularly high in soldiers who were immunologically
naïve and underwent intense exposure. If all relapses derived from the most
recent inoculum, then there should be no relationship between intensity of
exposure and number of relapses.
4.
Long-latency also occurs in the tropical frequent-relapse 'Chesson'
P. vivax
phenotypes
Four of seven volunteers receiving a single infected mosquito bite in
Coatney's series had relapses of the Chesson strain of
P. vivax
with variable
but long-latency periods - all exceeding 6 months after their preceding
relapse (
Coatney et al., 1950b
). It is not uncommon to see patients return-
ing from malaria endemic areas, where tropical phenotypes are prevalent
with relapses more than 3 months after either a primary infection or return
to the non-endemic area (of course, these might also be long-latency phe-
notypes, particularly if the interval is -8-10 months). This supports the
