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■Bio-mathematics, Statistics and Nano-Technologies: Mosquito Control Strategies

from the infection with a certain variant and neutralizes the parasites of that variant), or

general (i.e., variant-transcending as in [31]; resulting from the infection with any strain

and neutralization affects all strains equally) (see also [156]). The existing level of im-

munity was assumed to decay at some constant rate in the absence of re-infection. The

impact of variant-specific immunity was apparent in that, one can repeatedly see the clear-

ance of one parasite peak, while another grows immediately. However, incorporating only

rapidly accumulated variant-specific immunity was helpful to demonstrate the clearance

of individual parasite peaks but cannot explain age-associated variations in reinfection and

parasitaemia. This is because variant-specific immunity has to be short-lived [186] in or-

der to allow for effective clearance and also for reinfection. This suggests the need for

a general slowly accumulated immunity that decreases the growth of all variants; which

must be long-lived. Thus, incorporating both the rapidly-induced strain-specific immunity

which wipes out individual infections, and general immunity that accumulates slowly and

reduces the mean parasite growth rate with age, gives model outputs that are consistent

with the observed data. In general, the role of antigenic diversity whereby existing infec-

tions contribute significantly to protection, contrasts with the theory that NAI to malaria

is-strictly strain-specific and long-lasting [165].

5.2.8

Superinfection/ Reinfection and acquired immunity

In malaria-endemic areas, an individual can receive hundreds of infectious bites each

year, thereby increasing the risk of superinfection (Table 5.1) which results from consecu-

tive infectious bites [88], [80], [85]. In practice, an individual can host more than one plas-

modium species or variants of the same plasmodium species, at a time [182], [173], [165],

[81], [57], [187], [88] in endemic areas. In areas of low or moderate level of endemicity,

it is likely that re-inoculations would be infrequent within a short interval so that the first

infection would have become latent, or even have been cleared, before re-inoculation.

Several opinions of the mechanism associated with superinfection in malaria exist.

One idea from Macdonald’s model [143] was that successive infections are effectively

“stacked”, waiting to express themselves at the end of the previous infection. This idea

was also adopted in [72] by resetting the infection date of the individual, so that courses of

different infections proceed without interference, such that recovery from superinfection

happens when the course of the last infection is completed. Another related suggestion

by Dietz [144] is that infections arrive and run their course completely independent on

each other. Neither of these two models appears to be correct (see [40]). For the former

model, there is no evidence for an infection waiting for another to be completed. The latter

model by Dietz, on the other hand, ignored the concept of immunity and possible compe-

tition among parasites. Richie [84] in his suppression hypothesis postulated the tendency

of malarial species to exclude each other and thereby appear chronologically in the blood.

This he presumed to be caused by competition for host cells or nutrients, or by heterol-

ogous immunity. However, the repressed species bounce back after the previous species

has dwindled, and can result in prolonged infection. His hypothesis is supported by ex-

perimental data obtained from the simultaneous inoculation of two Plasmodium species

into laboratory animals; which show that one of either species is suppressed. This mecha-