| Summary: | I investigated the relationship between in-host ecology and transmission using the rodent malaria parasite <i>Plasmodium chabaudi</i> as an experimental laboratory model. This required the initial development of a novel quantitative reverse transcription PCR technique (qRT-PCR) to measure the in-host density of <i>P. chabaudi</i> transmission stages and provide better estimates of transmission investment. My doctoral research revealed that the majority of total parasite and transmission stage production occurs within the initial phase of infection, however, many individuals developing very low level long lasting chronic infections which are transmissible to vectors, confirming current findings in the field. During conspecific competition, a small degree of transmission investment plasticity was observed, but did not affect the competitive outcome. Competition success was greatly influenced by drug treatment when drug resistant and sensitive genotypes co-infected the same host. In this case, it was observed that strong drug dosage completely cleared the drug sensitive clone, releasing the resistant clone from competition and then resulted in its enhanced growth and increased transmission potential. Reduced drug dosage which did not completely clear the sensitive genotype also released the resistant clone from competition, but prevented its enhanced growth. These findings suggest that low drug treatment, which just alleviates host clinical symptoms but does not completely clear parasites, will preserve within host competition and many reduce the rate at which drug resistance spreads. This contradicts current medical thinking that incomplete drug treatment regimes will accelerate drug resistance evolution.
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