Premunition is the state in a disease where an existing infection protects the host from reinfection with the same species. The cause of premunition is not clearly understood. In this study, we hypothesized that kin-selection might be a contributing factor in premunition. To test this theory, sheep were infected either once with a linguiform or smooth vulval morphotype of Haemonchos contortus, twice with the same morphotype or twice with different morphotypes. All infections resulted in a similar number of adult parasites. However, there were differences in the morphotypes recovered providing potential evidence of kin selection. Negative interference competition might also contribute to the reduction of the incoming population. Allelopathic or physical interactions between the parasites may be the mechanism behind the observed phenomena.

Chronic Plasmodium falciparum malaria infections in a Sudanese village, in an area of seasonal and unstable malaria transmission, were monitored and genetically characterized to study the influence of persistent infection on the immunology and epidemiology of low endemicity malaria. During the October–December malaria season of 1996, 51 individuals out of a population of 420 had confirmed and treated P. falciparum malaria in the village of Daraweesh in eastern Sudan. In a cross-sectional survey carried out in December 1996, an additional 6 individuals were found to harbour a microscopically negative but polymerase chain reaction (PCR)-positive P. falciparum infection. On 1 January 1997, a cohort of 43 individuals aged from 9 to 53, recruited from this group of recently malaria-infected individuals agreed to donate fortnightly blood samples for the next 9 months, the first 6 of which constitute the long Sudanese dry season when transmission falls to undetectable levels. Each blood sample was tested for the presence of persistent malaria infection by microscopy and PCR. Parasite-positive samples were genotyped using PCR assays that detect allelic polymorphism at the MSP-1, MSP-2 and GLURP marker gene loci. Of 43 individuals 16 were found to maintain chronic P. falciparum infections which were continuously genetically characterized.