To test the hypothesis that the relatively high developmental temperature threshold of the parasitic nematode Elaphostrongylus rangiferi in the intermediate snail host is an adaptation to minimize larval mortality during winter, an experiment was set up in which snails of the species Arianta arbustorum were experimentally infected with the parasite. The snails were divided into 3 groups known to contain 1st, 2nd or 3rd-stage larvae, and incubated at 3 °C for an experimental period of 18 weeks. First-stage larvae showed a significantly higher survival rate within snails than 2nd or 3rd-stage larvae. We also found that snails carrying 1st-stage larvae survived better than snails with other larval stages. It is concluded that if the nematode has started development before the hibernation, this has a real and significant effect on the risk of dying. The high developmental threshold is therefore likely to be an adaptation to reduce the chance of hibernating as developing larvae during long periods of low temperatures.

The macroparasites Cephenemyia trompe (Modeer) and Hypoderma (=Oedemagena) tarandi (L.) (Diptera: Oestridae), Linguatula arctica Riley, Haugerud and Nilssen (Pentastomida: Linguatulidae), Elaphostrongylus rangiferi Mitskevich (Nematoda: Protostrongylidae), and abomasal nematodes (Nematoda: Trichostrongylidae) were sampled in semidomestic reindeer calves (Rangifer tarandus (L.)) (ca. 8 months of age) in northern Norway in 1988 (n=160) and 1989 (n=191). Each parasite showed an aggregated (clumped) distribution among the hosts and fitted the negative binomial distribution. Analyses of interspecific associations in intensities showed that there was no consistent covariation among the parasites apart from a weak correlation (Kendall's tau 0·104, P=0·007) between the 2 oestrids C. trompe and H. tarandi. This lack of covariation reveals that the parasites were distributed independently of each other, and suggests that innate host resistance is not a dominant factor that has a significant simultaneous effect on all parasites. The aggregated distribution of each parasite species is hypothesized to be caused by (1) random events and heterogeneities in host behaviour that create unequal transmission (exposure) rates, or (2) by heterogeneities in parasite specific immunocompetence among host individuals. Factors in hypothesis (1) are probably the most important at low transmission rates.