Understanding the coevolution of hosts and parasites is one of the key challenges for evolutionary biology. In particular, it is important to understand the processes that generate and maintain variation. Here, we examine a coevolutionary model of hosts and parasites where infection does not depend on absolute rates of transmission and defense but is approximately all-or-nothing, depending on the relative levels of defense and infectivity of the host and the parasite. We show that considerable diversity can be generated and maintained because of epidemiological feedbacks, with strains differing in the range of host and parasite types they can respectively infect or resist. Parasites with broad and narrow ranges therefore coexist, as do broadly and narrowly resistant hosts, but this diversity occurs without the assumption of highly specific gene interactions. In contrast to gene-for-gene models, cycling in strain types is found only under a restrictive set of circumstances. The generation of diversity in both hosts and parasites is dependent on the shape of the trade-off relationships but is more likely in long-lived hosts and chronic disease with long infectious periods. Overall, our model shows that significant diversity in infectivity and resistance range can evolve and be maintained from initially monomorphic populations.

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Monthly sampling of plaice caught off the north‐east coast of Scotland between February 1983 and May 1984 revealed a seasonal increase in condition factor, hepatosomatic index and serum glucose, which appeared to be related to the period of active feeding. The spleen indices followed a similar seasonal increase, although this was not statistically significant, while the kidney indices showed little change over the 16 months. The peak for the gonadosomatic index was in February/March 1984, but among these plaice (aged 4–5 years) there were still large numbers of immature males and females and there was no increase in 1983. Apart from the hepatosomatic index for January 1984, there was no significant difference between male and female plaice.

Rainbow trout fed diets containing 7.86 or 806 mg vitamin E kg-' for 22 weeks were exposed to virulent Yersiniu ruckeri by bath or injection. Mortalities were always least among those fed the highest concentration of vitamin E but serum antibody production was not affected by vitamin E levels.The relationship between diet and the immune response of fish is a topic of increasing interest (Landolt, 1989). Some attention has already been directed at vitamin E, an essential dietary component whose biological activity is principally associated with a-tocopherol. Blazer & Wolke (1984) found that rainbow trout fed diets deficient in a-tocopherol had reduced responses for both specific and non-specific resistance factors but Lall ct al. (1988) reported that diets low in vitamin E did not affect mortality rates or non-specific resistance to furunculosis in Atlantic salmon. Hardie et al. (1990), also working with Atlantic salmon, found that depleted fish had increased mortality rates when challenged with a virulent strain of Aeromonas salmonicida, but from a range of immunological tests, the only significant effect was a reduction in complement activity. The role of dietary vitamin E in disease resistance in salmonids is still not clearly established. Our objective therefore was to induce vitamin E deficiency in rainbow trout and examine the effect on resistance to the enteric redmouth (ERM) pathogen Yersinia ruckeri, compared with fish fed higher doses of the vitamin. Serum antibody titres were measured as indicators of immunocompetence.All female rainbow trout (Oncorhynchus mykiss, Walbaum) weighing 2.5 g, from an ERM-free hatchery, were reared in dechlorinated mains water at 13" C. They were fed on one of three diets prepared (Cowey et al., 1975) with the composition given in Table 1. This basal diet contained 7 mg vitamin E kg ' and the others were supplemented with 86 or 806 mg vitamin E kg-' to provide levels equivalent to commercial diets and megadose levels respectively. Diets, freshly prepared every 3 weeks and stored at -20" C, were fed at 20 g kg ~ I biomass day-I, given in four daily feeds. Vitamin E concentrations were measured by HPLC (McMurray et al., 1980) after extraction from the liver (Bieri, 1969) and diets (McMurray et al., 1980). Liver vitamin C (McGown et al., 1982), erythrocyte fragility and plasma pyruvate kinase (Bell et al., 1985) were measured. Histological examinations were made on 5 pm paraffin wax sections of liver, spleen and skeletal muscle stained with haematoxylin and eosin, and Perl's Prussian blue and Schmorl's reaction identified haemosiderin and lipofuscin. Y . ruckeri (FDL, Weymouth, ref. 13/86) used for challenge,

The formaldehyde-killed, whole-spherule vaccine, which is protective against lethal challenge of laboratory animals withCoccidioides immitis, was fractionated. It yielded a soluble, multicomponent, subcellular fraction termed the 27K vaccine. This vaccine, when it was accompanied by adjuvant, protected mice against lethal intranasal and intravenous challenge withC. immitis.