The prevalence of Trichostrongylus tenuis in red grouse was high and the distribution of parasites in their hosts highly aggregated. The prevalence and intensity of threadworms were greater in old birds than in young ones. There was no relationship between the body condition of individual grouse and their burden of adult worms. On the moor, T. tenuis eggs did not develop to third-stage infective larvae during the winter. In the summer, when development did occur, yields of third-stage larvae were dependent on temperature. Third-stage larvae moved laterally through the heather but were relatively short-lived and very few survived over winter. The proportion of larvae, ingested by captive grouse, which developed to adult worms varied with season and between individuals. Red grouse acquired little or no effective immunity to reinfection after challenge with infective larvae. Consequently, caecal threadworms produced a chronic infection in grouse: mature worms survived for over two years with very little mortality. Parasite fecundity decreased as the worms aged but not with intensity of infection. Third-stage larvae ingested by wild red grouse in the autumn were found to go into arrested development over the winter, resuming their development in the spring. Captive grouse with parasite burdens were later in starting to lay in spring and laid fewer eggs at a slower rate than uninfected hens. However developing larvae had greater effects than adult worms on egg production. Effects of developing larvae included inappetence and a reduced gain in body weight prior to laying. Consequently, overwintering larvae developing simultaneously in spring may reduce the breeding success of wild red grouse. This observation may also explain why outbreaks of trichostrongylosis are usually found in spring and summer. The transmission of T. tenuis is presumably influenced mainly by the density of infective larvae, which in turn was affected by weather, particularly temperature. A major regulatory constraint on this parasite is host mortality. Mortality, however, is unlikely to be linearly related to parasite intensity because developing larvae were more pathogenic than adult worms. Furthermore, there seemed to be no important intensity-dependent processes acting to regulate T. tenuis in red grouse populations. On the moor, T. tenuis eggs did not develop to third-stage infective larvae during the winter. In the summer, when development did occur, yields of third-stage larvae were dependent on temperature. Third-stage larvae moved laterally through the heather but were relatively short-lived and very few survived over winter. The proportion of larvae, ingested by captive grouse, which developed to adult worms varied with season and between individuals. Red grouse acquired little or no effective immunity to reinfection after challenge with infective larvae. Consequently, caecal threadworms produced a chronic infection in grouse: mature worms survived for over two years with very little mortality. Parasite fecundity decreased as the worms aged but not with intensity of infection. Third-stage larvae ingested by wild red grouse in the autumn were found to go into arrested development over the winter, resuming their development in the spring. Captive grouse with parasite burdens were later in starting to lay in spring and laid fewer eggs at a slower rate than uninfected hens. However developing larvae had greater effects than adult worms on egg production. Effects of developing larvae included inappetence and a reduced gain in body weight prior to laying. Consequently, overwintering larvae developing simultaneously in spring may reduce the breeding success of wild red grouse. This observation may also explain why outbreaks of trichostrongylosis are usually found in spring and summer. The transmission of T. tenuis is presumably influenced mainly by the density of infective larvae, which in turn was affected.