The survival and growth of secondary infections of Hymenolepsis diminuta (Rudolphi 1819) in the rat
Primary infections: 1. The older the rat at the time of infection with a multiple (50) worm infection of H. diminuta the more refractory it is to the survival of the parasites. 2. Mean worm weight is relatively constant at 25 and 50 dpi irrespective of the age of the host at infection. 3. The distribution of cestodes within the intestine at 0900 h is similar in all age groups of rats at both 25 and 50 dpi. 4. Rat age is a more important correlate than rat weight in determining worm recovery. Secondary infections: 5. Differences in growth of secondary populations of worms, following primary infections of various intensity and duration, cannot be detected at 25 dpi. 6. "Destrobilated" worms only occur in large numbers following long term, high intensity multiple worm infections. At 7 dpi they are distributed more anteriorly than "normal" worms. 7. Stunting of secondary populations of H. diminuta following 5-worm 21 day primaries is severe at 7 dpi but decreases as the infection progresses. This suggests an increase in duration of the lag phase of growth of secondary infections. 8. The rate of worm loss is not increased in secondary infections (50 worms) following 5-worm primaries of varying duration. Egg production: 9. Production of eggs from 50-worm secondary infections of H. diminuta is delayed by approximately one day when following 5-, 30- or 50-worm infections of at least 28 days duration. Similarly, total egg production is never as great, in toto, as that from a comparable primary infection. Immunology: 10. No T-cell responses (as measured by the MIF test) or B-cell responses (as measured by a number of techniques) could be implicated in the mechanism responsible for the stunting of secondary populations of H. diminuta. This does not exclude immunological involvement in the stunting phenomenon, however, as a number of more elaborate techniques with increased sensitivity were not used. 11. Lactating females, known to be immunodeficient, supported larger primary and secondary worms then comparable controls. The stunting of secondary worms when compared with primaries, however, was still apparent. Immunodeficient juvenile rats failed to cause stunting of secondary infections. 12. "Vaccination" of rats with homogenised whole worm produced conflicting data. "Vaccinated" rats either supported larger worms or worms of similar size to "non-vaccinated" controls. 13. Cellular populations within the intestine did not differ at 7 dpi between rats on different infection schedules. Immunomodulation: 14. Immunomodulation with C. parvum or BCG failed to influence the growth or survival of the cestodes when given on days -7, -1, 0, 27 or 28 relative to a 5-worm primary infection. 15. Concurrent infection with T. lewisi caused a slight though nonsignificant increase in the stunting of the cestodes. This is thought to be mediated by physiological conditions as the stunting was common to both primary and secondary infections.