Third stage larvae of Brugia pahangi irradiated with 10, 25 and 45 krads. of Co.SO were inhibited in their development beyond the juvenile adult stage, the fourth larval stage and third larval stage respectively. The higher two doses altered the migration pattern of most of the parasites, which were confined to the subcortical sinus of the infected lymph nodes. Hale parasites were more susceptible to irradiation than were females. Repeated infections with irradiated ».pahangi did not really change the architecture of the lymphatics of the e cats. Cats were repeatedly vaccinated with irradiated n.pahangi to determine whether attenuated parasites protected against challenge infections. Cats immunized with parasites irradiated with 10 krads. resisted 60.3 - 98.5% of the homologous challenge infections; and cats immunized with parasites irradiated with 25 krads. resisted 61 - 93% of challenge infections. The resistance in the immunized animals was mounted against all the stages of the life cycle. Two cats given heterologous challenges with Brugia patei resisted 78.6% and 65.3% of the challenge inoculations. One cat which was infected with normal parasites, and challenged after it had become amicrofilaraemic, also resisted challenge. Jirds vaccinated with parasites irradiated with 45 krads. resisted challenges, whilst vaccination with non-irradiated worms and parasites irradiated with 25 krads. did not protect these animals. Antibody responses to various homologous antigens were higher In cats given repeated infections than in cats given single infections. Antibodies against microfilariae were detected only when the animals had suppressed their microfilariae. No antibodies against adult stages could be detected in animals infected with irradiated larvae. The only significant change in the white blood cell population was eosinophilia. The highest eosinophilia occurred at the time of the onset of microfilaraemia. There were no significant changes in the serum components of cats infected with B.pahangi.