Date of Award


Document Type


Degree Name

Doctor of Philosophy (PhD)


Veterinary Medical Sciences - Pathobiological Sciences

First Advisor

Thomas R. Klei


Brugia pahangi infections in the jird (Meriones unguiculatus) is an accepted experimental model for the study of human lymphatic filariasis. Initial identification of parasite specific immune responses in jirds infected with B. pahangi are reported here. Antibody reactivity in sera from singly and multiply infected jirds against different stages of B. pahangi was determined using an indirect fluorescent antibody technique. All life cycle stages of the parasite were examined. Antibodies recognizing all stages were present in all serum samples. Removal of antibody reactivity by absorption of jird sera with B. pahangi antigen coated beads indicated that the antibodies were parasite specific. The surface was not recognized as immunogenic in jirds. Temporal occurrence of stage or organ specific antibody was not observed. Antibody responses of infected jirds to a soluble somatic extract of B. pahangi were further characterized by Western blot analysis. Antibody recognition of parasite antigens appeared to be independent of ELISA antibody titlers, lymphatic lesion severity, microfilaremia levels, inoculum size or numbers of adult parasites recovered. However, antibody recognition of 37 kD, 21 kD, 17 kD and 15 kD protein bands appeared to correspond with certain parasitological and/or host interactive events. Chronological association of antibody responses to these proteins were identical in singly and multiply infected jirds. No association between antibody recognition of antigens and severity of lymphatic lesions suggests that antibody is not directly involved in the pathogenesis of lymphatic lesions. The soluble somatic extract of B. pahangi was fractionated with lectin affinity chromatography and high performance liquid chromatography, yielding a glycoprotein pool and seven HPLC fractions. Pulmonary granulomatous inflammatory and in vitro lymphocyte blastogenic responses were measured and compared. Granulomas were induced by the glycoprotein pool and three HPLC fractions. A pulmonary eosinophilic perivascular inflammatory infiltrate appeared to be associated with granuloma size. Results indicate that the fractionation methods used yielded fractions that retained antigenicity and were both qualitatively and quantitatively different. Fractions containing antigens inducing a pulmonary granulomatous response were identified. Two fractions with suppressive properties were also identified. Some correlation between in vivo granulomatous responses and in vitro blastogenesis was observed.