Date of Award

1990

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Veterinary Medical Sciences - Pathobiological Sciences

First Advisor

Thomas R. Klei

Abstract

The effects of in utero and neonatal exposure to maternal Brugia pahangi infections on the development of homologous infections, immune responses, and pathologic lesions was studied in age-matched progeny of infected and uninfected female jirds. High IgG antibody titers to B. pahangi antigens were present in the sera of progeny from infected mothers. These neonatal titers to homologous antigens were shown to be of maternal origin, and did not alter the cellular responses of uninfected progeny as measured by in vitro antigen-stimulated blastogenesis and in vivo pulmonary granulomatous inflammatory responses to antigen-coated beads. Studies were conducted to measure age-related differences in susceptibility, lymphatic lesion formation, and antibody responses to B. pahangi infection in 2$-$, 6$-$, 10$-$, and 15-week old jirds from uninfected mothers. Significant reductions in quantities of testicular and intralymphatic worms recovered and antibody responses to solbule antigens in jirds infected at 2 weeks of age had no measurable effect on susceptibility or lymphatic lesion severity expressed as the ratio of intralymphatic thrombi formed per intralymphatic worm. Challenge infections in 2- or 4-week old progeny from B. pahangi-infected and uninfected female jirds yielded equivalent adult worm recoveries and microfilaremias. Lymphatic lesion severity expressed as the ratio of intralymphatic thrombi formed per intralymphatic worm recovered was similar in all groups. Offspring infected at either 2 or 4 weeks of age from infected mothers exhibited significantly lower serum IgG antibody titers to B. pahangi antigens compared to infected progeny of uninfected mothers at 5-8 weeks postinfection. Infected offspring from infected mothers displayed significantly fewer antigen-specific splenic plague-forming cells at 5 weeks postinfection than infected control progeny. Qualitative and quantitative reductions in serum antibody reactivity to B. pahangi antigens were also demonstrated by Western immunoblot at 8 weeks postinfection in infected progeny of infected females. These results suggest that a partial immune tolerance to B. pahangi antigens develops in infected offspring of infected female jirds. These modulated antibody responses had no measurable effect on the establishment of adult worms, microfilaremias, lymphatic lesion development, or antigen-specific pulmonary granulomatous inflammatory responses.

Pages

224

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