Etiology of ovarian dysfunction in chronic murine toxoplasmosis.

Ovarian dysfunction develops in Nya:NYLAR mice chronically infected with Toxoplasma gondii. To differentiate between primary ovarian failure and pituitary gonadotropin insufficiency, we (a) monitored ovarian responsiveness to pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin (hCG) and (b) assessed endogenous pituitary gonadotropin capacity by the degree of ovarian compensatory hypertrophy (OCH) developing after unilateral ovariectomy (ULO). PMSG stimulated vigorous folliculogenesis and estrogen synthesis, but not ovulation. HCG given 3 days after PMSG induced "superovulation" within 16 h. These observations indicate the absence of the critical preovulatory surge of endogenous luteinizing hormone (LH) from the pituitary. In addition, ULO did not result in compensatory hypertrophy of the contralateral ovary, an indication of follicle-stimulating hormone (FSH) insufficiency. We hypothesize that cytokines released peripherally in response to the parasite reached the hypothalamus and initiated a sequence of events that inhibited the pulsatile release of gonadotropin-releasing hormone (GnRH), leading to the subsequent impairment of the pituitary-ovarian axis.