This chapter provides an overview on immunological causes of male factor infertility. From a clinical standpoint, determining the site(s) of infection and/or inflammation is a key first step. Identifying causative organisms and providing appropriate medical treatment, including antibiotics and anti-inflammatory agents, are mainstays of therapy. The chapter presents specific sites of inflammation and infection within the male reproductive tract, characterizing each to provide a framework for arriving at the proper diagnosis, treatment, and counseling options for the affected patient. Some of the sites of inflammation include urethra, prostate, seminal vesicles, and vas deferens. Leukocytes initiate and maintain a complex series of steps in the immune system response. Nitric oxide is purported mediator of leukocyte damage to sperm. More specific testing for seminal leukocytes includes Bryan-Leishman staining, peroxidase (Endtz) test, and monoclonal antibodies directed against leukocyte surface molecules.

Infertility is due to a significant male factor alone, whereas combined male and female factors are present in an additional 20%. Thus, a male factor is involved in approximately 50% of infertile relationships. The primary goals of the evaluation of the male presenting with infertility are to identify: etiologic conditions, irreversible conditions, irreversible conditions not amenable to assisted reproductive techniques, medically significant pathologies, and genetic etiologies. Bilateral cryptorchidism results in a significant decrease in spermatogenesis, while the effect of unilateral cryptorchidism appears to be much milder. Approximately 50% of testicular cancer patients have subnormal sperm densities prior to chemotherapy. Of note, of those with oligo- or azoospermia, 75% normalized during surveillance. Diethylstilbestrol (DES) was given to pregnant women in the 1950s, and reports of epididymal cysts and cryptorchidism in males with prenatal DES exposure have raised concerns about effects on fertility. Exogenous androgens are well known to induce hypogonadotropic hypogonadism.