A. Immotile Cilia Syndromes
Immotile cilia syndromes are a heterogeneous group of disorders (1:20,000 males) in which sperm motility is reduced or absent. The sperm defects are due to abnormalities in the motor apparatus or axoneme of sperm and other ciliated cells. Normally, 9 pairs of microtubules are organized around a central pair within the sperm tail and are connected by dynein arms (ATPase) that regulate microtubule and therefore sperm tail motion. Various defects in the dynein arms cause deficits in ciliary and sperm activity. Kartagener syndrome is a subset of this disorder (1:40,000 males) that presents with the triad of chronic sinusitis, bronchiectasis, and situs inversus. Most immotile cilia cases are diagnosed in childhood with respiratory and sinus difficulties. Cilia present in the retina and ear may also be defective and lead to retinitis pigmentosa and deafness in Usher syndrome. Men with immotile cilia characteristically have nonmotile but viable sperm in normal numbers. Sperm nuclear material is thought to be unaffected. The diagnosis is made with electron microscopy of sperm.

B. Maturation Defects
After vasectomy reversal, normal sperm counts but low motility is often observed. This is thought to be due to elevated epididymal intratubular pressure and epididymal dysfunction, a consequence of time after vasectomy-induced blockage. As a result, sperm may not gain the usual maturation and motility capacities during transit through the epididymis.

C. Immunologic Infertility
Autoimmune infertility has been implicated as a cause of infertility in 10% of infertile couples. The testis is a curious organ in that sperm are highly antigenic, yet normally coexist within the host; it is an immunologically privileged site, probably owing to the blood-testis barrier, which consists of Sertoli cell tight junctions and locally downregulated cellular immunity. Autoimmune infertility may result from an abnormal exposure to sperm antigens after, for example, vasectomy, testis torsion, or biopsy, which then incites a pathologic immune response.

Clinically, antisperm antibodies (ASA) are found in 3-12% of men who undergo infertility evaluation. Antibodies may disturb sperm transport or disrupt normal sperm-egg interaction. Antibodies may cause clumping or agglutination of sperm, which inhibits passage, or may block normal sperm binding to the oocyte. Many assays are available to detect ASA. In the most widely used assay, polyacrylamide beads are coated with antihuman antibody and then exposed to motile sperm. Attachment of beads to sperm indicates antibody presence.

D. Infection
The agents most commonly responsible for male genital tract infections are listed in

Table 42-10. Various products of activated leukocytes can exist in infected semen. A significant correlation has been demonstrated between leukocytes in semen and the generation of superoxide anions, hydrogen peroxide, and hydroxyl radicals (reactive oxygen species), all of which can damage sperm membranes. Sperm are highly susceptible to the effects of oxidative stress because they possess little cytoplasm and therefore little antioxidant activity. Damage to sperm from oxidative stress has been correlated to loss of function. Although genital tract infection has been linked to infertility in epidemiologic studies, the correlation between individual organisms and infertility is unclear. Uncontrolled studies suggest that pregnancy rates may improve after treatment, but controlled studies do not confirm these findings. It is important to remember that seminal fluid that passes through the urethra is routinely contaminated with bacteria.