Mechanisms and effects of male genital tract infection on sperm quality and fertilizing potential: the andrologist's viewpoint

Abstract

There are several mechanisms acting in synergism that can impair sperm characteristics of patients with accessory gland infection. In some cases, conventional sperm variables are disturbed with oligo and/or asthenozoospermia. In other patients, these sperm variables may appear normal, but the functional capacity of spermatozoa may be impaired. In particular, changes in the composition of the sperm membrane may result in reduced acrosome reactivity and capacity to fuse with the oolemma, and oxidative damage of the sperm DNA may induce mutagenesis. Changes in the biochemical make-up of seminal plasma can also reduce the in-vivo fertilizing capacity of spermatozoa, and infection-related disruption of the blood-testis barrier can induce the generation of anti-sperm antibodies and immunological infertility. Many of these functional abnormalities will not become evident upon 'basic semen analysis', which explains why some authors are unable to link infection of the accessory sex glands to subfertility. Also, functional and anatomical damage acquired as a result of infection is often permanent and not reversible by (antibiotic) treatment. Clearly, there are many more aspects of male accessory gland infection that require investigation. Available data should stimulate clinicians to place more emphasis on the prevention of infection-related infertility than on its treatment, as the latter is often unsuccessful.

Paternal age and reproduction

“…Male genital tract infections can have an influence on semen parameters via different mechanisms (Comhaire et al, 1999), including a direct disruption of spermatogenesis by chronic orchitis (Schuppe et al, 2008) or histomorphological changes potentially leading to obstructive oligo-/azoospermia (Heshmat and Lo, 2006).…”

Characterization of 3-hydroxyisobutyrate dehydrogenase, HIBADH, as a sperm-motility marker

“…A large clinical study indicated that more than 80 % of infertile men have sperm-motility defects [7]. The causes of poor sperm motility include structural defects in the sperm tail, functional defects of the epididymis or other accessory sex glands, and abnormal metabolism in the testicular tissue and/or epididymis [8][9][10].…”

Effect of leukocytospermia and processing by discontinuous density gradient on sperm nuclear DNA fragmentation and mitochondrial activity

“…The mechanism by which leukocytes may determine decreased fertility potential is due to the release of reactive oxygen species (ROS), oxygen molecules with an unpaired electron [2,[4][5][6]. While baseline ROS concentration is essential during sperm capacitation and acrosome reaction [7,8], excessive ROS production will lead to oxidative stress [9,10], which in turn will decrease sperm functional integrity (mitochondrial activity, sperm-egg binding, and DNA integrity, for example) [11,12].…”