Common Features of Infections Producing Infertility
Infertility is presumably underestimated because diagnostic involves a specialist.
A review of the literature reveals that 60 to 80 million couples experience infertility worldwide and by 2 million couples (15%) in the United States wherein infection is the major cause. Annual reports suggests an occurrence of 3 million lower genital tract infections yearly in the United Stated. 30% of these infections cause pelvic inflammatory disease (PID) and that at least 20% result in infertility.
Portals of entry for these infections that are usually STDs, include genitalia, urinary meatus, mouth, rectum, and skin. Approximately one quarter of women presenting to an infertility clinic seeking to conceive were found to have a positive test for Ureaplasma urealyticum, Mycoplasma Hominis, Chlamydia trachomatis or Neisseria gonorrhoeae infection. Additionaly, almost 10% of the patients were Rubella non-imune at the time of presentation for infertility evaluation. The most serious form is Kartagener syndrome (KS), which accounts for 50% of all cases of Primary ciliary dyskinesia (PCD). Patients have lifelong chronic and recurrent infections, typically suffering from bronchitis, pneumonia, hemoptysis, sinusitis and infertility. Althought genital infections are often silent they can severly impair male infertility.
Some possible pathophysiologic mechanisms of the development of infertility linked with infection of the ejaculate are considered: its direct effect on the fertile properties of the seminal fluid due to a decrease in the number of spermatozoa, the suppression of their motility, changes in their morphology and fertilizing capacity, its direct influence due to the inhibition of spermatogenesis resulting from testicular damage, autoimmune processes induced by inflammation, secretory dysfunction of the male accessory sex glands as a consequence of the infection of the reproductive tract organs, leukocytospermia with its secondary influence on the ejaculate parameters, etc. Acute inflammation may cause transitory disturbances in sperm quality and secretion, yet the full impact of its timing and duration is unclear. Epididymitis secondary to urethritis produces azoospermia by obstruction.
As epididymitis progress, testicular infarction and infertility due to extensive scarring similar to that found in PID.
Gonococcal infection may produce seminiferous tubule breakage thereby leaking sperms into the interstitium ; antibodies to sperm then form impairing sperm motility. The importance of the pathogenic properties of microorgamisms for the localization of the inflammatory process in the urogenital tract of males and their role in the pathogenesis of male infertility are therefore requiring much greater and carefully designed studies.However one recent study has alleviated the apprehension regarding CMV producing infertility. CMV presence in the genital tract of subfertile patients is considerable, but findings do not suggest that sexual transmission is a frequent route of infection or that CMV infection is a significant cause of infertility.
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