1. Healthcare

259
Non-obstructive azoospermia: Is there evidence for an infectious origin?
Eur Urol Suppl 2014;13;e259 Print!
Print!
Pilatz A. 1 , Hossain H.2 , Schuppe H-C.1 , Haggeney T.3 , Schüttler C.4 , Diemer T.1 , Bergmann M. 3 , Chakraborty T.2 , Domann E. 2 , Weidner
W.1
1 Justus
Liebig University, Dept. of Urology, Pediatric Urology and Andrology, Gießen, Germany, 2 Justus Liebig University, Institute For
Medical Microbiology, Gießen, Germany, 3 Justus Liebig University, Institute of Veterinary Anatomy, Histology and Embryology, Gießen,
Germany, 4 Justus Liebig University, Institute For Medical Virology, Gießen, Germany
INTRODUCTION & OBJECTIVES: Infections and inflammatory conditions of the reproductive tract are accepted as major causes of fertility
disorders in males. These include asymptomatic focal inflammatory lesions frequently observed in testicular biopsies of azoospermic
patients undergoing testicular sperm extraction (TESE). However, little is known about a possible link between local infections and nonobstructive azoospermia.
MATERIAL & METHODS: The prospective study was approved by the local institutional review board (Ref. No. 26/11). From May 2011 to
September 2013 we evaluated 49 patients with non-obstructive azoospermia undergoing combined trifocal TESE and M-TESE. The
andrological workup included medical history, clinical investigation, sex hormone analysis, genetic analysis, semen analysis (WHO 2010
recommendations), standardized 2-glass test, testicular swabs taken from TESE and M-TESE incisions to collect testicular fluid, and
testicular histology (score count of spermatogenesis, assessment of testicular inflammation). The microbiological investigations consisted of
standard cultures, detection of sexually transmitted diseases (STD-PCR), 16S rDNA analysis, and a respiratory- and rash-based viral
multiplex-PCR panel.
RESULTS: 7/49 patients (15%) had a history of previous urogenital tract infections. 2-glass test and semen microbiology revealed the
presence of relevant bacterial pathogens in 17/49 patients (35%, 10× common urinary pathogens, 7× STDs). Analysis of testicular swabs
was negative for all viruses assessed, while only in one case 16S rDNA analysis revealed bacterial pathogens (Enterobacteriaceae).
Testicular histology showed Sertoli cell-only syndrome (n=22), mixed atrophy (n=14), hypospermatogenesis (n=10), and spermatogenic
arrest (n=3). Focal intratesticular lymphocytic infiltrates were diagnosed in 10/49 patients (20%). No significant associations were detected
between the three factors 1) microbiological/inflammatory findings in urine/semen, 2) score count of spermatogenesis, and 3) testicular
inflammatory lesions.
CONCLUSIONS: Although the medical history suggested previous urogenital tract infection/inflammation in 15% of cases and
microbiological examination revealed relevant bacterial pathogens in 37% of patients, all infection/inflammation-related variables
determined were neither associated with the outcome of testicular sperm retrieval, nor with focal intratesticular inflammation identified
histologically in 20% of patients.