This study characterized three cases of systematic sperm tail defects using electron microscopy and immunolocalisation of centrin 1 and tubulin and explored their impact on ICSI outcome. Structural sperm tail defects of possible genetic origin were suspected as the eosin test revealed a sperm viability of >70% despite severe asthenozoospermia or the absence of motility. In Patient 1, 80%-85% of axoneme cross sections was incomplete. The fluorescent signal of tubulin was weak along the entire tail; the signal of centrin 1 was normal. After ICSI, a female healthy baby was born. Patient 2 showed spermatozoa with tails reduced in length at different levels, axonemal and periaxonemal alterations and fragility of head-tail junction. Centrin 1 was altered in 80% of sperm. After ICSI, no embryos were obtained. Patient 3 showed tails reduced in length at light and fluorescence microscopy; ultrastructural study revealed a condition of dysplasia of fibrous sheath with heterogeneity of tails' length. The signal for centrin 1 was altered in 50% of spermatozoa; two embryos were transferred without pregnancy. The correct diagnosis of sperm pathology is important in case of systematic sperm defects as it enables the clinician to improve patient's management and to provide an adequate genetic counselling.
Keywords: ICSI; TEM; centrin 1; reduced motility; systematic sperm defects.
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