The presence of steroid binding sites in (or on) human spermatozoa was first suggested in the late 1970s, by studies showing that some steroids were able to influence sperm function. Subsequently, several effects exerted on spermatozoa by biological fluids, such as follicular fluid, were found to be probably linked to the action of steroids, and among them progesterone. Since the effects of progesterone on spermatozoa were rapid, dose-dependent and not affected by progesterone conjugation with high molecular weight proteins unable to cross the plasma membrane, the existence of a novel class of non-genomic progesterone receptors was strongly suspected. This hypothesis was further supported by the observation that some of the effects of progesterone on human spermatozoa were not abolished by inhibitors of the classical progesterone nuclear receptors, nor mimicked by progesterone genomic receptor agonists. Recently, surface progesterone binding sites were directly identified on the membranes of human spermatozoa, and their mechanism of action partially characterized.

A screening of 3196 semen analyses performed in our clinic from January 1986 to December 1990 revealed 314 (9.8%) patients whose semen was infected with Bacteroides ureolyticus. Investigating the relationship between the presence of B. ureobticus, the seminal microflora and the conventional semen parameters, we observed that the presence of this micro-organism in the semen was coupled (1) to an increased presence of Enterococcus species, (2) to an increased number of short-tailed spermatozoa and epithelial cells, and (3) to a decreased total fructose concentration (mg ejaculate -'). These results suggest that B. ureolyticus or its toxins may influence sperm morphology and function by yet unknown mechanisms and may also increase the number of epithelial cells by soft tissue infection in uiuo. The decreased fructose levels suggest that this anaerobic micro-organism might specifically colonize the seminal vesicles, while the normal zinc values recorded suggest a normal prostatic function. Overall, our data support the hypothesis that the presence of B. ureobticus is not associated with nongonococcal urethritis.

Summary The scope of this study was to evaluate the accuracy, precision and specificity of the sperm concentration measurements by the Strömberg‐Mika Cell Motion Analyser (SM‐CMA). Our data show that the instrument generally underscores the sperm concentration and therefore the uncorrected measurements must be corrected by the operator using the ‘mouse’‐driven option. In terms of precision, the system appears to have an excellent internal precision whereas its repeatability is influenced by the sperm concentration, the sample's homogeneity and the correction of the raw data. In order to increase the system's repeatability, we suggest that sperm counts should be carried out in various fields of the counting chamber, and the mean of the corrected values be taken as representative of the sperm concentration in the ejaculate if the various measurements show a homogenous (poissonian) distribution. The correction of the raw data with the ‘mouse’‐driven correction option was also shown to improve the system's reproducibility. Concerning specificity, our data evidenced that, without technical correction, the instrument failed to correctly classify certain spermatozoa as such, thereby grossly underscoring sperm counts. This finding was more evident at low sperm counts. Overall, the SM‐CMA requires additional laboratory time but the corrected sperm counts are comparable to manual counts and semi‐automated counts with the added option that it provides the andrologists with various motility characteristics not possible with the latter methodologies.

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