[Standards of microbiological diagnostics of spondylodiscitis]. / Standards der mikrobiologische Diagnostik der Spondylodiszitis.

In most cases spondylodiscitis is due to a monomicrobial infection caused by hematogenous dissemination of Staphylococcus aureus. There are, however, many other possible pathogens causing spondylodiscitis and the pathogen responsible can only be identified in approximately 50% of cases. This leads to delayed diagnosis and therapy and an increased morbidity and mortality rate. Failures in planning and performing material recovery are often the reason. As pathogen-specific antimicrobial treatment according to the results of susceptibility testing is the main component of interdisciplinary therapy, all available methods for identification of the pathogen, such as blood cultures, intraoperative and computed tomography (CT) guided biopsies of inflammatory fluids and tissues as well as molecular biological methods should be performed to optimize antimicrobial therapy.

Prognostic value of laryngeal electromyography in vocal fold paralysis.

OBJECTIVE: To analyze the value of electromyography in predicting recovery from acute neurogenic vocal fold paralysis. STUDY DESIGN: Prospective case series. SETTING: University-based hospital of otorhinolaryngology-head and neck surgery. PATIENTS: Ninety-eight patients (56 women, with a mean age of 62.2 years; 42 men, with a mean age of 39.8 years) with 111 paralyzed vocal folds. The causes were varied, with thyroid surgery (53 cases) and idiopathic palsy (18 cases) being the predominant factors. INTERVENTION: Prognostication was based on electromyography performed no earlier than 14 days after onset of palsy. Findings were classified as neurapraxy, axonotmesis, and neurotmesis. Prognosis is inherent in this classification, since neurapraxy is presumed to resolve completely within 8 to 12 weeks, whereas axonotmesis is most likely to be followed by impaired vocal fold mobility. MAIN OUTCOME MEASURES: Vocal fold mobility after 6 months. RESULTS: In 102 vocal folds, some palsy of various degree persisted after 6 months. Free mobility of the paralyzed vocal fold was restored in 9 cases. By means of laryngeal electromyography, defective recovery, defined as absence of completely free vocal fold mobility, was predicted correctly in 94.4% of cases (68/72). For complete recovery, prognosis was accurate in only 12.8% of cases (5/39). CONCLUSIONS: The detection of neural degeneration by laryngeal electromyography allows the prediction of poor functional outcome with sufficient reliability in an early phase of the disease process. Conversely, the absence of signs of degeneration does not imply that complete recovery is to be expected.

Restoration of normal implantation rates in mouse embryos with a hatching impairment by use of a new method of assisted hatching.

OBJECTIVE: To use a newly developed mouse model for embryos with a hatching defect to develop improved methods of assisted hatching. DESIGN: We had previously demonstrated that mouse embryos with reduced cell numbers, when resident within an intact zona, exhibit a hatching deficiency, and we used these "hatching-defective" embryos to demonstrate that hatching is mediated predominantly, if not entirely, by lysis of the zona pellucida. In the present study, the hatching-defective embryos were implanted into pseudo-pregnant females to determine if implantation rates were reduced. In addition, to compensate for reduced zona lysin production, the zonae of some embryos were circumferentially thinned with acid Tyrode's solution. The implantation rates and developmental potential of hatching-defective embryos subjected to zona thinning were compared with those of the hatching-defective embryos implanted without zona thinning. SETTING: University-based basic research laboratory. RESULTS: When hatching-defective embryos, created by destruction of 1/4 of the blastomeres at the four-cell stage, were implanted into pseudopregnant female mice, no pregnancies were established, and no implantation sites could be identified after transfer of 41 embryos. However, when hatching-defective embryos were subjected to zona thinning before ET, a normal rate of implantation was observed (18 implantation events of 49 embryos transferred). Fetuses appeared morphologically normal. The difference in implantation rates between hatching-defective embryos subjected to zona thinning and those not treated by zona thinning was highly significant by chi 2 analysis. CONCLUSION: Failure of embryos with cell numbers reduced by micromanipulation to implant and restoration of normal implantation and development after circumferential zona thinning demonstrates that the developmental defect of the manipulated embryos is confined to hatching, and thus, that this procedure establishes a useful model for defective hatching. High rates of implantation after circumferential thinning of the zona shows that this procedure of assisted hatching is highly effective. These findings have important implications for use of assisted hatching in human IVF because the assisted hatching procedure is safe and effective and increases the efficiency of the normal hatching mechanism. Thus, the procedure may be useful in a wide variety of circumstances for which assisted hatching by zona opening has been found to be ineffective.

A new mouse model for embryos with a hatching deficiency and its use to elucidate the mechanism of blastocyst hatching.

OBJECTIVE: To develop an experimental model for embryos with a defect specific to hatching, with the purpose of clarifying the mammalian embryo hatching mechanism. DESIGN: A microneedle was inserted under the zona pellucida (ZP) of mouse embryos, and either 1/2 or 1/4 of the blastomeres were mechanically destroyed. The remainder of embryos that developed into blastocysts were compared for hatching to controls wherein a microneedle was inserted and withdrawn without harming the embryo. Experiments were done to increase pressure within the perivitelline space to decrease the amount of ZP material to study the hatching mechanism. SETTING: University-based basic research laboratory. RESULTS: When 1/2 or 1/4 of the embryo was destroyed and the remaining cells developed into healthy blastocysts within the intact zona, hatching was significantly impaired, and zona thickness was markedly increased relative to controls. When a mineral oil droplet was inserted under the zona to enhance a possible mechanical component of hatching, manipulated embryos were not restored to normal hatching, and hatching of unmanipulated blastocysts was not improved. However, when the zona was circumferentially thinned by application of acid Tyrode's solution, the hatching defect in manipulated "3/4 embryos" was corrected. CONCLUSION: Because it is known that embryos with cells reduced by 1/2 or 1/4 have normal developmental potential, we conclude that the inability of such embryos to hatch from an intact zona constitutes a mouse model for a defect specific to hatching. Moreover, results from mineral oil droplet insertion and circumferential thinning of the zona indicate that normal hatching is accomplished predominantly, if not entirely, by zona lysis, not by pressure exerted against the zona by the expanding blastocyst.