The aim of the present study was to determine the prevalence of vancomycin-resistant enterococci (VRE) in Europe. Overall, 49 laboratories in 27 countries collected 4,208 clinical isolates of enterococci. Species identification, susceptibility testing, and van gene determination by polymerase chain reaction were performed in a central laboratory. Overall, 18 vanA and 5 vanB isolates of VRE were found. The prevalence of vanA VRE was highest in the UK (2.7%), while the prevalence of vanB VRE was highest in Slovenia (2%). Most vanA and vanB VRE were identified as Enterococcus faecium. Most VRE isolates originated from the patient's urogenital tract, skin, or digestive tract. VRE were equally distributed among clinical departments, with no clear preponderance in any single patient group. A total of 71 isolates containing the vanC gene were identified. The prevalence of vanC VRE was highest in Latvia and Turkey, where rates were 14.3 and 11.7%, respectively. Two-thirds of these isolates were identified as Enterococcus gallinarum and one-third as Enterococcus casseliflavus; the majority of these isolates were cultured from feces. Almost all isolates were obtained from hospitalized patients, mostly children. The highest prevalence of high-level gentamicin-resistant enterococci was seen in Turkey and Greece. In general, the distribution of this resistance type seemed unrelated to the occurrence of VRE. The prevalence of vanA/ vanB VRE in Europe is still low; the majority of the VRE isolates exhibit the vanC genotype and colonize the gastrointestinal tract of hospitalized children.

A PCR assay was developed for the diagnosis of invasive aspergillosis in immunocompromised patients. For this purpose, the complete nucleotide sequences of the genes encoding the 18S rRNA of Aspergillus nidulans, Aspergillus terreus, Aspergillus niger, and Aspergillus flavus were elucidated and aligned to the sequences of Aspergillusfumigatus and other clinically relevant prokaryotic and eukaryotic microorganisms. Genus-specific sequences could be identified in the V7 to V9 region of 18S rRNA. By using hot-start PCR, Southern blot hybridization, and restriction enzyme analysis, Aspergillus-specific and-sensitive determination was achieved. Five of six immunosuppressed mice experimentally infected with A. fumigatus developed infection, and rRNA could be detected in each case, even in livers with the absence of positive cultures. Aspergilus species were detected by PCR in four neutropenic patients with proven aspergillosis, although Aspergillus species had been isolated from only one bronchoalveolar lavage (BAL) fluid sample. Aspergillus species were detected by PCR in two more patients suspected of having infection. Positive PCR signals were obtained from the BAL samples of 3 of 8 neutropenic patients who had developed pulmonary infiltrates, but none were obtained from the samples of 14 nonimmunosuppressed patients. These results indicate the potential value of PCR to detect Aspergillus species in BAL samples and, therefore, to identify neutropenic patients at risk for invasive aspergillosis.

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The performance of a direct sandwich enzyme-linked immunosorbent assay (ELISA) for detecting Aspergillus galactomannan was compared with that of the Pastorex Aspergillus antigen latex agglutination (LA) test by using 532 serum samples from 61 patients at risk for invasive aspergillosis. The ELISA gave positive results earlier in the course of infection than did the LA test. A sensitivity of 70% and a specificity of 86% were obtained for the LA test and corresponding values of 90 and 84% were obtained for the ELISA when a series of serum samples was employed.

Ten patients with chronic Yersinia enterocolitica infections are described. The initial diagnosis was made by culture, significant agglutinin titres and indirect immunofluorescence (IF) on biopsies. During the chronic phase, culture and agglutinin titres were negative, but specific serum IgA and IgG antibodies reactive with at least two, i.e. the 36 kDa and the 46 kDa, virulence-associated released proteins were demonstrated in nine patients by immunoblot techniques. One patient had only IgG antibodies. The chronically elevated IgA production was the result of chronic stimulation of the gut-associated lymphoid tissue by virulent persistent Yersinia antigen, which was identified by IF with O-specific antiserum and monospecific antiserum to the 46 kDa released protein in biopsies. Virulent Yersinia bacilli were demonstrated in the intestinal mucosa and in the lymphoid tissue of the submucosa associated with macrophages in patients with chronic ileitis and arthritis, in granulomatous centres of lymph nodes in patients with chronic lymphadenopathy and in portal infiltrates in a patient with chronic hepatitis. Recognition of persistent Yersinia infections may have therapeutic implications.