The European, multicentre, quarterly point-prevalence study of community-acquired diarrhoea (EUCODI) analysed stool samples received at ten participating clinical microbiology laboratories (Austria, Finland, France, Germany, Greece, Ireland, Italy, Portugal, Romania, and the UK) in 2014. On four specified days, each local laboratory submitted samples from ≤20 consecutive patients to the Austrian Study Centre for further testing with the FilmArray GI Panel (BioFire Diagnostics, Salt Lake City, UT, USA). Of the 709 samples from as many patients received, 325 (45.8%) tested negative, 268 (37.8%) yielded only one organism, and 116 (16.4%) yielded multiple organisms. Positivity rates ranged from 41% (30 of 73 samples) in France to 74% (59 of 80 samples) in Romania. With the exception of Entamoeba histolytica and Vibrio cholerae, all of the 22 targeted pathogens were detected at least once. Enteropathogenic Escherichia coli, Campylobacter species, toxigenic Clostridium difficile, enteroaggregative E. coli, norovirus and enterotoxigenic E. coli were the six most commonly detected pathogens. When tested according to local protocols, seven of 128 positive samples (5.5%) yielded multiple organisms. Overall, the FilmArray GI Panel detected at least one organism in 54.2% (384/709) of the samples, as compared with 18.1% (128/709) when testing was performed with conventional techniques locally. This underlines the considerable potential of multiplex PCR to improve routine stool diagnostics in community-acquired diarrhoea. Classic culture methods directed at the isolation of specific pathogens are increasingly becoming second-line tools, being deployed when rapid molecular tests give positive results. This optimizes the yield from stool examinations and dramatically improves the timeliness of diagnosis.

Twelve cases of Mycobacterium bovis subsp. caprae infection have occurred in four humans, three cattle, and five red deer in western Austria since 1994. DNA-fingerprinting of the isolates suggested transmission in and between these species over several years. Contact with cattle, but not with goats, was found to be associated with three of four human cases

We investigated in detail the previously described capacity of pseudohyphae of Candida albicans to bind C3-coated particles. We show that the expression of the C3bi receptor of C. albicans was dependent upon the growth temperature of the fungi. C. albicans grown at 30°C bound strongly to EAC1423bi, whereas those cells grown at 38.5°C were completely devoid of this capacity. The molecule responsible for the attachment of EAC1423bi was heat labile and trypsin sensitive. Several, but not all, monoclonal antibodies to the a-chain of human complement receptor type 3 (CR3) stained C. albicans, and this reactivity was expressed in parallel with the capacity of C. albicans to bind EAC1423bi, i.e., both were dependent on the growth temperature of the fungi and were trypsin sensitive. In contrast to CR3, the binding of EAC1423bi to C. albicans did not require the presence of divalent cations. Rabbit immunoglobulin G antibodies directed against C. albicans inhibited the binding of EAC1423bi to C. albicans but not to human CR3. These inhibiting IgG antibodies recognized antigens expressed on the surface of pseudohyphae but not those of yeast cells. OKM-1, a monoclonal antibody to human CR3 inhibited the attachment of EAC1423bi to CR3 and also to C. albicans. OKM-1 precipitated a 130-kilodalton band from solubilized 12SI-labeled C. albicans. We conclude that the complement receptors on C. albicans and human CR3 were antigenically related but not identical and that they differed in their functional characteristics. Various human cells express, on their surfaces, molecules which are able to bind fragments of complement component 3, like C3b, C3bi, and C3dg. Whereas C3b binds well to complement receptor type 1 (CR1) (1, 8), membrane cofactor protein (3), and decay-accelerating factor (18) and binds weakly to CR3, C3bi can be bound by CR3 (33), CR4 (23a) and, with lower affinity, can be bound by CR1 and CR2. C3dg and C3dboth show a high affinity for CR2 (10, 32), and C3dg binds, although less strongly, to CR3. These C3binding membrane molecules differ in their respective functions. CR1 is important for the binding and clearance of C3-coated immune complexes (20) and seems to contribute to the phagocytosis of some complement-coated microorganisms (34, 35). CR3 and CR4 are the most important receptors for the ingestion of complement-coated particles by phagocytes (31). Decay-accelerating factor seems to protect cells from an attack by homologous complement (21), and CR2 acts as a receptor for growth-promoting signals on B cells (9, 22, 24, 25). C3-binding structures are not specific for human cells or mammalian cells in general but are also found in microorganisms pathogenic for humans. Mammalian cells infected with herpes simplex virus type 1 express, on their surface, glycoprotein C (gC) which is able to bind C3b (12). gC destabilizes in vitro the C3 convertase of the alternative pathway, suggesting that this gC might inhibit complement activation on the cell surface and thus protect the infected cell from complement-mediated lys...

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We describe the first cefixime-resistant Neisseria gonorrhoeae strain in Austria that caused treatment failure. It follows the first five cases in Europe of cefixime treatment failure, reported in Norway in 2010 and the United Kingdom in 2011. Effective treatment of gonorrhoea is crucial for public health control and, at present, requires substantially enhanced awareness, more frequent test-of-cure, interaction with experts after therapeutic failure, tracing and therapy of contacts, and surveillance of gonococcal antimicrobial resistance and treatment failures worldwide.