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Clostridium difficile is mainly considered a nosocomial pathogen associated with diarrhea and pseudomembranous colitis in hospitalized patients. Austrian hospitals reported 2761 cases of C. difficile infection (including 277 lethal outcomes) in 2007, compared with 777 cases (including 54 lethal outcomes) in 2003. The occurrence of community-acquired C. difficile infection is also increasingly reported. Recent studies have shown the occurrence of C. difficile in food and animals. The aim of the present study was to determine the occurrence of C. difficile in food and animals in Austria. Between March and July 2008, gut or fecal samples from 67 cows, 61 pigs and 59 broiler chickens were collected at Austrian abattoirs. Between February and April 2008 meat samples (51 beef [25 ground], 27 pork [17 ground] and 6 samples of chicken meat) were purchased at retail outlets. Of the 187 samples tested, eight yielded C. difficile: in cows 3/67 samples (4.5%) were positive, in pigs 2/61 (3.3%), in broiler chickens 3/59 (5%). Six of the eight isolates yielded toxigenic C. difficile (toxins A and B): 2/67 (3%) cow samples, 2/61 (3.3%) pig samples, 2/59 (3.4%) chicken samples. Genes for the binary toxin were detected in one of the two pig isolates, a PCR ribotype 126 strain. None of the 84 meat samples yielded C. difficile. The results of this Austrian study suggest that animal reservoirs are possible sources, via food, of human C. difficile infection.

Staphylococcus aureus is a major cause of infection in hospitals and the community. One third of the general population is colonized by the bacterium, constituting a risk factor for acquisition of infection with this pathogen. Worldwide, the increasing antibiotic resistance of S. aureus complicates treatment of infection and control measures. Soon after the introduction of methicillin, the first isolates resistant to this antibiotic were reported and named methicillin-resistant S. aureus (MRSA). During the past decade a major change in MRSA epidemiology has been observed: whereas in the past MRSA was almost exclusively regarded a hospital pathogen, the advent of community-acquired MRSA has led to infections in people without hospital-related risk factors. Recent evidence has also identified a link between colonization of livestock and MRSA carriage and infections in people who work with animals. Screening of pigs and pig farmers in the Netherlands revealed high prevalence of MRSA sequence type (ST) 398 and it has become clear that the emergence of ST398 is not just a Dutch problem, as reports on livestock colonization and human infections are appearing worldwide. In Austria, the ST398 lineage has been detected in dust samples from pig breeding facilities and in food samples. Since the first Austrian detection of this emerging lineage in 2006, 21 human isolates, partially associated with infections, have been observed. MRSA has to be regarded as a new emerging zoonotic agent and livestock may constitute a growing reservoir of the ST398 lineage. More information is needed so that control measures to reduce the impact of the emerging MRSA ST398 lineage on public health can be developed and implemented.

Mycoplasma gallisepticum is a flask-shaped organism that commonly induces chronic respiratory disease in chickens and infectious sinusitis in turkeys. Phenotypic switching in M. gallisepticum hemadsorption (HA) was found to correlate with phase variation of the GapA cytadhesin concurrently with that of the CrmA protein, which exhibits cytadhesin-related features and is encoded by a gene located downstream of the gapA gene as part of the same transcription unit. In clones derived from strain R low , detailed genetic analyses further revealed that on-off switching in GapA expression is governed by a reversible base substitution occurring at the beginning of the gapA structural gene. In HA ؊ variants, this event generates a stop codon that results in the premature termination of GapA translation and consequently affects the expression of CrmA. Sequences flanking the mutation spot do not feature any repeated motifs that could account for error-prone mutation via DNA slippage and the exact mechanism underlying this high-frequency mutational event remains to be elucidated. An HA ؊ mutant deficient in producing CrmA, mHAD3, was obtained by disrupting the crmA gene by using transposition mutagenesis. Despite a fully functional gapA gene, the amount of GapA detected in this mutant was considerably lower than in HA ؉ clonal variants, suggesting that, in absence of CrmA, GapA might be subjected to a higher turnover.Mycoplasma gallisepticum is a round flask-shaped organism commonly inducing chronic respiratory disease in chickens (14,26,32) and infectious sinusitis in turkeys (7). Like a large number of other mycoplasmas, this avian pathogen colonizes its host via the mucosal surfaces of the respiratory tract and must adhere to the epithelial cells to withstand clearance by the host. This intimate contact is mediated by a bleb-like structure (27, 28), a unipolar terminal organelle that is similar to the tip structure of the two human pathogens, M. pneumoniae and M. genitalium also involved in adhesion to host cells. Both mycoplasma species were shown to enter epithelial cells (2, 13), and recent in vitro assays have revealed that M. gallisepticum is likewise capable of establishing intracellular residence in nonphagocytic eukaryotic cells (29). During infection of highly immunocompetent hosts, the ability to enter and survive within host cells may provide these mycoplasmas with a survival strategy that relies first on adhesion. Cytadhesins and related components have been extensively studied in M. pneumoniae (17), and the data emerging from similar studies in M. gallisepticum suggest the occurrence of a family of cytadhesin genes conserved among pathogenic mycoplasmas that colonize widely divergent hosts. The identification and the characterization of M. gallisepticum surface-exposed components with adhesive properties are therefore of major importance in understanding the factors involved in promoting successful infection.In recent years, a large collection of data has underlined the versatility of the mycoplasma surface a...

bMycoplasma gallisepticum is an important avian pathogen that commonly induces chronic respiratory disease in chicken. To better understand the mycoplasma factors involved in host colonization, chickens were infected via aerosol with two hemadsorption-negative (HA ؊ ) mutants, mHAD3 and RCL2, that were derived from a low passage of the pathogenic strain R (R low ) and are both deficient in the two major cytadhesins GapA and CrmA. After 9 days of infection, chickens were monitored for air sac lesions and for the presence of mycoplasmas in various organs. The data showed that mHAD3, in which the crmA gene has been disrupted, did not promote efficient colonization or significant air sac lesions. In contrast, the spontaneous HA ؊ RCL2 mutant, which contains a point mutation in the gapA structural gene, successfully colonized the respiratory tract and displayed an attenuated virulence compared to that of R low . It has previously been shown in vitro that the point mutation of RCL2 spontaneously reverts with a high frequency, resulting in on-and-off switching of the HA phenotype. Detailed analyses further revealed that such an event is not responsible for the observed in vivo outcome, since 98.4% of the mycoplasma populations recovered from RCL2-infected chickens still display the mutation and the associated phenotype. Unlike R low , however, RCL2 was unable to colonize inner organs. These findings demonstrate the major role played by the GapA and CrmA proteins in M. gallisepticum host colonization and virulence.