Riemerella anatipestifer is a Gram-negative bacterium that can cause disease in a wide range of wild and domesticated birds, especially waterfowl. The presence of an antibiotic-resistance gene in R. anatipestifer has not yet been reported, indicating the need for investigation. In the present study, 40.5% of R. anatipestifer isolates were found to exhibit resistance to chloramphenicol, while 45.9% showed intermediate resistance and 13.5% were susceptible to chloramphenicol, an antibiotic that has been prohibited for use in food animals in Taiwan since 2003. The resistance gene was identified as the cat gene and cloned by library sequencing. The prevalence of the cat gene in Taiwanese R. anatipestifer isolates was 78.4%. The position of the cat gene was then determined within the novel plasmid, designated pRA0511. pRA0511 was sequenced and shown to be 11,435 bp in size with 10 open reading frames (ORFs). Proteins putatively encoded by these 10 ORFs included four drug-resistance-associated proteins. Two proteins designed as chloramphenicol acetyltransferases (CATs) were encoded by two non-adjacent ORFs, and the other two were TetX2 and a multi-drug ABC transporter permease/ATPase. The putative CAT protein had 62.9 to 79.5% homology to a known type B CAT. The pRA0511 plasmid is the first identified drug-resistance plasmid in R. anatipestifer, more specifically associated with chloramphenicol resistance.

The human gastric pathogen Helicobacter pylori has many virulence factors involved in pathogenesis, but the mechanisms regulating these virulence factors are not yet fully understood. In this study, we cloned HP1248, which is similar in sequence to Escherichia coli vacB, which was previously shown to be associated with the expression of virulence in Shigella and enteroinvasive E. coli. E. coli vacB encodes RNase R. RNase R is involved in the posttranscriptional regulation of mRNA stability. By global transcriptional microarray profiling of an H. pylori HP1248 deletion mutant, we defined six virulence-related genes which were posttranscriptionally downregulated by HP1248, including the motility-related genes HP1192 and flaB, the chemotaxis-related gene cheY, and the apoptosis-inducing genes HP0175, cagA, and gtt. In this study, recombinant HP1248 protein expressed in E. coli showed 3-to-5 exoribonuclease activity. Motility and apoptosis induction were increased in the H. pylori HP1248 deletion mutant. We also showed that HP1192 is associated with H. pylori motility, possibly through HP1248 regulation. Further, we suggested and studied the possible mechanisms of this specific regulation of virulent genes by HP1248. In addition, the expression level of HP1248 mRNA changed dramatically in response to a variety of altered environmental conditions, including pH and temperature. Hence, HP1248 in H. pylori seems to play a role in environmental sensing and in regulation of virulent phenotypes, such as motility and host apoptosis induction.Helicobacter pylori (27) is an important human pathogen, responsible for type B gastritis and peptic ulcers and for increasing the risk of gastric adenocarcinoma and mucosaassociated lymphoid tissue lymphoma of the stomach (6,32,35,42).Several bacterial factors, including flagella, various enzymes, and toxins, contribute to the full virulence of H. pylori (5,9,13,14,33). The motility of H. pylori is provided by flagella, the filaments of which consist of two flagellin types (38). The majority of the filament is composed of FlaA and FlaB (24). Motility in H. pylori is essential for colonization in gnotobiotic piglets (15). H. pylori infection can also induce apoptosis in gastric epithelial cells, lymphocytes, and macrophages (17,31,45) and could contribute to mucosal inflammation. In addition, the loss of activated macrophages is likely to decrease the effective immune response to the pathogen (17). Recently some apoptosis-inducing factors of H. pylori were examined (16, 25). However, the regulation mechanism of these virulence factors is not yet fully understood.In this study, we used an expression library of H. pylori (10) to clone a possible chlorhexidine resistance-related gene, HP1248. However, we suggested that the chlorhexidineresistant clone might be an overexpression artifact. On the other hand, HP1248 is similar to Escherichia coli vacB based on sequence similarity. Although its exact mechanism of action is unknown, vacB has been shown to encode RNase R and to be associated wi...

Background: In the past decades, the prevalence of candidemia has increased significantly and drug resistance has also become a pressing problem. Overexpression of CDR1, an efflux pump, has been proposed as a major mechanism contributing to the drug resistance in Candida albicans. It has been demonstrated that biological fluids such as human serum can have profound effects on antifungal pharmacodynamics. The aim of this study is to understand the effects of serum in drug susceptibility via monitoring the activity of CDR1 promoter of C. albicans.

No abstract