ColV plasmids have long been associated with the virulence of Escherichia coli, despite the fact that their namesake trait, ColV production, does not appear to contribute to virulence. Such plasmids or their associated sequences appear to be quite common among avian pathogenic E. coli (APEC) and are strongly linked to the virulence of these organisms. In the present study, a 180-kb ColV plasmid was sequenced and analyzed. This plasmid, pAPEC-O2-ColV, possesses a 93-kb region containing several putative virulence traits, including iss, tsh, and four putative iron acquisition and transport systems. The iron acquisition and transport systems include those encoding aerobactin and salmochelin, the sit ABC iron transport system, and a putative iron transport system novel to APEC, eit. In order to determine the prevalence of the virulence-associated genes within this region among avian E. coli strains, 595 APEC and 199 avian commensal E. coli isolates were examined for genes of this region using PCR. Results indicate that genes contained within a portion of this putative virulence region are highly conserved among APEC and that the genes of this region occur significantly more often in APEC than in avian commensal E. coli. The region of pAPEC-O2-ColV containing genes that are highly prevalent among APEC appears to be a distinguishing trait of APEC strains.Avian pathogenic Escherichia coli (APEC) strains are the etiologic agents of colibacillosis in birds, an important problem in the poultry industry (7). Along with uropathogenic E. coli (UPEC) and the E. coli strain causing neonatal meningitis or septicemias, APEC strains fall under the category of extraintestinal pathogenic E. coli (ExPEC) (39). ExPEC strains are characterized by the possession of virulence factors that enable their extraintestinal lifestyle and make them distinct from commensal and diarrheagenic E. coli strains (39). Among APEC strains, the iroBCDEN locus (11), shown to encode the siderophore salmochelin in Salmonella enterica (16), the aerobactin operon (51), and the yersiniabactin operon (21) are iron acquisition systems thought to contribute to virulence. Other putative APEC virulence factors include those contributing to complement resistance, such as the increased serum survival gene (iss) (31,33,37); tsh, the temperature-sensitive hemagglutinin gene (34); and the presence of ColV plasmids (37). In fact, it appears that large virulence plasmids, including ColV plasmids, are a defining feature of the APEC pathotype (37, 44).ColV and ColV plasmids have interested scientists for many years, with Gratia first describing ColV as "principle V" in 1925 (53). ColV plasmids, which encode ColV production, typically range in size from 80 to 180 kb (53) and encode traits such as aerobactin production (51) and complement resistance (31). Unlike other colicins, ColV itself is a small protein that is exported from the cell and behaves more like a microcin, disrupting the formation of cell membrane potential required for energy production (53). The ColV operon ...

In this study, a 101-kb IncF plasmid from an avian pathogenic Escherichia coli (APEC) strain (APEC O2) was sequenced and analyzed, providing the first completed APEC plasmid sequence. This plasmid, pAPEC-O2-R, has functional transfer and antimicrobial resistance-encoding regions. The resistance-encoding region encodes resistance to eight groups of antimicrobial agents, including silver and other heavy metals, quaternary ammonium compounds, tetracycline, sulfonamides, aminoglycosides, trimethoprim, and beta-lactam antimicrobial agents. This region of the plasmid is unique among previously described IncF plasmids in that it possesses a class 1 integron that harbors three gene cassettes and a heavy metal resistance operon. This region spans 33 kb and is flanked by the RepFII plasmid replicon and an assortment of plasmid maintenance genes. pAPEC-O2-R also contains a 32-kb transfer region that is nearly identical to that found in the E. coli F plasmid, rendering it transferable by conjugation to plasmid-less strains of bacteria, including an APEC strain, a fecal E. coli strain from an apparently healthy bird, a Salmonella enterica serovar Typhimurium strain, and a uropathogenic E. coli strain from humans. Differences in the G؉C contents of individual open reading frames suggest that various regions of pAPEC-O2-R had dissimilar origins. The presence of pAPEC-O2-R-like plasmids that encode resistance to multiple antimicrobial agents and that are readily transmissible from APEC to other bacteria suggests the possibility that such plasmids may serve as a reservoir of resistance genes for other bacteria of animal and human health significance.Antimicrobial resistance among bacterial pathogens of food animals can complicate veterinary therapy. Resistant animal pathogens may also be a threat to human health if these resistant bacteria enter the food supply or otherwise serve as reservoirs of resistance genes for human pathogens. Transmissible R plasmids that encode multidrug resistance would seem a likely means by which animal pathogens could acquire resistance genes or transmit them to human pathogens. This study examines an R plasmid encoding multidrug resistance in an avian pathogenic Escherichia coli (APEC) isolate. APEC strains are important and prevalent bacterial pathogens of poultry (3) and are frequently found to be resistant to multiple antimicrobial agents (21, 37), including ampicillin, tetracycline, aminoglycosides, fluoroquinolones, quaternary ammonium compounds, and heavy metals (37). Genes encoding such resistance are often found on large, transmissible R plasmids (20). Not surprisingly, multidrug-resistant APEC strains often carry conjugative plasmids (8). Interestingly, plasmids have been shown to be transferable from poultry to human isolates (23), suggesting that APEC strains and their plasmids might serve as reservoirs of resistance genes for bacteria that affect public health. In the present study, the first complete sequence of a transmissible APEC R plasmid is presented and analyzed. Additionally, an...

Aims:  To assess the abilities of 105 avian pathogenic Escherichia coli (APEC) and 103 avian faecal commensal E. coli (AFEC) to form biofilms on a plastic surface and to investigate the possible association of biofilm formation with the phylotype of these isolates. Methods and Results:  Biofilm production was assessed in 96‐well microtitre plates using three different media, namely, M63 minimal medium supplemented with glucose and casamino acids, brain–heart infusion broth, and diluted tryptic soy broth. Avian E. coli are highly variable in their ability to form biofilms. In fact, no strain produced a strong biofilm in all three types of media; however, most (75·7% AFEC and 55·2% APEC) were able to form a moderate or strong biofilm in at least one medium. Biofilm formation in APEC seems to be mostly limited to nutrient deplete media; whereas, AFEC are able to form biofilms in both nutrient deplete and replete media. Also, biofilm formation in E. coli from phylogenetic groups B2, D and B1 was induced by nutrient deplete conditions; whereas, biofilm formation by members of phylogenetic group A was strongest in a rich medium. Conclusions:  Biofilm formation by APEC and phylotypes B2, D and B1 is induced by nutrient deplete conditions, while AFEC are able to form biofilms in both nutrient rich and deplete media. Significance and Impact of the Study:  This is the first study to investigate biofilm formation by a large sample of avian E. coli isolates, and it provides insight into the conditions that induce biofilm formation in relation to the source (APEC or AFEC) and phylogenetic group (A, B1, B2 and D) of an isolate.