The biology of Escherichia coli in its primary niche, the animal intestinal tract, is remarkably unexplored. Studies with the streptomycin-treated mouse model have produced important insights into the metabolic requirements for Escherichia coli to colonize mice. However, we still know relatively little about the physiology of this bacterium growing in the complex environment of an intestine that is permissive for the growth of competing flora. We have developed a system for studying colonization using an E. coli strain, MP1, isolated from a mouse. MP1 is genetically tractable and does not require continuous antibiotic treatment for stable colonization. As an application of this system, we separately knocked out each two-component system response regulator in MP1 and performed competitions against the wild-type strain. We found that only three response regulators, ArcA, CpxR, and RcsB, produce strong colonization defects, suggesting that in addition to anaerobiosis, adaptation to cell envelope stress is a critical requirement for E. coli colonization of the mouse intestine. We also show that the response regulator OmpR, which had previously been hypothesized to be important for adaptation between in vivo and ex vivo environments, is not required for MP1 colonization due to the presence of a third major porin. Escherichia coli is one of the most extensively studied and bestcharacterized organisms. Its high growth rate, facile genetics, and simple nutritional requirements have made this bacterium an excellent model system for studying basic aspects of molecular biology and bacteriology and the primary host for DNA and protein engineering. The physiology of E. coli growth and survival under diverse conditions has been intensively studied, and a significant fraction of E. coli gene products and regulatory networks have been characterized. However, for such a well-studied organism, we know remarkably little about the biology of E. coli in its primary niche: the animal gastrointestinal tract.E. coli is generally the most abundant aerobe in the intestines of warm-blooded vertebrates, although its numbers vary considerably with animal host and geography (1-3). As a species, this bacterium has a remarkable genetic diversity; the number of genes in common among fully sequenced isolates is less than half the number of genes in any individual strain (4-6). Some E. coli strains are pathogenic, depending on the host and site of infection (3, 7-9), and have been intensively studied to understand the factors controlling their virulence. However, the majority of E. coli strains associated with animals are believed to be part of the normal flora of the intestine, growing asymptomatically as commensals.Most of our knowledge about E. coli colonization of the animal intestine comes from studies with streptomycin-resistant strains colonizing mice fed streptomycin continuously in their drinking water (10, 11). This streptomycin-treated mouse model has played a key role in the characterization of the growth of E. coli in the intestine a...

During a 12-month period, the clinical spectrum of extraintestinal disease due to Aeromonas species was determined for 56 patients in tropical Queensland (Australia). Forty-six patients acquired their infection in the community, six patients were infected in the hospital, and four patients were colonized. Demographic risk factors included male gender (67%) and Aboriginal ethnic background (35%). The disease ranged from deep-seated infection (four cases) to soft-tissue infection of varying intensity (48 cases). Among patients whose infections were community acquired, 22 required hospitalization and 27 suffered trauma-associated infection. Seventeen patients (63%) in the latter group had lacerations to the hands and feet that were contaminated with surface water or soil. The appearance of the wounds was not pathognomonic, and diagnosis was made by laboratory evaluation. Aeromonas was the sole pathogen in nine patients. Polymicrobial infections were due to Aeromonas and mainly Staphylococcus aureus and/or mixed enteric bacteria. Aeromonas hydrophila was the most common species isolated (71%), followed by Aeromonas sobria (25%). In nine cases, the empirical antibiotic regimen prescribed did not adequately cover infection due to Aeromonas. Infection was seen regularly throughout the year, but a cluster of cases also occurred during the tropical Australian wet season.

The normal intestinal microflora plays pivotal roles in aiding with digestion, stimulating the immune system, and providing protection from enteric pathogens. Despite the importance of these organisms, they are often an innocent bystander, caught in the crossfire during antibiotic treatments intended to target and eliminate invading infectious agents. The collateral damage of antibiotic therapy is a reduction in the population of beneficial bacteria as well as an increased risk for more severe infections, including Clostridium difficile. Additionally, the unpleasant condition termed antibiotic-associated diarrhea is an unfortunate consequence of such treatments. In an attempt to alleviate the intestinal distress, individuals are turning to probiotic supplements, which consist of non-pathogenic bacteria purported to provide various health benefits, such as digestive regularity, prevention of disease, and replenishment of the natural microbiota of the human intestinal tract. However, if the bacterial strains present in the physician-recommended probiotic supplements are overly sensitive to antibiotics, then they would fail to reestablish the intestinal microflora during the course of treatment. The purpose of this project was to test the hypothesis that bacterial strains contained within probiotics are resistant to a variety of common antibiotics. Antibiotic susceptibility was assessed for several over-the-counter probiotic supplements via the Kirby-Bauer Disk Diffusion method on medium specific for lactobacilli propagation. After measuring the zones of inhibition, the probiotics were surprisingly sensitive to two-thirds of the antibiotics tested, with the observed growth inhibition greatly exceeding predetermined standards for susceptibility. These results suggest that concomitantly taking probiotic supplements during a course of antibiotics is likely futile for replenishing the intestinal microbiota. We intend to expand the study to include additional antibiotics and supplements of varying formulations in an attempt to gain insight into which strains may exhibit the least sensitivity and be the most effective for recolonization of the gastrointestinal tract.