Background: A groundwater-associated outbreak affected approximately 1,450 residents and visitors of South Bass Island, Ohio, between July and September 2004. Objectives: To examine the microbiological quality of groundwater wells located on South Bass Island, we sampled 16 wells that provide potable water to public water systems 15–21 September 2004. Methods: We tested groundwater wells for fecal indicators, enteric viruses and bacteria, and protozoa (Cryptosporidium and Giardia). The hydrodynamics of Lake Erie were examined to explore the possible surface water–groundwater interactions. Results: All wells were positive for both total coliform and Escherichia coli. Seven wells tested positive for enterococci and Arcobacter (an emerging bacterial pathogen), and F+-specific coliphage was present in four wells. Three wells were positive for all three bacterial indicators, coliphages, and Arcobacter; adenovirus DNA was recovered from two of these wells. We found a cluster of the most contaminated wells at the southeast side of the island. Conclusions: Massive groundwater contamination on the island was likely caused by transport of microbiological contaminants from wastewater treatment facilities and septic tanks to the lake and the subsurface, after extreme precipitation events in May–July 2004. This likely raised the water table, saturated the subsurface, and along with very strong Lake Erie currents on 24 July, forced a surge in water levels and rapid surface water–groundwater interchange throughout the island. Landsat images showed massive influx of organic material and turbidity surrounding the island before the peak of the outbreak. These combinations of factors and information can be used to examine vulnerabilities in other coastal systems. Both wastewater and drinking water issues are now being addressed by the Ohio Environmental Protection Agency and the Ohio Department of Health.

Campylobacter jejuniis a globally distributed cause of human food-borne enteritis and has been linked to chronic joint and neurological diseases. We hypothesized thatC. jejuni11168 colonizes the gastrointestinal tract of both C57BL/6 mice and congenic C57BL/6 interleukin-10-deficient (IL-10^−/−) mice and that C57BL/6 IL-10^−/−mice experienceC. jejuni11168-mediated clinical signs and pathology. Individually housed mice were challenged orally withC. jejuni11168, and the course of infection was monitored by clinical examination, bacterial culture,C. jejuni-specific PCR, gross pathology, histopathology, immunohistochemistry, and anti-C. jejuni-specific serology. Ceca ofC. jejuni11168-infected mice were colonized at high rates: ceca of 50/50 wild-type mice and 168/170 IL-10^−/−mice were colonized. In a range from 2 to 35 days after infection withC. jejuni11168, C57BL/6 IL-10^−/−mice developed severe typhlocolitis best evaluated at the ileocecocolic junction. Rates of colonization and enteritis did not differ between male and female mice. A dose-response experiment showed that as little as 10⁶CFU produced significant disease and pathological lesions similar to responses seen in humans. Immunohistochemical staining demonstratedC. jejuniantigens within gastrointestinal tissues of infected mice. Significant anti-C. jejuniplasma immunoglobulin levels developed by day 28 after infection in both wild-type and IL-10-deficient animals; antibodies were predominantly T-helper-cell 1 (Th1)-associated subtypes. These results indicate that the colonization of the mouse gastrointestinal tract byC. jejuni11168 is necessary but not sufficient for the development of enteritis and that C57BL/6 IL-10^−/−mice can serve as models for the study ofC. jejunienteritis in humans.

Helicobacter hepaticus expresses a member of the cytolethal distending toxin (CDT) family of bacterial cytotoxins. To investigate the role of CDT in the pathogenesis of H. hepaticus , transposon mutagenesis was used to generate a series of isogenic mutants in and around the cdtABC gene cluster. An H. hepaticus transposon mutant with a disrupted cdtABC coding region no longer produced CDT activity. Conversely, a transposon insertion outside of the cluster did not affect the CDT activity. An examination of these mutants demonstrated that CDT represents the previously described granulating cytotoxin in H. hepaticus . Challenge of C57BL/6 interleukin 10 ^−/− mice with isogenic H. hepaticus mutants revealed that CDT expression is not required for colonization of the murine gut. However, a CDT-negative H. hepaticus mutant had a significantly diminished capacity to induce lesions in this murine model of inflammatory bowel disease.

The genome of the food-borne pathogen Campylobacter jejuni contains multiple highly mutable sites, or contingency loci. It has been suggested that standing variation at these loci is a mechanism for rapid adaptation to a novel environment, but this phenomenon has not been shown experimentally. In previous work we showed that the virulence of C. jejuni NCTC11168 increased after serial passage through a C57BL/6 IL-10^-/- mouse model of campylobacteriosis. Here we sought to determine the genetic basis of this adaptation during passage. Re-sequencing of the 1.64Mb genome to 200-500X coverage allowed us to define variation in 23 contingency loci to an unprecedented depth both before and after in vivo adaptation. Mutations in the mouse-adapted C. jejuni were largely restricted to the homopolymeric tracts of thirteen contingency loci. These changes cause significant alterations in open reading frames of genes in surface structure biosynthesis loci and in genes with only putative functions. Several loci with open reading frame changes also had altered transcript abundance. The increase in specific phases of contingency loci during in vivo passage of C. jejuni, coupled with the observed virulence increase and the lack of other types of genetic changes, is the first experimental evidence that these variable regions play a significant role in C. jejuni adaptation and virulence in a novel host.