Campylobacter jejuni is the leading cause of bacterial gastroenteritis in the developed world. Despite its prevalence, relatively little is known about C. jejuni's precise pathogenesis mechanisms, particularly in comparison to other well-studied enteric organisms such as Escherichia coli and Salmonella spp. Altered expression of phosphate genes in a C. jejuni stringent response mutant, together with known correlations between the stringent response, polyphosphate (poly-P), and virulence in other bacteria, led us to investigate the role of poly-P in C. jejuni stress survival and pathogenesis. All sequenced C. jejuni strains harbor a conserved putative polyphosphate kinase 1 predicted to be principally responsible for poly-P synthesis. We generated a targeted ppk1 deletion mutant (⌬ppk1) in C. jejuni strain 81-176 and found that ⌬ppk1, as well as the ⌬spoT stringent response mutant, exhibited low levels of poly-P at all growth stages. In contrast, wild-type C. jejuni poly-P levels increased significantly as the bacteria transitioned from log to stationary phase. Phenotypic analyses revealed that the ⌬ppk1 mutant was defective for survival during osmotic shock and low-nutrient stress. However, certain phenotypes associated with ppk1 deletion in other bacteria (i.e., motility and oxidative stress) were unaffected in the C. jejuni ⌬ppk1 mutant, which also displayed an unexpected increase in biofilm formation. The C. jejuni ⌬ppk1 mutant was also defective for the virulence-associated phenotype of intraepithelial cell survival in a tissue culture infection model and exhibited a striking, dose-dependent chick colonization defect. These results indicate that poly-P utilization and accumulation contribute significantly to C. jejuni pathogenesis and affect its ability to adapt to specific stresses and stringencies. Furthermore, our study demonstrates that poly-P likely plays both similar and unique roles in C. jejuni compared to its roles in other bacteria and that poly-P metabolism is linked to stringent response mechanisms in C. jejuni.

Water samples were collected from 36 locations within the Grand River Watershed, in Southwestern Ontario, Canada from July 2002 to December 2003 and were analyzed for total coliforms, fecal coliforms, Escherichia coli, Escherichia coli O157:H7, and thermophilic Campylobacter spp. A subset of samples was also analyzed for Cryptosporidium spp., Giardia spp., culturable human enteric viruses, and Clostridium perfringens. Storm and snowmelt events were sampled at two locations including a drinking water intake. For the majority of the events, the Spearman rank correlation test showed a positive correlation between E. coli levels and turbidity. Peaks in pathogen numbers frequently preceded the peaks in numbers of indicator organisms and turbidity. Pathogen levels sometimes decreased to undetectable levels during an event. As pathogen peaks did not correspond to turbidity and indicator peaks, the correlations were weak. Weak correlations may be the result of differences in the sources of the pathogens, rather than differences in pathogen movement through the environment. Results from this investigation have implications for planning monitoring programs for water quality and for the development of pathogen fate and transport models to be used for source water risk assessment.

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This report summarizes our experiences planning and implementing the transition to a new commercial line of hand hygiene products and their dispensing systems in a large academic health care facility in Toronto, Canada. Our lessons learned are organized into a practical guide made available in 2 different formats: this article and an illustrated peer-to-peer guide (http://www.baycrest.org/wp-content/uploads/HCE-PROG-HH_HighQuality.pdf).

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