Effectiveness of Aqueous Chlorine Dioxide in Minimizing Food Safety Risk Associated with Salmonella, E. coli O157:H7, and Listeria monocytogenes on Sweet Potatoes.

Sodium hypochlorite (NaOCl) is a commonly used sanitizer in the produce industry despite its limited effectiveness against contaminated human pathogens in fresh produce. Aqueous chlorine dioxide (ClO2) is an alternative sanitizer offering a greater oxidizing potency with greater efficacy in reducing a large number of microorganisms. We investigated the effect of aqueous chlorine dioxide treatment against human pathogens, Salmonella, Escherichia coli O157:H7, and Listeria monocytogenes seeded on sweet potatoes. Sweet potatoes were spot inoculated (4.2 to 5.7 log CFU/cm2) with multi-strain cocktails of Salmonella spp., E. coli O157:H7, and L. monocytogenes and treated for 10-30 min with 5 ppm aqueous ClO2 or water. Aqueous ClO2 treatment was significantly (p < 0.05) effective in reducing Salmonella with a reduction of 2.14 log CFU/cm2 within 20 min compared to 1.44 log CFU/cm2 for water treatment. Similar results were observed for L. monocytogenes with a 1.98 log CFU/cm2 reduction compared to 0.49 log CFU/cm2 reduction observed after 30 min treatment with aqueous ClO2 the water respectively. The maximum reduction in E. coli O157: H7 reached 2.1 Log CFU/cm2 after 20 min of treatment with aqueous ClO2. The level of the pathogens in ClO2 wash solutions, after the treatment, was below the detectable limit. While in the water wash solutions, the pathogens' populations ranged from 3.47 to 4.63 log CFU/mL. Our study indicates that aqueous ClO2 is highly effective in controlling cross-contamination during postharvest washing of sweet potatoes.

Loss of HCN2 leads to delayed gastrointestinal motility and reduced energy intake in mice.

Hyperpolarization-activated Cyclic Nucleotide-gated (HCN) channels are important regulators of excitability in neural, cardiac, and other pacemaking cells, which are often altered in disease. In mice, loss of HCN2 leads to cardiac dysrhythmias, persistent spike-wave discharges similar to those seen in absence epilepsy, ataxia, tremor, reduced neuropathic and inflammatory pain, antidepressant-like behavior, infertility, and severely restricted growth. While many of these phenotypes have tissue-specific mechanisms, the cause of restricted growth in HCN2 knockout animals remains unknown. Here, we characterize a novel, 3kb insertion mutation of Hcn2 in the Tremor and Reduced Lifespan 2 (TRLS/2J) mouse that leads to complete loss of HCN2 protein, and we show that this mutation causes many phenotypes similar to other mice lacking HCN2 expression. We then demonstrate that while TRLS/2J mice have low blood glucose levels and impaired growth, dysfunction in hormonal secretion from the pancreas, pituitary, and thyroid are unlikely to lead to this phenotype. Instead, we find that homozygous TRLS/2J mice have abnormal gastrointestinal function that is characterized by less food consumption and delayed gastrointestinal transit as compared to wildtype mice. In summary, a novel mutation in HCN2 likely leads to impaired GI motility, causing the severe growth restriction seen in mice with mutations that eliminate HCN2 expression.