Economic cost of illness due to Escherichia coli O157 infections in the United States.
ABSTRACT The Centers for Disease Control and Prevention (CDC) has estimated that Shiga toxin-producing Escherichia coli O157 (0157 STEC) infections cause 73,000 illnesses annually in the United States, resulting in more than 2,000 hospitalizations and 60 deaths. In this study, the economic cost of illness due to O157 STEC infections transmitted by food or other means was estimated based on the CDC estimate of annual cases and newly available data from the Foodborne Diseases Active Surveillance Network (FoodNet) of the CDC Emerging Infections Program. The annual cost of illness due to O157 STEC was $405 million (in 2003 dollars), including $370 million for premature deaths, $30 million for medical care, and $5 million in lost productivity. The average cost per case varied greatly by severity of illness, ranging from $26 for an individual who did not obtain medical care to $6.2 million for a patient who died from hemolytic uremic syndrome. The high cost of illness due to O157 STEC infections suggests that additional efforts to control this pathogen might be warranted.
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ABSTRACT: Abstract Escherichia coli O157:H7 is a foodborne pathogen that causes illness in humans worldwide. Cattle are the primary reservoir of this bacterium, with the concentration and frequency of E. coli O157:H7 shedding varying greatly among individuals. The term "super-shedder" has been applied to cattle that shed concentrations of E. coli O157:H7≥10(4) colony-forming units/g feces. Super-shedders have been reported to have a substantial impact on the prevalence and transmission of E. coli O157:H7 in the environment. The specific factors responsible for super-shedding are unknown, but are presumably mediated by characteristics of the bacterium, animal host, and environment. Super-shedding is sporadic and inconsistent, suggesting that biofilms of E. coli O157:H7 colonizing the intestinal epithelium in cattle are intermittently released into feces. Phenotypic and genotypic differences have been noted in E. coli O157:H7 recovered from super-shedders as compared to low-shedding cattle, including differences in phage type (PT21/28), carbon utilization, degree of clonal relatedness, tir polymorphisms, and differences in the presence of stx2a and stx2c, as well as antiterminator Q gene alleles. There is also some evidence to support that the native fecal microbiome is distinct between super-shedders and low-shedders and that low-shedders have higher levels of lytic phage within feces. Consequently, conditions within the host may determine whether E. coli O157:H7 can proliferate sufficiently for the host to obtain super-shedding status. Targeting super-shedders for mitigation of E. coli O157:H7 has been proposed as a means of reducing the incidence and spread of this pathogen to the environment. If super-shedders could be easily identified, strategies such as bacteriophage therapy, probiotics, vaccination, or dietary inclusion of plant secondary compounds could be specifically targeted at this subpopulation. Evidence that super-shedder isolates share a commonality with isolates linked to human illness makes it imperative that the etiology of this phenomenon be characterized.Foodborne Pathogens and Disease 12/2014; 12(2). DOI:10.1089/fpd.2014.1829 · 2.28 Impact Factor
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ABSTRACT: Our recent previous study reported the outstanding synergistic bactericidal activity of a combination of two natural antimicrobials: caprylic acid (CA) and citric acid (CTA). In the present study, the response surface methodology was used with the central composite design to build a model based on four factors, i.e., the CA concentration, CTA concentration, temperature, and treatment time, for the reduction of Escherichia coli O157:H7. This model was used to determine the optimum conditions for desirable responses and to evaluate the effects of experimental factors. The ranges of the four variables used in the design were as follows: CA concentration (0.25, 0.50, 0.75, 1.00, and 1.25 mM), CTA concentration (0.25, 0.50, 0.75, 1.00, and 1.25 mM), temperature (25, 30, 35, 40, and 45 °C), and time (1, 3, 5, 7, and 9 min). A second-order quadratic model of the effect of four variables was constructed and the experimental values agreed well with the values derived from model equation (R2 = 0.954). The adequacy of this model for predicting the magnitude of bacterial reduction was verified based on the validation data (R2 = 0.946). The optimum conditions for the combined treatment for microbial reduction were determined by ridge analysis, which were 1.0 mM CA and 0.8 mM CTA at 39.6 °C for 5.4 min. The CA concentration and temperature were the most significant variables. This study provides a comprehensive understanding of the bactericidal effects of the combined CA and CTA treatment. A distinct advantage of the proposed method is its cost-effectiveness. This treatment could be used as a preservative in the food industry because the two components are natural products.International Journal of Food Microbiology 03/2015; 197. DOI:10.1016/j.ijfoodmicro.2014.12.006 · 3.16 Impact Factor
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ABSTRACT: Enterohemorrhagic Escherichia coli produce ribotoxic Shiga toxins (Stx), which are responsible for kidney injury and development of hemolytic uremic syndrome. The endoplasmic reticulum (ER) stress response is hypothesized to induce apoptosis contributing to organ injury; however, this process has been described only in vitro. ER stress marker transcripts of spliced XBP1 (1.78-fold), HSP40 (4.45-fold) and CHOP (7.69-fold) were up-regulated early in kidneys of Stx2 challenged mice compared to saline controls. Anti-apoptotic Bcl2 decreased (-2.41-fold vs. saline) and pro-apoptotic DR5 increased (6.38-fold vs. saline) at later time points. Cytoprotective activated protein C (APC) reduced early CHOP expression (-3.3-fold vs. untreated), increased later Bcl2 expression (5.8-fold vs. untreated), and had early effects on survival but did not alter DR5 expression. Changes in kidney ER stress and apoptotic marker transcripts were observed in Stx2-producing C. rodentium challenged mice compared to mice infected with a non-toxigenic control strain. CHOP (4.14-fold) and DR5 (2.81-fold) were increased and Bcl2 (-1.65-fold) was decreased. APC reduced CHOP expression and increased Bcl2 expression, but did not alter mortality. These data indicate that Stx2 induces renal ER stress and apoptosis in murine models of Stx2-induced kidney injury, but decreasing these processes alone was not sufficient to alter survival outcome.