Stec

  • Posted: April 9th, 2012 - 4:31pm by Doug Powell

    The Columbia Tribune reports a Boone County, Missouri, 2-year-old infected with E. coli remained hospitalized this morning in Columbia as one of five Central Missouri residents battling the bacteria.

    Geni Alexander, public information officer for the Columbia/Boone County Department of Public Health and Human Services, said the 2-year-old is one of three Boone County residents with either a confirmed or suspected case of the illness.

    Alexander said health officials have determined that consumption of raw dairy products was the only common link for possible exposure among the three Boone County victims. She did not disclose the gender of the victims.

    "Each person was identified as a raw dairy consumer," Alexander said, "but we can't say they all got it from the same place."

    The Missouri Department of Health and Senior Services is investigating an increase in cases of Shiga toxin-producing E. coli in Central Missouri from late March through early April. In addition to the Boone County 2-year-old, state health officials reported Thursday that a 17-month-old toddler also developed symptoms of hemolytic uremic syndrome, or HUS, a severe condition that can lead to permanent kidney damage in some who survive the illness.

    Alexander said the victims of the three Boone County cases range in age from 2 to 31. The 17-month-old victim is not a Boone County resident, she said.

    "In public health, we always advise to stay away from those raw dairy products," she said.

    A table of raw milk related outbreaks is available at http://bites.ksu.edu/rawmilk.

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  • Posted: April 6th, 2012 - 5:59pm by Doug Powell

    The Missouri Department of Health and Senior Services (DHSS) is investigating an increase in cases of Shiga toxin-producing Escherichia coli (STEC) in Central Missouri during late March and early April, 2012. Five cases of E. coli O157:H7 have been identified during this time period. Two of the cases, a two-year old child and a 17-month old child, reportedly have developed hemolytic uremic syndrome (HUS).

    The investigation is ongoing and the source of the infections has not been identified.

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  • Posted: March 22nd, 2012 - 9:00pm by Doug Powell

    From researchers in Finland, writing in the April edition of Emerging Infectious Diseases. Edited bits below, the complete report is available at http://wwwnc.cdc.gov/eid/article/18/4/11-1310_article.htm.

    Shiga toxin–producing Escherichia coli (STEC) is a pathogen that causes gastroenteritis and bloody diarrhea but can lead to severe disease, such as hemolytic uremic syndrome (HUS). STEC serotype O78:H– is rare among humans, and infections are often asymptomatic.

    A boy born on Oct. 3, 2009, in Finland, the third child of healthy parents, was breast-fed and healthy. But by 2-weeks-old, he became irritable, started feeding poorly, and produced large volumes of watery feces with some blood. At 17-days-old he was taken to the Vaasa Central Hospital in Finland for medical care.

    A blood culture showed a gram-negative rod, which was identified as E. coli. Results of a test for the O157 antigen were negative. Because the neonate was severely ill, he was referred to the University Hospital in Pirkanmaa Hospital district, and the s E. coli train isolated from his blood was forwarded to the Helsinki University Hospital Laboratory, where the invasive strain from fecal specimens of the neonate and all 4 asymptomatic family members — the mother (31 years-old), father (32 years), sister (3 years), and brother (2 years) — was confirmed by detection of Stx. The 6 strains isolated from the blood and fecal samples of the neonate and from the fecal samples of his asymptomatic parents and 2 siblings showed a sorbitol-fermenting STEC serotype O78:H– that carried the virulence genes stx1 and hlyA.

    The boy recovered, but required a kidney transplantation, supplied by his father and performed in April 2011. The operation and posttransplantation period went without complications.

    HUS develops in ≈5%–15% of patients <10 years of age in whom E. coli O157:H7 infection is diagnosed and occurs 2–14 days after diarrhea onset. In contrast to the O157-related HUS cases, less information is available about the non–O157-related HUS cases. Some risk factors, including an elevated leukocyte count, administration of antimicrobial drugs, use of antimotility agents, and very young age, are associated with increased risk for HUS

    Ruminants, such as cattle and sheep, are the major reservoir of STEC. None of the family members, however, had contact with any farm animals, and the family had no pets. One of the family members of the neonate might have been infected with STEC by eating contaminated food, but these food items were not available for investigation. Moreover, because all the family members were asymptomatic, estimating the exact date of their infections is difficult. Secondary infections among family members most likely resulted from person-to-person transmission or from food given to the children with contaminated hands of other family members or from some other cross-contamination. Family clusters have been reported to be common. In Finland, ≈50% of STEC infections are family related.

    Handwashing practices may be of greater relevance than food as a source of infection in infants and very young children because the infection might result from an infected person or animal in the home. Prolonged excretion of STEC and intimate caring of infants by family members provide a risk for cross-infections. Therefore, to limit the risk for STEC infection, thorough handwashing before touching food or young babies is particularly necessary.

    Our findings demonstrate that contrary to earlier suggestions, STEC under certain conditions can invade the human bloodstream. Moreover, this study highlights the need to implement appropriate diagnostic methods for identifying the whole spectrum of STEC strains associated with HUS.

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  • Posted: March 10th, 2012 - 4:55pm by Doug Powell

    Is you is, or is you ain't, my constituency?

    The U.S. beef industry said last week beef is safer than it was 10 years ago, and cited survey data to show consumers agreed.

    Surveys still suck.

    “When asked whether someone is more likely to get sick from foodborne bacteria eating at home or at a restaurant, 65 percent of consumers answered “at a restaurant.” However, 72 percent of the experts attending the summit answered “at home.”

    “In fact, statistics back up the experts’ opinion showing between 60 percent and 70 percent of foodborne illnesses occur at home.”

    Got a reference for that? Or were the press release authors too busy inserting “dick fingers” and statements of nonsense like, “In fact.”

    “In fact, it isn’t beef safety consumers are concerned about. When asked which fresh food they might buy in the supermarket was their biggest safety concern, 48 percent of consumers answered “Fish and Seafood.” Only 10 percent said beef was their biggest safety concern.”

    Beef safety may have improved, but industry types can’t help but continue to cast stones. Beef types have lots to concern themselves with – non-O157 shiga-toxin producing E. coli, pink slime, cross-contamination, welfare and workplace issues -- instead of wasting rhetorical energy about who’s to blame for foodborne illness.

    It’s called playing to your constituency

    Jacob, C.J. and Powell, D.A. 2009. Where does foodborne illness happen—in the home, at foodservice, or elsewhere—and does it matter? Foodborne Pathogens and Disease, 6(9): 1121-1123.
http://www.liebertonline.com/doi/abs/10.1089/fpd.2008.0256
    Foodservice professionals, politicians, and the media are often cited making claims as to which locations most often expose consumers to foodborne pathogens. Many times, it is implied that most foodborne illnesses originate from food consumed where dishes are prepared to order, such as restaurants or in private homes. The manner in which the question is posed and answered frequently reveals a speculative bias that either favors homemade or foodservice meals as the most common source of foodborne pathogens. Many answers have little or no scientific grounding, while others use data compiled by passive surveillance systems. Current surveillance systems focus on the place where food is consumed rather than the point where food is contaminated. Rather than focusing on the location of consumption—and blaming consumers and others—analysis of the steps leading to foodborne illness should center on the causes of contamination in a complex farm-to-fork food safety system.

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  • Posted: March 1st, 2012 - 3:10pm by Doug Powell

    I sorta cringe, or maybe sigh, every time someone faithfully repeats the dogma that factory-farmed cattle are the source of E. coli O157:H7 and other shiga-toxin producing E. coli (STEC).

    All ruminants carry STEC naturally, and there are well-documented and tragic outbreaks involving deer, goats, sheep, elk and others.

    German researchers report on the occurrence of STEC in deer in Germany in the current issue of Epidemiology and Infection.

    Deer poop has been directly or indirectly linked to several outbreaks:

    1 dead and 14 sickened from E. coli O157:H7 from deer feces contaminating strawberries in Oregon in Aug. 2011;

    • deer feces were a possible source of E. coli O157 in Oregon hazelnuts that sickened 8 in March 2011;

    29 Minnesota high school students sickened with E. coli O103 and E. coli O145 after butchering and processing deer into venison in 2010;

    • deer meat was involved in at least two recognized E. coli outbreaks; and,

    an E. coli O157:H7 outbreak in Oct. 1996 that killed a 16-month-old and sickened 76 others who drank juice which contained unpasteurized apple cider that was probably contaminated with deer feces.

    In the current study, the Germans studied the virulence genes eae, e-hlyA and saa, thestx subtypes, pulsed-field gel electrophoresis (PFGE) patterns and serovars. In total, 120 samples of 60 animals were screened by real-time polymerase chain reaction (PCR). The PCR results showed a high detection rate of stx genes (83%). Mainly faecal samples, but also some lymphatic tissue samples, tested stx-positive. All isolates carried stx2, were eae-negative and carried e-hlyA in 38% and saa in 9% of samples. Serovars (O88:[H8], O174:[H8], O146:H28) associated with human diseases were also identified. In some animals, isolates from lymphatic tissue and faecal samples showed undistinguishable PFGE patterns. The examined deer were shown to be relevant reservoirs of STEC with subtype stx2b predominating.

    The complete paper is available at http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=8501556.

     

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  • Posted: February 24th, 2012 - 10:02pm by Doug Powell

    Stigi et al. report in the March, 2012, issue of Emerging Infectious Disease that in a survey of laboratories in Washington State, increased use of Shiga toxin assays correlated with increased reported incidence of non-O157 Shiga toxin–producing Escherichia coli (STEC) infections during 2005–2010.

    Despite increased assay use, only half of processed stool specimens underwent Shiga toxin testing during 2010, suggesting substantial underdetection of non-O157 STEC infections.

    Strains of Shiga toxin (Stx)–producing Escherichia coli (STEC) are differentiated by the O antigen on their outer membrane and are broadly classified as O157 or non-O157 STEC. The ability to produce Stx is a key virulence trait of STEC. STEC infections in humans often cause a self-limited diarrheal illness but can be complicated by hemorrhagic colitis or hemolytic uremic syndrome.

    Unlike other E. coli strains, serogroup O157 isolates do not ferment sorbitol and are readily identified by culture, appearing colorless on sorbitol MacConkey agar. Both O157 and non-O157 STEC can be identified by detecting Stx with nonculture assays that became commercially available in the United States in 1995. The Centers for Disease Control and Prevention (CDC) published formal STEC testing recommendations for clinical laboratories in 2009, advocating that all stool specimens submitted for routine bacterial pathogen testing be simultaneously cultured for O157 STEC and tested with a nonculture assay to detect Stx. Use of this testing protocol ensures timely identification of all STEC infections. Exclusive testing for Stx delays specific identification of O157 STEC and may impede prompt detection of common-source outbreaks.

    Non-O157 STEC infection has been a nationally notifiable condition since 2000. Although studies have documented the increased incidence of reported non-O157 STEC infections over the past decade, few have determined the proportion of laboratories that routinely test all submitted stool specimens for Stx and, to our knowledge, no study has quantified STEC testing practices by wwwnc.cdc.gov/eid/article/18/3/11-1358_article.htmproportion of stool specimens processed for bacterial culture. Our objectives, therefore, were to quantify statewide STEC testing practice by proportion of stool specimens processed for bacterial culture and to determine the contribution of enhanced STEC testing practice to increased reported incidence of non-O157 STEC infections.

    The complete report is available at: wwwnc.cdc.gov/eid/article/18/3/11-1358_article.htm.

     

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  • Posted: February 8th, 2012 - 10:58pm by Doug Powell

    The U.S. Food Safety and Inspection Service announced on Feb. 8 it is extending the implementation date for routine sampling of six additional shiga-toxin producing E. coli serogroups (O26, O45, O103, O111, O121 and O145) for 90 days, according to the North American Meat Processors Association. The date was extended from March 5 to June 4.

    NAMP says the extension was granted to give extra time to establishments so they could validate their test methods and detect these pathogens prior to entering the commerce stream.

    Initially, FSIS plans to sample raw beef manufacturing trimmings and other raw ground beef product components both imported and produced domestically, plus test the serogroups’ samples.

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  • Posted: January 23rd, 2012 - 11:19am by Ben Chapman

    Author: 
    Ben Chapman

    In January 1993 I was in 10th grade. I had just discovered the Violent Femmes and punk rock; was worried about figuring out calculus (I eventually did); and spent most of my time being uncool and longing to be cool. Probably pretty similar to every other awkward teenager. I didn't have a clue that a tragic foodborne illness outbreak was unfolding in the Pacific Northwest and that the event would eventually define a bunch of what I focus on every day.

    I had never even heard of Jack-in-the-Box.

    The outbreak was linked to four deaths, over to 700 illnesses and almost 200 hospitalizations. E. coli O157:H7 contaminated hamburger was then undercooked and served to thousands from 73 Jack-in-the-Box restaurants. Jack-in-the-Box will forever be linked to this event - and over the past 18 years has become a prominent force in food safety risk reduction.

    News of this outbreak hit on President Clinton's inauguration day and as Doug has written,

    Those two events, more than any other, dramatically changed the public discussion of food safety in the U.S. The Jack-in-the-Box outbreak had all the elements of a dramatic story: children were involved; the risk was relatively unknown and unfamiliar; and a sense of outrage developed in response to the inadequacy of the government inspection system. The newly inaugurated President Clinton made microbial food safety a Presidential issue.

    And the first focus went to E. coli O157:H7 - the serogroup linked to the Jack-in-the-Box illnesses. Food microbiologists and epidemiologists have seen lots of other equally dangerous shigatoxin-producing serogroups (shigatoxin is what makes E. coli O157:H7, along with its ability to stick to cells so devastating). Here's a list of the non-O157 STEC outbreaks we've been able to find going back to the mid-1990s.

    Later this afternoon I will be on my way to Lincoln, NE to meet with a group of academics, researchers, extension folks and regulators to talk about a large 5-year integrated project focused on reducing STECs from farm-to-fork that USDA NIFA has funded. Through the wonders of the Internet, Doug will be Skyping in.

    LINCOLN, Neb. -- The U.S. Department of Agriculture (USDA) announced today that it has awarded a research grant to the University of Nebraska-Lincoln (UNL) to help reduce the occurrence and public health risks from Shiga toxin-producing E. coli (STEC) along the entire beef production pathway. Dr. Chavonda Jacobs-Young, acting director of USDA's National Institute of Food and Agriculture (NIFA), is scheduled to award the $25 million grant to the UNL-lead research team today at the university in Lincoln.

    "Shiga toxin-producing E. coli are a serious threat to our food supply and public health, causing more than 265,000 infections each year," said Chavonda Jacobs-Young, acting NIFA director. "As non-O157 STEC bacteria have emerged and evolved, so too must our regulatory policies to protect the public health and ensure the safety of our food supply. This research will help us to understand how these pathogens travel throughout the beef production process and how outbreaks occur, enabling us to find ways to prevent illness and improve the safety of our nation's food supply."

    Dr. James Keen at UNL, along with a multi-institutional and multi-disciplinary team of researchers, educators and extension specialists, will use the $25 million grant to improve risk management and assessment of eight strains of STEC in beef. This work will include the O104 strain that caused the recent outbreak in Germany. The project will focus on identifying hazards and assessing exposures that lead to STEC infections in cattle and on developing strategies to detect, characterize and control these pathogens along the beef chain. This knowledge will then be used to find practical and effective STEC risk mitigation strategies. The five main objectives of the project include:

    Detection: develop and implement rapid detection technologies for pre-harvest, post-harvest and consumer environments.

    Biology: characterize the biological and epidemiological factors that drive outbreaks of STEC in pre-harvest, post-harvest, retail and consumer settings.

    Interventions: develop effective and economical interventions to lessen STEC risk from cattle, hides, carcasses, and ground and non-intact beef and compare the feasibility of implementing these interventions for large, small and very small beef producers.

    Risk analysis and assessment: develop a risk assessment model for STEC from live cattle to consumption to evaluate mitigation strategies and their expected public health impacts.

    Risk management and communication: translate research findings into user-friendly food-safety deliverables for stakeholders, food safety professionals, regulators, educators and consumers.

    For more check out the full PR here.
     

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  • Posted: December 23rd, 2011 - 10:49pm by Ben Chapman

    Author: 
    Ben Chapman

    Jack made it through his first child care season without much disease excitement --  just a little bit of pink eye and a couple of runny noses.  Child care facilities are notorious illness-spreading sites; children and care providers pass around pathogens like rotavirus, norovirus, Shigella and E. coli. As hand hygiene usually isn't the best in these facilities, outbreaks are often started by or extended by ill people (staff included) showing up while shedding. Cohorting (separating the already sick from the healthy) can be an effective way to limit spread.

    Except sick kids aren't always kept home and staff don't always stay away.

    In an early-release article in Pediatric Infectious Disease, investigators of an outbreak of E. coli O26:H11 linked to a Colorado child care center say that it could have been worse had health authorities hadn't pushed for cohorting. Part of the strategy was to test every staff member and child for STEC - those who were carrying the bug were separated from those who weren't. Sixty percent of the kids and staff at the center were carrying the outbreak strain (41 ill - 4 asymptomatically) and health authorities aggressively kept sick folks away until they stopped shedding.

    Some gems for child care providers from the abstract:

    - The median duration of shedding among symptomatic confirmed cases was 30.5 days.

    - The risk of being a case as in children <36 months was twice the risk among children 36-47 months.

    - Nearly half (49%) of the household contacts of confirmed cases developed a diarrheal illness.

    Outbreak of Shiga toxin-producing Escherichia coli serotype O26: H11 infection at a child care center in Colorado
    20.dec.11
    Pediatric Infectious Disease Journal
    Brown, Jennifer A. DVM, MPH; Hite, Donna S. BS; Gillim-Ross, Laura A. PHD; Maguire, Hugh F. PHD; Bennett, Janine K. MS; Patterson, Julia J. BA; Comstock, Nicole A. MSPH; Watkins, Anita K. MPH; Ghosh, Tista S. MD, MPH; Vogt, Richard L. MD
    Background: Shiga toxin-producing Escherichia coli (STEC) O26:H11 is an emerging cause of disease with serious potential consequences in children. The epidemiology and clinical spectrum of O26:H11 are incompletely understood. We investigated an outbreak of O26:H11 infection among children younger than 48 months of age and employees at a child care center.
    Methods: Every employee at the center (n=20) and every child <48 months (n=55) were tested for STEC and administered a questionnaire. Thirty environmental health inspections and site visits were conducted. A cohorting strategy for disease control was implemented.
    Results: Eighteen confirmed and 27 suspect cases were detected. There were no hospitalizations. The illness rate was 60% for children and for employees. The risk of being a case as in children <36 months was twice the risk among children 36-47 months (risk ratio: 2.10; 95% confidence interval: 1.00, 4.42). The median duration of shedding among symptomatic confirmed cases was 30.5 days (range: 14-52 days). Four (22%) confirmed cases were asymptomatic and 3 (17%) shed intermittently. Nearly half (49%) of the household contacts of confirmed cases developed a diarrheal illness. The outbreak was propagated by person-to-person transmission; cohorting was an effective disease control strategy.
    Conclusions: This was the largest reported outbreak of O26:H11 infection in the United States and the largest reported non-O157 STEC outbreak in a U.S. child care center. Non-O157 STEC infection is a differential diagnosis for outbreaks of diarrhea in child care settings. Aggressive disease control measures were effective, but should be evaluated for outbreaks in other settings.

     

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  • Posted: December 9th, 2011 - 4:12am by Doug Powell

     To all broken hearts: don't eat prepackaged cookie dough before it's baked.

    That’s the message health-types conclude from a June 2009 outbreak of shiga-toxin producing E. coli (primarily O157:H7) in Nestle Toll House cookie dough that sickened at least 77 people in 30 states. Thirty-five people were hospitalized – from cookie dough.

    The 2009 investigation, which involved extensive traceback, laboratory, and environmental analysis, led to a recall of 3.6 million packages of the cookie dough. However, no single source, vehicle, or production process associated with the dough could be identified for certain to have contributed to the contamination.

    The researchers could not conclusively implicate flour as the E. coli source, but it remains the prime suspect. They pointed out that a single purchase of contaminated flour might have been used to manufacture multiple lots and varieties of dough over a period of time as suggested by the use-by dates on the contaminated product.

    Flour does not ordinarily undergo a kill step to kill pathogens that may be present, unlike the other ingredients in the cookie dough like the pasteurized eggs, molasses, sugar, baking soda, and margarine. Chocolate was also not implicated in this outbreak since eating chocolate chip cookie dough was less strongly associated with these illnesses when compared with consuming other flavors of cookie dough.

    The study authors conclude that "foods containing raw flour should be considered as possible vehicles of infection of future outbreaks of STEC."

    During the investigation, three strains of STEC were discovered in one brand of cookie dough — although it wasn't the same strain involved in the outbreak.

    Manufacturers should consider using heat-treated or pasteurized flour, in ready-to-cook or ready-to-bake foods that may be consumed without cooking or baking, despite label statements about the danger of such risky eating practices, the authors conclude. In addition, manufacturers should consider formulating ready-to-bake prepackaged cookie dough to be as safe as a ready-to-eat food item.

    Eating uncooked cookie dough appears to be a popular practice, especially among adolescent girls, the study authors note, with several patients reporting that they bought the product with no intention of actually baking cookies. Since educating consumers about the health risks may not completely halt the habit of snacking on cookie dough, making the snacks safer may be the best outcome possible.

    A Novel Vehicle for Transmission of Escherichia coli O157:H7 to Humans: Multistate Outbreak of E. coli O157:H7 Infections Associated With Consumption of Ready-to-Bake Commercial Prepackaged Cookie Dough—United States, 2009
    http://www.oxfordjournals.org//our_journals/cid/prpaper.pdf

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