Tag Archives: Ruminant

Bambi poops in water, 4 kids get sick with E. coli O157, 2016

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In May 2016, an outbreak of Shiga toxin–producing Escherichia coli O157 infections occurred among children who had played in a stream flowing through a park. Analysis of E. coli isolates from the patients, stream water, and deer and coyote scat showed that feces from deer were the most likely source of contamination.

In the United States, recreational water is a relatively uncommon source of Shiga toxin–producing Escherichia coli (STEC) O157 outbreaks (1). We describe an outbreak of STEC O157 infections among children exposed to a contaminated stream in northern California, USA, and provide laboratory evidence establishing wildlife as the source of water contamination.

In May 2016, four cases of Shiga toxin (Stx) 1– and 2–producing E. coli O157 infection were reported to a local health department in northern California; investigation revealed a common source of exposure. The case-patients, ranging in age from 1 to 3 years, had played in a stream adjacent to a children’s playground within a city park. Exposure of the case-patients to the stream occurred on 3 separate days spanning a 2-week period. Two case-patients are known to have ingested water while playing in the stream. Two case-patients were siblings. All case-patients had diarrhea and abdominal cramps; bloody diarrhea was reported for 3. One case-patient was hospitalized with hemolytic uremic syndrome.

The stream is a second-order waterway located in a northern California community of ≈7,500 residents. At the time of exposures, stream flow was <30 ft3/s. The land upstream is not used for agricultural activities such as livestock production. The community is serviced by a public sewer system; inspection of sewer lines indicated no breach to the system.

Water samples were collected from the exposure site 7 days after the last case-patient was exposed and weekly thereafter for 17 weeks; samples were tested quantitatively for fecal indicator organisms. Throughout the study period, all water samples exceeded recreational water quality limits for E. coli and enterococci levels (2). Water samples were also cultured for STEC isolation and PCR detection of stx1 and stx2 (3). Stx1- and Stx2-producing E. coli O157 were isolated from stream water each week for the first 4 weeks. Additionally, an Stx2-producing E. coli non-O157 strain was isolated from the stream in the first week of sampling. Enrichment broth cultures of water samples were also positive by PCR for stx1 and stx2 for the first 4 weeks of sampling. Thereafter, both stx1 and stx2, or stx2 only, were intermittently detected in enrichment broth cultures for 9 additional weeks.

In the absence of an obvious source (e.g., upstream agricultural operation or sewer leak), wildlife was considered as a possible contributor to water contamination. Thirteen fresh wildlife scat specimens were collected along the stream for STEC culture and PCR. Of the 13 scat specimens, 8 originated from deer, 2 from raccoon, and 1 each from coyote, turkey, and river otter. Six scat specimens (4 deer, 1 coyote, 1 river otter) were positive for stx1 and stx2 or for stx2 by PCR (Technical Appendix[PDF – 16 KB – 1 page]). Stx1- and Stx2-producing E. coli O157 were isolated from deer scat and coyote scat. An Stx2-producing E. coli non-O157 strain was isolated from a deer scat specimen. The animal origin of the coyote and river otter scat specimens were definitively identified by partial DNA sequencing of mitochondrial cytochrome b (4).

To assess strain relatedness, we compared STEC O157 isolates from the case-patients, water, deer scat, and coyote scat by using pulsed-field gel electrophoresis (PFGE) and multilocus variable-number tandem-repeat analysis (MLVA) (5). PFGE patterns for XbaI-digested genomic DNA were highly similar among all isolates; only slight variations were found in the lower-sized bands (Figure). PFGE patterns for genomic DNA samples digested with BlnI also demonstrated a high degree of similarity (data not shown). Furthermore, MLVA profiles were identical for the case-patient, water, and deer scat isolates; only the coyote scat isolate differed from the main profile by 2 repeats at a single locus (VNTR_3).

This study provides laboratory evidence linking STEC O157 infections with the ingestion of recreational water that was probably contaminated by wildlife scat. Wild ruminants, including deer and elk, are known carriers of STEC and have been connected to outbreaks of human infections (6–9). We detected STEC in 50% of deer scat specimens collected from the stream bank. One of these specimens, found 1.5 miles upstream of the exposure site, contained an E. coli O157 isolate that was highly similar by molecular subtyping to case-patient and water isolates. These findings support the likelihood that feces from deer carrying STEC were the source of water contamination or, at the very least, contributed to the persistence of STEC in the water. It is unknown whether the STEC detected in coyote and river otter scat represents carriage or transitory colonization within these animals.

The common risk factor among the case-patients in this STEC O157 outbreak was exposure to a natural stream within a city park. After the outbreak was recognized, signs warning of bacterial contamination were posted along the stream. No further STEC O157 infections attributed to stream water exposure were reported.

Dr. Probert is the assistant director for the Napa-Solano-Yolo-Marin County Public Health Laboratory. His research interests focus on the development of molecular diagnostic tools for the detection of infectious agents.

Acknowledgment

We thank Frank Reyes, Keith Snipes, and Nailah Souder for their technical assistance; the County of Marin Health and Human Services and Environmental Health Services for information about the epidemiologic and environmental investigation; and the Microbial Diseases Laboratory Branch of the California Department of Public Health and the Santa Clara County Public Health Laboratory for the molecular subtyping data.

References

Heiman KE, Mody RK, Johnson SD, Griffin PM, Gould LH. Escherichia coli O157 outbreaks in the United States, 2003–2012. Emerg Infect Dis. 2015;21:1293–301. DOIPubMed

United States Environmental Protection Agency. 2012. Recreational water quality criteria. Office of Water 820-F-12–058 [cited 2017 Apr 13]. https://www.epa.gov/sites/production/files/2015-10/documents/rwqc2012.pdf

Probert WS, McQuaid C, Schrader K. Isolation and identification of an Enterobacter cloacae strain producing a novel subtype of Shiga toxin type 1. J Clin Microbiol. 2014;52:2346–51. DOIPubMed

Parson W, Pegoraro K, Niederstätter H, Föger M, Steinlechner M. Species identification by means of the cytochrome b gene. Int J Legal Med. 2000;114:23–8. DOIPubMed

Hyytia-Trees E, Lafon P, Vauterin P, Ribot EM. Multilaboratory validation study of standardized multiple-locus variable-number tandem repeat analysis protocol for Shiga toxin–producing Escherichia coli O157: a novel approach to normalize fragment size data between capillary electrophoresis platforms. Foodborne Pathog Dis. 2010;7:129–36. DOIPubMed

Fischer JR, Zhao T, Doyle MP, Goldberg MR, Brown CA, Sewell CT, et al. Experimental and field studies of Escherichia coli O157:H7 in white-tailed deer. Appl Environ Microbiol. 2001;67:1218–24. DOIPubMed

Keene WE, Sazie E, Kok J, Rice DH, Hancock DD, Balan VK, et al. An outbreak of Escherichia coli O157:H7 infections traced to jerky made from deer meat. JAMA. 1997;277:1229–31. DOIPubMed

Rounds JM, Rigdon CE, Muhl LJ, Forstner M, Danzeisen GT, Koziol BS, et al. Non-O157 Shiga toxin–producing Escherichia coli associated with venison. Emerg Infect Dis. 2012;18:279–82. DOIPubMed

Laidler MR, Tourdjman M, Buser GL, Hostetler T, Repp KK, Leman R, et al. Escherichia coli O157:H7 infections associated with consumption of locally grown strawberries contaminated by deer. Clin Infect Dis. 2013;57:1129–34. DOIPubMed

 Contaminated stream water as source for Escherichia coli O157 illness in children

05.may.17

William S. Probert, Glen M. Miller, and Katya E. Ledin

Emerging Infectious Diseases, vol. 23, no. 7, July 2017

https://wwwnc.cdc.gov/eid/article/23/7/17-0226_article

Goat prank closes NC high school football field for 6 months

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Whoever released 10-12 goats on a North Carolina high school football field last week probably didn’t figure the field would be closed for six months.

But that’s exactly the result for athletes at Burns High School in Lawndale, N.C., who aren’t too happy about having to find a new home for their games after a recent prank on the school’s football field.

Donna Carpenter, the school system’s public information officer, said a recent outbreak of E. coli in the county prompted the extended closure.

“We had some students who, as a prank, put some goats out on the football field,” Carpenter told ABCNews.com. ”You have to understand what’s been going on in this area. This county has a very large county fair. And this is a historically agricultural community.

“We have people who see and pet different animals, and there has been just shy of 100 cases of E. coli. There was a small child that passed away. Everybody was very on edge about E. coli.”

E. coli happens: cook burgers to 165F, whatever ruminant it came from

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Seventeen years ago, Gregg Jesperson ate a burger that was still pink at a mom-and-pop restaurant in northern Alberta (that’s in Canada), where he and his family were living at the time.

The medication he’ll have to take for life is one reason why he’s not going to forget what happened anytime soon.

Jesperson, now a teacher at Booth Memorial in St. John’s, ate the burger on a Thursday.

By Sunday, it was determined Jesperson had developed hemolytic uremic syndrome, or hamburger disease.

Jesperson was hospitalized almost four weeks, undergoing dialysis and being hooked up to a machine that withdraws plasma and replaces it.

After his release, it took him almost a year to regain his physical strength.

Jesperson, who always enjoyed a rare steak, says he wasn’t aware of the dangers of uncooked hamburger meat before that.

“I’m a big fella, fairly hardy and that, and it really knocked the piss right out of me,” he says.

These days, Jesperson gets nervous when he sees people served burgers that are a little pink.

If he grills one himself, he “cooks the bejeezus out of it.”

His advice is to do the same, and not to be afraid to send undercooked burgers back at a restaurant.

Better advice would be to use a tip-sensitive digital thermometer because color is a lousy indicator of safety.

But this story is a lot better than the misguided letter-writer to a New Brunswick newspaper (also in Canada) who insisted dangerous E. coli like O157 only “grows inside of dairy and beef cattle that are fed a high proportion of grain.” Way to recycle a 15-year-old myth.

Nosestretcher alert: Buying organic cow can help avoid E. coli

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Eager to capitalize on news of the day, Mary Forstbauer, an organic farmer in Chilliwack, B.C. who sells beef at farmer’s markets across Metro Vancouver, told News1130 E. coli is not as common in organically-raised cattle.

"Cows are meant to eat grass, not grains. Quite often, when they have a diet of grain, that causes their intestine to produce bacteria that’s not natural — which is the E. coli — and that would then contaminate some of the meat products.”

Just because this nugget has been repeated and amplified amongst foodies and on the Internet since 1998 doesn’t make it true.

E. coli happens. In ruminants. Like cattle.

Where does E. coli O157:H7 come from? Food Inc. and cookie dough versions

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Is E. coli O157:H7 associated with things other than feedlot cattle?

I had a few people call me recently, saying, I saw that movie, Food, Inc., which says that E. coli O157:H7 is predominately in feedlot cattle because of the grain they are fed, and that’s how the bug came to exist. So how did it get into Nestle cookie dough?

It’s sort of a mantra of raw milk enthusiasts and wannabe food safety types that E. coli O157:H7 is a product of feedlot cattle, and that grass-fed creatures are benign entities for the dinner plate.

A blogger yesterday wrote, “… hamburger tainted by e-coli, a virus that breeds in a cow’s stomach when it is feed grain instead of grass (which, of course, most cows are nowadays in order to fatten them quickly and cheaply).”

It’s a bacterium, not a virus.

Nicholas Kristof, a columnist for the N.Y. Times, wrote yesterday, on Sunday, June 21/09, that, “There is some evidence that pathogens, including E. coli, become much more common in factory farming operations. Move feedlot cattle out to a pasture for five days, and they will lose 80 percent of the E. coli in their gut, the film says.”

That evidence is about as strong as the whisps of evidence compiled by Danny Sugarman that The Doors’ frontman Jim Morrisson is still alive and didn’t die from excess in a Paris bathtub in 1971. But, every teenager goes through their Doors phase (I can only find the clip below in Spanish, but Canada’s The Guess Who stands up much better with the hindsight of time; they know they are drunken buffoons, and not a drunken buffoon trying to be a poet).

Scientific uncertainty can easily be exploited by the certainty of filmmakers, who cherry pick facts and flourish on rhetoric. And I guess if it’s repeated ad nauseum for 11 years by writers from the N.Y. Times to your-favorite-bullshit blogger it becomes fact.

That line, “Move feedlot cattle out to a pasture for five days, and they will lose 80 percent of the E. coli in their gut,” comes from a 1998 paper published in the journal Science by Diez-Gonzalez of Cornell University, and colleagues.

I had one of my colleagues, Rena Orr, write a review of the controversy back in Nov. 2000.

Since September 1998, there has been conflicting information on the effect of diet on E. coli shedding from cattle. The conflict arises in part from the effect of diet on the ability of E. coli to develop acid resistance. … Diez-Gonzalez et. al demonstrated that feeding a high-grain diet to cattle results in an acidic environment in the colon. Because the animals incompletely digested the starch in grains, some starch was able to reach the colon where it fermented, producing fermentation acids. The researchers believe an acidic environment selects for or induces acid resistance among the Escherichia coli population. … Diez-Gonzalez et al. concluded that if cattle were given hay for a brief period (five days) immediately before slaughter, the risk of foodborne E. coli infection would be significantly reduced because the acidity in the colon is greatly reduced. "Our studies indicate that cattle could be given hay for a brief period immediately before slaughter to significantly reduce the risk of food-borne E. coli infection."

The Science article received mainstream media attention, and was covered by the Associated Press and The New York Times, as well as scientific releases and reports. In the Irish Times, it was cited as the basis for concluding that because Irish cattle are fed a grass-based diet rather than grain, Ireland has a low incidence of E. coli O157:H7. Hancock et al. contend that this conclusion is unsupported or contradicted by several lines of evidence. The E. coli that contaminate beef typically originate from the hide, the hooves, or the equipment used in slaughter and processing rather than directly from the colon, and likely replicate in environments unlike the colon. Therefore, the induced acid resistance of E. coli contaminating beef is likely to be unrelated to the pH of its ancestral colonic environment. The E. coli O157:H7 bacterium uses several mechanisms to survive acid environments, some of which are innate and are not influenced by environment . Although acid resistance is likely a factor in an infective dose, induced acid resistance has not been shown to be a factor in E. coli O157:H7 infectivity by experimental (dose-inoculation) or observational (epidemiological) data . Therefore, acid resistance induced by exposure to weak acid may not influence the virulence of this pathogen.

Published data on E. coli O157:H7 tends to contradict or does not support the effects of the dietary change proposed by Diez-Gonzalez et al. In a recent study on three different grain diets (85% cracked corn, 15% whole cottonseed and 70% barley, or 85% barley), the fecal pH of the animals fed the corn diet was significantly lower (P < 0.05) than the fecal pH of the animals fed the cottonseed and barley and barley diets, likely resulting in a less suitable environment for E. coli O157:H7 in the hindgut of the corn fed animals (2000, Buchko et al). In the Journal of Food Protection, researchers concluded that changing from grain to a high roughage diet did not produce a change in the E. coli concentration that was large enough to deliver a drastic improvement in beef carcass hygiene. Sheep experiencing an abrupt diet change have higher concentrations and increased shedding of fecal E. coli O157:H7 for longer periods than sheep fed a consistent high-grain diet. Another study compared the duration of shedding E. coli O157:H7 isolates by hay-fed and grain-fed steers experimentally inoculated with E. coli O157:H7 as well as the acid resistance of the bacteria. The hay-fed animals shed E. coli O157:H7 longer than the grain-fed animals, and irrespective of diet, these bacteria were equally acid resistant.

These results suggest that the proposed dietary change would actually increase contamination with E. coli O157:H7. Also, the 1,000-fold reductions in total fecal E. coli demonstrated by Diez-Gonzales et al. are far greater than those recorded in cattle experiencing similar ration changes . Finally, extensive surveys show that grain-fed feedlot cattle have no higher E. coli O157:H7 infection prevalence than similarly aged dairy cattle fed forage (hay) diets. Abrupt feed change immediately before slaughter could have unexpected deleterious effects. The proposed diet change has the potential to increase the risk of bovine salmonella infections, a potential source of food poisoning. The dietary change results in sharply reduced volatile fatty acid concentrations in the large intestine as well as changes in the bacteria, allowing for colonization of Salmonella.

See, that’s a really long explanation. It’s not as soothing as, change cattle diet, disease prevented. And that was written nine years ago.

Mike Osterholm, director of the Center for Infectious Disease Research and Policy and professor in the School of Public Health at the University of Minnesota wrote a cleaner critique in 2007 in the Minneapolis-St. Paul Star Tribune:

"Russo cited conclusions from a 1998 study from Cornell University that cattle fed a diet of grass, not grain, had very few E. coli, and that those bacteria that survived in the cattle feces would not survive in the human when eaten in undercooked meat, particularly hamburger. This statement is based on a study of only three cows rotated on different diets and for which the researchers did not even test for E. coli O157:H7. Unfortunately, the authors extrapolated these incredibly sparse results to the entire cattle industry. The Cornell study is uncorroborated in numerous published scientific papers from renowned research groups around the world. Finally, work conducted by the Minnesota Department of Health as part of a national study on foodborne disease recently showed that eating red meat from local farms was a significant risk factor for E. coli infection. …

And as my colleague David Renter wrote in Sept. 2006,

"Cattle raised on diets of ‘grass, hay and other fibrous forage’ do contain E. coli O157:H7 bacteria in their feces as do other animals including deer, sheep, goats, bison, opossum, raccoons, birds, and many others.

"Cattle diet can affect levels of  E. coli O157:H7, but this is a complex issue that has been and continues to be studied by many scientists.  To suggest switching cattle from grain to forage based on a small piece of the scientific evidence is inappropriate and irresponsible.  Several pieces of evidence suggest that such a change would not eliminate and may even increase E. coli O157:H7 in cattle.

"The current spinach outbreak may be traced back to cattle manure, but there are many other potential sources.  Simplistically attacking one facet of livestock production may be politically expedient, but instead provides a false sense of security and ignores the biological realities of E. coli O157:H7. In 1999, for example, 90 children were felled by E. coli O157:H7 at a fair in London, Ont. The source? A goat at a petting zoo, hardly an intensively farmed animal."

Last time I looked, E. coli O157:H7 and about 60 other shiga-producing E. coli that are known to cause illness in humans are present in about 10 per cent of all ruminants – cattle, sheep, goats, deer, elk -– and I can point to outbreaks associated with all of those species. Pigs, chickens, humans, birds and rodents have all been shown to be carriers of shiga-producing E. coli but the resevoir appears to be ruminants. The final report of the fall 2006 spinach outbreak identifies nearby grass-fed beef cattle as the likely source of the E. coli O157:H7 that sickened 200 and killed 4.

How the E. coli O157:H7 got into the cookie dough remains to be seen. Biology is complex and constantly changing – even at farmer’s markets, which was the big solution of Food, Inc. But it’s only a movie.

That Cornell paper can be found here:

Diez-Gonzalez, Francisco, Todd R. Callaway, Menas G. Kizoulis, James B. Russell. Grain Feeding and the Dissemination of Acid-Resistance Escherichia coli from Cattle. Science: Sept 11, 1998. Volume 281, Number 5383, pages 1666-1668.