You see a cute chick, I see a Salmonella factory: 372 sick so far this year

Posted on June 3, 2017 by Douglas Powell

The U.S. Centers for Disease Control, many state departments of health and agriculture, and the U.S. Department of Agriculture’s Animal and Plant Health Inspection Service are investigating eight multistate outbreaks of human Salmonella infections linked to contact with live poultry in backyard flocks.

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These outbreaks are caused by several kinds of Salmonella bacteria: Salmonella Braenderup, Salmonella Enteritidis, Salmonella Hadar, Salmonella I 4,[5],12:i-, Salmonella Indiana, Salmonella Infantis, Salmonella Mbandaka, and Salmonella Typhimurium.

As of May 25, 2017, 372 people infected with the outbreak strains of Salmonella have been reported from 47 states.

Illnesses started on dates ranging from January 4, 2017 to May 13, 2017.

71 ill people have been hospitalized, and no deaths have been reported.

36% of ill people are children younger than 5 years.

Epidemiologic, traceback, and laboratory findings link the eight outbreaks to contact with live poultry, such as chicks and ducklings, which come from several hatcheries.

In interviews, 190 (83%) of 228 ill people reported contact with live poultry in the week before illness started.

People reported purchasing live baby poultry from several sources, including feed supply stores, websites, hatcheries, and from relatives.

Contact with live poultry and the areas where they live and roam can make people sick with Salmonella infections. Chicks, ducklings, and other live poultry that look healthy and clean can still carry Salmonella bacteria.

Outbreaks linked to contact with live poultry have increased in recent years as more people keep backyard flocks. In 2016, a record number of illnesses were linked to contact with backyard poultry.

Feed-to-farm-to-slaughter-to-267 sickened with Salmonella in Germany, 2013

Posted on April 3, 2016 by Douglas Powell

One of the largest and longest Salmonella outbreaks in Germany within the last 10 years occurred in central Germany in 2013.

To identify vehicles of infection, we analysed surveillance data, conducted a case-control study and food traceback. We identified 267 cases infected with Salmonella Infantis with symptom onset between 16 April and 26 October 2013 in four neighbouring federal states.

Results of our study indicated that cases were more likely to have eaten raw minced pork from local butcher’s shops [odds ratio (OR) 2·5, 95% confidence interval (CI) 1·1–5·8] and have taken gastric acid-reducing or -neutralizing medication (OR 3·8, 95% CI 1·3–13) than controls.

The outbreak was traced back to contaminated raw pork products found in different butcher’s shops supplied by one slaughterhouse, to pigs at one farm and to an animal feed producer. Characterization of isolates of human, food, animal, feed, and environmental origin by phage-typing and pulsed-field gel electrophoresis confirmed the chain of infection.

Insufficient hygiene standards in the slaughterhouse were the most probable cause of the ongoing transmission. We recommend that persons taking gastric acid suppressants should refrain from consuming raw pork products. Improving and maintaining adequate hygiene standards and process controls during slaughter is important to prevent future outbreaks.

A prolonged outbreak of Salmonella Infantis associated with pork products in central Germany, April–October 2013

Epidemiology and Infection / Volume 144 / Issue 07 / May 2016, pp 1429-1439

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=10259962&utm_source=Issue_Alert&utm_medium=RSS&utm_campaign=HYG

The effect of diet on E. coli 0157:H7 in cattle

Posted on March 28, 2015 by Douglas Powell

Fifteen years old, written for me by Rena Orr while I was a prof at Guelph, and I’m still citing it.

The gastrointestinal tract of animals and humans is an ideal habitat for the growth of mostly harmless bacteria. Escherichia coli (E. coli) is a normal inhabitant of the human gastrointestinal tract. The 0157:H7 strain of E. coli, however, is responsible for the illness known as hamburger disease. As few as 10 viable E. coli O157:H7 can cause infection. Victims may experience severe cramping and abdominal pain, watery or bloody diarrhea, vomiting or low-grade fever for an average of eight days. It can also cause kidney failure and death, primarily in children and immune compromised adults.

A small percentage of cattle are carriers of E. coli O157:H7. The prevalence of Shiga toxin‑producing Escherichia coli (STEC) in beef slaughter steers and heifers on P.E.I. was reported to be 4% (2000, Douglas Schurman). When meat is contaminated with cattle feces at slaughter, this strain of E. coli can enter the food chain. With the increasing use of hazard analysis and critical control point ( HACCP) plans, dietary management during the pre-slaughter period of beef production may play a role in reducing the incidence of E. coli O157:H7‑positive ruminants. Reducing the levels of E. coli O157:H7 organisms that enter slaughter plants would require two interrelated strategies: (i) reducing the number of cattle shedding E. coli O157:H7 and (ii) reducing the magnitude of shedding (CFU/gram) by those animals infected with the organism (1998, Cray Jr.).

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. The induction of acid resistance could increase the risk of human food‑borne illness. Normally, stomach acid is an effective barrier to infection by food‑borne pathogens because the organisms die in an acid environment. Acid resistant bacteria are able to survive this defence mechanism, reproduce, and produce the toxins that cause disease.

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.

On a diet of hay, there is no residual starch to be fermented in the colon. Thus, the acid level remains low and the E. coli remain acid‑sensitive. Acid‑sensitive E. coli are easily destroyed in the human stomach. Diez‑Gonzalez et al. concluded that if cattle were given hay for a brief period (five days) immediately before slaughter, the risk of food‑borne 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.” This finding was supported by studies on fecal shedding of E. coli 0157H7. Van Donkersgoed et al. concluded that feces and rumen content are sources of E. coli and Victor Gannon et al. showed that there were significantly fewer E. coli isolated from steers changed to an alfalfa hay diet for three weeks than for steers that stayed on silage/grain. The effect of dietary stress such as fasting has also been demonstrated to increase fecal shedding of E. coli O157:H7. 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 0157: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.

Several people interviewed in the media, including U.S. Agriculture Secretary Dan Glickman, Dr. Gary Weber of the National Cattlemen’s Beef Association and Dr. Robert Buchanan, a microbiologist at the Food and Drug Administration, and the authors, including Diez-Gonzalez, of a review article of recent research pointed out the need for further study to confirm that cattle feeding management practices may be manipulated to decrease the risk of foodborne illness from E. coli . Glickman said in a statement that the findings, if confirmed by additional research, “have the potential to greatly assist efforts to fight foodborne illness” and may lead the U.S. Department of Agriculture to recommend changes in the way cattle are fed. Peter Doris of the Ontario Cattlemen’s Association recommended a “cautious approach” on this issue. “Subjecting cattle to a special diet before slaughter is a problem in itself since most market‑ready cattle are sorted from pens in feedlots no more than 12 hours before they board the truck to the packing plant . Before we get to that point, we need to clarify if the research findings are valid”.

References

Buchko, S. J., R. A. Holley, S. J. Buchko, W. O. Olson, V. P. J. Gannon, and D. M. Veira. The Effect of Different Grain Diets on Fecal Shedding of Escherichia Coli O157:H7 by Steers Journal of Food Protection: October 2000 Vol. 63, No. 11, pp. 14671474

Brody, Jane E. The New York Times: September 11, 1998.

Cray Jr., William C., Thomas A. Casey, Brad T. Bosworth, and Mark A. Rasmussen. Effect of Dietary Stress on Fecal Shedding of Escherichia coli O157:H7 in Calves. Applied Environmental Microbiology: May 1998, p. 1975‑1979, Vol. 64, No. 5

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.

Douglas Schurman R., Harry Hariharan and Susan Heaney. Prevalence And Characteristics of Shiga Toxin‑producing Escherichia Coli in Beef Cattle Slaughtered on Prince Edward Island

Journal of Food Protection: November 2000. Vol. 63, No. 11, pp. 15831586.

Farm and Country: Scientists Debate Hay vs Corn. October 19, 1998

Gannon, Victor, Thomas Graham, Walter Olson, Roger Johnson: Fecal Shedding of

Escherichia coli O157:H7 during the Beef Cattle Production Cycle. Health Canada and

Agriculture and Agri‑Food Canada, Lethbridge Alberta and Health Canada, Guelph,

Ontario http://sun1.bham.ac.uk/bcm4ght6/res.html

Hancock, Dale D., Thomas E. Besser (College of Veterinary Medicine, Washington State University, Pullman, WA 99164, USA), Colin Gill (Agriculture and Agri‑Food Canada Research Center, Lacombe, Alberta, Canada T4L1W1), Carolyn Hovde Bochach (Department of Microbiology, Molecular Biology, and Biochemistry, University of Idaho, Moscow, ID 83844, USA): Cattle, Hay, and E. coli. Science, April 2, 1999 Volume 284, Number 5411, Page 49.

Hovde, Carolyn, et al. Applied and Environmental Microbiology: 65: 3233‑3235. 1999

Jordan, David, Scott McEwen. Effect of Duration of Fasting and a Short‑Term High Roughage Ration on the Concentration of Escherichia coli Biotype 1 in Cattle Feces. Journal of Food Protection 1998. Volume 61, No. 5, pages 531‑534.

Kudva, Indira T., Carl W. Hunt, Christopher J Williams, Ursula M. Nance, Carolyn J.

Hovde: Dietary Influences on the Shedding of Escherichia coli 0157:H7 by Ruminants.

Department of Microbiology, Molecular Biology and Biochemistry, Department of

Animal and Veterinary Sciences and Division of Statistics, University of Idaho, Moscow,

Idaho http://sun1.bham..ac.uk/bcm4ght6/res.html

O’Sullivan, Kevin. Irish Times: September 23, 1998.

Russell JB, F Diez‑Gonzalez, GN Jarvis. Invited review: effects of diet shifts on Escherichia coli in cattle. Journal of Dairy Science: 2000 Apr;83(4):863‑73

Tkalcic, Suzana, Barry G. Harmon, Cathy A. Brown, E. Mueller, A. Parks, T. Zhao, M.P.

Doyle: Effects of the Rumen Microenvironment on the Growth and Fecal Shedding of E

coli 0157:H7. The Department of Pathology and Department of Food Science and

Technology, University of Georgia. http://sun1.bham.ac.uk/bcm4ght6/res.html

Van Donkersgoed, Joyce, (Alberta Agriculture, Food and Rural Development, 11 Bruns

Road, Lacombe, Alberta, T4L 1P1), Tom Graham, Vic Gannon (Animal Diseases

Research Institute, Health Canada., Lethbridge Alberta). The Prevalence of Verotoxins,

coli O157:H7 and Salmonella in the Feces and Rumen of Cattle at Processing.

Porcine plasma? Feed is suspect in spread of deadly pig virus

Posted on April 1, 2014 by Douglas Powell

Scientists and regulators investigating the mysterious spread of a deadly virus plaguing the U.S. pork industry are stepping up their scrutiny of what the nation’s hog herd eats.

With a dearth of solid leads, investigators are exploring whether something in pig feed could be a conduit for porcine epidemic diarrhea virus, which has spread to 27 states and killed millions of young pigs since it was first identified in the U.S. last April. One focus of the inquiry: porcine plasma, a widely used feed ingredient made from the blood of slaughtered hogs and fed to piglets.

Scientists say the virus, one of the most devastating diseases to afflict U.S. livestock in years, is fatal only to young pigs, and poses no threat to human health or food safety. But it has rapidly increased costs for major hog-farm operators, such as Smithfield Foods Inc. and Maschoffs LLC, as prices for replacement pigs have soared to new highs.

Porcine plasma has been a mainstay of piglet diets in the U.S. since the 1990s, after scientists discovered it provided antibodies to protect young pigs from disease and helped them switch from feeding from their mother to the grain-heavy diet common on livestock farms.

Last month, the Canadian Food Inspection Agency disclosed that it had found plasma contaminated with the virus, after multiple hog farms in Ontario that were hit by PED, and another farm on Prince Edward Island with a suspected case, all reported that they bought feed from the same vendor, Ontario-based Grand Valley Fortifiers.

The Canadian agency said that the virus was present in plasma that originated in the U.S. and was obtained at the company that manufactured Grand Valley’s feed, which the agency has declined to identify. It said the plasma contained virus “capable of causing disease in pigs.”

Porcine plasma is one of more than 40 ingredients in typical piglet feed. “Many people think that feed is the most likely suspect,” said Greg Stevenson, a veterinary pathologist at Iowa State University who has studied the virus. “But practically speaking, we have no proof.”

Porcine plasma is made from blood captured in chilled vats at slaughterhouses. It is treated with an anticoagulant and spun in a centrifuge to separate the plasma from blood cells, then transported in insulated trucks to processing plants. The plasma is shot through a spray nozzle into a heated chamber to evaporate excess water, leaving a powder that is run through stainless-steel dryers, bagged and shipped to feed companies.

Rare burgers are not OK, whatever food porn says

Posted on December 12, 2012 by Douglas Powell

Butcher and Meat Hook co-owner Tom Mylan tells Grub Street New York when you move to outlaw hamburgers because of E. coli, “it’s a pretty clear sign that your food system is broken and you really need to start doing some heavier lifting rather than just pass some asinine piece of legislation that penalizes restaurants and eaters.

“If there’s E. coli present in your hamburgers, you can legislate to cook that burger to death, and you’re moving to make food more mediocre in a way. But anything that’s handled by the same person who touched the meat before it went on the grill to become incinerated, anything else they come into contact with still stands the chance of becoming contaminated.

“… E. coli is everywhere. The real problem with it now is that producers feed their cattle things they shouldn’t eat, like corn, for example, that promotes excessive E. coli production. But the other thing that has implications for the future of humanity, really, is that these farm animals are getting subtherapeutic antibiotics, and that’s building up strains of antibiotic-resistant super-bacteria.”

Such fantasies are endemic in the food porn industry, where people pay more for less. Shiga-toxin producing E. coli, like the O157:H7 strain, occur naturally in ruminants, and there are hundreds of outbreaks to document this.

Any chef or self-proclaimed food activist that relies on the 1998 Cornell study that linked corn consumption in cattle to E. coli production to satiate their own conspiracy theories ain’t serving food to me or my kids.

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

Posted on April 2, 2012 by Douglas Powell

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.

UK farmer fears roosting starlings may cause salmonella in dairy calves, milk

Posted on December 12, 2011 by Douglas Powell

The Brits love their birds.

But not so for a dairy farmer from the Somerset Levels who told BBC News
that roosting starlings and their salmonella-laden poop contaminating feed has led to the loss of 40 calves and is costing his business up to £40,000 a year.

He fears the droppings may also result in salmonella in his cattle’s dairy milk.

Thousands of starlings migrate from Baltic countries, such as Russia, to Somerset and other parts of the UK over the winter months.

In recent years their murmurations as they prepare to roost have become a major attraction for wildlife enthusiasts.

RSPB spokesman, Graham Madge, said, "The fact that starlings are visiting Somerset are not because the RSPB are encouraging them, it’s basically because these birds can find plenty of food in areas that are relatively warm for the winter.”

More on frozen mice as reptile food; first outbreak linked to MiceDirect started in Aug. 2008 in U.K.; over 400 now sick

Posted on July 30, 2010 by Douglas Powell

“I never thought that a mouse could have salmonella. It just never entered my mind.”

So says Steve Gilfillan, 51, a deputy sheriff in Council Bluffs, Iowa, who, according to the New York Times this morning, keeps “a couple hundred” garter snakes in several neat rows of roomy enclosures in his basement. The snakes, he said, are like part of the family, which leads to a certain familiarity.

“As far as precautions, I don’t know,” said Mr. Gilfillan, adding his three children helped feed and care for his pets. “Snakes got to eat and snakes got to poop and you got to clean it up. It’s just the nature of keeping them.”

More than 400 people, many of them snake owners or their children, in the United States and Britain, have been sickened by salmonella outbreaks, all traced to frozen mice sold over the Internet as food for exotic pets by a small Georgia company called MiceDirect.

The company announced this week a recall involving millions of frozen mice and said that it would begin irradiating future shipments to kill infectious bacteria.

MiceDirect also recalled frozen rats and baby chickens used as pet food by reptile fanciers, although those products had not been linked to the salmonella outbreaks.

Health officials said that owners of reptiles should be mindful that such pets, including snakes and turtles, often carry salmonella and have been the cause of outbreaks in the past. Rodents carry similar risks, whether kept as pets or used as food for other animals.

Snakes can become infected after eating tainted mice, although the snakes may show no signs of illness, said Dr. Casey Barton Behravesh, a veterinarian and epidemiologist with the Centers for Disease Control and Prevention. Snake owners can become sick from handling the frozen or thawed mice, handling infected snakes or cleaning feces from an enclosure.

Mr. Gilfillan and many other snake owners thaw mice to serving temperature in warm water. Dr. Barton Behravesh said people should not use a microwave oven, because the bacteria could spread to other food.

She also said that mice and reptiles should be kept out of the kitchen and away from areas where food is served. Reptile cages should not be cleaned in the kitchen sink, she said, and mice should not be kept in a freezer with food for humans.

And she said that reptile owners should wash their hands thoroughly after handling their pets or the rodents the pets eat.

The first salmonella outbreak linked to MiceDirect began in Great Britain in August 2008. Since then, more than 400 people have fallen ill there, about two-thirds of them have been children under 10, according to Chris Lane, a senior epidemiologist of the Health Protection Agency’s Center for Infections in London. Although the shipments of tainted mice were halted last year, people continue to get sick there, Mr. Lane said.

The first case in the United States appeared in January 2010, according Dr. Barton Behravesh. The C.D.C. has identified more than 30 cases in 17 states with the same strain as the British outbreak. She said the cases were not concentrated in one region but spread across the country. Half the victims were under 12.
Accounts from both sides of the Atlantic suggest that American authorities were slow to react to indications of a problem.

British investigators looking into the outbreak found that many of the victims came from families where snakes were kept as pets. They eventually began looking at the frozen mice fed to the snakes and found shipments from MiceDirect that contained the same strain of salmonella as that isolated from the victims.

British officials contacted MiceDirect, Mr. Lane said, and the company promised to act to prevent further contamination.

On July 21, 2010, the F.D.A. told the company that tests of its products and plant had found salmonella. Two days later, the agency said, MiceDirect agreed to a recall.

But the recall effort has been haphazard. The company’s recall notice was not prominently posted on its Web site until Thursday. And neither the company’s site nor the F.D.A.’s site gave clear instructions on what to do with mice that customers still had.

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