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Food Safety Lawyer Bill Marler to Speak at International Association for Food Protection 2014 Meeting in Indianapolis

The Seattle food safety attorney will discuss the infamous Jack in the Box E. coli case and how it changed the way we look at food safety

WHO: Bill Marler of Marler Clark, LLP is an accomplished personal injury and products liability attorney. He began litigating foodborne illness cases in 1993, when he represented Brianne Kiner, the most seriously injured survivor of the Jack in the Box E. coli O157:H7 outbreak.

Marler settled Brianne’s case for $15.6 million, creating a Washington state record for an individual personal injury action. He settled several other Jack in the Box E. coli outbreak cases for more than $1.5 million each.

At IAFP 2014, Marler will walk through the history of the Jack in the Box outbreak and how this terrible tragedy led to necessary changes in food safety – from supply to preparation.

WHAT: Opening Session Lecture – 20 Years Later, Where Were We, Where are We and Where are We Going? at The International Association for Food Protection (IAFP) Annual Meeting, which in 2014 is in Indianapolis, Indiana at the Indiana Convention Center.

WHEN: Sunday, April 3, 2014 from 6:00 PM

WHERE: 500 Ballroom (Indiana Convention Center)

The 1992–1993 Jack in the Box E. coli O157:H7 outbreak was one of the biggest outbreaks in the beef and restaurant industry. The story of Brianne Kiner, the most seriously injured survivor, and how Bill Marler came to represent her is recounted in the nonfiction novel Poisoned by Jeff Benedict.

“It is a privilege to speak at the IAFP and be given a chance to honor those who were sickened and those who died in the outbreak,” said Marler. At the Opening Session Lecture, Marler will also recognize the major breakthroughs over the past 20 years that have occurred in academics, government, and industry, in trying to make our food supply safer.

For media wishing to speak with Bill Marler, please contact Ginger Vaughan (ginger@quinnbrein.com) or Sam Jones (sam@quinnbrein.com) or call 206-842-8922. Also contact us if you would like to attend the conference as Marler’s guest.

Canada Offers Botulism Warnings

What is Infant Botulism?

Infant botulism is a very rare but serious form of illness that can affect children up to one year. It is caused by a bacterium called Clostridium botulinum. This bacteria forms “spores” that when swallowed may grow and produce a poison in the baby’s intestine.

C. botulinum can be found in both pasteurized and unpasteurized honey. Therefore, it is very important to never feed honey to a child under the age of one. As the spores are not easily destroyed by heat (for example by cooking or boiling), it should also not be added to infants’ food as a sweetener. C. botulinum can also be found in soil and dust.

What you should do?

–  Don’t give honey to infants younger than one year of age
–  Don’t add honey to their formula, food or water
–  Don’t put honey on their soother

Older children (more than one year old) can safely eat honey

Signs and Symptoms of Infant Botulism

Constipation is often the first sign of infant botulism that parents notice (although many other illnesses also can cause constipation). Contact your health care provider if your baby hasn’t had a bowel movement for several days.  Other symptoms can include:

–  weakness and/or lack of energy
–  too weak to cry or suck as usual
–  wobbly head because the neck is weak
–  lacks facial expression
–  weak arms and legs
–  has trouble breathing
–  unable to swallow

Botulism:  Marler Clark, The Food Safety Law Firm, is the nation’s leading law firm representing victims of Botulism outbreaks. The Botulism lawyers of Marler Clark have represented thousands of victims of Botulism and other foodborne illness outbreaks and have recovered over $600 million for clients.  Marler Clark is the only law firm in the nation with a practice focused exclusively on foodborne illness litigation.  Our Botulism lawyers have litigated Botulism cases stemming from outbreaks traced to carrot juice and chili.

If you or a family member became ill with Botulism after consuming food and you’re interested in pursuing a legal claim, contact the Marler Clark Botulism attorneys for a free case evaluation.

Who audits the auditors? How rockmelons can turn deadly

96% and a stellar audit rating did not stop a US rockmelon farm from selling contaminated melons that killed 33 people. How much responsibility should the auditor bear?

In 2011, whole rockmelons contaminated with Listeria monocytogenes sickened 147 and killed 33 people in the US. The rockmelons were traced to Jensen Farms in south-eastern Colorado. The two brothers who owned the farm were indicted with six federal misdemeanor charges for “introducing adulterated food into interstate commerce”. They each faced up to six years in prison plus up to US$1.5 million in fines.

After seeing their farm forced into bankruptcy, Eric and Ryan Jensen have just been sentenced with each receiving five years’ probation, six months of home detention and $150,000 each in restitution fees to victims. Victim families have already received $3.8 million from the Jensens’ insurance policy.

Now consumers have every right to expect that the rockmelon they purchase from the supermarket will not kill them and will not make them sick. But where does responsibility lie for this contamination disaster?

Prior to this case there is no record of whole, unprocessed rockmelons causing sickness. Then there is the matter of auditing.

The Jensen brothers moved their rockmelons through the distributor Frontera Produce to retailers including Walmart and Kroger. Apparently Frontera “required” the farm to be audited by PrimusLabs, a California-based food-safety consultant that provides “internationally recognized audits” for food producers such as Jensen Farms.

Jensen Farms contracted with PrimusLabs for an audit of both its farmlands and its packing house. PrimusLabs then hired a subcontractor, Bio Food Safety, to conduct the actual audit. Just six days before the Listeria outbreak began, Bio Food Safety’s auditor, James Dilorio, gave Jensen Farms 96/100 and a “superior” rating.

There is no question that Jensen Farms was the source of the outbreak and several problem areas have been highlighted. The packing room floor had water puddles, the conveyor and washing system was difficult to clean, the melons were washed in town water without added chlorine sanitizer, the farm-warm melons were not pre-cooled before going into cold storage …

However, if you had just received 96/100 for your food safety audit would you be looking for problems?

The Jensen brothers had no intention of causing anyone any harm – they just wanted to run their farm and make a living for their families. There is no way the brothers could have been charged with murder as there was absolutely no “intention to cause harm”. If the brothers were charged with a felony they could quite justifiably plead “not guilty” and hold their audit results up as proof that they were endeavoring to do the right thing. The matter could stay before the courts for decades.

To avoid this, the brothers were charged with a misdemeanor. Unlike felony convictions, misdemeanor convictions do not require proof of fraudulent intent or even of knowing or willful conduct. All that is required is that the person held a position of responsibility such that they could have prevented the violation. There is no need to even prove that the person knew of the violation – just that they could have stopped it.

The Jensen brothers could have stopped the contamination disaster so they had absolutely no option except to plead guilty.

With the farm bankrupt and each receiving five years’ probation, six months of home detention and $150,000 in restitution fees to victims, the brothers will now be able to sue the auditors, distributor and even the retailers.

Food safety is a basic consumer right and the responsibility for this safety needs to continue through the full distribution chain.

Walmart and Kroger required audits that they knew full well would generate a glowing inspection, all the while ignoring what was there to be seen. They used their market power to squeeze the supply chain of any profit that could have been invested in food safety while covering their own backs by setting the specifications for the “fresh fruits”.

The relationship between retailers and auditor is simply a conspiracy to keep product flowing through the chain of distribution at the lowest cost and an attempt to shield retailers from responsibility for the products they sell.

If the Jensen brothers had not met “Primus Certified” standards and so been “Primus Certified” they could not have sold and distributed their rockmelons in interstate commerce through Frontera.

They would also not be pleading guilty to federal misdemeanors and 33 people would not have died.

It is very easy to say that food processors should check their auditors – but how do you do that? And what can you do when the choice of auditor is dictated by those to whom you are selling your goods?

Food safety is a basic right and it is crucial that when foodborne disease outbreaks occur they are investigated and steps are taken to ensure that the problem cannot happen again.

Reprinted with permission of http://www.foodprocessing.com.au/articles/65435-Who-audits-the-auditors-How-rockmelons-can-turn-deadly.

Michigan Salmonella Outbreak Linked to Pints and Quarts Pub and Grill or C.F. Prime Chophouse & Wine Bar

Public Health Muskegon County is nearing the conclusion of the investigation of an outbreak of Salmonella that has sickened at least 29 people (25 Muskegon County, 4 Ottawa County). Laboratory testing revealed that most cases were caused by Salmonella Enteritidis, a common type of Salmonella associated most often with eggs and poultry. Those sickened had in common a history of consuming meals containing chicken and/or lettuce at Pints and Quarts Pub and Grill or C.F. Prime Chophouse & Wine Bar, which share the same kitchen, in Roosevelt Park between Oct. 30 and Nov. 2, 2013.

“We conducted over 100 interviews with food service workers, restaurant patrons, and others,” explained Ken Kraus, Director of Public Health Muskegon County. “We spoke with those who were ill as well as those who did not get sick to gather as much information as possible about what may have happened during this 4-day period.”

In addition to conducting interviews and gathering food consumption histories, all food-borne illness outbreaks include reviewing food handling processes, exploring the possibility of food cross contamination as well as checking food supply sources.

Human E. coli O157:H7 Illnesses Reduced 50% to 85% with Cattle Vaccine

The University of Glasgow reported today:

Vaccinating cattle against the E. coli O157 bacterium could cut the number of human cases of the disease by 85%, according to scientists.

The bacteria, which cause severe gastrointestinal illness and even death in humans, are spread by consuming contaminated food and water, or by contact with livestock faeces in the environment. Cattle are the main reservoir for the bacterium.

The vaccines that are available for cattle are rarely used, but could be significant.

The research was lead by a team of researchers at the University of Glasgow in collaboration with the University of Edinburgh, the Royal Veterinary College, Scotland’s Rural College, Health Protection Scotland, and the Scottish E. coli O157/VTEC Reference Laboratory.

The study, published in the online journal PNAS, used veterinary, human and molecular data to examine the risks of E. coli O157 transmission from cattle to humans, and to estimate the impact of vaccinating cattle.

The risk of E. coli O157 infection is particularly significant when the cattle are ‘super-shedding’ – excreting extremely high numbers of bacteria in their faeces for a limited period of time. Vaccines against the bacteria exist that can reduce super-shedding.

As a consequence, the researchers predict that vaccinating cattle could reduce human cases by nearly 85 percent, far higher than the 50 percent predicted by studies simply looking at the efficacy of current vaccines in cattle.

These figures provide strong support for the adoption of vaccines by the livestock industry, and work is now underway to establish the economic basis for such a programme of vaccination. In addition, research is continuing in Scotland by the same collaborative grouping to develop even more effective vaccines that would further reduce the impact on human disease.

Lead author, Dr Louise Matthews, Senior Research Fellow in the Institute of Biodiversity, Animal Health and Comparative Medicine, said: “E. coli O157 is a serious gastrointestinal illness. The economic impact is also serious – for instance studies in the US suggest that healthcare, lost productivity and food product recalls due to E. coli O157 can cost hundreds of millions of dollars each year.

“Treating cattle in order to reduce the number of human cases certainly makes sense from a human health perspective and, while more work is needed to calculate the cost of a vaccination programme, the public health justification must be taken seriously.”

In Scotland, an average of 235 culture positive cases of E. coli O157 infection per year (i.e. people who had the organism in their stools) were notified to Health Protection Scotland from 2008 to 2012.

The vaccines that are available currently have poor take-up: one version in the US is not fully licensed because medicines for veterinary use must show that animal health is improved. This is problematic because E. coli O157 does not harm cattle and assessing the impact of treatment involves coordination between human and veterinary health practitioners.

Senior author Professor Stuart Reid of the Royal Veterinary College added: “We increasingly recognise the fact that we share a common environment with the animals we keep – and inevitably the pathogens they harbour. This study is an excellent example the interface between veterinary and human medicine and of the concept of ‘One Health’ in action – controlling infections in animals can have a major impact on public health.”

One year ago Kansas State reported:

A commercial vaccine for cattle can effectively reduce levels of E. coli by more than 50 percent, a Kansas State University study has found. The vaccine is also effective using two doses instead of the recommended three doses, which can help cut costs for the beef industry.

David Renter, associate professor of epidemiology, is the principal investigator on a project that researched the effectiveness of products used to prevent the shedding of E. coli O157:H7 in cattle. The research appears in a recent online version of the journal Vaccine and helps improve current preventative methods for addressing food safety concerns.

While E. coli O157:H7 does not affect cattle, it causes foodborne disease in humans. Vaccines and other products may be given to cattle to help prevent the spread of the bacteria.

“We wanted to test how well these products work to control E. coli O157:H7 in a commercial feedlot with a large population of cattle that were fed in the summer and may be expected to have a high level of E. coli O157:H7,” Renter said.

Other Kansas State University researchers involved include T.G. Nagaraja, university distinguished professor of microbiology; Nora Bello, assistant professor of statistics; Charley Cull, doctoral student in pathobiology, Oakland, Neb.; and Zachary Paddock, doctoral student in pathobiology, Manhattan, Kan. Abram Babcock, an August 2010 Kansas State University doctoral graduate, also was involved in the research.

Using a commercial feedlot setting, the researchers studied more than 17,000 cattle during an 85-day period. They studied two products: a vaccine and a low-dose direct-fed microbial.

“What’s unique about this study is the number of animals we used, the research setting and that we used commercial products in the way that any cattle producer could use them,” Renter said. “We didn’t want it to be any different than the way somebody would use the products in a commercial feedlot.”

The researchers found that the vaccine reduced the number of cattle that were shedding E. coli O157:H7 in feces by more than 50 percent. E. coli shedding was reduced by more than 75 percent among cattle that were high shedders of E. coli. While the vaccine label suggests that it is given in three doses, the researchers found that two doses of the vaccine significantly reduced E. coli.

“Showing that level of efficacy with two doses is really important because a shift to two doses from three could significantly cut costs for the beef industry,” Renter said. “In terms of logistics, it can be difficult for commercial feedlot production systems to vaccinate animals three times. Both of these benefits help when considering how the vaccine can be adopted and implemented in the industry.”

The researchers also discovered that the low-dose direct-fed microbial product did not work as well as the vaccine. Renter said while the study used a lower dose of the direct-fed microbial and could find no evidence that it reduced E. coli shredding, it is possible that the direct-fed microbial product is more effective at a higher dose.

“This vaccine is an option for reducing E. coli,” Renter said. “We have shown that this vaccine works and that it is a tool that could be adopted in the industry.”

Westside Market – Marler Clark Calls for Hepatitis A Vaccinations for All Foodservice Workers – Again

New Yorkers are again being urged to stand in line and get Hepatitis A vaccines or Immune Globulin (Ig) shots to prevent the infection and further spread of hepatitis A after being exposed to a hepatitis A infected foodservice worker – this time at the Westside Market.

Hardly a month passes without a warning from a health department somewhere that an infected food handler is the source of yet another potential hepatitis A outbreak. Absent vaccinations of food handlers, combined with an effective and rigorous hand washing policy, there will continue to be more hepatitis A outbreaks. It is time for health departments across the country to require vaccinations of foodservice workers, especially those that serve the very young and the elderly.

Hepatitis A is a communicable disease that spreads from person-to-person. It is spread almost exclusively through fecal-oral contact, generally from person-to-person, or via contaminated food or water. Hepatitis A is the only foodborne illness that is vaccine preventable.  According to the Centers for Disease Control and Prevention (CDC), since the inception of the vaccine, rates of infection have declined 92 percent.

The Centers for Disease Control (CDC) estimate that 83,000 cases of hepatitis A occur in the United States every year, and that many of these cases are related to food-borne transmission. In 1999, over 10,000 people were hospitalized due to hepatitis A infections and 83 people died. In 2003, 650 people became sickened, 4 died and nearly 10,000 people got Ig shots after eating at a Pennsylvania restaurant. Not only do customers get sick, but also businesses lose customers or some simply go out of business.

Although the CDC has not yet called for mandatory vaccination of foodservice workers, it has repeatedly pointed out that the consumption of worker-contaminated food is a major cause of food-borne illness in the United States.

Hepatitis A continues to be one of the most frequently reported, vaccine-preventable diseases in the United States, despite the FDA-approval of hepatitis A vaccine in 1995. Widespread vaccination of appropriate susceptible populations would substantially lower disease incidence and potentially eliminate indigenous transmission of hepatitis A infections. Vaccinations cost about $50. The major economic reason that these preventative shots have not been used is because of the high turnover rate of foodservice employees. Eating out becomes a whole lot less of a gamble, if all foodservice workers faced the same requirement.

According to the CDC, the costs associated with hepatitis A are substantial. Between 11% and 22% of persons who have hepatitis A are hospitalized. Adults who become ill lose an average of 27 days of work. Health departments incur substantial costs in providing post-exposure prophylaxis to an average of 11 contacts per case. Average costs (direct and indirect) of hepatitis A range from $1,817 to $2,459 per case for adults and from $433 to $1,492 per case for children less than 18 years of age. In 1989, the estimated annual direct and indirect costs of hepatitis A in the United States were more than $200 million, equivalent to more than $300 million in 1997 dollars.  A new CDC report shows in 2010 just over 10 percent of people between the ages of 19 and 49 years old got a Hepatitis A shot.

Hepatitis A:  Marler Clark, The Food Safety Law Firm, is the nation’s leading law firm representing victims of Hepatitis A outbreaks. The Hepatitis A lawyers of Marler Clark have represented thousands of victims of Hepatitis A and other foodborne illness outbreaks and have recovered over $600 million for clients.  Marler Clark is the only law firm in the nation with a practice focused exclusively on foodborne illness litigation.  Our Hepatitis A lawyers have litigated Hepatitis A cases stemming from outbreaks traced to a variety of sources, such as green onions, lettuce and restaurant food.  The law firm has brought Hepatitis A lawsuits against such companies as Subway, McDonald’s, Chipotle, Quiznos, Chi-Chi’s and Carl’s Jr.

NYC HEALTH DEPARTMENT WARNS PATRONS OF AN UPPER WEST SIDE MARKET AT 97TH AND BROADWAY OF POSSIBLE EXPOSURE TO HEPATITIS A FROM AUGUST 9th TO AUGUST 22nd

Customers who ate Chopped, Ready-to-Eat Fruit from the Westside Market (2589 Broadway btwn. 97th and 98th) Between Those Dates Should Get Hepatitis A Vaccine as a Precautionary Measure

No Current Reports of Hepatitis A in Customers

August 22, 2013 – In response to a case of hepatitis A in a food handler at Westside Market located at 2589 Broadway between 97th and 98th street, on the Upper West Side, the Health Department is urging patrons who ate chopped, ready-to-eat fruit either in-store, through catering or delivery between August 9th and August 22nd to get hepatitis A vaccination as a precautionary measure. Fruits involved include those packaged in plastic containers and sold in the refrigerated case immediately to the left as you enter the store and includes watermelon cut into halves and quarters; peeled whole pineapples; and shelled and cut coconut. Hepatitis A is spread by eating food (even though it might look clean) that has been contaminated with traces of fecal matter from an infected person. Symptoms include jaundice (yellowing of eyes and skin), fatigue, abdominal pain, nausea, and diarrhea. People typically develop symptoms of hepatitis A

infection about one month (range is 15 to 50 days) after they are exposed to the virus. However, if people are vaccinated within 14 days of exposure, it can prevent the disease from occurring.

Any person who ate chopped, ready-to-eat fruit from the Westside Market either in-store, through catering or delivery from August 9th to August 22nd is considered at risk and is recommended to receive a preventive vaccine. The Health Department has already worked with the store to ensure all of the remaining ready-to-eat fruit with expiration dates within the at-risk time period have been destroyed.

The Westside Market is cooperating fully with the Health Department, and estimates that it sells approximately 100 ready-to-eat fruit containers per day.

People can visit their regular doctor to receive this shot. The Health Department will offer free hepatitis A vaccinations starting tomorrow at MS 258: Community Action School located at 154 West 93rd Street New York, NY 10025 at the following times:

Friday, August 23: 2pm – 8pm Saturday, August 24: 10am – 2pm Sunday, August 25: 2pm – 6pm

Monday, August 26: 2pm – 8pm

*(Those with insurance, please bring your insurance card with you)

People who were exposed but have already received two doses of hepatitis A vaccine sometime in their life do not need another shot; all others should be vaccinated. Pregnant women are urged to consult with their doctor to discuss whether to receive vaccine or a different preventive treatment.

“We are asking these store patrons to get this vaccination as a precautionary measure,” said Health Commissioner Dr. Thomas Farley. “If people experience symptoms, they should see a doctor immediately. This incident serves as an important reminder to always wash your hands thoroughly to prevent the spread of disease.”

About Hepatitis

Hepatitis type A is a liver disease caused by a virus. It is spread from person to person by putting something in the mouth (even though it might look clean) that has been contaminated with traces of fecal matter from an infected person. There are no special medicines or antibiotics that can be used to treat a person once the symptoms appear. While some people who have chronic liver disease or a weakened immune system could experience more severe illness and require hospitalization, hepatitis A is rarely fatal (fewer than 1% of cases).

In order for the vaccine to be most effective, people who have been exposed to hepatitis A should be vaccinated within 14 days. The earlier the vaccine is given, the more effective it is in preventing the disease.

About the Investigation

The Health Department investigates all cases of hepatitis A in New York City. The Department was notified of this case on August 21, began the investigation, and inspected today. An average of 65 cases of hepatitis A occur in New York City each year, with 1-2 occurring in food handlers.

If you would like vaccination location and hours or incident updates sent directly to your phone, you may text HEPA to 877877.

Tracking Twitter may enhance monitoring of food safety at restaurants

A new system could tell you how likely it is for you to become ill if you visit a particular restaurant by ‘listening’ to the tweets from other restaurant patrons.

The University of Rochester researchers say their system, nEmesis, can help people make more informed decisions, and it also has the potential to complement traditional public health methods for monitoring food safety, such as restaurant inspections. For example, it could enable what they call “adaptive inspections,” inspections guided in part by the real-time information that nEmesis provides.

The system combines machine-learning and crowdsourcing techniques to analyze millions of tweets to find people reporting food poisoning symptoms following a restaurant visit. This volume of tweets would be impossible to analyze manually, the researchers note. Over a four-month period, the system collected 3.8 million tweets from more than 94,000 unique users in New York City, traced 23,000 restaurant visitors, and found 480 reports of likely food poisoning. They also found they correlate fairly well with public inspection data by the local health department, as the researchers describe in a paper to be presented at the Conference on Human Computation & Crowdsourcing in Palm Springs, Calif., in November.

The system ranks restaurants according to how likely it is for someone to become ill after visiting that restaurant.

“The Twitter reports are not an exact indicator – any individual case could well be due to factors unrelated to the restaurant meal – but in aggregate the numbers are revealing,” said Henry Kautz, chair of the computer science department at the University of Rochester and co-author of the paper. In other words, a “seemingly random collection of online rants becomes an actionable alert,” according to Kautz, which can help detect cases of foodborne illness in a timely manner.

nEmesis “listens” to relevant public tweets and detects restaurant visits by matching up where a person tweets from and the known locations of restaurants. People will often tweet from their phones or other mobile devices, which are GPS enabled. This means that tweets can be “geotagged”: the tweet not only provides information in the 140 characters allowed, but also about where the user was at the time.

If a user tweets from a location that is determined to be a restaurant (by using the locations of 24,904 restaurants that had been visited by the Department of Health and Mental Hygiene in New York City), the system will continue to track this person’s tweets for 72 hours, even when they’re not geotagged, or when they are tweeted from a different device. If a user then tweets about feeling ill, the system captures the information that this person is now ill and had visited a specific restaurant.

The correlation between the Twitter data and the public inspection data means that about one third of the inspection scores could be reliably predicted from the Twitter data. The remainder of the scores show some disagreement. “This disagreement is interesting as the public inspection data is not perfect either,” argued co-author Adam Sadilek, formerly a colleague of Kautz at Rochester and who is now at Google. “The adaptive inspections could reveal the real risk, which is currently hidden for both methods.”

This work builds on earlier work by Kautz and Sadilek that used Twitter to find out how likely a specific user was to have flu-like symptoms, and also to find the influence of different lifestyle factors on health. At the heart of all this work is the algorithm that Sadilek developed to distinguish between tweets that suggest a person tweeting is sick and those that don’t. This algorithm is based on machine-learning, or as Sadilek described it, “it’s like teaching a baby a new language,” only in this case it’s a computational algorithm that is being taught.

In their new system, nEmesis, they brought in an extra layer of complexity to improve the algorithm; they used crowdsourcing. For any one person, it would be exhausting and time-consuming to look through thousands of tweets to categorize them. The end results might not even be very accurate if their judgment is not quite right.

Instead the researchers turned to Amazon’s Mechanical Turk system to reach out to a crowd of readily available workers. These were paid small amounts of money to categorize some tweets that could then be used to train the algorithm. They ensured the pool of tweets they were going use was of high accuracy by having more than one worker look at each tweet and incentivizing the right answer by paying the workers when their answer agreed with that of the majority and deducting money when it didn’t. The algorithm was then able to learn from the training samples how to spot tweets that show people that are likely to have foodborne illnesses.

Of course, the system only considers people who tweet, who might not even be a representative sample of the whole population or of the population visiting a restaurant. But the Twitter data can be used together with knowledge gained from other sources to detect foodborne illness in a timely manner. It provides an extra layer – a passive level of monitoring – which is cost-effective. And the information that nEmesis offers can benefit both Twitter and non-Twitter users.

Rochester researchers Sean Brennan, graduate student, and Vincent Silenzio, associate professor of psychiatry, are also both part of the team that worked on nEmesis.

Everything You Never Wanted to Know About Listeria, But Need To

An Introduction to Listeria

Listeria (pronounced liss-STEER-ē-uh) is a gram-positive rod-shaped bacterium that can grow under either anaerobic (without oxygen) or aerobic (with oxygen) conditions. [4, 18] Of the six species of Listeria, only L. monocytogenes (pronounced maw-NO-site-aw-JUH-neez) causes disease in humans. [18] These bacteria multiply best at 86-98.6 degrees F (30-37 degrees C), but also multiply better than all other bacteria at refrigerator temperatures, something that allows temperature to be used as a means of differentiating Listeria from other contaminating bacteria. [18]

Called an “opportunistic pathogen,” Listeria is noted to cause an estimated 2,600 cases per year of severe invasive illness. [26] Perhaps not surprisingly then, “foodborne illness caused by Listeria monocytogenes has raised significant public health concern in the United States, Europe, and other areas of the world.” [3] As one noted expert observed, summarizing the history of these bacteria and their significance for public health,

Although L. monocytogenes was recognized as an animal pathogen over 80 years ago, the first outbreak confirming an indirect transmission from animals to humans was reported only in 1983, in Canada’s Maritime provinces. In that outbreak, cabbages, stored in the cold over the winter, were contaminated with Listeria through exposure to infected sheep manure. A subsequent outbreak in California in 1985 confirmed the role of food in disseminating listeriosis. Since then Listeria has been implicated in many outbreaks of food-borne illness, most commonly from exposure to contaminated dairy products and prepared meat products, including turkey and deli meats, pâté, hot dogs and seafood and fish. [4]

Given its widespread presence in the environment and food supply, the ingestion of Listeria has been described as an “exceedingly common occurrence.” [18]

The Incidence of Listeria Infections

Listeria bacteria are found widely in the environment in soil, including in decaying vegetation and water, and may be part of the fecal flora of a large number of mammals, including healthy human adults. [4, 18] According to the FDA, “studies suggest that 1-10% of humans may be intestinal carriers of Listeria.” [14] Another authority notes that the “organism has been isolated from the stool of approximately 5% of healthy adults.” [18] Overall, seasonal trends show a notable peak in total Listeria cases and related-deaths from July through October. [3]

Ingested by mouth, Listeria is among the most virulent foodborne pathogens, with up to 20% of clinical infections resulting in death. [3] These bacteria primarily cause severe illness and death in persons with immature or compromised immune systems. [13, 18] Consequently, most healthy adults can be exposed to Listeria with little to any risk of infection and illness. [4, 11]

A study published in 1995 projected Listeria infection-rates to the U.S. population, suggesting that an estimated 1,965 cases and 481 deaths occurred in 1989 compared with an estimated 1,092 cases and 248 deaths in 1993, a 44% and 48% reduction in illness and death, respectively. [25] In comparison, a USDA study published in 1996 estimated that there had been 1,795-1860 Listeria-related cases in 1993, and 445-510 deaths, with 85-95% of these attributable to the consumption of contaminated food. [28] Listeriosis-related mortality rates decreased annually by 10.7% from 1990 through 1996, and by 4.3% from 1996 through 2005. [3]

Among adults 50 years of age and older, infection rates were estimated to have declined from 16.2 per 1 million in 1989 to 10.2 per 1 million in 1993. [25] Perinatal disease decreased from 17.4 cases per 100,000 births in 1989 to 8.6 cases per 100,000 births in 1993. [25] Neonatal infections are often severe, with a mortality rate of 25-50%. [4]

According to the CDC’s National Center for Zoonotic, Vector-Borne, and Enteric Diseases:

Listeriosis was added to the list of nationally notifiable diseases in 2001. To improve surveillance, the Council of State and Territorial Epidemiologists has recommended that all L. monocytogenes isolates be forwarded to state public health laboratories for subtyping through the National Molecular Subtyping Network for Foodborne Disease Surveillance (PulseNet). All states have regulations requiring health care providers to report cases of listeriosis and public health officials try to interview all persons with listeriosis promptly using a standard questionnaire about high risk foods. In addition, FoodNet conducts active laboratory- and population-based surveillance. [7]

In 2006, public health officials from 48 states reported 1,270 foodborne disease outbreaks, with a confirmed or suspect source in 884 of the outbreaks (70%). [8] Only one of the outbreaks with a confirmed source was attributed to Listeria, with this outbreak involving eleven hospitalizations and one death. [8] The next year, of 17,883 lab-confirmed infections, the CDC attributed 122 to Listeria. [9] In 2009, there were 158 confirmed Listeria infections, representing an incidence-rate of .34 cases for every 100,000 persons in the United States. [10] Such data revealed an incidence-rate of 0.27 cases per 100,000 persons, a decrease of 42% compared with 1996—1998. [10] But, according to CDC’s Technical Information website, it is estimated that there are 1,600 cases of Listeria infection annually in the United States, based on data through 2008. [7]

The 2009 numbers represented a reported 30% decrease in the number of infections compared to the 1996—1998 rates of infection. [10] Although the nature and degree of underreporting is subject to dispute, all agree that the confirmed cases represent just the tip of the iceberg. [6, 13] Indeed, one study estimates the annual incidence rate for Listeria to be around 1,795-1,860 cases per 100,000 persons, with 445-510 of the cases ending in death. [28]

Finally, in a study of FoodNet laboratory-confirmed invasive cases—where infection is detected in blood, cerebrospinal fluid, amniotic fluid, placenta or products of conception—the number of listeriosis cases decreased by 24% from 1996 through 2003. [33] During this same period, pregnancy-associated disease decreased by 37%, while cases among those fifty years old and older decreased by 23%. [33]

The Prevalence of Listeria in Food and the Environment

Listeria is a common presence in nature, found widely in such places as water, soil, infected animals, human and animal feces, raw and treated sewage, leafy vegetables, effluent from poultry and meat processing facilities, decaying corn and soybeans, improperly fermented silage, and raw (unpasteurized) milk. [18, 23, 27]  Foods commonly identified as sources of Listeria infection include  improperly pasteurized fluid milk, cheeses (particularly soft-ripened varieties, such as traditional Mexican cheeses, Camembert and ricotta), ice cream, raw vegetables, fermented raw-meat sausages, raw and cooked poultry, and cooked, ready-to-eat (RTE) sliced meats—often referred to as “deli meats”. [18, 21, 23, 28] One study found that, over a five-year period of testing, in multiple processing facilities, Listeria monocytogenes was isolated from 14% of 1,080 samples of smoked finfish and smoked shellfish. [16]

Ready-to-eats foods have been found to be a notable and consistent source of Listeria. [14, 21] For example, a research-study done by the Listeria Study Group found that Listeria monocytogenes grew from at least one food specimen in the refrigerators of  64% of persons with a confirmed Listeria infection (79 of 123 patients), and in 11% of more than 2000 food specimens collected in the study. [21] Moreover, 33% of refrigerators (26 of 79) contained foods that grew the same strain with which the individual had been infected, a frequency much higher than would be expected by chance. [21] A widely cited USDA study that reviewed the available literature also summarized that:

In samples of uncooked meat and poultry from seven countries, up to 70 percent had detectable levels of Listeria [13].  Schuchat [23] found that 32 percent of the 165 culture-confirmed listeriosis cases could be attributed to eating food purchased from store delicatessen counters or soft cheeses.  In Pinner [21] microbiologic survey of refrigerated foods specimens obtained from households with listeriosis patients, 36 percent of the beef samples and 31 percent of the poultry samples were contaminated with Listeria.

The prevalence of Listeria in ready-to-eat meats has not proven difficult to explain. [26, 29] As one expert in another much-cited article has noted:

The centralized production of prepared ready-to-eat food products…increases the risk of higher levels of contamination, since it requires that foods be stored for long periods at refrigerated temperatures that favour the growth of Listeria. During the preparation, transportation and storage of prepared foods, the organism can multiply to reach a threshold needed to cause infection. [4]

The danger posed by the risk of Listeria in ready-to-eat meats has prompted the USDA to declare the bacterium an adulterant in these kinds of meat products and, as a result, to adopt a zero-tolerance policy for the presence of this deadly pathogen. [7, 29]

A USDA Baseline Data Collection Program done in 1994 documented Listeria contamination on 15.0% of broiler-chicken carcasses [30]. Subsequent USDA data-collection did not test for the prevalence of Listeria in chicken or in turkeys. [31, 32]

Transmission and Infection

Except for the transmission of mother to fetus, human-to-human transmission of Listeria is not known to occur. [18] Infection is caused almost exclusively by the ingestion of the bacteria, most often through the consumption of contaminated food. [18, 21, 23] The most widely-accepted estimate of foodborne transmission is 85-95% of all Listeria cases. [23, 28]

The infective dose—that is, the amount of bacteria that must be ingested to cause illness—is not known. [4, 18, 26] In an otherwise healthy person, an extremely large number of Listeria bacteria must be ingested to cause illness—estimated to be somewhere between 10–100 million viable bacteria (or colony forming units “CFU”) in healthy individuals, and only 0.1–10 million CFU in people at high risk of infection. [4, 18, 26] Even with such a dose, a healthy individual will suffer only a fever, diarrhea, and related gastrointestinal symptoms. [4, 18].

The amount of time from infection to the onset of symptoms—typically referred to as the incubation period—can vary to a significant degree.  Symptoms of Listeria infection can develop at any time from 2 to 70 days after eating contaminated food. [4, 5] According to one authoritative text,

The incubation period for invasive illness is not well established, but evidence from a few cases related to specific ingestions points to 11 to 70 days, with a mean of 31 days. In one report, two pregnant women whose only common exposure was attendance at a party developed Listeria bacteremia with the same uncommon enzyme type; incubation periods for illness were 19 and 23 days. [18]

Adults can get listeriosis by eating food contaminated with Listeria, but babies can be born with listeriosis if their mothers eat contaminated food during pregnancy. [4, 24] The mode of transmission of Listeria to the fetus is either transplacental via the maternal blood stream or ascending from a colonized genital tract. [24] Infections during pregnancy can cause premature delivery, miscarriage, stillbirth, or serious health problems for the newborn. [18, 24]

Incidence of Listeria infection in HIV-positive individuals is higher than in the general population. [17, 18] One study found that:

The estimated incidence of listeriosis among HIV-infected patients in metropolitan Atlanta was 52 cases per 100,000 patients per year, and among patients with AIDS it was 115 cases per 100,000 patients per year, rates 65–145 times higher than those among the general population. HIV-associated cases occurred in adults who were 29–62 years of age and in postnatal infants who were 2 and 6 months of age. [17]

Pregnant women make up around 30% of all infection cases, while accounting for 60% of cases involving the 10- to 40-year age group. [18]

Those Most Susceptible to Infection

Several segments of the population are at increased risk and need to be informed so that proper precautions can be taken. [19,20, 27] The body’s defense against Listeria is called “cell-mediated immunity” because the success of defending against infection depends on our cells (as opposed to our antibodies), especially lymphocytes called “T-cells.” [12] Therefore, individuals whose cell-mediated immunity is suppressed are more susceptible to the devastating effects of listeriosis, including especially HIV-infected individuals, who have been found to have a Listeria-related mortality of 29%. [12, 17, 18]

Pregnant women naturally have a depressed cell-mediated immune system. [18, 24] In addition, the immune systems of fetuses and newborns are very immature and are extremely susceptible to these types of infections. [24] Other adults, especially transplant recipients and lymphoma patients, are given necessary therapies with the specific intent of depressing T-cells, and these individuals become especially susceptible to Listeria as well. [7, 18, 27]

According to the CDC and other public health organizations, individuals at increased risk for being infected and becoming seriously ill with Listeria include the following groups:

  • Pregnant women: They are about 20 times more likely than other healthy adults to get listeriosis. About one-third of listeriosis cases happen during pregnancy.
  • Newborns: Newborns rather than the pregnant women themselves suffer the serious effects of infection in pregnancy.
  • Persons with weakened immune systems
  • Persons with cancer, diabetes, or kidney disease
  • Persons with AIDS: They are almost 300 times more likely to get listeriosis than people with normal immune systems.
  • Persons who take glucocorticosteroid medications (such as cortisone)
  • The elderly [11, 20, 21]

Symptoms of Listeria infection

When a person is infected and develops symptoms of Listeria infection, the resulting illness is called listeriosis. [4, 11, 18] Only a small percentage of persons who ingest Listeria fall ill or develop symptoms. [18] For those who do develop symptoms as a result of their infection, the resulting illness is either mild or quite severe—sometimes referred to as a “bimodal distribution of severity.” [13, 28]

On the mild end of the spectrum, listeriosis usually consists of the sudden onset of fever, chills, severe headache, vomiting, and other influenza-type symptoms. [18, 28]  Along these same lines, the CDC notes that infected individuals may develop fever, muscle aches, and sometimes gastrointestinal symptoms such as nausea or diarrhea. [11] When present, the diarrhea usually lasts 1-4 days (with 42 hours being average), with 12 bowel movements per day at its worst. [18]

Most healthy adults and children who consume contaminated food experience only mild to moderate symptoms. The infection is usually self-limited, since, in healthy hosts, exposure to Listeria stimulates the production of tumour necrosis factor and other cytokines, which activate monocytes and macrophages to eradicate the organism.  Few people with normal immune function go on to have more severe, life-threatening forms of listeriosis, characterized by septic shock, meningitis and encephalitis. [4]

As already noted, when pregnant, women have a mildly impaired immune system that makes them susceptible to Listeria infection. [19] If infected, the illness appears as an acute fever, muscle pain, backache, and headache. [18, 24] Illness usually occurs in the third trimester, which is when immunity is at its lowest. [18] Infection during pregnancy can lead to premature labor, miscarriage, infection of the newborn, or even stillbirth. [24, 28] Twenty-two percent of such infections result in stillbirth or neonatal death. [18]

Newborns may present clinically with early-onset (less than 7 days) or late-onset forms of infection (7 or more days). [3] Those with the early-onset form are often diagnosed in the first 24 hours of life with sepsis (infection in the blood). [3, 18] Early-onset listeriosis is most often acquired through trans-placental transmission. [18, 24] Late-onset neonatal listeriosis is less common than the early-onset form. [4, 18, 24] Clinical symptoms may be subtle and include irritability, fever and poor feeding. [24] The mode of acquisition of late-onset listeriosis is poorly understood. [18, 24]

Diagnosis and Treatment of Listeria Infections

Because there are few symtpoms that are unique to listeriosis, doctors must consider a variety of potential causes for infection, including viral infections (like flu), and other bacterial infections that may cause sepsis or meningitis. [4, 18, 19]

Early diagnosis and treatment of listeriosis in high-risk patients is critical, since the outcome of untreated infection can be devastating. This is especially true for pregnant women because of the increased risk of spontaneous abortion and preterm delivery. Depending on the risk group, rates of death from listeriosis range from 10% to 50%, with the highest rate among newborns in the first week of life. [4]

Methods typically used to identify diarrhea-causing bacteria in stool cultures interfere or limit the growth of Listeria, making it less likely to be identified and isolated for further testing. [18] On the other hand, routine methods are effective for isolating Listeria from spinal fluid, blood, and joint fluid. [4, 18] Magnetic-resonance imaging (MRI) is used to confirm or rule out brain or brain stem involvement. [18]

Listeriosis is usually a self-limited illness—which means that a majority of infected individuals will improve without the need for medical care. [4, 11, 14, 18] But for those patients with a high fever, a stool culture and antibiotic-treatment may be justified for otherwise healthy individuals. [4, 18] Although there have been no studies done to determine what drugs or treatment duration is best, ampicillin is generally considered the “preferred agent.” [18] There is no consensus on the best approach for patients who are allergic to penicillins.[18]

Invasive infections with Listeria can be treated with antibiotics. [18] When infection occurs during pregnancy, antibiotics given promptly to the pregnant woman can often prevent infection of the fetus or newborn. [18, 24] Babies with listeriosis receive the same antibiotics as adults, although a combination of antibiotics is often used until physicians are certain of the diagnosis.

Complications of Listeria infection

For those persons who suffer a Listeria infection that does not resolve on its own, the complications (or sequelae) can be many. [4, 28] The most common is septicemia (bacterial pathogens in the blood, also known as bacteremia), with meningitis being the second most common. [4, 18] Other complications can include inflammation of the brain or brain stem (encephalitis), brain abscess, inflammation of the heart-membrane (endocarditis), and localized infection, either internally or of the skin. [18]

Death is the most severe consequence of listeriosis, and it is tragically common. [3] For example, based on 2009 FoodNet surveillance data, 89.2% of Listeria patients ended up in the hospital, the highest hospitalization rate for pathogenic bacterial infection. [10] In persons 50 years of age and older, there was a 17.5% fatality rate—also the highest relative to other pathogens. [10, 18]

The Economic Impact of Listeria Infections

The USDA Economic Research Service (ERS) published its first comprehensive cost estimates for sixteen foodborne bacterial pathogens in 1989. [22]  Five years later, it was estimated that, in 1993, there were 1,795 to 1,860 Listeria infections that required hospitalization, with 295-360 of these cases involving pregnant women. [28]  Based on these estimates, the medical costs that Listeria infections had caused each year were said to run from $61.7 to $64.8 million, including those individuals who ultimately died as a result of their infections. [28] For these same acute cases, productivity costs were estimated to run from $125.8 to $154.4 million a year. [28] The productivity costs associated with Listeria-related chronic illness was estimated to be an additional $38 million a year. [28] In sum, “[e]stimates of total costs for the 1,795 to 1,860 cases of listeriosis range from $232.7 million to $264.4 million annually.” [28]

In 2000, USDA updated the cost-estimates for four pathogens:  Campylobacter, Salmonella, E. coli O157:H7, and Listeria monocytogenes. [28a] The 2000 estimates were based on the CDC’s then newly-released estimates of annual foodborne illnesses, and put the total cost in the United States for these four pathogens at $6.5 billion a year. [28a] For Listeria specifically, it was estimated that costs amounted to $2.3 billion per year, based on 2,493 cases, which involved 2,298 hospitalizations and 499 deaths. [28a]  More recently, in 2007, it was estimated that the worldwide cost of all foodborne disease was $1.4 trillion per year. [6]

Real Life Impacts of Listeria Infection

Because Listeria infection is most severe in elderly persons, pregnant women and newborns, the symptoms of infection vary greatly.

  • In older adults or immunocompromised individuals, septicemia (Listeria bacteria in the blood stream) and meningitis are the most common indicators of illness.
  • In pregnant women, a mild, flu-like illness can be followed by miscarriage, premature delivery or stillbirth.
  • In newborns, bacteremia (Listeria bacteria in the blood stream) and meningitis are the most common indicators of Listeria infection.

Antimicrobial Resistance in Bacteria

Antimicrobial resistance in bacteria is an emerging and increasing threat to human health. [1, 4] Physicians are increasingly aware that antimicrobial resistance is increasing in foodborne pathogens and that, as a result, patients who are prescribed antibiotics are at increased risk for acquiring antimicrobial-resistant foodborne infections. [1] Indeed, “increased frequency of treatment failures for acute illness and increased severity of infection may be manifested by prolonged duration of illness, increased frequency of bloodstream infections, increased hospitalization or increased mortality.” [3]

The use of antimicrobial agents in the feed of food animals is estimated by the FDA to be over 100 million pounds per year. [4]  It is estimated that 36% to 70% of all antibiotics produced in the United States are used in a food animal feed or in prophylactic treatment to prevent animal disease. [3, 4, 18] In 2002, the Minnesota Medical Association published an article by David Wallinga, M.D., M.P.H. who wrote:

According to the [Union of Concerned Scientists], 70 percent of all the antimicrobials used in the United States for all purposes—or about 24.6 million pounds annually—are fed to poultry, swine, and beef cattle for nontherapeutic purposes, in the absence of disease. Over half are “medically important” antimicrobials; identical or so closely related to human medicines that resistance to the animal drug can confer resistance to the similar human drug. Penicillin, tetracycline, macrolides, streptogramins, and sulfonamides are prominent examples. [33]

The use of antibiotics in feed for food animals, on animals prophylactically to prevent disease, and the use of antibiotics in humans unnecessarily must be reduced. [1, 25] European countries have reduced the use of antibiotics in animal feed and have seen a corresponding reduction in antibiotic-resistant illnesses in humans. [1, 4]

The Prevention of Listeria infection

Given its widespread presence in the environment, and the fact that the vast majority of Listeria infections are the result of consuming contaminated food or water, preventing illness and death is necessarily (and understandably) a food safety issue.

L. monocytogenes presents a particular concern with respect to food handling because it can grow at refrigerator temperatures (4°C to 10°C), temperatures commonly used to control pathogens in foods. Freezing also has little detrimental effect on the microbe. Although pasteurization is sufficient to kill Listeria, failure to reach the desired temperature in large packages can allow the organism to survive. Food can also be contaminated after processing by the introduction of unpasteurized material, as happens during the preparation of some cheeses. Listeria can also be spread by contact with contaminated hands, equipment and counter tops. [4]

The use of irradiation to reduce Listeria to safe levels in foods has many proponents. [26] As noted by an eminent CDC researcher, Robert V. Tauxe,

Ready-to-eat meats, such as hot dogs, have already been subjected to a pathogen-killing step when the meat is cooked at the factory, so contamination is typically the result of in-plant contamination after that step. Improved sanitation in many plants has reduced the incidence of infection by half since 1986, but the risk persists, as illustrated by a large hot dog-associated outbreak that occurred in 1999. Additional heat treatment or irradiation of meat after it is packaged would eliminate Listeria that might be present at that point. [26]

The CDC provides a comprehensive list of recommendations and precautions to avoid becoming infected with Listeria, which are as follows:

· Thoroughly cook raw food from animal sources, such as beef, pork, or poultry to a safe internal temperature. For a list of recommended temperatures for meat and poultry, visit http://www.fsis.usda.gov/PDF/IsItDoneYet_Magnet.pdf.

· Rinse raw vegetables thoroughly under running tap water before eating.

· Keep uncooked meats and poultry separate from vegetables and from cooked foods and ready-to-eat foods.

· Do not drink raw (unpasteurized) milk, and do not eat foods that have unpasteurized milk in them.

· Wash hands, knives, countertops, and cutting boards after handling and preparing uncooked foods.

· Consume perishable and ready-to-eat foods as soon as possible.

Recommendations for persons at high risk, such as pregnant women and persons with weakened immune systems, in addition to the recommendations listed above, include:

· Meats

o Do not eat hot dogs, luncheon meats, cold cuts, other deli meats (e.g., bologna), or fermented or dry sausages unless they are heated to an internal temperature of 165°F or until steaming hot just before serving.

o Avoid getting fluid from hot dog and lunch meat packages on other foods, utensils, and food preparation surfaces, and wash hands after handling hot dogs, luncheon meats, and deli meats.

o Do not eat refrigerated pâté or meat spreads from a deli or meat counter or from the refrigerated section of a store. Foods that do not need refrigeration, like canned or shelf-stable pâté and meat spreads, are safe to eat. Refrigerate after opening.

· Cheeses

o Do not eat soft cheese such as feta, queso blanco, queso fresco, brie, Camembert, blue-veined, or panela (queso panela) unless it is labeled as made with pasteurized milk. Make sure the label says, “MADE WITH PASTEURIZED MILK.”

· Seafood

o Do not eat refrigerated smoked seafood, unless it is contained in a cooked dish, such as a casserole, or unless it is a canned or shelf-stable product. Refrigerated smoked seafood, such as salmon, trout, whitefish, cod, tuna, and mackerel, is most often labeled as “nova-style,” “lox,” “kippered,” “smoked,” or “jerky.” These fish are typically found in the refrigerator section or sold at seafood and deli counters of grocery stores and delicatessens. Canned and shelf stable tuna, salmon, and other fish products are safe to eat.

Recommendations to keep food safe:

· Be aware that Listeria monocytogenes can grow in foods in the refrigerator. Use an appliance thermometer, such as a refrigerator thermometer, to check the temperature inside your refrigerator. The refrigerator should be 40°F or lower and the freezer 0°F or lower.

· Clean up all spills in your refrigerator right away–especially juices from hot dog and lunch meat packages, raw meat, and raw poultry.

· Clean the inside walls and shelves of your refrigerator with hot water and liquid soap, then rinse.

· Divide leftovers into shallow containers to promote rapid, even cooling. Cover with airtight lids or enclose in plastic wrap or aluminum foil. Use leftovers within 3 to 4 days.

· Use precooked or ready-to-eat food as soon as you can. Do not store the product in the refrigerator beyond the use-by date; follow USDA refrigerator storage time guidelines:

o Hot Dogs – store opened packages no longer than 1 week and unopened packages no longer than 2 weeks in the refrigerator.

o Luncheon and Deli Meat – store factory-sealed, unopened packages no longer than 2 weeks. Store opened packages and meat sliced at a local deli no longer than 3 to 5 days in the refrigerator. [11]

Additional preventive steps and precautions can be found on the websites of most State Departments of Health, including, for example, the Minnesota Department of Health. [20] There is also excellent information to be found at the Extension Service website of the Institute of Food and Agricultural Sciences at University of Florida. [27]

References

  1. Angulo, F.J., et al., “Antimicrobial Use in Agriculture: Controlling the Transfer of Antimicrobial Resistance to Humans,” SEMINARS IN PEDIATRIC INFECTIOUS DISEASES, Vol. 15, No. 2, pp. 78-85 (April 2004).
  2. Angulo, F.J., et al., “Evidence of an Association Between Use of Anti-microbial Agents in Food Animals and Anti-microbial Resistance Among Bacteria Isolated from Humans and the Human Health Consequences of Such Resistance, JOURNAL OF VETERINARY MEDICINE, Series-B, Vol. 51, Issue 8-9, pp. 374-79 (Oct. 2004).
  3. Bennion, J.R., et al., “Decreasing Listeriosis Mortality in the United States, 1990-2005,” CLINICAL INFECTIOUS DISEASES, Vol. 47, No. 7, pp. 867-74 (2008), available online at http://cid.oxfordjournals.org/content/47/7/867.long
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  5. Bryan, Frank, “Procedures to Investigate Foodborne Illness,” International Association for Food Protection, p. 119 (5th ed. 1999).
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  10. CDC, “Preliminary FoodNet Data on the Incidence of Infection with Pathogens Transmitted Commonly through Food—10 States, 2009,” MORBIDITY AND MORTALITY WEEKLY REPORT, Vol. 59, No. 14, pp. 418-22 (April 16, 2010) available online at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5914a2.htm
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  19. Mayo Clinic.  (2009). Listeria infection (listeriosis). Retrieved November 1, 2009 from Mayo Clinic website:  http://www.mayoclinic.com/health/Listeria-infection/DS00963.
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  29. USDA Food Safety and Inspection Service (FSIS), “Assessing the Effectiveness of theListeria monocytogenes Interim Final Rule, Summary Report,” (Sept. 28, 2004), available online at http://www.fsis.usda.gov/Oppde/rdad/frpubs/97-013F/LM_Assessment_Report_2004.pdf
  30. USDA FSIS, NATIONWIDE BROILER CHICKEN MICROBIOLOGICAL BASELINE DATA COLLECTION PROGRAM, July 1994—July 1995, (April 1996), full report available online at http://www.fsis.usda.gov/OPHS/baseline/broiler1.pdf
  31. USDA FSIS, THE NATIONWIDE MICROBIOLOGICAL BASELINE DATA COLLECTION PROGRAM: YOUNG CHICKEN SURVEY, July 2007—June 2008, full report available online at http://www.fsis.usda.gov/PDF/Baseline_Data_Young_Chicken_2007-2008.pdf
  32. USDA FSIS, THE NATIONWIDE MICROBIOLOGICAL BASELINE DATA COLLECTION PROGRAM: YOUNG TURKEY SURVEY, Aug. 2008—July 2009, at http://www.fsis.usda.gov/PDF/Baseline_Data_Young_Turkey_2008-2009.pdf
  33. Voetsch, AC, et al., “Reduction in the Incidence of Invasive Listeriosis in Foodborne Diseases Active Surveillance Network Sites, 1996-2003,” CLINICAL INFECTIOUS DISEASES, Vol. 44, No. 4, pp. 513-20 (CDC Control & Prevention Emerging Infections Program, Foodborne Diseases Active Surveillance Network Working Group 2007).
  34. Wallinga, D, “Antimicrobial Use in Animal Feed:  An Ecological and Public Health Problem,” MINNESOTA MEDICINE, Vol. 85, No. 10 pp. 12-16 (Oct. 2002).

Everything You Need to Know About Hepatitis A

An Introduction to Hepatitis A

Exposure to the hepatitis A virus can cause an acute infection of the liver that is typically mild and resolves on its own. [11, 17] The symptoms and duration of illness vary a great deal, with many persons showing no symptoms at all. [11] Fever and jaundice are two of the symptoms most commonly associated with a hepatitis A infection. [17]

It has been written that the “earliest accounts of contagious jaundice are found in ancient China.” [11] According to the CDC,

The first descriptions of hepatitis (epidemic jaundice) are generally attributed to Hippocrates. Outbreaks of jaundice, probably hepatitis A, were reported in the 17th and 18th centuries, particularly in association with military campaigns. Hepatitis A (formerly called infectious hepatitis) was first differentiated epidemiologically from hepatitis B, which has a long incubation period, in the 1940s. Development of serologic tests allowed definitive diagnosis of hepatitis B. In the 1970s, identification of the virus, and development of serologic tests helped differentiate hepatitis A from other types of non-B hepatitis.

Until 2004, hepatitis A was the most frequently reported type of hepatitis in the United States. In the pre-vaccine era, the primary methods used for preventing hepatitis A were hygienic measures and passive protection with immune globulin (IG). Hepatitis A vaccines were licensed in 1995 and 1996. These vaccines provide long-term protection against hepatitis A virus (HAV) infection. [7]

Consequently, hepatitis A is the only common vaccine-preventable foodborne disease in the United States. [7, 12] This virus is one of five human hepatitis viruses that primarily infect the human liver and cause human illness. [11] Unlike hepatitis B and C, hepatitis A does not develop into chronic hepatitis or cirrhosis, which are both potentially fatal conditions, [7, 11, 17] Nonetheless, infection with the hepatitis A virus (HAV) can lead to acute liver failure and death. [12, 17]

The Incidence of Hepatitis A Infections

Hepatitis A is much more common in countries with underdeveloped sanitation systems and, thus, is a risk in most of the world. [11, 16] An increased transmission rate is seen in all countries other than the United States, Canada, Japan, Australia, New Zealand, and the countries of Western Europe. [9] Nevertheless, infections continue to occur in the United States, where approximately one-third of the population has been previously infected with HAV. [6, 12]

Each year, approximately 30,000 to 50,000 cases of hepatitis A occur in the United States. [5, 7] Historically, acute hepatitis A rates have varied cyclically, with nationwide increases every 10 to 15 years. [13] The national rate of HAV infections has declined steadily since the last peak in 1995. [5, 6] Although the national incidence—1.0 case per 100,000 population—of hepatitis A was the lowest ever recorded in 2007, it is estimated that asymptomatic infections and underreporting kept the documented incidence-rate lower than it actually is. In fact, it is estimated that there were 25,000 new infections in 2007. [6, 22]

Although the rates of HAV infection have declined over the years, rates are twice as high among American Indians and Alaskan Natives. [1] Hispanics are also twice as likely to be infected compared to non-Hispanic Whites in the United States. [19]. Rates among American Indians and Alaskan Natives have decreased dramatically, largely as a result of increased vaccination of children in both urban and rural communities. [1]

In 2007, the CDC reported a total of 2,979 acute symptomatic cases of hepatitis A. [6] Of these, information about food and water exposure was known for 1,047 cases, leading to an estimate that 6.5% of all infections were caused by exposure to contaminated water or food. [6] In 2,500 of the cases, no known risk factor was identified. [6]

Estimates of the annual costs (direct and indirect) of hepatitis A in the United States have ranged from $300 million to $488.8 million in 1997 dollars. [5] In one study conducted in Spokane, Washington, the combined direct and indirect costs for each case of hepatitis A from all sources ranged from $2892 to $3837. [2, 13] In a 2007 Ohio study, each case of HAV infection attributable to contaminated food was estimated to cost at least $10,000, including medical and other non-economic costs. [21] Nationwide, adults who become ill miss an average of 27 workdays per illness, and 11-to-22 percent of those infected are hospitalized. [6, 7] All of these costs are entirely preventable given the effectiveness of a vaccination in providing immunity from infection. [7, 13]

How is Hepatitis A transmitted?

Hepatitis A is a communicable (or contagious) disease that often spreads from person to person. [11] Person-to-person transmission occurs via the “fecal-oral route,” while all other exposure is generally attributable to contaminated food or water. [11, 16] Food-related outbreaks are usually associated with contamination of food during preparation by a HAV-infected food handler. [6, 7, 12] The food handler is generally not ill because the peak time of infectivity—that is, when the most virus is present in the stool of an infected individual—occurs two weeks before illness begins. [12]

Fresh produce contaminated during cultivation, harvesting, processing, and distribution has also been a source of hepatitis A. [12, 25] In 1997, frozen strawberries were the source of a hepatitis A outbreak in five states. [15] Six years later, in 2003, fresh green onions were identified as the source of a hepatitis A outbreak traced to consumption of food at a Pennsylvania restaurant. [25] Other produce, such as blueberries and lettuce, has been associated with hepatitis A outbreaks in the U.S. as well as other developed countries. [3, 4]

HAV is relatively stable and can survive for several hours on fingertips and hands and up to two months on dry surfaces. [11, 17] The virus can be inactivated by heating to 185°F (85°C) or higher for one minute, or disinfecting surfaces with a 1:100 dilution of sodium hypochlorite (household bleach) in tap water. [8, 13, 24] It must be noted, however, that HAV can still be spread from cooked food if it is contaminated after cooking. [12]

Although ingestion of contaminated food is a common means of spread for hepatitis A, it may also be spread by household contact among families or roommates, sexual contact, or by direct inoculation from persons sharing illicit drugs. [12, 17] Children are often asymptomatic, or have unrecognized infections, and can pass the virus through ordinary play, unknown to their parents, who may later become infected from contact with their children. [11, 18, 22]

Symptoms of Hepatitis A Infection

Hepatitis A may cause no symptoms at all when it is contracted, especially in children. [12] Asymptomatic individuals will only know they were infected (and have become immune, given that you can only get hepatitis A once) by getting a blood test later in life. [17] Approximately 10 to 12 days after exposure, HAV is present in blood and is excreted via the biliary system into the feces. [7, 11] Although the virus is present in the blood, its concentration is much higher in feces. [11] HAV excretion begins to decline at the onset of clinical illness, and decreases significantly by 7 to 10 days after onset of symptoms. [11] Most infected persons no longer excrete virus in the feces by the third week of illness; children may excrete HAV longer than adults. [11, 20]

Seventy percent of hepatitis A infections in children younger than six years of age are asymptomatic; in older children and adults, infection tends to be symptomatic with more than 70% of those infected developing jaundice. [7] Symptoms typically begin about 28 days after contracting HAV, but can begin as early as 15 days or as late as 50 days after exposure. [7, 11, 12] The symptoms include muscle aches, headache, anorexia (loss of appetite), abdominal discomfort, fever, and malaise. [[7, 11, 17]

After a few days of typical symptoms, jaundice (also termed “icterus”) sets in. [11, 17] Jaundice is a yellowing of the skin, eyes and mucous membranes that occurs because bile flows poorly through the liver and backs up into the blood. [17] The urine will also turn dark with bile and the stool light or clay-colored from lack of bile. [7, 11, 17] When jaundice sets in, initial symptoms such as fever and headache begin to subside. [17]

In general, symptoms usually last less than 2 months, although 10% to 15% of symptomatic persons have prolonged or relapsing disease for up to 6 months. [13, 14] It is not unusual, however, for blood tests to remain abnormal for six months or more. [11] The jaundice so commonly associated with hepatitis A can also linger for a prolonged period in some infected persons—sometimes as long as eight months or more. [11, 17] Additionally, pruritus, or severe “itchiness” of the skin, can persist for several months after the onset of symptoms. These conditions are frequently accompanied by diarrhea, anorexia, and fatigue. [7, 17]

Relapse is possible with hepatitis A, typically within three months of the initial onset of symptoms. [14] Although relapse is more common in children, it does occur with some regularity in adults. [11, 14] The vast majority of persons who are infected with hepatitis A fully recover, and do not develop chronic hepatitis. [17] Persons do not carry hepatitis A long-term as with hepatitis B and C. [5, 7]

Fulminant Hepatitis A

Fulminant hepatitis A is a rare but devastating complication of HAV infection. [10] As many as 50% of individuals with acute liver failure may die or require emergency liver transplantation. [23] Elderly patients and patients with chronic liver disease are at higher risk for fulminant hepatitis A. [11, 23] In parallel with a declining incidence of acute HAV infection in the general population, however, the incidence of fulminant HAV appears to be decreasing. [23]

HAV infects the liver’s parenchymal cells (internal liver cells). [10, 11] Once a cell has been penetrated by the viral particles, the hepatitis A virus releases its own toxins that cause, in essence, a hostile takeover of the host’s cellular system. [11, 22] The cell then produces new viral components that are released into the bile capillaries or tubes that run between the liver’s parenchymal cells. [11] This process results in the death of liver cells, called hepatic necrosis. [11, 23]

The fulminant form of hepatitis occurs when this necrotic process kills so many liver cells—upwards of three-quarters of the liver’s total cell count—that the liver can no longer perform its job. [10, 23] Aside from the loss of liver function, fulminant hepatic failure can lead to encephalopathy and cerebral edema. [10] Encephalopathy is a brain disorder that causes central nervous system depression and abnormal neuromuscular function. [10, 11] Cerebral edema is a swelling of the brain that can result in dangerous intracranial pressure. [10] Intracranial hypertensions leading to brain stem death and sepsis with multiple organ failure are the leading causes of death in individuals with fulminant hepatic failure. [10, 23]

How is Hepatitis A Infection Diagnosed?

The various human hepatitis viruses cause very similar illnesses. [11] Therefore, neither the individual nor the healthcare provider can tell by symptoms or signs if a given individual is suffering from hepatitis A unless laboratory tests are performed. [7, 17]

Fortunately, blood tests are widely available to accurately diagnose hepatitis A, including tests for antibodies, or the affected person’s immune response to hepatitis A proteins. [7] This immune response is conclusively demonstrated by the presence of Immunoglobulin M (IgM) antibodies, indicating acute disease, and immunoglobulin G (IgG), indicating a past infection. [11, 13] The IgG antibodies are present for life, indicating immunity. [13] Following is some guidance for the interpretation of the test results:

  • IgM negative / IgG negative: Most persons with these results have never contracted hepatitis A. Antibodies of the IgM variety develop five to ten days prior to the onset of symptoms.
  • IgM positive / IgG negative: This result indicates acute hepatitis A.
  • IgM positive / IgG positive: This result indicates that acute hepatitis A occurred within the last six months. By six months, the IgM reverts to negative.
  • IgM negative / IgG positive: Persons with this result are immune to hepatitis A. They have either been infected with the virus months or years in the past (with or without symptoms), or they have been vaccinated for hepatitis A. However, if they are currently ill, it is not likely to be due to hepatitis A.

Treatment for Acute Hepatitis A Infection

Once a clinical infection is established, there is no specific treatment for hepatitis A. Affected individuals generally suffer from loss of appetite, so the main concern is ensuring a patient receives adequate nutrition and avoids permanent liver damage. [7, 17] An individual’s perception of the severity of fatigue or malaise is the best determinant of the need for rest. [17]

Treatment of those suffering from fulminant hepatic failure depends largely on the affected person’s status. [23, 26] Those who have not become encephalopathic generally undergo an intense course of supportive treatment. [10, 23] But for those whose liver failure is so complete that it has lead to encephalopathy or cerebral edema, timely liver transplantation is often the only option. [10, 14] Unfortunately, many individuals with irreversible liver failure do not receive a transplant because of contraindications or the unavailability of donor livers. [11, 23]

Real Life Impacts

The number of acute hepatitis A infections in the U.S. drastically fell in the first part of the 21st Century, largely in part because hepatitis A vaccination was recommended for persons in groups shown to be at high risk for infection and children living in communities with high rates of disease beginning in 1996. By 2006, hepatitis A vaccine had been incorporated into the Advisory Committee on Immunization Practices’ recommended childhood vaccination schedule. [27]

Despite a decrease in the number of hepatitis A cases reported annually, anyone who has not been vaccinated is at increased risk for contracting hepatitis A infection. Persons over the age of 50, those with chronic liver disease, and immunocompromised individuals who have not been vaccinated against hepatitis A remain most at risk for developing fulminant hepatitis, a rare but devastating complication of a hepatitis A infection that can lead to the need for a liver transplant, or death.  See, 27 year history of Hepatitis A outbreaks at Outbreak Database.

How to Prevent Hepatitis A Infection

Hepatitis A is totally and completely preventable. [12] Although outbreaks continue to occur in the United States, no one should ever get infected if preventive measures are taken. [7, 12] For example, food handlers must always wash their hands with soap and water after using the bathroom, changing a diaper, and certainly before preparing food. [12, 24] Food handlers should always wear gloves when handling or preparing ready-to-eat foods, although gloves are not a substitute for good hand washing. Ill food-handlers should be excluded from work. [14, 24]

After exposure, immune globulin (IG) is 80% to 90% effective in preventing clinical hepatitis A when administered within 2 weeks of last exposure. [9] Although efficacy is greatest when IG is administered early in the incubation period, when administered later, IG is still likely to make the symptoms less severe. [9, 11] Given the lack of appropriately designed studies comparing the post exposure efficacy of vaccine with that of IG, the Advisory Committee on Immunization Practices (ACIP) recommends IG exclusively for post-exposure. [9] Hepatitis A vaccine, if recommended for other reasons, could be given at the same time. [9, 13]

In 2006, the ACIP recommended routine hepatitis A vaccination for all children ages 12-23 months, that hepatitis A vaccination be integrated into the routine childhood vaccination schedule, and that children not vaccinated by two years of age be vaccinated subsequently. [9, 13] The vaccine is recommended for the following persons:

  • Travelers to areas with increased rates of hepatitis A
  • Men who have sex with men
  • Injecting and non-injecting drug users
  • Persons with clotting factor disorders (e.g. hemophilia)
  • Persons with chronic liver disease
  • Persons with occupational risk of infection (e.g. those who work with hepatitis A-infected primates or with hepatitis A virus in a laboratory setting)
  • Children living in regions of the U.S. with increased rates of hepatitis A
  • Household members and other close personal contacts (such as regular babysitters) of adopted children newly arriving from countries with high or intermediate rates of hepatitis A. [9]

The vaccine may also help protect household contacts of those persons infected with hepatitis A. [9, 20] Although generally not a legal requirement at this time, vaccination of food handlers would be expected to substantially diminish the incidence of hepatitis A outbreaks. [12] Persons traveling to a high-risk area less than four weeks after receiving the initial dose of hepatitis A vaccine, or travelers who choose not to be vaccinated against hepatitis A should receive a single dose of Immune Globulin, which provides protection against hepatitis A infection for up to three months. [9, 11, 18]

References

1.         Bialek, Stephanie, et al., “Hepatitis A Incidence and Hepatitis A Vaccination among American Indians and Alaska Natives, 1990–2001,” American Journal of Public Health.Vol. 94, No. 6, pp. 996-1001 (2004). Full text of article is available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1448379/pdf/0940996.pdf.

2.         Bownds, Lynne, et al., “Economic Impact of a Hepatitis A Epidemic in a Mid-Sized Urban Community: The Case of Spokane, Washington,” Journal of Community Health, Vol. 28, No. 4, pp. 233-246 (2003). Abstract available online at http://www.ncbi.nlm.nih.gov/pubmed/12856793

3.         Butot S, et al., “Effects of Sanitation, Freezing and Frozen Storage on Enteric Viruses in Berries and Herbs,” International Journal of Food Microbiology, Vol. 126, pp. 30-35 (2008). Full text of article is available at http://www.prograd.uff.br/virologia/sites/default/files/bulot_et_al_2008_inactivation.pdf

4.         Calder, L, et al., “An Outbreak of Hepatitis A Associated with Consumption of Raw Blueberries,” Epidemiology and Infection, Vol. 131, No. 1, 745-751 (2003) at  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2870016/pdf/12948375.pdf

5.         CDC Summary, “Disease Burden from Viral Hepatitis A, B, and C in the United States, 2004-2009, at http://www.cdc.gov/hepatitis/pdfs/disease_burden.pdf

6.         CDC, “Surveillance for Acute Viral Hepatitis — United States, 2007, Morbidity and Mortality Weekly Report, Surveillance Summaries, Vol. 58, No. SS03 (May 22, 2009) at http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5803a1.htm

7.         CDC, “Hepatitis A,” in EPIDEMIOLOGY AND PREVENTION OF VACCINE-PREVENTABLE DISEASES (also known as “The Pink Book”), Atkinson W, Wolfe S, Hamborsky J, McIntyre L, editors, 12th edition. Chapter available online at http://www.cdc.gov/vaccines/pubs/pinkbook/hepa.html

8.         CDC, “Updated recommendations from Advisory Committee on Immunization Practices (ACIP) for use of hepatitis A vaccine in close contacts of newly arriving international adoptees,” Morbidity and Mortality Weekly Report, Vol. 58, No. 36, (Sept. 18, 2009), http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5836a4.htm

9.         CDC, “Update: Prevention of Hepatitis A after Exposure to Hepatitis A Virus and in International Travelers, Updated ACIP Recommendations,” Morbidity and Mortality Weekly Report, Vol. 56, No. 41, pp. 1080-84 (Oct. 19, 2007), online at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5641a3.htm.

10.       Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure:  Pathophysiology and Management,” World Journal of Gastroenterology, Vol. 12, No. 46, pp. 7405-7412 (Dec. 14, 2006). Full article is available online at http://www.wjgnet.com/1007-9327/12/7405.pdf

11.       Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” in Mandell, Douglas, & Bennett’s PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES, Fifth Edition, Chap. 161, pp. 1920-40 (2000).

12.       Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” Clinical Infectious Diseases, Vol. 38, 705-715 (March 1, 2004). Full text online at http://www.cdc.gov/hepatitis/PDFs/fiore_ha_transmitted_by_food.pdf

13.       Fiore, Anthony, et al., Advisory Committee on Immunization Practices (ACIP), Prevention of Hepatitis-A Through Active or Passive Immunization: Recommendations, Morbidity & Mortality Weekly Review, Vol. 55, Report 407, (May 19, 2006) at http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5507a1.htm

14.       Gilkson Miryam, et al., “Relapsing Hepatitis A. Review of 14 cases and literature survey,” Medicine, Vol. 71, No. 1, 14-23 ( Jan. 1992). Abstract of article online at http://www.ncbi.nlm.nih.gov/pubmed/1312659

15.       Hutin YJF, et al., “A Multistate, Foodborne Outbreak of Hepatitis A,” New England Journal of Medincine, Vol. 340, pp. 595–602 (1999). Full text of article is online at http://www.nejm.org/doi/full/10.1056/NEJM199902253400802

16.       Jaykus Lee Ann, “Epidemiology and Detection as Options for Control of Viral and Parasitic Foodborne Disease,” Emerging Infectious Diseases, Vol. 3, No. 4, pp. 529-39 (October-December 1997). Full text of the article is available online at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2640072/pdf/9366607.pdf

17.       Mayo Clinic Staff, “Hepatitis A,” (last updated Sept. 1, 2011). Articles available online at http://www.mayoclinic.com/health/hepatitis-a/DS00397 .

18.       Piazza, M, et al., “Safety and Immunogenicity of Hepatitis A Vaccine in Infants: A Candidate for Inclusion in Childhood Vaccination Program,” Vaccine. Vol. 17, pp. 585-588 (1999). Abstract at http://www.ncbi.nlm.nih.gov/pubmed/10075165

19.       Rawls, R.A. and Vega, K.J., “Viral Hepatitis in Minority America,” Journal of Clinical Gastroenterology, Vol. 39, No. 2, pp. 144–151 (Feb. 2005). Abstract is at  http://www.ncbi.nlm.nih.gov/pubmed/15681912

20.       Sagliocca, Luciano, et al., “Efficacy of Hepatitis A Vaccine in Prevention of Secondary Hepatitis A Infection: A Randomized Trial,” Lancet, Vol. 353, 1136-39 (1999). Abstract at http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(98)08139-2/abstract

21.       Scharff, RL, et al., “Economic Cost of Foodborne Illness in Ohio,” Journal of Food Protection, Vol. 72, No. 1, pp. 128-136 (2009). Abstract available online at http://www.ingentaconnect.com/content/iafp/jfp/2009/00000072/00000001/art00018

22.       Schiff, E.R., “Atypical Manifestations of hepatitis-A,” Vaccine, Vol. 10, Suppl. 1, pp. 18-20 (1992). Abstract at http://www.ncbi.nlm.nih.gov/pubmed/1475999

23.       Taylor, Ryan, et al., “Fulminant Hepatitis A Virus Infection in the United States: Incidence, Prognosis, and Outcomes,” Hepatology, Vol. 44, 1589-1597 (2006). Full text http://deepblue.lib.umich.edu/bitstream/2027.42/55879/1/21439_ftp.pdf

24.       Todd, Ewan C. D., et al., “Outbreaks Where Food Workers Have Been Implicated in the Spread of Foodborne Disease. Part 6. Transmission and Survival of Pathogens in the Food Processing and Preparation-environment,” Journal of Food Protection, Vol. 72, 202-219 (2009). Full text of the article is available online at http://courses.washington.edu/eh451/articles/Todd_2009_food%20processing.pdf

25.       Wheeler, C, et al., “An Outbreak of Hepatitis A Associated with Green Onions,” New England Journal of Medicine, Vol. 353, 890-897 (2005). Full text of article available at http://www.nejm.org/doi/full/10.1056/NEJMoa050855

26.       Willner, IR, et al., “Serious Hepatitis A: An Analysis of Patients Hospitalized During an Urban Epidemic in the United States,” Annals of Internal Medicine, Vol. 128, No. 2, pp. 111-114 (Jan. 15, 1998). Full text of the article is available at http://www.annals.org/content/128/2/111.full.pdf+html

27.       CDC. “Prevention of Hepatitis A through Active or Passive Immunization:  Recommendations of the Advisory Committee on Immunization Practices (ACIP),”  Morbidity and Mortality Weekly Report, Vol. 55, (RR07), pp. 1-23 (May 29, 2006) online at http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5507a1.htm