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Network of germ sleuths heads off nearly 276,000 foodborne illnesses a year

OHIO STATE UNIVERSITY

CDC-led PulseNet spots outbreaks early, encourages safer practices 

110868_webAn elderly woman in Phoenix. A Toledo toddler. An accountant in Indianapolis. All poisoned by food. Quickly uncovering that their illnesses are connected can make all the difference in halting a deadly outbreak.

About 276,000 cases of foodborne illness are avoided each year because of PulseNet, a 20-year-old network coordinated by the Centers for Disease Control and Prevention, new research has found. PulseNet links U.S. public health laboratories so that they can speedily share details about E. coli, Salmonella and other bacterial illnesses.

The averted illnesses translate to $507 million in annual savings on medical bills and lost productivity, according to a study led by Robert L. Scharff of The Ohio State University and Craig Hedberg of the University of Minnesota.

PulseNet has created a climate that encourages better business practices and swift response to trouble, Scharff said, and that likely explains most of the avoided illnesses in the study.

In the face of public scrutiny, lawsuits and lost revenue, businesses have responded with better self-policing, he said.

“Companies are saying, ‘We can’t have this risk. This risk is too big for us,'” said Scharff, an associate professor of consumer sciences.

“What’s exciting for me is this shows the power of information in the market to force change on industry. It’s not just a way of tracking illness, but of allowing markets to work better.”

Scharff worked with experts from the CDC and elsewhere to assign a value to PulseNet, both in terms of illnesses prevented and dollars saved. The team analyzed data from 1994 to 2009.

The results, published in conjunction with PulseNet’s 20th anniversary, appear in the American Journal of Preventive Medicine.

PulseNet’s annual price tag is $7.3 million, according to the analysis. The network includes 83 state and federal laboratories where microbiologists uncover DNA fingerprints of illness-causing bacteria that tie cases together and confirm outbreaks.

“If more agencies used information as a tool instead of trying to fight the markets, I think we would all be better off,” said Scharff, also an economist who is part of Ohio State’s Food Innovation Center.

Tainted food is responsible for about 48 million illnesses, 128,000 hospitalizations and 3,000 deaths in the United States each year.

PulseNet’s purpose is to use DNA fingerprinting techniques to link illnesses that are likely to have a shared cause, even if the cases are widely dispersed. Food moves far and wide in the modern world and the first clues of an outbreak aren’t always clustered geographically.

Until now, health officials have not been able to assign a value to the service.

“PulseNet has been very impactful. We’ve known this for many years, but it’s been anecdotal. This gives us some hard figures,” said John Besser, deputy chief of the CDC’s enteric diseases laboratory branch.

PulseNet identifies about 1,750 clusters of disease a year, including nearly 250 that span multiple states.

“PulseNet is an integral part of our food-safety system and it helps improve the quality and safety of all the food that we eat,” said Besser, who formerly worked with PulseNet in Minnesota, one of the first states to embrace the program.

“Part of that effect is containing outbreaks, but a really significant portion of the benefit is giving feedback to the food industry and the regulatory agencies so they can make food safer,” he said.

Besser said he’s hopeful the federal government will be able to sustain PulseNet as changes in laboratory testing methods evolve. Placing a value on the service should help, he said.

To participate in PulseNet, state, county and city labs evaluate samples from people sickened by food and look for the DNA fingerprint of the bacteria, molecular subtyping that goes deeper than simply naming the responsible pathogen.

Salmonella cases, for example, arise all the time. And most are sporadic, meaning the strain of bacteria in one person’s stool sample isn’t likely to match the strain in the sample across town, or across the country. When they do match, there could be big trouble.

Scharff and his colleagues found that in states that put more DNA data into the system, the chance of future illnesses declined significantly.

Their work focused on E. coli, Listeria and Salmonella – the bacteria that have been analyzed by the network the longest. The team used two models. One was designed to capture indirect effects of PulseNet – the food contamination that never happened because the network exists.

This was possible because states have adopted PulseNet to differing degrees and at different times, opening the door for a calculation based on how rates of illness differ by PulseNet participation level.

“The more that a state uploads into the system, the lower reported illnesses will be,” Scharff said.

The second model estimated the direct effects of product recalls when outbreaks arise and are linked to a specific food. Faster identification of outbreaks, resulting in more timely recalls, led to 16,994 fewer Salmonella cases and 2,819 fewer E. coli cases a year at a savings of $37 million, the study found.

Though the study provides estimates of illness reduction, it’s unclear how many illnesses are being prevented because of improvements in fields, factories and slaughterhouses or how many are avoided due to better-informed government and consumer actions.

It is also impossible to know about spillover effects – reductions in foodborne illnesses from pathogens not included in this analysis.

“The calculations probably underestimate the impact of PulseNet,” Scharff said. “We did not examine whether illnesses from pathogens outside of the three in question were reduced as a result of industry efforts, though they likely were.”

The economic model also may not fully include all of the costs.

“We used a very conservative economic method of measuring health costs,” he said. The study did not assign a dollar value to losses from premature death and reduced quality of life, a number that could be quite large, the researchers wrote.

On the other side, “we aren’t able to estimate the cost to industry from remedial actions,” he said. “These could be significant for affected companies, but are lower than the costs of having foodborne illnesses associated with their products.”

###

Financial support for the research came from the CDC, through the Association of Public Health Laboratories.

Scharff, Hedberg and Besser’s collaborators on the study were Donald Sharp and Peter Gerner-Smidt of the CDC and Timothy Jones of the Tennessee Department of Health.

CONTACT: Robert Scharff, (614) 292-4549; Scharff.8@osu.edu

Written by: Misti Crane, (614) 292-5220; Crane.11@osu.edu

With Norovirus in the News, What do You Need to Know

norovirusAn Introduction to Norovirus

The Centers for Disease Control and Prevention (CDC) estimates that noroviruses cause nearly 21 million cases of acute gastroenteritis annually, making noroviruses the leading cause of gastroenteritis in adults in the United States. [5, 9, 13, 31]  According to a relatively recent article in the New England Journal of Medicine,

The Norwalk agent was the first virus that was identified as causing gastroenteritis in humans, but recognition of its importance as a pathogen has been limited because of the lack of available, sensitive, and routine diagnostic methods. Recent advances in understanding the molecular biology of the noroviruses, coupled with applications of novel diagnostic techniques, have radically altered our appreciation of their impact. Noroviruses are now recognized as being the leading cause of epidemics of gastroenteritis and an important cause of sporadic gastroenteritis in both children and adults. [16]

Of the viruses, only the common cold is reported more often than a norovirus infection—also referred to as viral gastroenteritis. [3]

Nature has created an ingenious bug in norovirus. [21] The round blue ball structure of norovirus is actually a protein surrounding the virus’s genetic material. [16, 33] The virus attaches to the outside of cells lining the intestine, and then transfers its genetic material into those cells. [33] Once the genetic material has been transferred, norovirus reproduces, finally killing the human cells and releasing new copies of itself that attach to more cells of the intestine’s lining. [12, 15, 33]

Norovirus (previously called “Norwalk-like virus” or NLV) is a member of the family Caliciviridae. [15, 33] The name derives from the Latin for chalice—calyx—meaning cup-like, and refers to the indentations of the virus surface. [33] The family of Caliciviridae consists of several distinct groups of viruses that were first named after the places where outbreaks occurred. [30] The first of these outbreaks occurred in 1968 among schoolchildren in Norwalk, Ohio. [16] The prototype strain was identified four years later, in 1972, and was the first virus identified that specifically caused gastroenteritis in humans. [16, 33] Other discoveries followed, with each strain name based on the location of its discovery—e.g., Montgomery County, Snow Mountain, Mexico, Hawaii, Parmatta, Taunton, and Toronto viruses. [15, 21] A study published in 1977 found that the Toronto virus was the second most common cause of gastroenteritis in children. [27] Eventually this confusing nomenclature was resolved, first in favor of calling each of the strains a Norwalk-like virus, and then simply, a norovirus – the term used today. [16, 33]

Humans are the only host of norovirus, and norovirus has several mechanisms that allow it to spread quickly and easily. [15] Norovirus infects humans in a pathway similar to the influenza virus’ mode of infection. [5, 15, 33] In addition to their similar infective pathways, norovirus and influenza also evolve to avoid the immune system in a similar way. [21] Both viruses are driven by heavy immune selection pressure and antigenic drift, allowing evasion of the immune system, which results in outbreaks. [21, 30] Norovirus is able to survive a wide range of temperatures and in many different environments. [15, 33] Moreover, the viruses can spread quickly, especially in places where people are in close proximity, such as cruise ships and airline flights, even those of short duration. [14, 15] As noted by the CDC in its Final Trip Report, noroviruses can cause extended outbreaks because of their high infectivity, persistence in the environment, resistance to common disinfectants, and difficulty in controlling their transmission through routine sanitary measures. [10]

Norovirus outbreaks can result from the evolution of one strain due to the pressure of population immunity. [12, 32] Typically, norovirus outbreaks are dominated by one strain, but can also involve more than one strain. [9, 11, 15] For example, some outbreaks associated with shellfish have been found to contain up to seven different norovirus strains. [30, 38] Swedish outbreak studies also reveal a high degree of genetic variability, indicating a need for wide detection methods when studying these outbreaks. [23]

By way of further example, in 2006, there was a large increase in the number of norovirus cases on cruise ships. Norovirus cases were increasing throughout Europe and the Pacific at the same time. [36] One issue with cruise ships is the close contact between people as living quarters are so close, and despite education efforts, there still seems to be a lack of public understanding regarding how the illness is spread. [7, 14] On the other hand, reporting occurs much more quickly in these situations because of the close proximity and concentration of illness, allowing for the quicker detection of outbreaks. [8] Cruise ship outbreaks often occur when new strains of norovirus are appearing, providing a good indicator system for new norovirus strains. [7, 8] In this case, two new variants appeared within the global epidemic genotype, suggesting a strong pressure for evolution against the human immune system. [12] This points to the need for an international system of guidelines in tracing norovirus outbreaks. [36]

How is Norovirus transmitted?

Norovirus causes nearly 60% of all foodborne illness outbreaks. [31] Norovirus is transmitted primarily through the fecal-oral route, with fewer than 100 norovirus particles needed to cause infection. [10, 15, 33] Transmission occurs either person-to-person or through contamination of food or water.  [1, 15, 33] CDC statistics show that food is the most common vehicle of transmission for noroviruses; of 232 outbreaks of norovirus between July 1997 and June 2000, 57% were foodborne, 16% were spread from person-to-person, and 3% were waterborne. [6, 31] When food is the vehicle of transmission, contamination occurs most often through a food handler improperly handling a food directly before it is eaten. [4, 9, 10]

Infected individuals shed the virus in large numbers in their vomit and stool, shedding the highest amount of viral particles while they are ill.  [5, 33] Aerosolized vomit has also been implicated as a mode of norovirus transmission. [24] Previously, it was thought that viral shedding ceased approximately 100 hours after infection; however, some individuals continue to shed norovirus long after they have recovered from it, in some cases up to 28 days after experiencing symptoms. [28, 31, 35] Viral shedding can also precede symptoms, which occurs in approximately 30% of cases. [16] Often, an infected food handler may not even show symptoms. [9] In these cases, people can carry the same viral load as those who do experience symptoms. [5, 9, 33]

A Japanese study examined the ability of asymptomatic food handlers to transfer norovirus. Approximately 12% of asymptomatic food handlers were carriers for one of the norovirus genotypes. [28] This was the first report of norovirus molecular epidemiology relating asymptomatic individuals to outbreaks, suggesting that asymptomatic individuals are an important link in the infectivity pathway. [15, 28] Asymptomatic infection may occur because some people may have acquired immunity, which explains why some show symptoms upon infection and some do not. [16, 28, 33] Such immunity does not last long, though. [16, 21, 28] These discoveries reveal just how complicated the pathway of norovirus infection is, as well as how difficult it is to define the true period of infectivity. [30] Furthermore, it remains unclear why some people do not become sick with norovirus even when they are exposed. [16, 21, 32] Very little is known about the differences in hygiene practices, behaviors, and personal susceptibility between those who become infected and those who do not, which brings up the potential for more research. [17] Discrepancies exist in the published research about infective doses for norovirus, with earlier studies having used a much higher dose to trigger immune responses. [16]

Symptoms & Risks of Norovirus Infection

Norovirus illness usually develops 24 to 48 hours after ingestion of contaminated food or water. [5, 16, 33] Symptoms typically last a relatively short amount of time, approximately 24 to 48 hours. [5, 25] These symptoms include nausea, vomiting, diarrhea, and abdominal pain.  Headache and low-grade fever may also accompany this illness. [5, 25, 33]  People infected with norovirus usually recover in two to three days without serious or long-term health effects. [5, 25]

Although symptoms usually only last one to two days in healthy individuals, norovirus infection can become quite serious in children, the elderly, and immune-compromised individuals. [10, 18, 33] In some cases, severe dehydration, malnutrition, and even death can result from norovirus infection, especially among children and among older and immune-compromised adults in hospitals and nursing homes. [25, 30] In England and Wales, 20% of those over the age of 65 die due to infectious intestinal illness other than Clostridium difficile. [18] Recently, there have been reports of some long-term effects associated with norovirus, including necrotizing entercolitis, chronic diarrhea, and post-infectious irritable bowel syndrome, but more data is needed to support these claims. [37]

Diagnosing a Norovirus Infection

Diagnosis of norovirus illness is based on the combination of symptoms, particularly the prominence of vomiting, little fever, and the short duration of illness. [5, 25, 33] If a known norovirus outbreak is in progress, public health officials may obtain specimens from ill individuals for testing in a lab. [5, 9] These lab tests consist of identifying norovirus under an electron microscope. A reverse transcriptase polymerase chain reaction test (RT-PCR assay) also can detect norovirus in food, water, stool samples, and on surfaces. These tests isolate and replicate the suspected virus’ genetic material for analysis. [25, 33] An ELISA can also be performed, which detects antigens. They are easier to perform than RT-PCR, but less sensitive and can also result in many false negatives. [9, 11]

Treating a Norovirus Infection

There is no specific treatment available for norovirus. [16, 33] In most healthy people, the illness is self-limiting and resolves in a few days; however, outbreaks among infants, children, elderly, and immune-compromised populations may result in severe complications among those affected.  [16, 27, 30, 33] Death may result without prompt measures. [5, 16, 25, 33] The replacement of fluids and minerals such as sodium, potassium and calcium – otherwise known as electrolytes – lost due to persistent diarrhea is vital. This can be done either by drinking large amounts of liquids, or intravenously. [16, 25]

Recent research has looked into the potential for developing a norovirus vaccine. [9, 16, 37] Researchers indicate that coming up with a norovirus vaccine would be similar to vaccinating for influenza, by using screening in order to select for the most prevalent strains. This is a quite challenging process. [37] Other challenges include the fact that cell culture and small-animal models are limited, host pre-exposure histories are complicated, and there is always the potential for the evolution of novel immune escape variants, rendering the vaccine useless. [13, 33] Furthermore, scientists would likely face a lack of funding to develop a vaccine because vaccine development is expensive. [12, 21]

Preventing Norovirus Infection

Common settings for norovirus outbreaks include restaurants and events with catered meals (36%), nursing homes (23%), schools (13%), and vacation settings or cruise ships (10%). [6] Proper hand washing is the best way to prevent the spread of norovirus. [9, 17, 25]

The good news about norovirus is that it does not multiply in foods as many bacteria do. [5, 31, 33] In addition, thorough cooking destroys this virus.  [5, 25] To avoid norovirus, make sure the food you eat is cooked completely. [5, 9, 10] While traveling in in areas that have polluted water sources, raw vegetables should be washed thoroughly before being served, and travelers should drink only boiled drinks or carbonated bottled beverages without ice. [9, 16]

Shellfish (oysters, clams, mussels) pose the greatest risk and any particular serving may be contaminated with norovirus; there is no way to detect a contaminated oyster, clam, or mussel from a safe one. [5, 31] Shellfish become contaminated when their waters become contaminated—e.g., when raw sewage is dumped overboard by recreational or commercial boaters).  [19, 33] Shellfish are filter feeders and will concentrate virus particles present in their environment. With shellfish, only complete cooking offers reliable protection; steaming does not kill the virus or prevent its transmission. [19] Some researchers suggest that norovirus monitoring in shellfish areas could be a good preventive strategy as well. [22] Waterborne norovirus outbreaks are ubiquitous, but difficult to recognize. Improved analysis of environmental samples would have the potential to significantly improve the detection for norovirus in shellfish waters. [20]

Finally, and as briefly mentioned earlier, outbreaks of norovirus infections have become synonymous with cruise ships. [7, 8, 36] Healthcare facilities also experience a high incidence of norovirus outbreaks.  [6, 30, 35]The CDC has published information regarding the prevention of norovirus outbreaks on cruise ships and in healthcare facilities on its website. [6, 7] Once a case has occurred, even more stringent hygienic measures than normal are required in order to prevent an outbreak, particularly on an enclosed space such as a cruise ship. [17]

References (more…)

Hepatitis A Infection in Waterloo, Seneca County, New York McDonalds Employee

The Seneca County Health Department has confirmed a case of Hepatitis A in a food service worker employed at the McDonalds located at 2500 Mound Rd. Waterloo, NY. Public health officials are stressing there is a low risk of contracting illness, however, individuals who have not been previously vaccinated for Hepatitis A and who consumed food/drink from McDonalds on the following dates should consider treatment.

If you ate at McDonald’s at 2500 Mound Rd. Waterloo, NY on 10/31 you should attend the 11/14/15 clinic.

If you ate at McDonald’s at 2500 Mound Road Waterloo, NY on any of the following dates you should attend either the 11/14 or the 11/15 clinic.

Monday, November 2nd, 2015

Tuesday, November 3rd, 2015

Thursday, November, 5th 2015

Friday, November 6th 2015

Sunday, November 8th 2015

Clinics will be held offering Hepatitis A Vaccine

Saturday, November 14, 2015- 1:00 pm-8:00 pm

Sunday, November 15, 2015 – 10:00 am-4:00 pm

Mynderse Academy Gymnasium

105 Troy Street

Seneca Falls, NY 13148

To preregister for a clinic www.health.state.ny.us/gotoclinic/50

For other additional questions: New York State Department of Health Hotline: 1-844-364-6397

Waterloo/Seneca Falls Hepatitis A FAQ

What happened at the McDonalds in Waterloo?

A worker at the McDonalds on Route 414 and Mound Road in Waterloo NY, a short distance from Exit 41 off the NYS Thruway, worked while they may have been shedding Hepatitis A virus, before the worker was diagnosed with the illness. Because of how Hepatitis A is spread, this may have put customers and coworkers at that McDonalds at risk of acquiring Hepatitis A.

What is Hepatitis A?

Hepatitis A is a contagious liver disease that results from infection with the Hepatitis A virus. It can range in severity from a mild illness lasting a few weeks to a severe illness lasting several months. Hepatitis A is usually spread when a person ingests fecal matter — even in microscopic amounts — from contact with objects, food, or drinks contaminated by the feces, or stool, of an infected person.

What are the symptoms of Hepatitis A?

Some people with Hepatitis A do not have any symptoms. Children in particular may not show symptoms. If you do have symptoms, they may include the following:

Fever
Fatigue
Loss of appetite
Nausea
Vomiting
Abdominal pain
Dark urine
Clay-colored bowel movements
Joint pain
Jaundice (a yellowing of the skin or eyes)
What if I am too late to get the treatment, or choose to not get treated?

Monitor yourself for signs and symptoms of Hepatitis A over the next 4-6 weeks. If you have any symptoms, contact your physician and be sure to tell them that you may have been exposed to Hepatitis A.

Has my child already been vaccinated for Hepatitis A?

The vaccine for Hepatitis A for children is recommended, but not required for school entry. If you do not know if your child has received the Hepatitis A vaccine, you should contact your child’s heathcare provider.

Is the Hepatitis A vaccine effective?

Yes, the Hepatitis A vaccine is highly effective in preventing Hepatitis A virus infection. Protection begins approximately 2 to 4 weeks after the first injection. A second injection in 6 monhts results in long-term protection.

Is the Hepatitis A vaccine safe?

Yes, the Hepatitis A vaccine is safe. No serious side effects have resulted from the Hepatitis A vaccine. Soreness at the injection site is the most common side effect reported. As with any medicine, there are very small risks that a serious problem could occur after someone gets the vaccine. However, the potential risks associated with Hepatitis A are much greater than the potential risks associated with the Hepatitis A vaccine. Before the Hepatitis A vaccine became available in the Unites States, more than 250,000 people were infected with Hepatitis A virus each year. Since the licensure of the first Hepatitis A vaccine in 1995, millions of doses of Hepatitis A vaccine have been given in the United States and worldwide.

Who should not receive the Hepatitis A vaccine?

People who have ever had a serious allergic reaction to the Hepatitis A vaccine or who are known to be allergic to any part of the Hepatitis A vaccine should not receive the vaccine. Tell those working at the clinic or your doctor if you have any severe allergies. Also, the vaccine is not licensed for use in infants under age 1 year.

If you are pregnant, it is OK to get the vaccine or immune globulin.

What is immune globulin?

Immune globulin is a substance made from human blood plasma that contains antibodies that protect against infection. It is given as a shot and provides short-term protection (approximately 3 months) against Hepatitis A. Immune globulin can be given either before exposure to the Hepatitis A virus (such as before travel to a country where Hepatitis A is common) or to prevent infection after exposure to the Hepatitis A virus. Immune globulin must be given within 2 weeks after exposure for the best protection.

How severe is Hepatitis A?

Almost all people who get Hepatitis A recover completely and do not have any lasting liver damage, although they may feel sick for months. Hepatitis A can sometimes cause liver failure and death, although this is rare and occurs more commonly in persons 50 years of age or older and persons with other liver diseases, such as Hepatitis B or C.

If I get Hepatitis A, when will symptoms start?

Symptoms will usually develop within 2-6 weeks after being exposed to the Hepatitis A virus. Most see symptoms start right around 4 weeks after exposure.

How is Hepatitis A treated? Is there a cure for Hepatitis A?

There are no special treatments for Hepatitis A. Most people with Hepatitis A will feel sick for a few months before they begin to feel better. A few people will need to be hospitalized. During this time, doctors usually recommend rest, adequate nutrition, and fluids. People with Hepatitis A should check with a health professional before taking any prescription pills, supplements, or over-the-counter medications, which can potentially damage the liver. Alcohol should be avoided.

Are there specific dates when this individual worked while possibly infectious?

Yes. These dates are Thursday October 29, Saturday October 31, Monday November 2, Tuesday November 3, Thursday November 5, Friday November 6, and Sunday November 8.

How likely am I to get sick? Who is at the highest risk?

Most people do not get sick when an employee at a restaurant has Hepatitis A. However, if an infected food handler is infectious and has poor hygiene, the risk goes up for patrons of that restaurant. The job duties of the ill employee involved front end duties—cashier, handling drinks, putting food on trays. This makes risk low, but there is still risk present.

Those at risk would be individuals who consumed food handled by the ill employee, or individuals who may have put their fingers in their mouth after handling objects handled by the ill employee. If you only used the bathroom at the McDonalds, you are at no risk.

Can anything be done to prevent getting sick?

If you were recently exposed to Hepatitis A virus and have not been vaccinated against Hepatitis A, you might benefit from an injection of either immune globulin or Hepatitis A vaccine. However, the vaccine or immune globulin must be given within the first 2 weeks after exposure to be effective. To this end, the Seneca County Health Department is setting up clinics to provide preventative treatment to individuals who visited the Waterloo McDonalds. (For those getting vaccine, a second vaccine in 6 months, at your physician, will result in maximum protection.)

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 and Carl’s Jr.

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

Salmonella Bacteria Induced Reactive Arthritis or Reiter’s Syndrome

inflammation-in-jointsWhat is Reactive Arthritis or Reiter’s Syndrome?

Reactive Arthritis refers to a group of arthritic diseases that includes a subset formally know as “Reiter’s Syndrome” The old term Reiter’s syndrome has fallen into disfavor.  In recent medical literature Reiter’s Syndrome is simply referred to as Reactive Arthritis which may or may not be accompanied by extraintestinal manifestations.

Reactive Arthritis is the name used to describe an uncommon, but potentially debilitating group of symptoms that follows a gastrointestinal, genitourinary, or viral infection. The most common gastrointestinal bacteria involved are Salmonella, Campylobacter, Yersinia, Shigella, E. coli, and Vibrio. The most common genitourinary causes are sexually transmitted diseases such as Chlamydia and Gonorrhea. The most common viral causes are the common flu, HIV, and Parvovirus.

The specific triad of arthritis, conjunctivitis, and urethritis was known as Reiter’s Syndrome. In many patients, however, only one or two of these symptoms many be present, such as arthritis and urethritis or arthritis and conjunctivitis. [1] A reactive arthritis may develop after a person eats food that has been tainted with the pathogenic bacteria. Many patients will get severe bloating, abdominal pain, and watery diarrhea. However in some patients, the initial infection may be milder and not easily recognized, but the reactive arthritis may still occur. Reactive arthritis typically involves inflammation of one joint (monoarthritis) or several joints (oligoarthritis), preferentially affecting those of the lower extremities.  The most common joints affected are the knees and ankles. The pattern of joint involvement is usually asymmetric. Inflammation can also be commonly seen at an enthesis (a place where ligaments and tendons attach to bone), especially the front of the knee or the back of the ankle where the Achilles attaches to the calcaneal bone.   This is referred to as an enthesopathy. It causes local swelling and pain with walking or exercise.

Salmonella has been the most frequently studied bacterium associated with reactive arthritis. Overall, studies have found rates of Salmonella-associated reactive arthritis to vary between 6% and 30%. [1] The frequency of post-infectious Reiter’s syndrome specifically, however, has not been well described. In a Washington State study of an outbreak of foodborne Salmonella gastroenteritis, 29% of patients developed arthritis, but only 3% developed the triad of symptoms associated with Reiter’s syndrome. [2] In addition, individuals of Caucasian descent may be more likely than those of Asian descent to develop reactive arthritis, [3] and children may be less susceptible than adults to reactive arthritis following infection with Salmonella. [4]

The frequency of acute reactive arthritis from other bacteria varies widely. The occurrence of new joint pain alone after enteric infection is reported to be between 1 and 4% in adults with Campylobacter or Shigella infections. [5]   In another study, it has been reported to occur in 0.6% to 24% of Campylobacter gastroenteritis patients. [6]   After Shigella infection the percentage of patients who exhibit subsequent reactive arthritis ranges from 1.5% to 7%. [7]

A clear association has been made between reactive arthritis and a genetic marker called the Human Leukocyte Antigen (HLA) B27 genotype. HLA is a major histocompatibility complex in humans; these are proteins present on the surface of all body cells that contain a nucleus, and are in especially high concentrations in white blood cells (leukocytes). It is thought that HLA-B27 may affect the elimination of the infecting bacteria or an individual’s immune response. [1] HLA-B27 has been shown to be a predisposing factor in one-half to over two-thirds of individuals with reactive arthritis. [8,1] While HLA-B27 does not appear to predispose to the initial infection itself, it increases the risk of developing arthritis that is more likely to be severe and prolonged. This risk may be slightly greater for Salmonella and Yersinia-associated arthritis than with Campylobacter, but more research is required to clarify this. [1]

Why Have Some Forms of Reactive Arthritis Been Called Reiter’s Syndrome?

One could also ask, “Why isn’t Reiter’s syndrome called Reiter’s syndrome anymore?”  The answer is that the syndrome, or group of symptoms, is named for Hans Reiter who described a soldier with the triad of urethritis (burning and pain with urination), conjunctivitis (redness and pain of the eye), and arthritis (swelling and pain of the joints) after having bloody diarrhea in 1916.  However, the history of this constellation of signs actually predates his description.  And what is disturbing is that Reiter was a high-ranking Nazi official who was responsible for medical experiments in concentration camps. [9, 10]   As a result, the term Reiter’s syndrome has fallen out of favor and Reactive Arthritis is preferred to describe the post-infectious arthritis which may be accompanied by extra-articular manifestations (such as urethritis and conjunctivitis).

What are the Symptoms of Reactive Arthritis?

The three most common symptoms of Reiter’s syndrome are arthritis, conjunctivitis, and urethritis. The onset of symptoms typically occurs one to four weeks following the initial infection and may present acutely or develop slowly over time. It can occasionally occur years after the initial infection. In many patients the urethritis and conjunctivitis symptoms are usually mild, symmetric, and bilateral. [11, 12] Bacterial cultures are negative and the inflammation typically resolves within 10 days without treatment.

Urethritis, a urinary tract inflammation, is often accompanied by symptoms such as a penile discharge in males, pain with urination, or blood in the urine. Females may also present with an inflammation of the cervix or pain during intercourse. Urethritis in either males or females may also be present without symptoms but can show up on a urine test with your doctor. [8]

Ophthalmic, or eye, manifestations occur in approximately one-third of individuals with Salmonella-associated arthritis. [8]  The involvement of the eye in reactive arthritis is most commonly manifested as conjunctivitis, an inflammation of the mucous membrane that covers the eyeball. Conjunctivitis usually appears within a few weeks of the onset of arthritis. Conjunctivitis and uveitis often presents with redness of the eyes, eye pain and irritation, blurred vision and a yellowish discharge. Conjunctivitis is present in up to 50% of affected individuals and can develop at any time during the course of the disease, although it is more common in reactive arthritis associated with genitourinary or Shigella infections. [13]

Anterior uveitis, an inflammation of the inner eye, is the second most common ocular symptom of Reiter’s syndrome, occurring in up to 12% of affected persons. [12] Uveitis is most often acute, unilateral, and recurrent. [14, 15]  It is more frequent in those who are HLA-B27 positive and in individuals with sacroiliitis, an inflammation of the sacroiliac (sacrum and ilium) joint or region. [13] Other ocular conditions also have been associated with Reiter’s, including scleritis, cataract, glaucoma, keratitis, papillitis, retinal and disc edema, and retinal vasculitis. [16]

The arthritis associated with Reiter’s syndrome generally occurs rapidly, with joints becoming hot and swollen; large effusions, or collections of fluid, can develop in the knee joint or ankle. [1, 8] Wrists, fingers and other joints can be affected, although with less frequency. Joint pain without inflammation may also occur at sites other than those affected by inflammation. A condition called enthesopathy also commonly occurs, in which the tendon that attaches to the bone becomes inflamed. [8, 13] Enthesopathies occur in 5 to 21% of individuals with Salmonella-associated arthritis. [8] The heel is the most common site with the development of heel pain and Achilles tendonitis, but pain at the insertion of the patellar (kneecap) tendon into the tibia, the larger of the two bones in the lower leg, may also occur. Some individuals with reactive arthritis may develop heel spurs, bony growths that cause chronic foot pain. Arthritis from reactive arthritis can also affect the joints of the back, causing spondylitis, an inflammation of the vertebrae and the attached disks and ligaments in the spinal column, and asymmetric sacroiliitis. [15] Patients will present with pain and morning stiffness in the lower back or neck. Pain will be worse after rest or sleep and better after walking for a while.

The duration of reactive arthritis symptoms can vary greatly. The literature suggests that the majority of affected individuals recover within a year although reactive arthritis can become chronic. [13, 17] Up to 50% of those with reactive arthritis may have recurrent bouts of arthritis and 15 to 30% develop chronic arthritis or sacroiliitis. [15] In one study, 18 (67%) of 27 individuals who developed reactive arthritis after a Salmonella infection continued to have symptoms at five years of follow-up. [17] Symptoms were severe enough to force a change in work for four individuals and another four had objective damage to joints radiographically.

Other symptoms of reactive arthritis may include a painless skin rash on the penis in men called circinate balanitis. Skin rashes on the soles of the feet and, less often, on the palms of the hands or elsewhere may also occur; these rashes are called keratoderma blennorrhagicum (or keratosis blennorrhagica) and are similar to psoriasis. They often begin as clear vesicles (blisters) on a red base and progress to macules (flat lesions), papules (raised lesions), and nodules (firm bumps). [13] In addition, some people develop mouth ulcers that come and go. In some cases, these ulcers are painless and go unnoticed.

How is Reactive Arthritis or Reiter’s Syndrome diagnosed?

Diagnosis of reactive arthritis (including the condition formerly called Reiter’s syndrome) is mainly clinical.  There are no validated diagnostic criteria, however some guidance for diagnosis is available. [18, 19, 20, 10]   In 1995, the Third International Workshop on Reactive Arthritis established criteria for diagnosing reactive arthritis.  The main criteria involve the pattern of joint involvement and the timing of the onset of the condition (such as soon after an infection).  Diagnosis of Reiter’s syndrome has essentially been replaced with diagnosis of the broader category in which it resides:  Reactive Arthritis.

The diagnostic criteria of the Third International Workshop on Reactive Arthritis are:

  • The arthritis should predominantly involve the lower limb, involve one or only a few joints and not equally involve both sides of the body (asymmetric).
  • There should be evidence or a history of preceding infection.  Although it is ideal to have a culture that is positive for an infectious agent that is recognized to be associated with this condition (such as Salmonella or Chlamydia), if the patient has documented diarrhea or urethritis in the prior 4 weeks, laboratory confirmation is not required.
  • If there is no clear clinical infection, then laboratory confirmation (perhaps with serology or a culture) is essential.
  • The patient should not have evidence that the joint itself is infected (i.e., septic arthritis).  Also, other causes of monoarthritis (such as gout) or oligoarthritis (such as rheumatoid arthritis) should be ruled out.

Interestingly, the above criteria do not require laboratory tests (such as HLA-B27).  Features that have been considered part of Reiter’s syndrome such as conjunctivitis, iritis, skin lesions, noninfectious urethritis, and certain types of cardiac and neurological abnormalities are not required for a diagnosis of reactive arthritis.

How is Reiter’s Syndrome treated?

Testing for and treating any underlying infection is often attempted but in many cases the underlying infection is self limited or can no longer be found. If the inciting infectious agent can be determined it must be treated aggressively with antibiotics.

Symptomatic treatment with high doses of a nonsteroidal anti-inflammatory drug (NSAID) and steroid injections into affected joints can be helpful for patients with reactive arthritis. [8] NSAIDs can reduce joint inflammation and are commonly used to treat patients with reactive arthritis. Some traditional NSAIDs, such as aspirin and ibuprofen, are available without a prescription, but others that are more effective for reactive arthritis, such as indomethacin and voltaren, must be prescribed by a doctor. Less is known about whether a new class of NSAIDs, called COX-2 inhibitors, is effective for reactive arthritis, but they may reduce the risk of gastrointestinal complications associated with traditional NSAIDs. [21] For people with severe joint inflammation, injections of corticosteroids directly into the affected joint may reduce inflammation. Doctors usually give these injections only after trying unsuccessfully to control arthritis with NSAIDs. In some cases, short courses of oral steroids, such as methylprednisolone or prednisone, may also be required.

A small percentage of patients with reactive arthritis have severe symptoms that cannot be controlled with any of the above treatments. For these people, medicine that suppresses the immune system, such as sulfasalazine or methotrexate, may be effective. [22, 23, 21]  If the symptoms do not respond to these agents a newer group of medications, called biologics, can often be very effective. Biologic agents can be either injectables (such as etanercept or adalimumab) or given intravascularly (such as infliximab or rituximab).   These agents can be very immunosuppressive and are very expensive so are not used as first-line treatments.

Topical corticosteroids, which come in a cream or lotion, can be applied directly on the skin lesions associated with reactive arthritis. Topical corticosteroids reduce inflammation and promote healing. [21]

Antibiotics to eliminate the bacterial infection that triggered the reactive arthritis may be prescribed. The specific antibiotic prescribed depends on the type of bacterial infection present. It is important to follow instructions about how much medicine to take and for how long; otherwise the infection may persist. Typically, an antibiotic is taken for 7 to 10 days or longer. [21] Currently, however, there is no evidence to suggest that antibiotic treatment is beneficial once reactive arthritis has occurred. [1]

Exercise, when introduced gradually, may help improve joint function. In particular, strengthening and range-of-motion exercises will maintain or improve joint function. Strengthening exercises builds up the muscles around the joint to better support it. Muscle-tightening exercises that do not move any joints can be done even when a person has inflammation and pain. Range-of-motion exercises improve movement and flexibility and reduce stiffness in the affected joint. For patients with spine pain or inflammation, exercises to stretch and extend the back can be particularly helpful in preventing long-term disability. Aquatic exercise also may be helpful. Before beginning an exercise program, patients should talk to a health professional who can recommend appropriate exercises. [21]

What Is the Prognosis for People Who Have Reiter’s Syndrome or Reactive Arthritis?

Most people with reactive arthritis recover fully from the initial flare of symptoms and are able to return to regular activities 2 to 6 months after the first symptoms appear. In some cases, the symptoms of arthritis may last up to 12 months, although these symptoms are usually very mild and do not interfere with daily activities. Approximately 20% of people with reactive arthritis will have chronic (long-term) arthritis, which usually is mild.

Studies show that between 15% and 50% of patients will develop symptoms again sometime after the initial flare has disappeared. [15, 21] Back pain and arthritis are the symptoms that most commonly reappear. Up to one-third of affected individuals will have chronic, severe arthritis that is difficult to control with treatment and may cause joint deformity. [13, 24, 21, 15] One study found that two-thirds of individuals who developed reactive arthritis after a Salmonella infection continued to have symptoms at five years of follow-up. [17] Symptoms were severe enough to force a change in work for four of 18 individuals and another four had objective damage to joints radiographically.

Overall, a relapsing course appears less common in enteric-infection-related disease than in Chlamydia-associated reactive arthritis (of genitourinary origin). HLA-B27 contributes to the development of chronic disease and therefore, the prognosis is less favorable in those who are HLA-positive. [1, 24]

How can Reactive Arthritis be prevented?

Because Reactive Arthritis is the result of a prior infection, no one specific measure can be prescribed for the prevention of Reiter’s syndrome or Reactive Arthritis.

Bacteria known to cause Reactive Arthritis are sensitive to heat and other common disinfection procedures, including pasteurization of milk, adequate cooking of meat and poultry, and chlorination or ozonation of water.  The most reliable method to ensure such bacteria as Salmonella, Campylobacter, and Shigella are killed during the cooking process is to use a digital food thermometer.  General sanitary techniques of hand washing and clean drinking water have decreased the incidence of these infections in industrialized countries but they are still very prevalent in less developed countries and the third world.

References

  1. Hill Gaston JS, Lillicrap MS.  (2003).  Arthritis associated with enteric infection. Best Practices & Research Clinical Rheumatology.  17(2):219-239, article abstract and paid-access to full text available online at http://www.bprclinrheum.com/article/S1521-6942(02)00104-3/abstract
  1. Dworkin MS, Shoemaker PC, Goldoft MJ, Kobayashi JM.  (2001).  “Reactive arthritis and Reiter’s syndrome following an outbreak of gastroenteritis caused by Salmonella enteritidis.  Clin. Infect. Dis. 33(7):1010-1014, available online at http://cid.oxfordjournals.org/content/33/7/1010.full
  1. McColl GJ, Diviney MB, Holdsworth RF, McNair PD, Carnie J, Hart W, McCluskey J.  (2000).  HLA-B27 expression and reactive arthritis susceptibility in two patient cohorts infected with Salmonella Typhimurium.  Australian and New Zealand Journal of Medicine 30(1):28-32, article abstract and paid-access to full text available online at http://onlinelibrary.wiley.com/doi/10.1111/j.1445-5994.2000.tb01050.x/abstract
  1. Rudwaleit M, Richter S, Braun J, Sieper J.  (2001).  Low incidence of reactive arthritis in children following a Salmonella outbreak. Annals of the Rheumatic Diseases. 60(11):1055-1057, available online at http://ard.bmj.com/content/60/11/1055.full
  1. Rees JR, Pannier MA, McNees A, Shallow S, Angulo FJ, Vugia DJ.  (2004).  Persistent diarrhea, arthritis, and other complications of enteric infections: a pilot survey based on California FoodNet surveillance, 1998-1999. Clin. Infect. Dis. 38(Suppl 3):S311-S317, available online at http://cid.oxfordjournals.org/content/38/Supplement_3/S311.full.pdf+html
  1. Pope JE, Krizova A, Garg AX, Thiessen-Philbrook H, Ouimet JM.  (2007).  Campylobacter reactive arthritis:  a systematic review.  Seminars in Arthritis and Rheumatism (in press as of July 2007), available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909271/?tool=pubmed
  1. Hannu T, Mattila L, Siitonen A, Leirisalo-Repo.  (2005).  Reactive arthritis attributable to Shigella infection:  a clinical and epidemiological nationwide study.  Annals of Rheumatologic Diseases.  64:594-598, available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1755450/
  1. Barth WF, Segal K.  (1999).  “Reactive arthritis (Reiter’s syndrome).”  American Family Physician.  60(2):499-503, 507, available at http://www.aafp.org/afp/1999/0801/p499.html
  1. Panush RS, Paraschiv D,  Dorff RE.  (2003).  The tainted legacy of Hans Reiter.  Seminars in Arthritis and Rheumatology.  32:231-236, article abstract and paid-access to full text available online at http://www.journals.elsevierhealth.com/periodicals/ysarh/article/S0049-0172(02)70103-0/abstract
  1. Petersel DL, Sigal LH.  (2005).  Reative arthritis.  Infectious Disease Clinics in North America.  19:863-883, article abstract and paid-access to full text available online at http://www.id.theclinics.com/search/quick
  1. Lee DA, Barker SM, Su WP, Allen GL, Liesegang TJ, Ilstrup DM. (1986). The clinical diagnosis of Reiter’s syndrome. Ophthalmic and nonophthalmic aspects. Ophthalmology. 93(3):350–356, article abstract available online at http://www.ncbi.nlm.nih.gov/pubmed/3486396
  1. Ostler HB, Dawson CR, Schachter J, Engleman EP. (1971). Reiter’s syndrome. Am J Ophthalmol. 71(5):986–991.
  1. Kataria RK, Brent LH.  (2004).  Spondyloarthropathies.  American Family Physician 69 (12):2853-2860, available at http://www.aafp.org/afp/2004/0615/p2853.html
  1. Lau CS, Burgos-Vargas R, Luothrenoo W, Mok MY, Wordsworth P, Zeng QY. (1998). Features of spondyloarthritis around the world. Rheum Dis Clin North Am. 24(4):753-770, article abstract and paid-access to full text available online at http://www.ncbi.nlm.nih.gov/pubmed/9891709
  1. Yu DT, Peng TF. (2001). Reiter’s syndrome. In: Ruddy S, Harris ED Jr, Sledge CB, eds. Kelley’s Textbook of rheumatology. 6th ed. Philadelphia: Saunders, 2001:1055-70.
  1. Kiss S, Letko E, Qamruddin S, Baltatzis S, Foster CS.  (2003).  Long-term progression, prognosis, and treatment of patients with recurrent ocular manifestations of Reiter’s syndrome.  Ophthalmology.  110(9):1764-1769, article abstract available online at http://www.ncbi.nlm.nih.gov/pubmed/13129875
  1. Thomson GT, DeRubeis DA, Hodge MA, Rajanayagam C, Inman RD.  (1995).  Post-Salmonella reactive arthritis: late clinical sequelae in a point source cohort.  The American Journal of Medicine.  98(1):13-21, article abstract and paid-access to full text available online at http://www.amjmed.com/article/S0002-9343(99)80076-X/abstract
  1. Braun J, Kigsley G, van der Heijde D et al. (2000).  On the difficulties of establishing a consensus on the definition of and diagnostic investigations for reactive arthritis.  Results and discussion of a questionnaire prepared for the 4th International Workshop on Reactive Arthritis, Berlin, Germany, 3-6 July 1999.  Journal of Rheumatology. 27:2185-92, article abstract available online at http://www.ncbi.nlm.nih.gov/pubmed/10990232
  1. Hannu T, Inman R, Granfors K, Lerisalo-Repo M. (2006).  Reactive arthritis or post-infectious arthritis?  Best Practices and Research Clinical Rheumatology 20:419-33, article abstract available online at http://www.ncbi.nlm.nih.gov/pubmed/16777574
  1. Kingsley G, Sieper J. (1996).  Third International Workshop on Reactive Arthritis.  23-26 September 1995, Berlin, Germany.  Annals of Rheumatic Diseases 55:564-84, availbe online at http://ard.bmj.com/content/55/8/564.full.pdf?sid=8224781d-9d45-403d-b846-1cdf67466d5a
  1. National Institutes of Health. (2011). Questions and Answers about Reactive Arthritis. NIH Publication No. 09-5039, available online at http://www.niams.nih.gov/Health_Info/Reactive_Arthritis/default.asp
  1. Clegg DO, Reda DJ, Weisman MH, Cush JJ, Vasey FB, Schumacher HR Jr, Budiman-Mak E, Balestra DJ, Blackburn WD, Cannon GW, Inman RD, Alepa FP, Mejias E, Cohen MR, Makkena R, Mahowald ML, Higashida J, Silverman SL, Parhami N, Buxbaum J, Haakenson CM, Ward RH, Manaster BJ, Anderson RJ, Henderson WG, et al. (1996). Comparison o fsulfasalazine and placebo in the treatment of reactive arthritis (Reiter’s syndrome). A Department of Veterans Affairs Cooperative Study. Arthritis Rheum. 39(12):2021-7, abstract available online at http://www.ncbi.nlm.nih.gov/pubmed/8961907.
  1. Creamer P, Lim K, George E, Dieppe P. (1994). Acute inflammatory polyarthritis in association with tamoxifen. Br J Rheumatol. 33(6):583-5, abstract and paid-access to full text available online at http://rheumatology.oxfordjournals.org/content/33/6/583.abstract.
  1. Leirisalo-Repo M, Helenius P, Hannu T, Lehtinen A, Kreula J, Taavitsainen M, Koskimies S.  (1997).  Long-term prognosis of reactive Salmonella arthritis. Annals of Rheumatic Disease.  56(9):516-520, available online at http://ard.bmj.com/content/56/9/516.full.pdf?sid=dc192ce4-4995-493e-85a0-90bbc3840350

Salmonella: Marler Clark, The Food Safety Law Firm, is the nation’s leading law firm representing victims of Salmonella outbreaks. The Salmonella lawyers of Marler Clark have represented thousands of victims of Salmonella 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 Salmonella lawyers have litigated Salmonella cases stemming from outbreaks traced to a variety of foods, such as cantaloupe, tomatoes, ground turkey, salami, sprouts, cereal, peanut butter, and food served in restaurants. The law firm has brought Salmonella lawsuits against such companies as Cargill, ConAgra, Peanut Corporation of America, Sheetz, Taco Bell, Subway and Wal-Mart.

South Carolina Gives 4,809 Hepatitis A Vaccines After Hardee’s Exposure

2g91hmtyHardee’s should reimburse the State of South Carolina for the expense.

As of September 25th, the South Carolina Department of Health and Environmental Control announced it has provided 4,809 vaccinations through its hepatitis A vaccine clinics in Spartanburg and Greenville.

Vaccinations are being offered to individuals who might have been exposed to hepatitis A at two Hardee’s restaurants located in Spartanburg County. The restaurants are located at 12209 Greenville Highway in Lyman and 1397 E. Main St. in Duncan.

To serve customers and staff, DHEC will operate a clinic at the Spartanburg County Health Department on Saturday, September 26th from 9 a.m. to noon. Clinic operations will continue on Monday, September 28th.

Customers and staff who, as of September 25th, ate at the Lyman-area restaurant September 11th through September 15th, or the Duncan-area restaurant September 11th through September 13th, should receive post-exposure treatment for hepatitis A. Post-exposure treatment is recommended for individuals if it can be administered less than two weeks from their date of consuming anything from the restaurants.

Customers and staff who ate at the restaurants between August 31st and September 10th are not likely to benefit from post-exposure treatment. Anyone who ate at these Hardee’s restaurants between these dates should watch for symptoms of infection, such as nausea, vomiting, and jaundice, which is yellowing of the eyes and skin. Seek medical care if symptoms develop.

Marler Clark has filed a Class Action lawsuit against Hardee’s in South Carolina. Here are some historical examples of other Class Actions involving those who received shots:

  • Approximately 1,300 persons as part of a class action on behalf of persons who received IG shots due to an HAV outbreak in June and July 2000 in Spokane, Washington, which was associated with food served at a Carl’s Jr. fast-food restaurant;
  • More than 1,500 individuals in a class action related to a previous HAV outbreak at the D’Angelo’s in Swansea, Massachusetts in 2001;
  • Approximately 9,000 persons who received IG shots due to an outbreak of HAV at a Chi-Chi’s restaurant near Pittsburgh, Pennsylvania in 2003;
  • Approximately 3,800 persons as part of a class action on behalf of persons who received IG shots due to an HAV exposure in June 2004 at a Friendly’s restaurant in Arlington, Massachusetts;
  • Approximately 850 persons as part of a class action on behalf of persons who received IG shots due to an HAV exposure at a Quizno’s in Boston, Massachusetts in 2004;
  • Over 3,000 persons who received IG shots due to potential HAV exposure in January 2007 at a Houlihan’s restaurant in Geneva, Illinois;
  • More than 5,000 persons who were required to get vaccinations against HAV following exposure at a McDonald’s restaurant in Milan, Illinois in 2009;
  • Approximately 3,000 claimants who dined at The Olive Garden Italian Restaurant in Fayetteville, North Carolina who thereby were required to get vaccinations against HAV following their potential exposure to hepatitis A;
  • All persons who consumed food and drink at a McDonald’s Restaurant in Northport, Alabama on March 14, 2012 or on March 16, 2012, and who thereby were required to get vaccinations against HAV following their potential exposure to HAV;
  • More than 700 claimants who consumed food or drink purchased at a Papa John’s restaurant in Charlotte, North Carolina in March and April 2014, and who thereby were required to get vaccinations against HAV following their potential exposure to hepatitis A;
  • Approximately 2,400 persons who received HAV vaccines in 2014 due to exposure at a Charlotte, North Carolina Papa Johns;
  • Approximately 2,700 persons who received HAV vaccines in 2014 due to exposure at a Springfield, Missouri Red Robin; and
  • Presently Marler Clark is class counsel for nationwide putative HAV class involving as many as 25,000 claimants.

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 and Carl’s Jr.

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

Seattle Food Safety Law Firm: 22 Years of E. coli Experience

The E. coli lawyers of Marler Clark have many years of experience working with clients on E. coli outbreak lawsuits.

E. coli are bacteria that can cause serious, sometimes fatal, infections in humans.  The Centers for Disease Control and Prevention (CDC) estimates that E. coli causes 2,000 hospitalizations in the United States each year.

Ten percent of E. coli victims develop hemolytic uremic syndrome (HUS), which can cause kidney failure, damage to the central nervous system, and ultimately death.

The Marler Clark E. coli lawyers have unmatched experience representing victims of E. coli and HUS.  We have represented hundreds of victims of E. coli outbreaks traced to foods such as hamburgers, spinach, raw milk, water, and food served at restaurants.  The Marler Clark E. coli lawyers are the only lawyers in the nation with a practice focused exclusively on plaintiff foodborne illness litigation.

Our E. coli lawyers have represented victims of notable E. coli outbreaks such as the 2006 Dole Spinach E. coli outbreak, the 2007 Cargill beef E. coli outbreak, and the landmark 1993 Jack in the Box E. coli outbreak. Contact us today to learn more about our services.

Washington Pork Outbreak Continues

first-chinese-bbqThe Salmonella outbreak linked to pork products has grown to 134 cases in 10 counties around the state. Consumers are advised to cook pork thoroughly.

The case count has continued to grow as state health officials work with Public Health — Seattle & King County along with other local, state, and federal partners on the disease investigation. The federal Centers for Disease Control and Prevention (CDC) sent its team of “disease detectives” to the state to help. Investigators are interviewing the most recent cases and comparing information to early cases, which were first reported in the spring.

Disease investigators are searching for possible contamination and exposure sources from a wide range of possible venues, including restaurants, markets, slaughter facilities, and farms/ranches. Salmonella bacteria are commonly found in animals used for food, and proper storage, handling, preparation, and cooking can help prevent the illness known as salmonellosis.

Most of the illnesses have been confirmed with the outbreak strain of Salmonella bacteria, and early testing shows a connection to a slaughter facility in Graham, WA. Samples were collected at Kapowsin Meats in Pierce County last week. Testing confirms the outbreak strain was present. The business, which is regulated by the United States Department of Agriculture Food Safety and Inspection Service, has cooperated with the investigation. There may be other sources and disease investigators are searching for the origin of the Salmonella bacteria in the outbreak.

The 134 cases include residents of Clark (2), Cowlitz (1), Grays Harbor (1), King (84), Kitsap (1), Mason (2), Pierce (12), Snohomish (24), Thurston (2), and Yakima (5) counties.

Exposure for many of the ill people apparently was whole roasted pigs, served at private events and restaurants. State health officials have issued guidance for cooking whole roasted pigs, with an emphasis on making sure the meat is cooked thoroughly. In addition to proper handling and preparation, thorough cooking can help prevent possible illness. A meat thermometer should be used to ensure an internal temperature of 145 degrees in the thickest cut of the meat.

Salmonellosis, the illness caused by infection with Salmonella, can cause severe and even bloody diarrhea, fever, chills, abdominal discomfort, and vomiting. Serious bloodstream infections may also occur. Annually, 600-800 cases of salmonellosis are reported among Washington residents.

Proper food handling, preparation, and cooking are the best precautions to take to prevent illness. Following food safety guidance can help prevent food-borne illness. Health officials warn consumers to use a food thermometer to make sure all meats and fish are cooked to a safe internal temperature; guidance can be found on the Department of Health website. Other food safety tips include washing hands thoroughly with soap and water before and after preparing food, especially raw meats.

To avoid cross-contamination, don’t place cooked food on a plate that previously held raw meat of any kind. It’s also important to wash and then sanitize cutting boards, knives, and countertops that come into contact with raw meat by using a solution of bleach water (1 teaspoon bleach per gallon of water) or antibacterial cleaner.

Contact with live animals— including pigs or other livestock at home, in petting zoos, at local fairs and elsewhere — can create exposure to Salmonella and other bacteria. Thorough hand washing after contact with live animals is an important tool in preventing the spread of disease.

The Department of Health website (www.doh.wa.gov) is your source for a healthy dose of information. Also, find us on Facebook and follow us on Twitter.

22 Years of E. coli Lawsuits with Marler Clark

MCthefoodsafetylawfirmMarler Clark, The Food Safety Law Firm, is the nation’s leading law firm representing victims of E. coli outbreaks and hemolytic uremic syndrome (HUS). The E. coli lawyers of Marler Clark have represented thousands of victims of E. coli and other foodborne illness infections 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 E. coli lawyers have litigated E. coli and HUS cases stemming from outbreaks traced to ground beef, raw milk, lettuce, spinach, sprouts, and other food products. The law firm has brought E. coli lawsuits against such companies as Jack in the Box, Dole, ConAgra, Cargill, and Jimmy John’s. We have proudly represented such victims as Brianne Kiner, Stephanie Smith and Linda Rivera.

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

20 Years of Salmonella Lawsuits with Marler Clark

MCthefoodsafetylawfirmMarler Clark, The Food Safety Law Firm, is the nation’s leading law firm representing victims of Salmonella outbreaks. The Salmonella lawyers of Marler Clark have represented thousands of victims of Salmonella 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 Salmonella lawyers have litigated Salmonella cases stemming from outbreaks traced to a variety of foods, such as cantaloupe, tomatoes, ground turkey, salami, sprouts, cereal, peanut butter, and food served in restaurants. The law firm has brought Salmonella lawsuits against such companies as Cargill, ConAgra, Peanut Corporation of America, Sheetz, Taco Bell, Subway and Wal-Mart. If you or a family member became ill with a Salmonella infection, including Reactive Arthritis or Irritable bowel syndrome (IBS), after consuming food and you’re interested in pursuing a legal claim, contact the Marler Clark Salmonella attorneys for a free case evaluation.

Food Safety News: Call for Op-eds and Subscribers

op-ed_406x250Food Safety News does not take a vacation, nor does it take time off to attend this or that summer conference. But people do, so this is a time of opportunity for you. We’d like to invite you to try your hand as one of our contributing opinion-editorial writers.

If you choose to accept our invitation, you could be joining some of the best-known food safety people in government, industry and academia whom we count among our contributors.

We have been the go-to publication for sharing ideas with the food safety world, and we’ve run editorials from high-profile players in the food industry, insightful academics, and leaders at FDA, USDA and CDC, alongside everyday people, with something to say about food safety.

At most times of the year, if you submit an op-ed to Food Safety News, it is a good bet there is a line ahead of you. For the rest of the summer, there is not likely to be much waiting since those who are usually in line seem to have scattered for vacations and conferences.

We don’t pay our contributing writers because then we could not call them “contributing” writers. But we can’t help noticing that our contributing writers are often the same people getting the big job offers and opportunities for exotic foreign travel.

We don’t want to oversell ourselves, but there are advantages to becoming known.

Becoming a Food Safety News contributing writer is not difficult, but there are few things you should know.

You should have something to say about food safety. This is important because we are called Food Safety News. We are sure your grandma’s sugar cookie recipes were great, but unless she poisoned people with them and then learned some lessons you want to share, it won’t be a fit.

In other words, you want to have a food safety angle and your topic should interest our large, broad audience. Somewhere around a half-million people check in on Food Safety News every month.

With a submission, first-time contributors also need to submit a photo, a short biography, and links for their author’s file at Food Safety News. This is the area shown after someone clicks on your byline. Links to websites, email, and twitter accounts are most common.

Food Safety News does not impose any minimum or maximum word counts on contributing writers. However, most probably fall in the 600- to 1,200-word range.

Either Managing Editor Cathy Siegner or I are available if you want to run your idea past us before you start writing. Or, if you’ve already written something, just turn it in to Cathy (I tend to lose things).

Either of us would be happy to take any questions you have. Think of how accomplished you’ll feel sharing your thoughts with a few hundred thousand of your associates in food safety rather than just sitting on a beach somewhere!

Contact us via email as listed below:

Dan Flynn, Editor in Chief
Food Safety News
dflynn@foodsafetynews.com

Cathy Siegner, Managing Editor
Food Safety News
csiegner@foodsafetynews.com

(To sign up for a free subscription to Food Safety News, click here.)