Carbon

AP reports that Police in a seaside community on Mexico’s Baja California peninsula said Wednesday that two Americans have been found dead in their hotel room. 

Police said the deaths occurred in the community of El Pescadero on Tuesday. The town is located between Todos Santos and the resort of Los Cabos, in Baja California Sur state.

U.S. officials said they were aware of the case but could not comment on it because of privacy concerns. There was no immediate information on the names or hometowns of the victims.

According to a police officer, paramedics received a report Tuesday that the Americans were unconscious in their room. They were dead by the time paramedics arrived. The suspected cause of death was inhalation of gas. 

There have been several cases of such deaths in Mexico due to poisoning by carbon monoxide or other gases. Such gases are often produced by improperly vented or leaky water heaters and stoves.

In October, three U.S. citizens found dead at a rented apartment in Mexico, apparently victims of gas inhalation.

The Mexico City police department said the three were found unresponsive Oct. 30 in an upscale neighborhood. They had apparently rented the dwelling for a short visit. Post-mortem examinations suggested the two men and one woman died of carbon monoxide poisoning. 

In Mexico, proper gas line installations, vents and monitoring devices are often lacking. 

In 2018, a gas leak in a water heater caused the deaths of an American couple and their two children in the resort town of Tulum, south of Playa del Carmen.

An inspection revealed that the water heater at the rented condominium was leaking gas. Prosecutors said the gas leak was perhaps caused by a lack of maintenance or the age of the equipment.

The Food and Drug Administration is investigating two new outbreaks. Sources of the pathogens involved have not yet been identified.

In an outbreak of infections of Salmonella Paratyphi B var. L(+) tartrate+ there are 31 confirmed patients. The FDA reports that it has begun traceback efforts but has not reported what food or foods are being traced.

In an outbreak of infections from the microscopic cyclospora parasite, 28 patients have been confirmed. As with the Salmonella outbreak, the FDA has begun traceback efforts but has not reported what food or foods are being traced. 

Well, its more than a half a loaf.

Yesterday I had the great opportunity to speak to Food and Drug officials at their annual conference.  In the audience were a smattering of “GET THE ‘F’ OUT OF THE FDA” t-shirts. The hundreds of t-shirts that I had sent to the conference were returned to me unopened – no one wanted to offend the Commissioner and the FDA’s top leadership. My guess is that if the t-shirts had been given out, there might have been a sea of light blue.

The talk with the great Brian Ronholm ranged over my 30 years litigating nearly every major – and many minor foodborne illness cases in the United States and around the world.  Given the audience, and the return of the t-shirts, I was surprised when he asked me about my t-shirt campaign (see below) and my desire to restructure the FDA into a separate Food and Human Nutrition and Drugs and Medical Devices.  I made my pitch that all aspects of food should be reorganized under a separate Commissioner with another separate Commissioner for drugs to a rousing round of applause.  It is certainly clear that the rank and file – although not the leadership – sees that we would be better served by separating the functions.

Well, it seems that the House of Representatives are paying attention (perhaps it was the delivery of hundreds of t-shirts to House and Senate members over that last months?). Here is what House Appropriations just released directing a restructuring – skip to page 79.

Human Foods Program Restructuring.—The Committee directs FDA to unify the foods program under an expert, empowered Deputy Commissioner for Foods with full line authority over CFSAN, the food and feed-related activities of the Center for Veterinary Medicine (CVM), and all the food-related components of the Office of Regulatory Affairs, including inspection and compliance, food-related laboratories, import oversight, State partnerships, training, and information technology.

Here is the full document – http://tinyurl.com/3z8cdcv9

Gotta love the t-shirts.

The good folks at Netflix have been kind enough to allow us to do another “red carpet premiere” at the historic Lynwood Theater on Bainbridge Island on July 2 at 5:30 PM after the documentary’s successful premiere at Tribeca.

The tickets are free and can be “purchased” at this Eventbright Link – or can be reserved by emailing jdueck@marlerclark.com. There is seating for only 200.

Please join us for the premiere of the new movie Poisoned, based on the book by Jeff Benedict, which chronicles the events surrounding the worst food-poisoning epidemic in US history: the deadly Jack in the Box E. coli infections in 1993. Tickets are complimentary but we are collecting donations for Helpline House, please donate here 

There will be books available to be purchased and signed courtesy of Eagle Harbor Books. There really will be a red carpet and photos available by Hallie Kathryn along with free Poisoned t-shirts.

The showing will be from 5:30 – 6:45 followed by Q+ A moderated by Herb Weisbaum with Bill and Jeff from 6:45-to 7:15. A community gathering and celebration at Treehouse will follow. 

On December 24, 1992, six-year-old Lauren Rudolph was hospitalized with excruciating stomach pain. Less than a week later she was dead. Doctors were baffled: How could a healthy child become so sick so quickly? After a frenzied investigation, public-health officials announced that the cause was E. coli O157:H7, and the source was hamburger meat served at a Jack in the Box restaurant. During this unprecedented crisis, four children died and over seven hundred others became gravely ill. Poisoned delivers a jarringly candid narrative of the fast-moving disaster, drawing on access to confidential documents and exclusive interviews with the real-life characters at the center of the drama—the families whose children were infected, the Jack in the Box executives forced to answer for the tragedy, the physicians and scientists who identified E. coli as the culprit, and the legal teams on both sides of the historic lawsuits that ensued. Poisoned reveals the evolution and history of America’s food supply system, as well as the untold stories of the victims of notorious outbreaks, and spotlights high-profile criminal prosecutions for those responsible. Poisoned will go directly to the source, following the distribution trail from start to finish, examining where the process breaks down, as well as the bureaucratic red tape and collusion among lobbyists and lawmakers that work against addressing this life-or-death problem.

See you there. Any questions, shoot me an email at bmarler@marlerclark.com.

Even if you cannot attend, consider a donation – Helpline House, please donate here 

AN INTRODUCTION TO E. COLI BACTERIA

Escherichia coli (or E. coli) is the most prevalent infecting organism in the family of gram-negative bacteria known as enterobacteriaceae. [1]  E. coli bacteria were discovered in the human colon in 1885 by German bacteriologist Theodor Escherich. [2] Dr. Escherich also showed that certain strains of the bacterium were responsible for infant diarrhea and gastroenteritis, an important public health discovery. Although E. coli bacteria were initially called Bacterium coli, the name was later changed to Escherichia coli to honor its discoverer. [2]

E. coli is often referred to as the best or most-studied free-living organism. [1, 3] More than 700 serotypes of E. coli have been identified. [1,4] The “O” and “H” antigens on the bacteria and their flagella distinguish the different serotypes. [4] It is important to remember that most kinds of E. coli bacteria do not cause disease in humans. [1, 2] Indeed, some E. coliare beneficial, while some cause infections other than gastrointestinal infections, such as urinary tract infections. [1] 

The E. coli that are responsible for the numerous reports of contaminated foods and beverages are those that produce Shiga toxin, so called because the toxin is virtually identical to that produced by Shigella dysenteria type 1. [4]  The best-known and also most notorious E. coli bacteria that produce Shiga toxin is E. coli O157:H7. [1, 4] The Centers for Disease Control and Prevention (CDC) has estimated that every year at least 2,000 Americans are hospitalized, and about 60 die as a result of E. coli infection and its complications. [4, 5] A study published in 2005 estimated the annual cost of E. coli O157:H7 illnesses to be $405 million (in 2003 dollars), which included $370 million for premature deaths, $30 million for medical care, and $5 million for lost productivity. [5]

E. COLI O157:H7

E. coli O157:H7—a foodborne pathogen

E. coli O157:H7 is one of thousands of serotypes of Escherichia coli. The testing done to distinguish E. coli O157:H7 from its other E. coli counterparts is called serotyping. [6]  

Pulsed-field gel electrophoresis (PFGE), sometimes also referred to as genetic fingerprinting, is used to compare E. coliO157:H7 isolates to determine if the strains are distinguishable. [3, 7] A technique called multilocus variable number of tandem repeats analysis (MLVA) is used to determine precise classification when it is difficult to differentiate between isolates with indistinguishable or very similar PFGE patterns. [8]  

E. coli O157:H7 was first recognized as a pathogen in 1982 during an investigation into an outbreak of hemorrhagic colitis associated with consumption of hamburgers from a fast-food chain restaurant. [9]  Retrospective examination of more than three thousand E. coli cultures obtained between 1973 and 1982 found only one isolate with serotype O157:H7, and that was a case in 1975.[4, 9]  In the ten years that followed, there were approximately thirty outbreaks recorded in the United States. [10]  This number is likely misleading, however, because E. coli O157:H7 infections did not become a reportable disease in any state until 1987, when Washington became the first state to mandate its reporting to public health authorities. [11, 12]  Consequently, an outbreak would not be detected if it was not large enough to prompt investigation.[11, 13]

E. coli O157:H7’s ability to induce injury in humans is a result of its ability to produce numerous virulence factors, most notably Shiga toxin (Stx), which is one of the most potent toxins known to man. [4, 14, 15]  Shiga toxin has multiple variants (e.g., Stx1, Stx2, Stx2c), and acts like the plant toxin ricin by inhibiting protein synthesis in endothelial and other cells. [16]   Endothelial cells line the interior surface of blood vessels and are known to be extremely sensitive to E. coliO157:H7, which is cytotoxigenic to these cells. [16]

In addition to Shiga toxin, E. coli O157:H7 produces numerous other putative virulence factors, including proteins which aid in the attachment and colonization of the bacteria in the intestinal wall, and which can lyse red blood cells and liberate iron to help support E. coli metabolism. [17]

E. coli O157:H7 evolved from enteropathogenic E. coli serotype O55:H7, a cause of non-bloody diarrhea, through the sequential acquisition of phage encoded Stx2, a large virulence plasmid, and additional chromosomal mutations. [18, 19] The rate of genetic mutation indicates that the common ancestor of current E. coli O157:H7 clades likely existed some 20,000 years ago. [20]  E. coli O157:H7 is a relentlessly evolving organism, constantly mutating and acquiring new characteristics, including virulence factors that make the emergence of more dangerous variants a constant threat. [21, 22] The prospect of emerging pathogens as a significant public health threat has been emphasized by the CDC for some time.[23] As Robert Tauxe of the CDC notes:

After 15 years of research, we know a great deal about infections with E. coli O157:H7, but we still do not know how best to treat the infection, nor how the cattle (the principal source of infection for humans) themselves become infected. [23]

Although foods of a bovine origin are the most common cause of both outbreaks and sporadic cases of E. coli O157:H7 infections, outbreaks of illnesses have been linked to a wide variety of food items.  For example, produce has been the source of substantial numbers of outbreak-related E. coli O157:H7 infections since at least 1991. [13, 24]  Outbreaks have been linked to alfalfa, clover and radish sprouts, lettuce, and spinach. [31, 32]Other vehicles for outbreaks include unpasteurized juices, yogurt, dried salami, mayonnaise, raw milk, game meats, hazelnuts, and raw cookie dough. [10, 13, 30] 

NON-O157 STEC

Non-O157 Shiga Toxin-Producing E. coli

E. coli are classified by their O and H antigens (e.g., E. coli O157:H7, E. coli O26:H11) and broadly categorized as Shiga toxin-producing E. coli (STEC) O157 or non-O157 STEC.  For many years, most recognized STEC outbreaks were associated with STEC O157. Despite the dominance of STEC O157, at least 150 non-O157 strains of E. coli are known to cause human illness and have been associated with outbreaks.

In the US, documented outbreaks of non-O157 E. coli include 10 involving O111; 6 involving O26; 3 involving O45; 2 involving O145, O104, and O6; and one each involving O51; O103; O27; and, O84. Non-O157 STEC outbreaks are rare but tend to primarily be due to contaminated food and person-to-person transmission.  

Non-O157 STEC infections are under-recognized and under-reported due to inadequate epidemiological and laboratory surveillance.  In the United States, E. coli O157:H7 became nationally notifiable in 1994, whereas non-O157 STEC infections were not reportable until 2000. [55] Screening for non-O157 STEC remains rare.  This is no surprise since by 2007 only 66% of clinical labs screened all stool samples for E. coli O157:H7 and fewer than 10% of labs ever conducted on-site testing for non-O157 STEC.  As with E. coli O157:H7, non-O157 STEC cases tend to occur during the summer months. 

Non-O157 STEC can be difficult to identify in laboratory screening for E. coli O157 because they do not ferment sorbitol.  Most stool cultures suspected to contain STEC are first screened for Shiga toxin; a positive test could be either E. coli O157:H7 or non-O157 STEC.  Unfortunately, some labs will discard Shiga toxin-positive cultures after reporting to the referring doctor without identifying the strain. State laboratories can send STEC cultures to the CDC to determine the serotype.  Some states, such as Minnesota and Connecticut have begun studies of their own to identify non-O157 STEC.

In recent years, improved diagnostic assays for non-O157 STEC have contributed to an increased appreciation of the severity of disease caused by these strains, including hemolytic uremic syndrome (HUS).  Notably, the number of non-O157 STEC cases reported to CDC’s FoodNet has risen steadily each year; from 2000-2006, there was an overall 4-fold increase in incidence (0.12 cases per 100,000 to 0.42 cases per 100,000 population) at FoodNet sites. The most common serogroups reported to cause foodborne illness in the United States are O26, O111, O103, O121, O45, and O145. [56] These six serotypes account for 75% of human infections.

Worldwide, non-O157 STEC outbreaks emerged in the 1980s, and the first reported outbreaks in the United States occurred in the 1990s. [57, 55] The number of reported outbreaks due to non-O157 STECs remains relatively low in the United States, but experts agree that documented outbreaks probably represent the “tip of the iceberg.”  From 1983-2002, seven non-O157 STEC outbreaks were reported in the United States. [55] During the following five-year period from 2003-2007, CDC documented an additional five non-O157 STEC outbreaks (CDC Outbreak Surveillance Data, http://www.cdc.gov/foodborneoutbreaks/outbreak_data.htm).  

An extraordinary non-O157 outbreak occurred in Germany beginning in May 2011.  The STEC involved was extremely rare: E. coli O104:H4. It was also extremely virulent.  Ultimately, the outbreak sickened nearly 4,000 people and killed more than 50.  This strain was not only resistant to many antibiotics, but it also possessed a novel mechanism for sticking to intestinal cells.  Other unusual aspects of this outbreak were that it affected a disproportionately large percentage of women.  Further, nearly a quarter of those infected developed HUS and of those the vast majority was women.  It appears that this non-O157 STEC acquired its virulence factors and antibiotic resistance through horizontal gene acquisition rather than point mutations or descent from prior generations of bacteria. [65] The outbreak was ultimately traced to contaminated seeds of fenugreek from Egypt, sold as sprouts by an organic farm in Germany.

A study of non-O157 STEC concluded that these strains may account for up to 20 to 50% of all STEC infections in the United States. [57] The prevalence of non-O157 STEC infections is placing an increasing burden on society and the health care system in the United States.

PREVALENCE

E. coli O157:H7 bacteria and other pathogenic E. coli mostly live in the intestines of cattle, but E. coli bacteria have also been found in the intestines of chickens, deer, sheep, and pigs. [1, 35] A 2003 study on the prevalence of E. coli O157:H7 in livestock at 29 county and three large state agricultural fairs in the United States found that E. coli O157:H7 could be isolated from 13.8% of beef cattle, 5.9% of dairy cattle, 3.6% of pigs, 5.2% of sheep, and 2.8% of goats. [36] Over 7% of pest fly pools also tested positive for E. coli O157:H7. [36] Shiga toxin-producing E. coli does not make the animals that carry it ill. [1] The animals are merely the reservoir for the bacteria. [35]

According to a study published in 2011, an estimated 93,094 illnesses are due to domestically acquired E. coli O157:H7 each year in the United States. [25] Estimates of foodborne-acquired O157:H7 cases result in 2,138 hospitalizations and 20 deaths annually. [25] 

What makes E. coli O157:H7 remarkably dangerous is its very low infectious dose, and how relatively difficult it is to kill these bacteria. [4, 27]  “E. coli O157:H7 in ground beef that is only slightly undercooked can result in infection.” [4] As few as 20 organisms may be sufficient to infect a person and, as a result, possibly kill them. [28]  And unlike generic E. coli, the O157:H7 serotype multiplies at temperatures up to 44° Fahrenheit, survives freezing and thawing, is heat-resistant, grows at temperatures up to 111 F, resists drying, and can survive exposure to acidic environments. [27, 28]  And, finally, to make it even more of a threat, E. coli O157:H7 bacteria are easily transmitted by person-to-person contact. [4, 13]  

Trace-back and source identification

E. coli O157:H7 and other non-O157 STECs are now routinely “fingerprinted” as part of surveillance of foodborne disease. [52] This surveillance was first initiated in response to the major outbreak of E. coli O157:H7 infections in 1993.  As described by the CDC on the PulseNet website:

In 1993, a large outbreak of foodborne illness caused by the bacterium Escherichia coli O157:H7 occurred in the western United States. In this outbreak, scientists at CDC performed DNA “fingerprinting” by pulsed-field gel electrophoresis (PFGE) and determined that the strain of E. coli O157:H7 found in patients had the same PFGE pattern as the strain found in hamburger patties served at a large chain of regional fast-food restaurants. Prompt recognition of this outbreak and its cause may have prevented an estimated 800 illnesses. As a result, CDC developed standardized PFGE methods and in collaboration with the Association of Public Health Laboratories (APHL), created PulseNet so that scientists at public health laboratories throughout the country could rapidly compare the PFGE patterns of bacteria isolated from ill persons and determine whether they are similar.

(For more information, go here: http://www.cdc.gov/pulsenet/whatis.htm#role)

When a sample is taken from food that is contaminated with bacteria, such as E. coli O157:H7, Listeria, Salmonella, or Campylobacter, the sample is tested (or cultured) to obtain and identify the bacterial isolate. [52]  Similarly, if a person consumes contaminated food, and becomes infected as a result, a stool sample can be cultured to obtain and identify the bacterial isolate.  These bacterial isolates are then broken down into component parts to create a DNA “fingerprint.” [52, 53] The “fingerprint” can then be compared and matched up to the “fingerprint” of isolates from other persons who consumed the contaminated food. [52] When “fingerprints” match, the match is proof that the contaminated food was the source of the illness. 

The process of obtaining the DNA “fingerprint” is called Pulse Field Gel Electrophoresis (PFGE). [52] The PFGE technique is used to separate the DNA of the bacterial isolate into smaller pieces.  The DNA is placed in a flat gel matrix of agarose, a polysaccharide obtained from agar, and exposed to an alternating electric field. [52, 53] Individual pieces of DNA, or bands, will migrate across the gel, creating a bar code-like pattern unique to each strain. [53] By performing the procedure, scientists can identify hundreds of strains of E. coli O157:H7 as well as strains of Listeria, Salmonella, and Campylobacter. [52]

TRANSMISSION

Cattle as Reservoirs

Beef and dairy cattle are known reservoirs of E. coli O157:H7 and non-O157 STEC strains. [58, 59] In reviews of STEC occurrence in cattle worldwide, the prevalence of non-O157 STECs ranged from 4.6 to 55.9% in feedlot cattle, 4.7 to 44.8% in grazing cattle, and 0.4 to 74% in dairy cattle feces.  The prevalence in beef cattle going to slaughter ranged from 2.1 to 70.1%.  While most dairy cattle-associated foodborne disease outbreaks are linked to milk products, dairy cattle still represent a potential source of contamination of beef products when they are sent to slaughter at the end of their useful production life (termed “cull” or “spent” dairy cows); this “dairy beef” is often ground and sold as hamburger. 

The high prevalence of E. coli O157 and non-O157 STEC in some cattle populations, combined with the lack of effective on-farm control strategies to reduce carriage, represents a significant risk of contamination of the food supply and the environment.  Non-O157 STEC are also harbored in other ruminants, including swine. [60]

Beef Products

Numerous Shiga toxin-producing E. coli serotypes known to cause human illness are of bovine origin, thus putting the beef supply at-risk.  Both E. coli O157:H7 and non-O157 STEC may colonize the gastrointestinal tract of cattle, and potentially contaminate beef carcasses during processing.  Although not as well studied, the risk factors for contamination of beef products from cattle colonized with non-O157 STECs are probably the same or very similar to E. coli O157:H7.  For example, cattle hides contaminated with E. coli O157:H7 during slaughter and processing are a known risk factor for subsequent E. coli O157:H7 contamination of beef products.  One study showed that the prevalence of non-O157 STEC (56.6%) on hides is nearly as high as that found for E. coli O157:H7 (60.6%). [62] 

A review of published reports from over three decades found that non-O157 STEC were more prevalent in beef products compared with E. coli O157. [61]  In this study, the prevalence of non-O157 STEC ranged from 1.7 to 58% in packing plants, from 3 to 62.5% in supermarkets, and an average of 3% in fast food restaurants.  In a recent survey of retail ground beef products in the United States, 23 (1.9%) of 1,216 samples were contaminated with non-O157 STEC. [63] In another study, researchers found a 10 to 30% prevalence of non-O157 STEC in imported and domestic boneless beef trim used for ground beef. [64] 

Environmental Sources of E. coli

E. coli O157:H7 bacteria and other pathogenic E. coli are believed to mostly live in the intestines of cattle, but these bacteria have also been found in the intestines of chickens, deer, sheep, and pigs. [1, 35] A 2003 study on the prevalence of E. coli O157:H7 in livestock at 29 county and three large state agricultural fairs in the United States found that E. coliO157:H7 could be isolated from 13.8% of beef cattle, 5.9% of dairy cattle, 3.6% of pigs, 5.2% of sheep, and 2.8% of goats. [36] Over seven percent of pest fly pools also tested positive for E. coli O157:H7. [36] Shiga toxin-producing E. coli does not make the animals that carry it ill, the animals are merely the reservoir for the bacteria. [35] [1]

Products Implicated in Previous Non-O157 STEC Outbreaks

There is a paucity of information on the vehicles of transmission for human non-O157 STEC infections, but contaminated raw dairy products, produce, and water have been implicated in the United States. [55] A review of non-O157 STEC in Connecticut showed that exposures, including ground beef, were similar in both non-O157 STEC and E. coli O157:H7 cases, suggesting that the routes of transmission are similar (CDC 2007).  Considering the relatively high prevalence of both E. coli O157:H7 and non-O157 STEC in cattle populations and their products, it is not surprising that ground beef and other beef products could be a common food vehicle.  

Non-O157 STEC outbreaks attributed to ground beef and its sausage products have been documented outside the United States including Argentina, Australia, Germany, and Italy.  These beef-related outbreaks involved 8 STEC serogroups (O1, O2, O15, O25, O75, O86, O111, and O160).  HUS cases were reported in five of the six outbreaks, mostly striking children, and the elderly.

SYMPTOMS

What happens after the Shiga toxin-producing E. coli are ingested?

The colitis caused by E. coli O157:H7 is characterized by severe abdominal cramps, diarrhea that typically turns bloody within 24 hours, and sometimes fever. [4]  The incubation period—that is, the time from exposure to the onset of symptoms—in outbreaks is usually reported as 3 to 4 days but may be as short as 1 day or as long as 10 days. [4, 13, 26] Infection can occur in people of all ages but is most common in children. [26]  

Unlike other E. coli pathogens, which remain on intestinal surfaces, Shiga toxin-producing bacteria, like O157:H7, are invasive. [1] After ingestion, E. coli bacteria rapidly multiply in the large intestine and then bind tightly to cells in the intestinal lining.  [1, 26] This snug attachment facilitates absorption of the toxins into the small capillaries within the bowel wall.  [1, 33, 45] Once in the systemic circulation, Shiga toxin becomes attached to weak receptors on white blood cells, thus allowing the toxin to “ride piggyback” to the kidneys where it is transferred to numerous avid (strong) Gb3 receptors that grasp and hold on to the toxin. [33]

Inflammation caused by the toxins is believed to be the cause of hemorrhagic colitis, the first symptom of E. coliinfection, which is characterized by the sudden onset of abdominal pain and severe cramps. [29, 42] Such symptoms are typically followed within 24 hours by diarrhea, sometimes fever. [1, 4]

As the infection progresses, diarrhea becomes watery and then may become grossly bloody; that is, bloody to the naked eye.  E. coli symptoms also may include vomiting and fever, although fever is an uncommon symptom. 

On rare occasions, E. coli infection can cause bowel necrosis (tissue death) and perforation without progressing to hemolytic uremic syndrome (HUS)—a complication of E. coli infection that is now recognized as the most common cause of acute kidney failure in infants and young children.  In about 10 percent of E. coli cases, the Shiga toxin attachment to Gb3 receptors results in HUS.  

The duration of an uncomplicated illness can range from one to twelve days. [4, 23]  In reported outbreaks, the rate of death is 0-2%, with rates running as high as 16-35% in outbreaks involving the elderly, like those that have occurred at nursing homes. [23]

Shiga toxin–producing E. coli (STEC) cause approximately 100,000 illnesses, 3,000 hospitalizations, and 90 deaths annually in the United States.  [39, 54] As noted, most reported STEC infections in the United States are caused by E. coliO157:H7, with an estimated 73,000 cases occurring each year. [39] According to the CDC: 

Non-O157 STEC bacteria also are important causes of diarrheal illness in the United States; at least 150 STEC serotypes have been associated with outbreaks and sporadic illness. In the United States, six non-O157 serogroups (O26, O45, O103, O111, O121, and O145) account for the majority of reported non-O157 STEC infections. [54]

Persons with non-O157 STEC tend to have less severe illness, but some non-O157 STEC members can cause very severe infections, including those that result in HUS and death.  Non-O157 STEC that cause HUS overwhelmingly produce Shiga toxin 2 with or without Shiga toxin 1.  As with E. coli O157:H7, more severe disease results from Shiga toxin 2 production by non-O157 STEC.

COMPLICATIONS

A Life-Threatening Complication—Hemolytic Uremic Syndrome 

E. coli O157:H7 infections can lead to a severe, life-threatening complication called the hemolytic uremic syndrome (HUS). [4, 13]  HUS accounts for most of the acute deaths and chronic injuries caused by the bacteria. [3] HUS occurs in 2-7% of victims, primarily children, with onset five to ten days after diarrhea begins. [23, 44] “E. coli serotype O157:H7 infection has been recognized as the most common cause of HUS in the United States, with 6% of patients developing HUS within 2 to 14 days of onset of diarrhea.” [44, 45] And it is the most common cause of renal failure in children. [26, 45, 48]  

Approximately half of the children who suffer HUS require dialysis, and at least 5% of those who survive have long term renal impairment. [44] The same number suffers severe brain damage. [46]  While somewhat rare, serious injury to the pancreas, resulting in death or the development of diabetes, also occurs. [47] There is no cure or effective treatment for HUS. [47] And, tragically, children with HUS too often die, with a mortality rate of five to ten percent. [26]

Once Shiga toxins attach to receptors on the inside surface of blood vessel cells (endothelial cells), a chemical cascade begins that results in the formation of tiny thrombi (blood clots) within these vessels. [33, 45]  Some organs seem more susceptible, perhaps due to the presence of increased numbers of receptors, and include the kidney, pancreas, and brain. [26, 33]  Consequently, organ injury is primarily a function of receptor location and density. [33, 54]

Once they move into the interior of the cell (cytoplasm), Shiga toxins shut down protein machinery, causing cellular injury or death. [33, 46] This cellular injury activates blood platelets too, and the resulting “coagulation cascade” causes the formation of clots in the very small vessels of the kidney, leading to acute kidney failure.

The red blood cells are either directly destroyed by Shiga toxin (hemolytic destruction), or are damaged as cells attempt to pass through partially obstructed micro-vessels. [33, 46] Blood platelets become trapped in the tiny blood clots, or they are damaged and destroyed by the spleen. [46] 

When fully expressed, HUS presents with the triad of hemolytic anemia (destruction of red blood cells), thrombocytopenia (low platelet count), and renal failure (loss of kidney function). [33, 45] Although recognized in the medical community since at least the mid-1950s, HUS first captured  the public’s widespread attention in 1993 following a large E. coli outbreak in Washington State that was linked to the consumption of contaminated hamburgers served at a fast-food chain. [6, 28] Over 500 cases of E. coli  were reported; 151 were hospitalized (31%), 45 persons (mostly children) developed HUS (9%), and three died. [6, 28]

Of those who survive HUS, at least five percent will suffer end stage renal disease (ESRD) with the resultant need for dialysis or transplantation. [47]  But, “[b]ecause renal failure can progress slowly over decades, the eventual incidence of ESRD cannot yet be determined.” [33]  Other long-term problems include the risk for hypertension, proteinuria (abnormal amounts of protein in the urine that can portend a decline in renal function), and reduced kidney filtration rate. [33, 47]  Since the longest available follow-up studies of HUS victims are 25 years, an accurate lifetime prognosis is not available and remains controversial. [47]  

Other Complications from Infection 

IBS is a chronic disorder characterized by alternating bouts of constipation and diarrhea, both of which are generally accompanied by abdominal cramping and pain. [50] Suffering an E. coli O157:H7 infection has been linked to the development of post-infectious irritable bowel syndrome (IBS).  This link was demonstrated by the Walkerton Health Study (WHS), which followed one of the largest O157:H7 outbreaks in the history of North America. [49] In this outbreak, contaminated drinking water caused over 2,300 people to be infected, resulting in 27 recognized cases of HUS, and 7 deaths. The WHS followed 2,069 eligible study participants. Among its findings, WHS noted that, “Between 5% and 30% of patients who suffer an acute episode of infectious gastroenteritis develop chronic gastrointestinal symptoms despite clearance of the inciting pathogens.” [49]

Not surprisingly, E. coli O157:H7 infection is associated with long-term emotional disruption as well, not just for the victim, but for entire families. [51]   A recent study reported that “parents experienced long-term emotional distress and substantive disruption to family and daily life” following an E. coli O157:H7 infection in the family. [51]

DIAGNOSIS

How is an E. coli Infection Diagnosed?

Infection with E. coli O157:H7 or other Shiga toxin-producing E. coli is usually confirmed by the detection of the bacteria in a stool specimen from an infected individual. [1, 54] Most hospitals labs and physicians know to test for these bacteria, especially if the potentially infected person has bloody diarrhea.  Still, it remains a good idea to specifically request that a stool specimen be tested for the presence of Shiga toxin-producing E. coli. [54]

TREATMENT

Treatment for an E. coli Infection

In most infected individuals, symptoms of a Shiga toxin-producing E. coli infection last about a week and resolve without any long-term problems. [1, 42] Antibiotics do not improve the illness, and some medical researchers believe that these medications can increase the risk of developing HUS. [43] Therefore, apart from supportive care, such as close attention to hydration and nutrition, there is no specific therapy to halt E. coli symptoms. [42]  The recent finding that E. coliO157:H7 initially speeds up blood coagulation may lead to future medical therapies that could forestall the most serious consequences. [34] Most individuals who do not develop HUS recover within two weeks. [33, 42] 

PREVENTION

What can we do to protect our families from E. coli?

Since there is no fail-safe food safety program, consumers need to “drive defensively” as they navigate from the market to the table.  It is no longer enough to take precautions only with ground beef and hamburgers; anything ingested by family members can be a vehicle for infection.  Shiga toxin-producing E. coli are so widely disseminated that a wide variety of foods can be contaminated.  Direct animal-to-person and person-to-person transmission is not uncommon.  Following are steps you can take to protect your family.  

  1. Practice meticulous personal hygiene.  This is true not only for family members (and guests), but for anyone interfacing with the food supply chain.  Remember that E. coli bacteria are very hardy (e.g., can survive on surfaces for weeks) and that only a few are sufficient to induce serious illness.  Since there is no practical way of policing the hygiene of food service workers, it is important to check with local departments of health to identify any restaurants that have been given citations or warnings.  The emerging practice of providing sanitation “report cards” for public display is a step in the right direction.
  1. Be sure to clean and sanitize all imported and domestic fruits or vegetables.  All can be carriers of disease.  If possible, fruits should be skinned, or at least vigorously scrubbed and/or washed. Vegetables (and of course meat) should be cooked to a core temperature of at least 160 degrees Fahrenheit for at least 15 seconds. If not cooked, fruits and vegetables should be washed to remove any dirt or other material, and then soaked in chlorinated water (1 teaspoon of household bleach in one quart of water, soaked for at least 15 minutes).  They can then be rinsed in clean water to remove the chlorine taste.  This will remove most, but not all, bacteria.  In the case of leafy vegetables, bacteria may not be limited to the leaf’s surface, but can reside within the minute circulatory system of the individual vegetable leaves.
  1. Be careful to avoid cross contamination when preparing and cooking food, especially if beef is being served.  This requires being very mindful of the surfaces (especially cutting boards) and the utensils used during meal preparation that have meet uncooked beef and other meats.  This even means that utensils used to transport raw meat to the cooking surfaces should not be the same that are later used to remove the cooked meat (or other foodstuffs) from the cooking surfaces.
  1. Do not allow children to share bath water with anyone who has any signs of diarrhea or “stomach flu”.  And keep any toddlers still in diapers out of all bodies of water (especially wading and swimming pools).
  1. Do not let any family members touch or pet farm animals.  Merely cleaning the hands with germ “killing” wipes may not be adequate!
  1. Wear disposable gloves when changing the diapers of any child with any type of diarrhea.  Remember that E. coliO157:H7 diarrhea initially is non-bloody, but still very infectious.  If gloves are not available, then thorough hand washing is a must.
  1. Remember that achieving a brown color when cooking hamburgers does not guarantee that E. coli bacteria have been killed.  This is especially true for patties that have been frozen.  Verifying a core temperature of at least 160 degrees Fahrenheit for at least 15 seconds is trustworthy.  Small, disposable meat thermometers are available, a small investment compared to the medical expense (and grief) of one infected family member.
  1. Avoid drinking (and even playing in) any non-chlorinated water.  There is an added risk if the water (well, irrigation water or creek/river) is close to, or downstream from any livestock.

References

1.         Eisenstein, Barry and Zaleznik, Dori, “Enterobacteriiaceae,” in Mandell, Douglas, & Bennett’s PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES, Fifth Edition, Chap. 206, pp. 2294-2310 (2000).

2          Feng, Peter, et al., “Enumeration of Escherichia coli and the Coliform Bacteria,” in BACTERIOLOGICAL ANALYTICAL MANUAL (8th Ed. 2002), available online at http://www.cfsan.fda.gov/~ebam/bam-4.html.

3.         James M. Jay, MODERN FOOD MICROBIOLOGY at 21 (6th ed. 2000).  

4.         Griffin, Patricia and Tauxe, Robert, “The Epidemiology of Infections Caused by Escherichia coli O157:H7, Other Enterohemorrhagic E. coli, and the Associated Hemolytic Uremic Syndrome,” EPIDEMIOLOGICAL REVIEW, Vol. 13, pp. 60-98 (1991).

5.         Frenzen, Paul D., et al., “Economic Cost of Illness due to Escherichia coli O157 Infections in the United States,” JOURNAL OF FOOD PROTECTION, Vol. 68, pp. 2623-2630 (2005).

6.         Bell, B.P., et al., “A multistate outbreak of Escherichia coli O157:H7-associated bloody diarrhea and hemolytic uremic syndrome from hamburgers:  the Washington experience.” JOURNAL OF AMERICAN MEDICAL ASSOCIATION, Vol. 272, pp. 1349-1353 (1994).

7.         Bala Swaminathan, et al., “PulseNet: Molecular Subtyping Network for Foodborne Bacterial Disease Surveillance, United States,” EMERGING INFECTIOUS DISEASES Vol. 7, No. 3, pp. 382-89 (May-June 2001).

8.         Konno T. et al., “Application of a multilocus variable number of tandem repeats analysis to regional outbreak surveillance of Enterohemorrhagic Escherichia coli O157:H7 infections,” JAPANESE JOURNAL OF INFECTIOUS DISEASE, Vol. 64, No. 1, pp. 63-5 (January 2011).

9.         Riley, LW, et al., “Hemorrhagic colitis associated with a rare Escherichia coli serotype,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 308, No. 12, pp. 681, 684-85 (1983).

10.       Feng, Peter, “ Escherichia coli Serotype O157:H7: Novel Vehicles of Infection and Emergence of Phenotypic Variants,” EMERGING INFECTIOUS DISEASES, Vol. 1, No. 2, at 47 (April-June 1995).

11.       Keene, William E.,  et al., “A Swimming-Associated Outbreak of Hemorrhagic Colitis Caused by Escherichia coli O157:H7 and Shigella Sonnei,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 331, at 579 (Sept. 1, 1994).  

12.       Ostroff, Stephen M., et al., “Infections with Escherichia coli O157:H7 in Washington State: The First Year of Statewide Disease Surveillance,” JOURNAL OF AMERICAN MEDICAL ASSOCIATION, Vol. 262, No. 3, at 355 (July 21, 1989).

13.       Rangel, Josefa M., et al., “Epidemiology of Escherichia coli O157:H7 Outbreaks, United States, 1982-2002,” EMERGING INFECTIOUS DISEASES, Vol. 11, No. 4, 603 (April 2005).

14.       Johannes, L, “Shiga toxins, from cell biology to biomedical applications,” NATIONAL REVIEW OF MICROBIOLOGY, Vol. 8, pp. 105-16 (2010).

15.       Suh, J.K., et al., “Shiga Toxin Attacks Bacterial Ribosomes as Effectively as Eucaryotic Ribosomes,” BIOCHEMISTRY, Vol. 37, No. 26, pp. 9394–398 (1998).

16.       Sandvig, K, “Pathways followed by ricin and Shiga toxin into cells,” HISTOCHEMISTRY AND CELL BIOLOGY, vol. 117, no. 2, pp. 131-141 (2002).  

17.       Welinder-Olsson, C and Kaijser, B, “Enterohemorrhagic Escherichia coli (EHEC),” SCANDINAVIAN JOURNAL OF INFECTIOUS DISEASE, Vol. 37, pp. 405-16 (2005).  

18.       Kaper, J.B. and Karmali, M.A., “The Continuing Evolution of a Bacterial Pathogen,” PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCE, Vol. 105, No. 12, pp. 4535-4536 (March 2008).

19.       Wick, L.M., et al., “Evolution of genomic content in the stepwise emergence of Escherichia coli O157:H7,” JOURNAL OF BACTERIOLOGY, Vol. 187, pp. 1783–1791 (2005).

20.       Zhang, W, et al., “Probing genomic diversity and evolution of Escherichia coli O157 by single nucleotide polymorphisms,” GENOME RESEARCH, Vol. 16, pp. 757–67 (2006).  The full-text of this article is available online at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1473186/pdf/757.pdf

21.       Robins-Browne, R.M., “The relentless evolution of pathogenic Escherichia coli,” CLINICAL INFECTIOUS DISEASES, Vol. 41, pp. 793–94 (2005).

22.       Manning S.D., et al., “Variation in virulence among clades of Escherichia coli O157:H7 associated with disease outbreaks, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCE, Vol. 105, No. 12, pp. 4868-73 (2008). 

23.       Tauxe, Robert A., “Emerging Foodborne Diseases: An Evolving Public Health Challenge, “ EMERGING INFECTIOUS DISEASES, Vol. 3, No. 4, pp. 425-427 (Oct.-Dec. 1997).

24.       CDC, “Multistate Outbreak of Escherichia coli O157:H7 Infections Associated with Eating Ground Beef—United States, June-July 2002,” MORBIDITY AND MORTALITY WEEKLY REVIEW, Vol. 51, at 638 (2002) reprinted in JOURNAL OF AMERICAN MEDICAL ASSOCIATION, Vol. 288, No. 6, 690 (Aug. 14, 2002).

25.       Scallan, E, et al., “Foodborne illness acquired in the United States –major pathogens, EMERGING INFECTIOUS DISEASES, Vol. 17, No. 1, (Jan. 2011), available at:  http://www.cdc.gov/EID/content/17/1/7.htm.

26.       Su, Chinyu Su &Brandt,  Lawrence “Escherichia coli O157:H7 Infection in Humans,” ANNALS OF INTERNAL MEDICINCE, Vol.123, Issue 9, pp. 698-707 (1995).

27.       Juneja, V.K., et al., “Thermal Destruction of Escherichia coli O157:H7 in Hamburger,” JOURNAL OF FOOD PROTECTION, Vol. 60, No. 10, pp. 1163-1166 (1997).

28.       Griffin, Patricia M.,  et al., “Large Outbreak of Escherichia coli O157:H7 Infections in the Western United States: The Big Picture,” in RECENT ADVANCES IN VEROCYTOTOXIN-PRODUCING ESCHERICHIA COLI INFECTIONS, at 7 (M.A. Karmali & A. G. Goglio eds. 1994).

29.       Boyce, T.G., et al., “Escherichia coli O157:H7 and the hemolytic-uremic syndrome,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 333, pp. 364-368 (1995).

30.       Breuer, T, et al., “A multistate outbreak of Escherichia coli O157:H7 infections linked to alfalfa sprouts grown from contaminated seeds,” EMERGING INFECTIOUS DISEASES, Vol. 7, pp. 977-982 (2001).

31.       Friedman, M.S., et al., “Escherichia coli O157:H7 Outbreak Associated with an Improperly Chlorinated Swimming Pool,”  CLINICAL INFECTIOUS DISEASE, Vol. 29, No. 2, pp. 298-303 (1999).  

32.       Cody, S.H., et al., “An outbreak of Escherichia coli O157:H7 infection from unpasteurized commercial apple juice,”  ANNALS OF INTERNAL MEDICINE, Vol. 130, No. 3, pp. 202-9 (1999).

33.       Siegler, Richard, “The Hemolytic Uremic Syndrome,” PEDIATRIC NEPHROLOGY, Vol. 42, p. 1505 (Dec. 1995)

34.       Chandler, W.L., et al., “Prothrombotic Coagulation Abnormalities Preceding the Hemolytic-Uremic Syndrome,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 346, No. 1, pp. 23-32 (2002).

35.       Elder, R.O., et al., “Correlation of enterohemorrhagic Escherichia coli O157 prevalence in feces, hides, and carcasses of beef cattle during processing,” USDA Agricultural Research Service, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES (2000). http://www.pnas.org/content/97/7/2999.long

36.       Keen, J.E., et al., “Shiga-toxigenic Escherichia coli O157 in agricultural fair livestock, United States,” EMERGING INFECTIOUS DISEASES, Vol. 12, No. 5, pp. 780-86 (2003).

37.       King, L.J., Testimony on CDC Food Safety Activities and the Recent E. coli Spinach Outbreak, Hearing Before the Committee on Health, Education, Labor and Pensions, United States Senate,  Nov. 15, 2006, available online at http://www.hhs.gov/asl/testify/t061115.html.  

38.       McCarthy, T.A., et al., “Hemolytic-Uremic Syndrome and Escherichia coli O121 at a Lake in Connecticut, 1999,” PEDIATRICS, vol. 108, pp. e59-59 (2001).

39.       Mead, Paul M., et al., “Food-related Illness and Death in the United States,”  EMERGING INFECTIOUS DISEASES, Vol. 5, pp. 607-625 (1999).

40.       Olsen, S.J., et al., “A Waterborne Outbreak of Escherichia coli O157:H7 Infections and Hemolytic Uremic Syndrome: Implications for Rural Water Systems,”  MORBIDITY AND MORTALITY WEEKLY REVIEW, Vol. 8, No. 4 (April 2002). The full text of article is available online at http://www.cdc.gov/ncidod/EID/vol8no4/00-0218.htm.  

41.       Slutsker, L, et al., “A nationwide case-control study of Escherichia coli O157:H7 infection in the United States,” JOURNAL OF INFECTIOUS DISEASE, Vol. 177, pp. 962-966 (1998).  

42.       Tarr, Philip, “Escherichia coli O157:H7:  Clinical, Diagnostic, and Epidemiological Aspects of Human Infection,”  CLINICAL INFECTIOUS DISEASE, Vol. 20, pp. 1-10 (1995).

43.       Wong, C.S., et al., “The risk of the hemolytic uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 342, pp.1930-36 (2000). 

44.       Safdar, Nasia, et al., “Risk of Hemolytic Uremic Syndrome After Treatment of Escherichia coli O157:H7 Enteritis: A Meta-analysis,” JOURNAL OF AMERICAN MEDICAL ASSOCIATION, Vol. 288, No. 8, pp. 996 (Aug. 28, 2002).  

45.       Garg, Amit X, et al., “Long-term Renal Prognosis of Diarrhea-Associated Hemolytic Uremic Syndrome: A Systematic Review, Meta-Analysis, and Meta-regression, “ JOURNAL OF AMERICAN MEDICAL ASSOCIATION, Vol. 290, No. 10, p. 1360 (Sept. 10, 2003).

46.       Siegler, Richard, “Postdiarrheal Shiga Toxin-Mediated Hemolytic Uremic Syndrome,” JOURNAL OF AMERICAN MEDICAL ASSOCIATION, Vol. No. 10, p. 1379 (Sept. 10, 2003).

47.       Robitaille, Pierre, et al., “Pancreatic Injury in the Hemolytic Uremic Syndrome, PEDIATRIC NEPHROLOGY, Vol. 11, pp. 631-32 (1997).

48.       Bell, Beth, et al., “Predictors of Hemolytic Uremic Syndrome in Children During a Large Outbreak of Escherichia coli O157:H7 Infections,” PEDIATRICS, Vol. 100, No. 1, p. 1 (July 1, 1997), full text available online at http://www.pediatrics.org/cgi/content/full/100/1/e12.

49.       Marshall, J., et al., “Incidence and Epidemiology of Irritable Bowel Syndrome After a Large Waterborne Outbreak of Bacterial Dysentery,” GASTROENTEROLOGY, Vol. 131, pp. 445-50 (2006).

50.       Hungin, A., et al., “Irritable Bowel Syndrome in the United States: Prevalence, Symptom Patterns and Impact,” ALIMENTARY PHARMACOLOGY AND THERAPEUTICS, Vol. 21, No. 11, pp. 1365-75, (2005). Online at http://www.ncbi.nlm.nih.gov/pubmed/15932367

51.       Pollock, KG, et al., “Emotional and behavioral changes in parents of children affected by hemolytic-uremic syndrome associated with verocytotoxin-producing Escherichia coli: a qualitative analysis,” PYSCHOSOMATICS, Vol. 50, No. 3, pp. 263-9 (May-June 2009).

52.       Boxrud, D., “Genetic Testing,” Food Safety News, August 31, 2006, online at http://www.foodsafetynews.com/2009/08/genetic-testing-1/

53.       Boxrud D, et al., “Comparison of multiple-locus variable-number tandem repeat analysis, pulsed-field gel electrophoresis, and phage typing for subtype analysis of Salmonella enterica serotype Enteritidis,” JOURNAL OF CLINICAL MICROBIOLOGY, Vol. 45, No. 2, pp. 536-43 (Feb. 2007).

54.       CDC, “Recommendations for Diagnosis of Shiga Toxin–Producing Escherichia coli Infections by Clinical Laboratories,” MORBIDITY AND MORTALITY WEEKLY REVIEW, Vol. 88, No. RR-12 (Oct. 16, 2009), available online at http://www.cdc.gov/mmwr/PDF/rr/rr5812.pdf

55.       CDC,“Shiga toxin-producing Escherichia coli:  burden and trends.” FOODNET NEWS, Winter 2008. Available at: http://www.cdc.gov/FoodNet/news/2008/January_FoodNet_News.pdf  

56.       Brooks, J. T., E. G. Sowers, J. G. Wells, K. D. Greene, P. M. Griffin, R. M. Hoekstra, and N. A. Strockbine.,“Non-O157 Shiga Toxin-Producing Escherichia coli Infections in the United States, 1983-2002.” J. INFECT DIS. 192:1422-9 (2005) available online at http://www.foodpoisonjournal.com/uploads/file/466536_web%5B1%5D.pdf

57.       Johnson, K. E., C. M. Thorpe, and C. L. Sears. “The Emerging Clinical Importance of Non-O157 Shiga Toxin-Producing Escherichia coli” CLIN INFECT DIS. 43:1587-95 (2006) available online at http://cid.oxfordjournals.org/content/43/12/1587.full.pdf+html

58.       Hussein, H. S. “Prevalence and pathogenicity of shiga toxin-producing Escherichia coli in beef cattle and their products.” J ANIM SCI. 85:E63-72 (2007) available online at http://jas.fass.org/content/85/13_suppl/E63.full.pdf

59.       Hussein, H. S. and T. Sakuma, “Prevalence of shiga toxin-producing Escherichia coli in dairy cattle and their products.” J DAIRY SCI. 88:450-65 (2005) abstract available online at http://www.ncbi.nlm.nih.gov/pubmed/15653509

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65.       Rasko, D.A. et al. “ Origins of the E. coli Strain Causing an Outbreak of Hemolytic-Uremic Syndrome in Germany.”  N ENGL J MED 365:709-717 (2011) available online at http://www.nejm.org/doi/full/10.1056/NEJMoa1106920

Tonight is the big night for the Tribeca premiere of “Poisoned” and the short red carpet walk. After the showing of the film there will be a Q and A. The movie also will be showing twice on Saturday at Tribeca.

For those who do not want to brave the smokey skies of NYC, the movie will go online through Tribeca and at some point through Netflix. Here is how to access the online version though Tribeca in the coming weeks:

TRIBECA AT HOME

At Home Virtual Screenings will take place June 19 – July 2

  • WAYS TO WATCH:
    • Browser:watch.tribecafilm.com
      • Members can use their login credentials (email & password) to access the At Home portal. The activation link can be found in your confirmation email.
      • Single ticket holders can redeem their 9-digit voucher code for their screening. This code can be found in the confirmation email. 
    • App: “Tribeca At Home”/ Available on Apple TV, Fire TV, Roku
    • TV:
      • Download the OTT app for Apple TV (Gen4 and above), Fire TV, or Roku
      • Chromecast [3rd generation or later Chromecast stick] from a computer using the Chrome browser or an Android device to your TV.
      • Airplay from a computer, iPhone or iPad to your Apple TV (Gen 4 and above) or to any Smart TV bearing the “AirPlay” badge.
      • Connect your laptop to your TV via HDMI, VGA, or DVI cables.
    • Computer:
      • PCs running Windows 7+ [Browsers: Google Chrome, Firefox, Microsoft Edge, Opera]
      • Intel-based Macs running macOS 10.12+  [Browsers: Google Chrome, Firefox, Safari, Opera]
      • *Internet Explorer is not supported
    • iPhone / iPad / Android:
      • Android: use Chrome on Android 6.0 or later
      • iPhone/iPad: use Safari on iOS 11.2 or later 
    • Please note that screen mirroring cannot be used to watch Tribeca At Home. If you attempt to screen mirroring, you will see a black screen with audio playing. Airplay, Chromecast or HDMI cable are the best methods to watch on a television screen if you do not have one of the TV apps.
  • Tribeca At Home FAQ
    • What is a “Watch Window”?
      • A watch window is how long you have to watch a film once you press ‘PLAY’. For Tribeca At Home, this watch window will be 72 hours after you first initiate playback.
    • Can I pause or rewind during the watch window?
      • Yes, you have complete access to the entire program during your watch window.
    • How many times can I watch a film with my At Home Festival Pass?
      • Vouchers have a 72 hour watch window in place. Once the PLAY button has been pressed, 72 hours later the film’s availability will expire – regardless of whether or not the film has been watched in full. You will not be able to start the film again once the watch window has expired.
    • Can I watch the films from anywhere in the USA?
      • Tribeca At Home will be available to access in all 50 states of the USA. At the request of the filmmakers, certain titles might have geo-blocking restrictions. These restrictions will be noted on all relevant content. 
    • Can I watch films on multiple devices throughout my home?
      • You may have up to two devices (i.e. your laptop and OTT device) logged into your account at a time under the same IP address (i.e. the same household/location). Concurrent stream restriction means you are only able to actively stream content on a single device at a time.
    • What if I move from one location to another during the festival?
      • Single-IP restriction means that you can only watch content from a single IP address at a given time. If you move locations but are using the same device, you will have no issue watching films. If you move locations and are watching on a new device, you will need to deactivate the old device before the system will allow you to login on the new device.
      • User activity will be tracked and monitored and accounts will be deactivated if abuse is found (you may not share your account with friends or family who do not reside in the same location as you).

If you cannot resolve any issue redeeming your At Home screening, please contact us at athome@tribecafilm.com.

Remember, by law and with the USDA stamp of approval – meat producers can sell knowing that the product may well be tainted with a pathogen that sickens over 1,000,000 yearly.  This is because USDA/FSIS does not consider Salmonella an adulterant – see below.

The USDA FSIS has been investigating this outbreak for a month. To date the suspect product is ground beef, but who produced it is still a mystery. In Illinois, patients are reported in Chicago as well as Cook, DuPage, Kane, Lake, McHenry, and Will counties.

According to the Illinois Department of Health, state and federal officials are investigating this new outbreak of Salmonella infections related to ground beef.

So far the Illinois Department of Health has identified 26 confirmed cases. A source of ground beef has not yet been found. Illness onset dates range from April 25 to May 18, but additional patients are expected to be identified because it can take more than four weeks for confirmation testing and reporting to be concluded.

In addition to the Illinois patients, there are patients in other states, but the Illinois officials did not report what states are involved. A report from the CDC on the expanded scope of the outbreak is likely today.

As of this afternoon, June 7, neither the U.S. Centers for Disease Control and Prevention nor the USDA Foos Safety and Inspection Service have released any information about the outbreak.

it is Food Safety and Inspection Service (FSIS) Mission Statement: Protecting the public’s health by ensuring the safety of meat, poultry, and processed egg products.

USDA/FSIS has the authority to deem Salmonella and other pathogens adulterants – they just need to use it.

Americans will bring a food product (beef, port or poultry) into their homes or eat food out that is likely teeming with Salmonella that the manufacturer – by law and with the USDA stamp of approval – knowingly can sell knowing that it may well be tainted with a pathogen that sickens over 1,000,000 yearly.  This is because USDA/FSIS does not consider Salmonella an adulterant.

Personally, as I said to the Los Angeles Times some time ago, “I think that anything that can poison or kill a person should be listed as an adulterant [in food].”

Ignoring Salmonella in meat makes little, if any, sense.

Even after the Court’s twisted opinion in Supreme Beef v. USDA, where it found Salmonella “not an adulterant per se, meaning its presence does not require the USDA to refuse to stamp such meat ‘inspected and passed’, ” our government’s failure to confront the reality of Salmonella, especially antibiotic-resistant Salmonella, is inexcusable.

The Wisconsin Supreme Court in Kriefall v Excel called it as it saw it – at least with respect to E. coli – but the analysis is spot on for Salmonella as well:

The E. coli strain that killed Brianna and made the others sick is a “deleterious substance which may render [meat] injurious to health.” There is no dispute about this. Thus, under the first part of 21 U.S.C. § 601(m)(1), meat that either “bears or contains” E. coli O157:H7 (the “deleterious substance”) is “adulterated.” That E. coli O157:H7 contamination can be rendered non-“injurious to health” by cooking thoroughly, as discussed below, does not negate this; Congress used the phrase “may render,” not “in every circumstance renders.” Moreover, if the E. coli bacteria is not considered to be “an added substance,” because it comes from some of the animals themselves and is not either applied or supplied during the slaughtering process (although we do not decide this), it cannot be said that the E. coli strain “does not ordinarily render [the meat on or in which it appears] injurious to health.” Accordingly, meat contaminated by E. coli O157:H7 is also “adulterated” under the second part of § 601(m)(1).

Now, why would Salmonella be different? According to the CDC, it is estimated that 1.4 million cases of salmonellosis occur each year in the United States. Of those cases, 95 percent are related to foodborne causes. Approximately 220 of each 1,000 cases result in hospitalization, and 8 of every 1,000 cases result in death. About 500 to 1,000 deaths – 31 percent of all food-related deaths – are caused by Salmonella infections each year.

So, where do we stand with the existing USDA/FSIS law on adulteration?

Here is the law:

21 U.S.C. § 601(m)(4) – SUBCHAPTER I – INSPECTION REQUIREMENTS; ADULTERATION AND MISBRANDING – CHAPTER 12 – MEAT INSPECTION – TITLE 21—FOOD AND DRUGS

(m) The term “adulterated” shall apply to any carcass, part thereof, meat or meat food product under one or more of the following circumstances:

(1) if it bears or contains any poisonous or deleterious substance which may render it injurious to health; but in case the substance is not an added substance, such article shall not be considered adulterated under this clause if the quantity of such substance in or on such article does not ordinarily render it injurious to health; …

(3) if it consists in whole or in part of any filthy, putrid, or decomposed substance or is for any other reason unsound, unhealthful, unwholesome, or otherwise unfit for human food;

(4) if it has been prepared, packed, or held under insanitary conditions whereby it may have become contaminated with filth, or whereby it may have been rendered injurious to health; …

Here is the law specifically related to poultry:

Title 21 – FOOD AND DRUGS CHAPTER 10 – POULTRY AND POULTRY PRODUCTS INSPECTION

(g) The term “adulterated” shall apply to any poultry product under one or more of the following circumstances:

(1) if it bears or contains any poisonous or deleterious substance which may render it injurious to health; but in case the substance is not an added substance, such article shall not be considered adulterated under this clause if the quantity of such substance in or on such article does not ordinarily render it injurious to health; …

(3) if it consists in whole or in part of any filthy, putrid, or decomposed substance or is for any other reason unsound, unhealthful, unwholesome, or otherwise unfit for human food;

(4) if it has been prepared, packed, or held under insanitary conditions whereby it may have become contaminated with filth, or whereby it may have been rendered injurious to health;

Hmmm. It is hard to read the above and not think that the words equate to all E. coli as well as Salmonella — frankly, all pathogens in food.

I know, I am just a lawyer, but don’t ya think that when food with animal feces (and a dash of E. coli O157:H7) in it is considered an adulterant, that other animal feces (with dashes of other pathogens, like Salmonella) in them, should be considered adulterated too?  But, hey, that is just me.

Another odd governmental fact is that the FDA does not seem to make a distinction between pathogens it considers adulterants or not.

FDA’s enabling legislation – Sec. 402. [21 USC §342] of the Food, Drug & Cosmetic Act also defines “Adulterated Food” as food that is:

(a) Poisonous, insanitary, or deleterious ingredients.

(1) If it bears or contains any poisonous or deleterious substance which may render it injurious to health; but in case the substance is not an added substance such food shall not be considered adulterated under this clause if the quantity of such substance in such food does not ordinarily render it injurious to health;

(2) If it bears or contains any added poisonous or added deleterious substance … that is unsafe within the meaning of section 406;

(3) if it consists in whole or in part of any filthy, putrid, or decomposed substance, or if it is otherwise unfit for food;

(4) if it has been prepared, packed, or held under insanitary conditions whereby it may have become contaminated with filth, or whereby it may have been rendered injurious to health …

It would be interesting, and perhaps entertaining, to have House and Senate hearings focusing on what should and should not be considered adulterants in our food. I can see panels of scientists from various fields, FDA, USDA and FSIS officials, beef, poultry, fish and produce industry representatives, and consumers discussing this.

And so now onto some history to ruin your appetite.

In 1971 the American Public Health Association (APHA) sued the USDA on the grounds that its mark of inspection (“USDA inspected for wholesomeness”) was misleading because, even though the USDA had put its stamp of approval on meat—literally—it did not, for example, test the meat for bacteria. Moreover, APHA argued that raw meat was commonly contaminated with Salmonella, which posed a risk to the public health. According to APHA, the USDA should instead require that meat carry both a warning label and cooking instructions. The USDA opposed the APHA, helped ably (and predictably) by the meat industry. As quoted by Marion Nestle in her great book, Safe Food, the USDA’s position was that, given how many foods are contaminated with Salmonella, “it would be unjustified to single out the meat industry and ask that the [USDA] require it to identify its raw products as being hazardous to health.” Nestle at 66. (Note to Reader: No, I am really not making this up.)

In 1974, the DC Circuit Court of Appeals upheld the position of the USDA and the meat industry, doing so in a way that was as nonsensical as it was sexist. The court stated that: “The presence of salmonellae on meat does not constitute adulteration within this definition [of ‘adulterated,’ provided in 21 U.S.C. § 601 (m)]….As it said in its letter of August 18, 1971 ‘the American consumer knows that raw meat and poultry are not sterile and, if handled improperly, perhaps could cause illness.” In other words, American housewives and cooks normally are not ignorant or stupid and their methods of preparing and cooking of food do not ordinarily result in salmonellosis.’” APHA v. Butz, 511 F.2d 331, 334 (1974).

This remained the position of the USDA and the meat industry until 1994 when, in an act of both common-sense and bravado, Michael Taylor, then FSIS Administrator, announced that E. coli O157:H7 would be deemed an adulterant in raw ground beef. The Agency did not, however, change its tune with regard to any other pathogens, especially Salmonella. Indeed, in 1999, when FSIS announced it inane distinction between E. coli O157:H7 in “intact” meat versus “non-intact” meat, the Agency continued to focus on how a given meat was “customarily cooked” as a chief determinant of whether it must be treated as an adulterant. Thus, for example, because it decided that “intact steaks and roasts are customarily cooked in a manner that ensures that these products are not contaminated with E. coli O157:H7,” there was no need to treat this deadly pathogen as an adulterant on intact cuts of meat. Of course, this FSIS policy is also one that appears to have been silently jettisoned by the Agency of late.

The Agency’s position on Salmonella and meat came back to haunt it in a big way when FSIS tried to shut down Supreme Beef Processors, Inc. for repeatedly failing Salmonella performance standards that, according to the Agency, was proof that the ground beef being made there was being processed under “insanitary conditions.” Supreme Beef sued the USDA and not only won an injunction, but it succeeded in having the Salmonella regulations struck down as being “beyond the authority granted the Secretary [of the USDA] by the Federal Meat Inspection Act.” Supreme Beef v. USDA, 275 F.3d 432, 434 (5th Cir. 2001). Explaining its holding, the Court wrote:

The difficulty in this case arises, in part, because Salmonella, present in a substantial proportion of meat and poultry products, is not an adulterant per se, 21 meaning its presence does not require the USDA to refuse to stamp such meat “inspected and passed.” 22 This is because normal cooking practices for meat and poultry destroy the Salmonella organism, 23 and therefore the presence of Salmonella in meat products does not render them “injurious to health” 24 for purposes of § 601(m)(1). Salmonella-infected beef is thus routinely labeled “inspected and passed” by USDA inspectors and is legal to sell to the consumer.

Supreme Beef, 275 F.2d at 438-39. And, of course, not surprisingly, the court in this case was quick to cite the decision in APHA v. Butz, and to note that even now the “USDA agrees that Salmonella is not an adulterant per se.” Id. at 439 n. 21.

In my view the Supreme Beef decision is poorly reasoned and ill-informed. (For example, could not someone at the Court figure out that it is impossible for meat to be “infected” with Salmonella, and the proper term here is “contaminated”?) But the real lesson of Supreme Beef is that the USDA was, and continues to be, an Agency that is unable to decide whose side it is on. Sometimes it puts on its public safety hat, and sometimes—actually, most often—it puts on its pro-meat industry hat. And, unfortunately, these roles are too often contradictory. That is why USDA policy when it comes to meat safety is also too often contradictory.

Perhaps it is just time for the FSIS to take the the position that all pathogens that can kill you in meat are adulterants.  You have the authority – you just need to use it.

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 cases 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.  

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 postexposure 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 Medicine, 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

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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.

We in the U.S. tend to think about food safety from our perspective. Given that I am involve in cases around the world, I thought I would give my readers a bit broader perspecitive.

1,600, 000 – People get sick due to unsafe food in one day, on average

340 – Children under 5 years of age die due to preventable foodborne diseases, on average, every day 

200 – Diseases caused by unsafe food, ranging from diarrhoea to cancers

France

According to Sante Publique reports, as of 04/25/2022, 55 confirmed cases have been identified, of which 53 are linked to STEC O26 strains, and 2 to STEC O103 strains. Earlier reports on 04/13/2022, indicated that another 26 other cases of HUS and STEC infections notified to Public Health France with investigations are ongoing.

These 55 cases occurred in 54 children and 1 adult, who presented symptoms between 18/01/2022 (week 3) and 25/03/2022 (week 12). The epidemic peak is in week 7 (14/02 to 20/02) and week 9 (28/02 to 06/03), with 10 cases each of these weeks. These 55 cases occurred in 12 regions of metropolitan France: Hauts-de-France (12 cases), Ile-de-France (9 cases), New Aquitaine (8 cases), Pays de la Loire (7 cases), Brittany ( 6 cases), Grand Est (3 cases), Auvergne-Rhône-Alpes (2 cases), Occitanie (2 cases), Provence-Alpes-Côte d’Azur (2 cases), Center Val-de-Loire (2 cases) , Bourgogne Franche-Comté (1 case) and Normandy (1 case).

The 54 sick children are aged from 1 to 17 years with a median age of 7 years; 24 (44%) are female; 47 (87%) presented with HUS, 7 (13%) with STEC gastroenteritis. Two children died. The adult did not present with HUS.

The epidemiological, microbiological and traceability investigations carried out since that date have confirmed a link between the occurrence of these grouped cases and the consumption of frozen pizzas from the Buitoni brand Fraîch’Up range contaminated with STEC bacteria.

The total number of cases of HUS linked to the consumption of these pizzas seems to have stabilized since the withdrawal-recall.

French prosecutors have searched a Buitoni frozen pizza factory in northern France, the suspected source of an E. coli outbreak, as well as the headquarters of its owner Nestle France.

South Africa

In 2017 and 2018, the world’s largest and deadliest outbreak of listeriosis occurred in multiple provinces of South Africa (Figure 1). The outbreak was caused by contaminated polony, a ready-to-eat, processed meat product. Ready-to-eat, processed meats are a well-known vehicle for listeriosis outbreaks (Thomas et al., 2020). The Minister of Health declared that there was an outbreak of listeriosis on December 5, 2017, and, on March 4, 2018, further identified Tiger Brands’ polony products as the cause of the outbreak. The Minister of Health instructed Tiger Brands to recall all polony products the same day. See generally, Minister of Health September 3, 2018, Media Statement. The Ministry of Health based its conclusions on the investigative findings of the Joint Public Health Emergency Co-ordinating Committee, which was established for the specific purpose of identifying the cause of the outbreak and developing measures to prevent further illnesses and other outbreaks associated with processed meat products generally. Id. The relevant epidemiologic findings are set forth in the paragraphs that follow.

Figure 1. Incidence of Laboratory-Confirmed Listeriosis Cases during the Outbreak Period, According to South African Districts (Thomas et al., 2020).

Cases were reported from across the country, with most cases reported from Gauteng Province (58%). Women accounted for 55% of total cases. The ages of cases ranged from birth to 93 years. Neonates (aged £ 28 days) were the most affected age group, accounting for 43% of cases. This was followed by adults of 15 to 49 years of age, accounting for 32% of cases. The disease outcome was known for 806/1,060 (76%) of cases; 27% (216/806) had the known outcome “died” (Smith et al., 2019).

Listeriosis is a serious foodborne infection with a case-fatality rate (“death rate”) of 20-30% (Thomas et al., 2020). People primarily affected by listeriosis have impaired cell-mediated immunity. This includes those who are pregnant, elderly, or immunocompromised from conditions such as HIV, chronic disease, or immunosuppressive therapy (Thomas et al., 2020). The specific outbreak strain associated with the outbreak was Lm ST6. There are two ways that listeriosis can manifest: febrile gastroenteritis and invasive listeriosis (Coulombier). Invasive listeriosis is characterized by bacteraemia, meningitis, pneumonia, endocarditis, and sepsis (Smith et al., 2019).

A total of 1,060 cases were reported during the period of January 11, 2017, to July 17, 2018 (Figure 2)[1]. The outbreak period was defined as a duration of time during which case numbers exceeded and remained above a weekly threshold of five cases per epidemiological week (Thomas et al., 2020). At the peak of the outbreak (mid-November 2017), 41 listeriosis cases were reported in a single week. Prior to this outbreak, listeriosis was not a reportable disease in South Africa; therefore, information is not available on the prevalence, epidemiology, and description of clusters/outbreaks on listeriosis. Due to the lack of surveillance data, the baseline number of listeriosis cases was estimated from counts of listeriosis cases in 2016.

It is known that in 2015 and 2016, clusters of listeriosis occurred in South Africa. The 2015 listeriosis cluster involved 7 cases total, and the predominant strain was Lm ST6. However, researchers did not have sufficient epidemiologic evidence to connect the 2015 cluster to any specific food product (Shuping et al., 2015). For the 2016 cluster, retrospective analysis of Lm cases from the years 2012-2016 was used to calculate the expected case numbers for years 2013, 2014, 2015, and 2016 in the Gauteng province (Mathebula et al., 2016)[2]. Because there were only 3 cases in the 2016 cluster, researchers needed to estimate the baseline number of cases.

When determining if a cluster of diseases is classified as an outbreak or epidemic, it is essential to know what the baseline number of illnesses is in the population of interest. An epidemic refers to an increase in the number of cases of a disease, above what is normally expected in that population in that area, and an outbreak is defined the same but is often used for a more limited geographic area (Centers for Disease Control and Prevention [CDC], 2012).

Figure 2. Distribution of Laboratory-Confirmed Cases of Listeriosis, According to Outbreak Week and Major Events (January 1, 2017 to August 21, 2018) (Thomas et al., 2020).

Case definitions are used in outbreak investigations to help identify cases who are associated with the outbreak. A case definition includes criteria such as the subject population, implicated location, time, clinical features, and/or laboratory test results if available (CDC, 2012). The initial case definition for the primary listeriosis outbreak included all cases of listeriosis that occurred in South Africa from 2017 to 2018. The initial case definition was appropriate due to the lack of whole-genome sequencing (WGS) data at the beginning of the investigation. Multilocus sequencing typing (MLST) was used later to analyse the WGS results from all viable isolates obtained from case-patients. Researchers discovered that 93% of the clinical isolates collected from cases during the outbreak period were Lm ST6 (Thomas et al., 2020; Gerner-Smidt). The case definition later included sequence typing information to increase the likelihood of identifying a common source (Besser). This finding also showed that the outbreak strain of Listeriosis was definitively the Lm ST6 strain.

Further, we note that investigators thoroughly analysed the theoretical possibility that Lm ST6 was coming from more than just Tiger Brands’ polony products. In short, after conducting environmental investigations at all 157 ready-to-eat meat production facilities in South Africa, there was no Lm ST6 in any other products or facilities except Tiger Brands.

Together with the NCID’s clear statements that Tiger Brands polony products were the source of the outbreak, based on epidemiologic and environmental evidence, the constellation of all evidence conclusively establishes that Tiger Brands’ polony products were in fact the sole source. There is no additional analysis that will materially change these facts.

Based on its investigation findings, the Minister of Health issued a recall of Tiger Brand’s ready-to-eat meat products produced at the Enterprise facility. The Minister of Health also recalled all ready-to-eat meat products produced at Rainbow Foods, but epidemiologic and environmental findings during the investigation showed that this was a precautionary measure only—i.e., the Listeria identified at the Rainbow Foods’ production facility on environmental testing was not Lm ST6, and therefore had no causal association with illness in the outbreak. See Minister of Health March 4, 2017 Statement. Shortly after Tiger Brands’ recall, the outbreak essentially stopped (Figure 3).

Figure 3. Epidemic curve of laboratory-confirmed listeriosis cases by date of clinical specimen collection (n=1 038) and sequence type (ST) (n=564), South Africa, 01 January 2017 to 5 June 2018 (n=1049)

The environmental and epidemiologic investigative findings establish the likely causal nexus between Tiger Brands’ polony products and most all Listeriosis cases that occurred in South Africa before, during, and after the outbreak period. (Coulombier).  As stated above, 93% of clinical isolates that underwent sequencing were shown to be Lm ST6, the strain that was both epidemiologically associated with illness and repeatedly found in the production environment at the Enterprise facility, and nowhere else. But not all isolates could be sequenced, due to the lack of laboratory resources and personnel available (Besser). Based on the high percentage of Lm ST6 clinical isolates, it is highly likely that a similar percentage of non-sequenced isolates would have been Lm ST6 if sequencing could have been done (Coulombier). As further support that there was no difference between the distribution of sequence types among the non-sequenced samples and the distribution of sequence types observed in the sequenced samples, the process of selecting case isolates to be sequenced was not biased. Therefore, it is a statistically valid and provable fact that, in the absence of evidence to the contrary—i.e., sequencing that showed that a clinical isolate was not Lm ST6–a listeriosis patient diagnosed during the outbreak period had a > 90% probability of being related to the outbreak even without confirmed laboratory results (Gerner-Smidt).

After detecting the outbreak, the Centre for Enteric Diseases, a part of the National Institute for Communicable Diseases, conducted a nested case-control study that provided evidence that cases with Lm ST6 infections were more likely to have eaten polony than those with non- Lm ST6 infections (Thomas et. al, 2020). In outbreak investigations, case-control analysis is performed to estimate the odds ratio for the association between specific food items and the outbreak-associated illness. For this nested case-control study, case patients were those with Lm ST6 infections, and control patients were people infected by another strain of LM (i.e., not Lm ST6) during the outbreak period. Results from this study show that the odds ratio was 8.55 with a 95% confidence interval of 1.66 – 43.35. An odds ratio is a measure of association between the odds of becoming ill from consuming a specific food item versus the odds of becoming ill without having consumed the specific food item (Coulombier). An odds ratio of 8.55 signifies that the odds of having eaten polony in Lm ST6 cases is 8.55 times greater than the odds of having eaten polony in non-Lm ST6 cases. Based on the calculated confidence interval, this result is statistically significant because the confidence interval does not include the null value of 1. Therefore, 95% of the time, the true odds ratio fell within this interval.

Prior to the study, food history interviews were conducted to generate a hypothesis as to which food item could have been the source of the outbreak (Coulombier). The food histories were conducted with the use of a standardized questionnaire that inquired as to food consumed by a case-patient over the four weeks prior to onset of symptoms. Open-ended questions were posed to Listeriosis cases to understand each case’s food habits, such as where they purchase food, name of restaurants patronized, and use (and name) of informal food vendors. Closed-ended questions were posed to determine each case’s exposure to specific food items associated with outbreaks in the past and locally consumed foods thought to pose a high risk for listeriosis such as processed meats (e.g., biltong), cold meats (e.g., ham, polony), soft cheeses, raw milk, and raw vegetables. Brand preferences were also captured in the form.  The combination of open and closed-ended questions was and continues to be standard practice for the conduct of epidemiologic investigations internationally and provided investigators with high value data for consideration alongside other epidemiologic and environmental information.

The food history interviews were completed by November 1, 2017. The epidemiologic methods utilized throughout this investigation, including the case-control, were robust and mirrored those used in high-level investigations throughout the world. The investigators’ multi-disciplinary investigative methods were fully appropriate for the outbreak circumstances (Besser).

On January 13, 2018, febrile gastroenteritis developed in 10 children from a nursery in Gauteng Province. Several stool samples were collected from the children, and one yielded Lm ST6. Sandwiches prepared and eaten at the nursery were the only common food exposure, and polony was the common ingredient. Polony was recovered from the nursery refrigerator, and Lm ST6 was identified in the polony produced at Tiger Brands Enterprise Facility in Polokwane (Thomas et al., 2020).

On February 2, 2018, an environmental investigation took place at the Tiger Brands Enterprise Facility in Polokwane following the discovery at the nursery (Gerner-Smidt). Of 317 environmental samples taken from the Polokwane facility, 47 tested positive for Listeria monocytogenes, and of the 47 that tested positive, 34 were subtyped as the outbreak Lm ST6 strain. Additionally, two of 13 samples of unopened polony loaves collected at the facility tested positive for Listeria monocytogenes, and both were subtyped as the outbreak Lm ST6 strain.

These facts stand in stark contrast to the investigations at all other South African ready-to-eat meat producers, during which investigations no Lm ST6 was recovered in any food or environmental sample.

The fact that the public health investigation involved environmental inspections and sampling at the production facilities of other ready-to-eat meat producers is remarkable. Indeed, the public health investigation of this outbreak was unprecedented in scope, even internationally, as it is, in our experience, unprecedented to engage in such robust investigation of producers whose products are not epidemiologically associated with an outbreak. Thus, the only epidemiologic evidence establishes that Tiger Brands, and Tiger Brands alone, produced product contaminated by Lm ST6 during the outbreak period. By incorporating findings from the epidemiologic, environmental, microbiologic, and traceback data, investigators provided conclusive evidence that the source of the outbreak was polony produced fromTiger Brands Enterprise Foods Polokwane production facility, and that there were no other possible causes.

Further, and as set forth previously, the Minister of Health identified Tiger Brands’ polony products as the source of the outbreak on March 4, 2018, and instructed Tiger Brands to recall all its ready-to-eat meat products. At the point in time that Tiger Brands’ polony products were taken off of store shelves and were no longer widely available for purchase and consumption in South Africa, the outbreak ended and listeriosis cases in South Africa shortly returned to their pre-outbreak baseline. As Figure 3 demonstrates, by mid-April 2018 (6 weeks after recall), fewer than 5 cases were reported weekly. Regarding those individuals who became ill between the date of Tiger Brands’ recall and mid-April 2018, listeriosis cases continued to become ill by consumption of Tiger Brands’ polony products that were purchased before the date of the recall, which was to be expected given the lengthy incubation period for listeriosis generally (from 3 days to over one month), or from Tiger Brands’ polony products that were simply not removed from store shelves in time.

Following the findings by the NICD, Tiger Brands conducted its own internal investigation into the outbreak. During this internal investigation, based on information set forth in the discovery conducted to-date and Tiger Brands’ various public statements, Tiger Brands confirmed the presence of the Lm ST6 outbreak strain in both its products and various locations in the production environment at the Enterprise facility. Tiger Brands issued several public statements to this effect.

In a SENS statement dated 19 March 2018, Tiger Brands issued the following public statement:

“On 15 March 2018, Tiger Brands received confirmation from independent laboratory tests corroborating the DoH’s findings of the presence of LST6 in the environment at its Polokwane Enterprise Foods manufacturing Facility. In addition, there was a positive detection of LST6 on the outer casing of two samples.”

On 26 March 2018, Tiger Brands issued a public statement on its website reiterating the independent laboratory results announced in the SENS statement of 19 March 2018 as aforementioned which confirmed the presence Lm ST6 in the Tiger Brands Polokwane Facility. In the 26 March press statement, Tiger Brands CEO, Mr Lawrence Mac Dougall commented on this discovery and, inter alia, stated as follows:

“We are investing all our time and energy into not only understanding the cause of the LST6 detection, but also how it could have come into our facility.”

In a statement to shareholders dated 23 May 2018, Mr Mac Dougall stated that:

“The detection of the presence of Listeria ST6 in our factory in Polokwane was disappointing to us given our compliance with best practices and prevailing standards.”

In a SENS statement dated 25 April 2018, Tiger Brands reported that it had received independent laboratory test results following its own internal investigation which confirmed the presence of the Lm ST6 in samples of ready-to-eat meat products manufactured at the Polokwane Facility:

“The purpose of this announcement is to update shareholders on the results of the independent laboratory re-testing which was carried out in respect of the presence of LST6 in the above samples which were manufactured at the Enterprise Polokwane processing facility. On 24 April 2018, Tiger Brands received confirmation of the presence of LST6 in these samples.”

From both the NICD’s and Tiger Brands’ investigations into the outbreak, there is no evidence that the outbreak had any source other than Tiger Brands’ polony products. There is no epidemiologic support for that proposition, and there is no environmental support for that proposition because NICD found no other positive Lm ST6 samples at any other facility that produces ready-to-eat meat. In fact, Tiger Brands has, in unequivocal terms, admitted to this responsibility. For example, in the request Further Trial Particular, Tiger Brands affirmed its responsibility for Lm ST6 cases:

“Tiger Brands statement of 24 April 2018 was correct. Tiger Brands learnt that laboratory tests had found ST6 in ready-to-eat meat products from its Enterprise Foods manufacturing facility in Polokwane. It accepts that the laboratory findings were correct.”

“Tiger Brands does not know to what products the contamination extended or over what period it occurred. It accepts, however, that ST6 contaminated products from its Polokwane facility probably infected some of the people who suffered from listeriosis during the outbreak.”

“The defendants accept the test results that L. monocytogenes was detected in the polony water coolers at the Polokwane facility.”

Further, and following the Supreme Court of Appeal’s ruling in the third-party subpoena’s litigation, Tiger Brands issued the following statement to the press:

“On Friday, 4 February 2022, the Supreme Court of Appeal overturned the earlier order of the Gauteng Division of the High Court, Johannesburg which required various third parties to hand over epidemiological information relating to the listeriosis outbreak.”

“The 2018 listeriosis outbreak affected many South Africans. We are saddened by the impact it has had on the lives of the victims and those who have lost loved ones from the outbreak. Tiger Brands reiterates its commitment to ensure that a resolution of the matter is reached in the shortest possible time, in the interest of all parties, particularly the victims of listeriosis.”

That Tiger Brands is liable for the manufacture and sale of contaminated polony products that injured people is beyond doubt; the scientific findings from the multi-disciplinary investigation allow only this conclusion, and the functional life of the outbreak ended when Tiger Brands was ordered to withdraw its products from the market. The epidemiologic implications of NICD’s sequencing effort are conclusive, which is the preliminary point made by SAAFOsT, in which organization Tiger Brands is a custodian member, in its December 2017 statement that:

“This is undoubtedly one of the worst listeriosis cases in global history. A large percentage (74%) of all the clinical isolates belong to the same sequence type i.e. ST6—this means that these isolates originate from a single source, most likely a food product on the market.”

What SAAFOsT did not have the benefit of then knowing, however, was that sampling at Tiger Brands’ Polokwane facility would validate in every respect the epidemiologic implications from NICD’s sequencing efforts on human isolates.