Famous Anthony’s “About Us” Page in its website tells the story of a family run, Roanoke institution that has been taken to its knees in bankruptcy because one employee was not vaccinated against hepatitis A. Sadder still are the 50 customers sickened, some so severely that they required liver transplants, and in four instances they died, including two members of the same family.

As its About Page says:

We are often asked what makes us famous.  We’ve always been known for our food and service, but to us, it’s our customer (you!) that makes us famous.  Since 1986 we’ve been an integral part of the community and our story has been woven by our customers, spanning many generations of families.  It’s their stories that makes ours.   

We are still family owned and operated and you can often find Mr. Anthony out and about in the restaurants.  So come by and give us a visit.  As our customers say, visit once and you’re family.

My guess is that Mr. Anthony wishes that he had taken the About Page to heart and protected his family by offering vaccinations to all employees or seeking free vaccines from the local health department.  But, he did not and now it is too late for many customers and for his 40 year old business.

An outbreak of hepatitis A occurred in the early fall of 2021 in Roanoke City, Virginia. The health department was notified about the outbreak on September 21, 2021, after the first case was reported by a local hospital. The Roanoke City Health Department, along with the Virginia Department of Health, investigated this outbreak. Three different Famous Anthony’s locations were ultimately found associated with this outbreak: 6499 Williamson Road, Roanoke; 4913 Grandin Road, Roanoke; and 2221 Crystal Springs Avenue, Roanoke. A public posting was made by the Virginia Department of Health on September 24, 2021, about this outbreak and the potential exposure risk. 

As of November 2021, a total of 52 primary cases (41 confirmed and 11 probable) were identified in this outbreak. Two secondary cases were also identified. Cases ranged from 30 to 82 years of age (median 63). In all, 57 percent of cases were male. Thirty-three cases included hospitalizations, and at least 4 cases involved deaths. Exposures to the Famous Anthony’s food establishments occurred between August 10 and 27, 2021. Illness onsets occurred between August 25 and October 15, 2021.

A cook, who also had risk factors associated with hepatitis A, was found to be infected with hepatitis A while working at multiple Famous Anthony’s restaurant locations. This index case’s mother and adult son also tested positive for hepatitis A. Following an inspection, the inspector noted, “due to the etiology of Hepatitis A transmission, it is assumed the infectious food handler did not perform proper hand washing or follow glove use policy.” It was determined that person-to-person spread was the most likely mode of transmission in this outbreak. Environmental contamination was also considered a possible mode of transmission. 

Exposure to hepatitis A virus (“HAV”) can cause an acute infection of the liver that is typically mild and resolves on its own.[1] The symptoms and duration of illness vary a great deal, with many persons showing no symptoms at all.[2] Fever and jaundice are two of the symptoms most associated with HAV infection.[3]

Hepatitis A is the only common vaccine-preventable foodborne disease in the United States.[4] This virus is one of five human hepatitis viruses that primarily infect the human liver and cause human illness.[5] Unlike hepatitis B and C, hepatitis A does not develop into chronic hepatitis or cirrhosis, which are both potentially fatal conditions.[6]Nonetheless, infection with the hepatitis A virus (HAV) can lead to acute liver failure and death.[7]

Hepatitis A is a communicable (or contagious) disease that often spreads from person to person.[8] Person-to-person transmission occurs via the “fecal-oral route,” while all other exposure is generally attributable to contaminated food or water.[9] Food-related outbreaks are usually associated with contamination of food during preparation by a HAV-infected food handler.[10] 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.[11]

According to Lin & Fang[12], the recent upsurgence of hepatitis A transmitted from person-to-person has raised alarm among public health officials. Although hepatitis A is primarily foodborne, hepatitis A virus (HAV) can also be transmitted through close contact. The authors point to increasing rates of person-to-person transmission of hepatitis A across the world since 2015, which international health organizations now recognize as a reemerging health threat. 

In the United States, the increase in hepatitis A outbreaks from 2016 to the present are thought to be at least partially related to people using drugs and being homeless; however, both medical and nonmedical factors account for the observed increase of hospitalization and deaths. Of particular concern is the rising risk of morbidity during this wave of outbreaks. Recent studies cited by Lin & Fang show that more than half (52%) of patients were hospitalized, of whom 10% required intensive care, 4% developed fulminant hepatitis, and 1% died. This is in sharp contrast to past studies, where serious hepatic complications associated with acute hepatitis A were rarely reported. Nonetheless, these findings highlight the importance of HAV vaccinations for at-risk populations. 

As recommended in the United States by the Advisory Committee on Immunization Practices (ACIP), from a public health perspective, HAV vaccination is the most effective prevention strategy to control a person-to-person transmitted hepatitis A outbreak. HAV vaccines are highly immunogenic, and >95% of immunocompetent individuals achieve seroconversion within 4 weeks after the first dose. Despite the benefits of vaccination, several barriers and missed opportunities to vaccination were identified from the experiences during the hepatitis A outbreaks. Hofmeister et. al[13]cite recent research describing that information on HAV vaccination status was missing in nearly two-thirds of study participants, and nearly 90% of those with available information had not previously received HAV vaccines. Citing another study reporting a hepatitis A outbreak in San Diego County, no hepatitis A case patients had ever received a full series of HAV vaccinations.

HAV is relatively stable and can survive for several hours on fingertips and hands, and up to two months on dry surfaces.[14] 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 household bleach in tap water.[15] HAV can still be spread from cooked food if it is contaminated after cooking.[16]

Hepatitis A may cause no symptoms at all when it is contracted, especially in children.[17] 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.[18] Approximately 10 to 12 days after exposure, HAV is present in blood and is excreted via the biliary system into the feces.[19] Although the virus is present in the blood, its concentration is much higher in feces.[20] HAV excretion begins to decline at the onset of clinical illness, and decreases significantly by 7 to 10 days after onset of symptoms.[21] Most infected persons no longer excrete virus in the feces by the third week of illness. Children may excrete HAV longer than adults.[22]

Seventy percent of HAV 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.[23] 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.[24] The symptoms include muscle aches, headache, anorexia (loss of appetite), abdominal discomfort, fever, and malaise.[25]

After a few days of typical symptoms, jaundice (also termed “icterus”) sets in.[26] 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.[27] The urine will also turn dark with bile and the stool light or clay-colored from lack of bile.[28] When jaundice sets in, initial symptoms such as fever and headache begin to subside.[29]

In general, symptoms usually last less than two months, although 10% to 15% of symptomatic persons have prolonged or relapsing disease for up to 6 months.[30] It is not unusual, however, for blood tests to remain abnormal for six months or more.[31] The jaundice so commonly associated with HAV can also linger for a prolonged period in some infected persons, sometimes as long as eight months or more.[32] 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.[33]

Relapse is possible with hepatitis A, typically within three months of the initial onset of symptoms.[34] Although relapse is more common in children, it does occur with some regularity in adults.[35] The vast majority of persons who are infected with hepatitis A fully recover, and do not develop chronic hepatitis.[36] Persons do not carry HAV long-term as with hepatitis B and C.[37]

Fulminant hepatitis A, or acute liver failure, is a rare but devastating complication of HAV infection.[38] As many as 50% of individuals with acute liver failure may die or require emergency liver transplantation.[39] Elderly patients and patients with chronic liver disease are at higher risk for fulminant hepatitis A.[40] In parallel with a declining incidence of acute HAV infection in the general population, however, the incidence of fulminant HAV appears to be decreasing.[41]

HAV infects the liver’s parenchymal cells (internal liver cells).[42] Once a cell has been penetrated by the viral particles, the hepatitis A releases its own toxins that cause, in essence, a hostile takeover of the host’s cellular system.[43] The cell then produces new viral components that are released into the bile capillaries or tubes that run between the liver’s parenchymal cells.[44] This process results in the death of liver cells, called hepatic necrosis.[45]

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.[46] Aside from the loss of liver function, fulminant hepatic failure can lead to encephalopathy and cerebral edema.[47] Encephalopathy is a brain disorder that causes central nervous system depression and abnormal neuromuscular function.[48] Cerebral edema is a swelling of the brain that can result in dangerous intracranial pressure.[49] Intracranial hypertensions leading to a brain stem death and sepsis with multiple organ failure are the leading causes of death in individuals with fulminant hepatic failure.[50]

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

[2]           Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[3]           Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[4]           Id.; See also 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.

[5]           Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[6]           Id.

[7]           Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” supra note 7; Mayo Clinic Staff, “Hepatitis A,” supra note 1. 

[8]           Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[9]           Id.; See also 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

[10]         Fiore, Anthony, supra note 7; CDC, “Hepatitis A,” supra note 5; See also 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.

[11]         Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” supra note 7. 

[12]         Lin, K. Y., & Fang, C. T. (2021). Public health responses to person-to-person hepatitis A outbreaks. The Journal of Infectious Diseases, 223(3), 359-361.

[13]          Hofmeister, M. G., Xing, J., Foster, M. A., Augustine, R. J., Burkholder, C., Collins, J., … & Spradling, P. R. (2021). Hepatitis A person-to-person outbreaks: Epidemiology, morbidity burden, and factors associated with hospitalization—Multiple States, 2016–2019. The Journal of Infectious Diseases, 223(3), 426-434.

[14]         Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[15]         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, 2006), http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5836a4.htm; 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 29, 2006) at http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5507a1.htm; 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, 202-19 (2009). Full text of the article is available online at http://courses.washington.edu/eh451/articles/Todd_2009_food%20processing.pdf.

[16]         Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” supra note 7.

[17]         Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” supra note 7

[18]         Mayo Clinic Staff, “Hepatitis A,” supra note 1. 

[19]         CDC, “Hepatitis A,” supra note 5; Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1

[20]         Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1

[21]         Id.

[22]         Id.; See also 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.

[23]         CDC, “Hepatitis A,” supra note 5.

[24]         Id.: See also Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” supra note 7.

[25]         CDC, “Hepatitis A,” supra note 5; Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[26]         Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[27]         Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[28]         CDC, “Hepatitis A,” supra note 5; Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Mayo Clinic Staff, “Hepatitis A,” supra note 1. 

[29]         Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[30]         Fiore, Anthony, et al., Advisory Committee on Immunization Practices (ACIP), Prevention of Hepatitis-A Through Active or Passive Immunization: Recommendations,” supra note 20; 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.

[31]         Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[32]         Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[33]         CDC, “Hepatitis A,” supra note 5; Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[34]         Gilkson Miryam, et al., “Relapsing Hepatitis A. Review of 14 cases and literature survey,” supra note 37.

[35]         Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Gilkson Miryam, et al., “Relapsing Hepatitis A. Review of 14 cases and literature survey,” supra note 37.

[36]         Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[37]         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; CDC, “Hepatitis A,” supra note 5.

[38]         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.

[39]         Taylor, Ryan, et al., “Fulminant Hepatitis A Virus Infection in the United States: Incidence, Prognosis, and Outcomes,” Hepatology, Vol. 44, 1589-1597. Full text http://deepblue.lib.umich.edu/bitstream/2027.42/55879/1/21349_ftp.pdf.

[40]         Id.: See also Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[41]         Taylor, Ryan, et. al., “Fulminant Hepatitis A Virus Infection in the United States: Incidence, Prognosis, and Outcomes,” supra note 46. 

[42]         Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45; Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[43]         Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Schiff, E.R., “Atypical Manifestations of hepatitis-A,” supra note 23. 

[44]         Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45.

[45]         Id.; See also Taylor, Ryan, et. al., “Fulminant Hepatitis A Virus Infection in the United States: Incidence, Prognosis, and Outcomes,” supra note 46. 

[46]         Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45; Taylor, Ryan, et. al., “Fulminant Hepatitis A Virus Infection in the United States: Incidence, Prognosis, and Outcomes,” supra note 46.

[47]         Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45.

[48]         Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supranote 45; Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[49]         Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45.

[50]         Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45; Taylor, Ryan, et. al., “Fulminant Hepatitis A Virus Infection in the United States: Incidence, Prognosis, and Outcomes,” supra note 46.

ophs-esteban2-profile

Dr. Jose Emilio Esteban as been appointed and confirmed as the U.S. Department of Agriculture Food Safety and Inspection Service (FSIS) Under Secretary for Food Safety.Hanukkah

Dr. Esteban was appointed as Chief Scientist of the U.S. Department of Agriculture Food Safety and Inspection Service (FSIS) in August 2018. In this capacity, Dr. Esteban serves as the primary scientific advisor on matters of public health and food safety that affect the mission of the Agency, with primary responsibility for scientific initiatives within the Office of Public Health Science (OPHS). Dr. Esteban’s efforts directly support FSIS’ Strategic Goals 1: Prevent Foodborne Illness and Protect Public Health, and 2: Modernize Inspection Systems, Policies, and the Use of Scientific Approaches.

In 2002, Dr. Esteban joined OPHS as the Director of the Western Laboratory. In this role, he directed the implementation of the sampling program and was responsible for the physical plant, equipment and personnel infrastructure. In 2008, he was appointed as the FSIS Science Advisor for Laboratory Services, where he harmonized the operation of all three FSIS laboratories, maintained operations to meet with the ISO17025 standard and coordinated emergency response.

Prior to joining FSIS, Dr. Esteban worked in several positions at the Centers for Disease Control and Prevention (CDC). From 1994 to 2002, he was as an Epidemic Intelligence Service Officer; a Staff Epidemiologist in the National Center for Environmental Health; and an Assistant Director for the CDC Food Safety Office.

He received his Doctorate in Veterinary Medicine from Mexico’s National University, a Master of Business Administration Degree from the Panamerican Institute, and a Master of Preventive Veterinary Medicine Degree, as well as a Doctorate in Epidemiology from the University of California at Davis.

Dr. Esteban, here is some Christmas reading:

Remember this as you prepare Christmas dinner for your family and as you read this post – 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.

In a few days millions of Americans will bring a food product (a turkey) into their homes 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.

I would pay to watch it.

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.

Let the meat industry sue you.  I know a good lawyer to defend you.

Dr. Esteban – I will see you in the New Year.

caesar-salad-10-1200

A produce nightmare at retail – the only thing those consumers will remember is your father’s restaurant

Your father had a great idea for a restaurant when he was still alive.  After 20 years of working seven days a week, your father built an impressive chain of ten restaurants.  The restaurants were the place where first dates bloomed, where engagements happened, where anniversaries and birthdays were celebrated, and where, in the overflowing banquet rooms, passings were celebrated.  Business deals were made over long lunches, and a few affairs began and ended in the leather-seated bar.  Your father’s restaurants reflected him, but more importantly, they reflected a high standard of quality within the community.  All the reviews were glowing.  The restaurants set a standard that competitors could only envy.

Your father cared about the safety of the food he served his customers.  For the most part, it was because he saw his customers as friends and family.  However, he also understood how a sickened customer (or customers) could, with one meal, ruin the brand he had worked tirelessly to create.  He paid attention to the cleanliness of all his restaurants and the training of his employees.  Your father was at times an annoying stickler as to the quality of all the food that entered his restaurant.  He took pride in never having a negative health department inspection.

A Caesar salad has been one of your father’s restaurants’ signature dishes.  Your father took pride in the table-side preparation.  All the ingredients were hand-selected from nearby farmers and suppliers that your father had known since the first restaurant opened.  The heads of romaine were stripped of the outside leaves and thoroughly washed just before the lunch rush with the same process repeated shortly before dinner.  Your father always worried about the raw eggs in the dressing even though he knew the rancher that supplied the eggs.  However, he was a quick adapter when pasteurized eggs became available.

Growing up, at times you were annoyed when your father talked about the risks of hepatitis A due to inadequate employee handwashing, or Salmonella from undercooked eggs, the dreaded E. coli in undercooked beef, or a growing problem of leafy greens and E. coli.  A Jack in the Box was never considered a toy. By the time you began working in the restaurants in high school you were well-steeped in food safety, the cold chain, and third-party audits.

When your father died in the middle of your second year in college as an English major, you did not hesitate to come home to try and step into his very large shoes.  Your mother had died a few years earlier and your siblings had no interest in the business, save for what it did to fund their education and lifestyles.

Your father’s memorial service was enormous; all expertly catered by the general managers of each of the ten restaurants. A senator gave the eulogy. Stories were told about the meaning of the restaurants to the communities they served.  The foodbanks and homeless shelters came forward with how many times your father provided gourmet food to those less fortunate.

As you said your goodbyes and thank yous, the managers hung back.  Sitting in the very first restaurant’s bar, the enormity of your task was becoming more and more apparent.  You now realized that you not only were responsible for your father’s legacy and the tens of thousands of customers, but the ten managers and the hundreds of employees and their families.  Feeling a bit unprepared, you listened to the managers offering both their condolences and their support. You thanked them and after they left, you sat there for some time wishing your father would walk through the door.

You learned a long time ago that the restaurant business is 24/7/365 – almost.  From overseeing the expanded purchasing staff to hiring and firing decisions, things came at you like a firehose.  At best of times, you only had time to make a snap decision on a supplier change or to rely on the managers to manage.  At two in the morning, you were often awakened by the decisions that needed to be made the next day and the days after.

Perhaps it was exhaustion, or perhaps it was the desire to try something new and a bit simpler, but when a new salesperson somehow got a meeting with you one day, she pitched triple-washed, chopped bagged romaine that would equal the quality of your father’s signature salad.  Intrigued, you ordered a box and asked a trusted manager to test the product.  The results were glowing.  No more time stripping leaves and washing and cutting, it was open the bag and put it in the bowl.  The price was a bit higher, but it seemed that you would make it up in labor and convenience.  The decision made, your forgot to ask about where the product was grown.  You let the disappointed romaine suppliers know that their product was no longer needed.

And then the unthinkable happened.  The Friday after a holiday Monday, the local health department called that there were a handful of patients, mostly older, but some children who were hospitalized with E. coli, two in kidney failure, that seemed to have a connection to meals served at three of your restaurants in the prior week.  Testing was still being done, and other states were also reporting E. coli cases.  Thus far, no product had been identified.

Your heart sank.  Over the next days, various local, state, and federal health agencies found that nearly 100 people were sickened in several states, but that nearly 35 people were linked to your restaurants, including now two dead children, at least six more with acute kidney failure, and a dozen of others hospitalized. Thus far, still no product had been identified.

You immediately closed all restaurants, threw out all perishable foods, and began a thorough cleaning.  The health authorities then announced that the likely source of all the infections was the triple-washed, chopped bagged romaine that you recently purchased.  The traceback to the growing location showed that the lettuce was grown within a stone’s throw of a cattle feedlot which was the likely source of the E. coli.

Even after you shut the restaurants for a week (still paying all employees) and the health authorities said salad was safe to eat, the fact that your father’s restaurants were linked to severe illnesses and deaths kept customers away.  Sales were down between 70 to 80%.  Every day, the news talked about the struggles of the victims and how it was clear that the romaine was grown in an unsafe place.  As the days and weeks wore on, sales did not improve.  The decision was made to close three restaurants, but the news picked that up, and sales in the other seven stores dropped further.  Within three months, still paying both employees and suppliers, it became apparent that more restaurants would need to close.  Then, the lawsuits started.

Sitting in the bar in the last remaining restaurant, you thought back on the decision to order the triple-washed, chopped bagged romaine, and as you sat there, you wondered what your father would say if he walked through the door.

What is Vibrio parahaemolyticus?

Vibrio parahaemolyticus is a Gram-negative, curved-rod-shaped mobile bacterium that inhabits marine and estuarine environments throughout the world. It is a major foodborne pathogen that causes life threatening diseases in humans after the consumption of raw or undercooked seafood.[1]

Vibrio genus was first described by an Italian physician, Filippo Pacini in 1854.[2] He discovered the first Vibriospecies, Vibrio cholera, the causative agent of cholera while studying outbreaks of cholera disease in Italy. Although Dr. Pacini pointed out that cholerae was contagious, his discovery was largely ignored by the world’s scientific community for the next 30 years. During an active Vibrio outbreak, in Calcutta, India, another scientist, Robert Koch, successfully isolated Vibrio from pure culture and was finally recognized as an important public health discovery.

Vibrio genus consist of 142 species that are marine originated, and new species continue to be identified. Vibrio sp. infects any living being including animals and humans. Recently, the worldwide ocean warming and climate changes have enabled the emergence of foodborne pathogenic strains with several virulence factors in marine environments. The geographic areas where V. parahaemolyticus infections were originally reported were related to areas with high seafood consumption, particularly in Asia, but are expanding worldwide.[3]

As a member of the Vibrionaceace family and Vibrio genus, Vibrio parahaemolyticus has been in limelight for the rising vibriosis and foodborne cases worldwide. It was first identified in 1951 by Tsunesaburi Fujino from Research Institute of Microbial Diseases (RIMD), Osaka University from an acute gastroenteritis outbreak. The outbreak occurred in a southern suburb of Osaka, Japan due to consumption of “shirasu,” a type of dried sardine which resulted in 20 deaths and 272 infected patients at that time.

Where Does Vibrio parahaemolyticus Come From?

Vibrio parahaemolyticus is a human pathogen that is widely distributed in the marine environments. This organism is frequently isolated from a variety of raw seafoods, particularly shellfish. [4] Consumption of raw or undercooked seafood contaminated with V. parahaemolyticus may lead to development of acute gastroenteritis characterized by diarrhea, headache, vomiting, nausea, and abdominal cramps. This pathogen is a common cause of foodborne illnesses in many Asian countries, including China, Japan and Taiwan, and is recognized as the leading cause of human gastroenteritis associated with seafood consumption in the United States. 

Although the gastroenteritis caused by V. parahaemolyticus infection is often self-limited, the infection may cause septicemia that is life-threatening to people having underlying medical conditions such as liver disease or immune disorders. Two deaths were reported among three cases of wound infections caused by V. parahaemolyticus in Louisiana and Mississippi after Hurricane Katrina in 2005.

The degree of V. parahaemolyticus contamination in raw shellfish is also known to relate to the water temperatures. Therefore, it is more likely to detect V. parahaemolyticus in oysters harvested in the spring and the summer than in the winter.[5]

What are the Symptoms of Vibriosis?

The food poisoning caused by V. parahaemolyticus (“vibriosis”) usually occurs in summer (from June to October), and is predominantly associated with different kinds of seafood, including crab, shrimp, shellfish, lobster, fish, and oysters.[6] Once consumers eat undercooked, contaminated seafood, illness is inevitable. The typical clinical symptoms of V. parahaemolyticus poisoning are acute dysentery and abdominal pain, accompanied by nausea, vomiting, fever, chills, and watery diarrhea that may contain blood and/or mucous. Severely low blood pressure (hypotension) often develops progressively and can lead to shock. Some severely affected patients become unconscious, develop convulsions, become pale or cyanotic, and if untreated can die. The distinct pathologic changes that occur within the body include erosive gastritis and internal organ damage (liver, spleen lungs).

What is the Treatment of Vibriosis?

Early treatment of Vibrio parahaemolyticus poisoning (“vibriosis”) is vital and commonly includes antibiotics and oral rehydration.[7] Volume repletion is the most important element of therapy in patients with Vibrio gastroenteritis. The gastroenteritis caused by V. parahaemolyticus tends to be mild and self-limited. Antimicrobial therapy is reasonable in more severe cases, since among patients with cholera, antibiotic therapy is known to decrease the duration of diarrhea and the excretion of infectious organisms.

Because of the potential severity of illness, it is recommended that some subpopulations, including patients suffering severe physical or immunodeficiency diseases should avoid eating seafood during high risk seasons.

[1]           Wang, R., Zhong, Y., Gu, X., Yuan, J., Saeed, A. F., & Wang, S. (2015). The pathogenesis, detection, and prevention of Vibrio parahaemolyticus. Frontiers in microbiology, 6, 144. https://www.frontiersin.org/articles/10.3389/fmicb.2015.00144/full

[2]           Letchumanan, V., Loo, K. Y., Law, J. W. F., Wong, S. H., Goh, B. H., Ab Mutalib, N. S., & Lee, L. H. (2019). Vibrio parahaemolyticus: The protagonist of foodborne diseases. Progress In Microbes & Molecular Biology, 2(1). https://journals.hh-publisher.com/index.php/pmmb/article/view/59

[3]           Matsuda, S., Hiyoshi, H., Tandhavanant, S., & Kodama, T. (2020). Advances on Vibrio parahaemolyticus research in the postgenomic era. Microbiology and Immunology, 64(3), 167-181.

[4]           Su, Y. C., & Liu, C. (2007). Vibrio parahaemolyticus: a concern of seafood safety. Food microbiology, 24(6), 549-558.

[5]           Id.

[6]           Wang, R., Zhong, Y., Gu, X., Yuan, J., Saeed, A. F., & Wang, S. (2015). The pathogenesis, detection, and prevention of Vibrio parahaemolyticus. Frontiers in microbiology, 6, 144. https://www.frontiersin.org/articles/10.3389/fmicb.2015.00144/full

[7]           Wang, R., Zhong, Y., Gu, X., Yuan, J., Saeed, A. F., & Wang, S. (2015). The pathogenesis, detection, and prevention of Vibrio parahaemolyticus. Frontiers in microbiology, 6, 144. https://www.frontiersin.org/articles/10.3389/fmicb.2015.00144/full

I need to restart my world travel. I missed a great presentation at a recent conference in Sweden

An outbreak of Escherichia coli-associated haemolytic uremic syndrome linked to consumption of an unexpected food vehicle, France 2022

C. Krug 1 N. Jourdan-Da Silva 2, M. Tourdjman 3, P. Mariani-Kurkdjian 4, A. Cointe 5, S. Lefevre 6, S. Belichon 7, C. Postic 8, N. Fredriksen 9, M. Bernabe 10, H. Herber 11, D. Sergentet 12, S. Ganet 13, A. Bondat 14, I. Horrigue 15, F. Chereau 16, H. Noël 17, H. de Valk 18, S. Bonacorsi 19, F. Weill 20, G. Jones 21

1 ECDC Fellowship Programme, Field Epidemiology path (EPIET), European Centre for Disease Prevention and Control (ECDC), Solna, Sweden 1, 2, 3, 15, 16, 17, 18, 21 Santé publique France, Saint-Maurice, France 4, 5, 19 National associated reference centre for Escherichia coli, Department of Microbiology, Robert-Debré Hospital, AP-HP, Paris, France 6, 20 Institut Pasteur, National reference centre for Escherichia coli, Shigella and Salmonella, Paris, France 7, 8, 9 General Directorate for Food (DGAL), Paris, France 10, 11 Directorate General for Competition Policy, Consumer Affairs and Fraud Control (DGCCRF), Paris, France 12, 13, 14 National reference laboratory for STEC (LNR, VetAgroSup)

BACKGROUND

In February 2022, Santé publique France identified an excess of paediatric haemolytic uremic syndrome cases. We conducted epidemiological, microbiological, and trace-back investigations to identify the outbreak source and implement control measures.

METHODS

We defined cases as Shiga toxin-producing Escherichia coli (STEC) O26:H11 or O103:H2 infection with outbreak strains identified by whole genome sequencing (WGS) and symptom onset since Jan 1, 2022. We interviewed case caretakers about food exposures before symptom onset. Supermarket loyalty card information was requested to identify purchases and guide trace-back investigations. Stool and food isolates were characterized by multilocus variable-number tandem- repeat analysis and WGS at the National reference centre. We conducted a case-control study including O26:H11 cases and controls from parents registered on GrippeNet.fr (online population-based surveillance system).

RESULTS

We identified 55 cases nationwide with onset between 18 January and 25 March (median age 7 years; sex ratio M/F: 1.3). Two children died. Eighty-eight percent (35/40) of cases with available information reported consumption of Brand X frozen pizza. Ninety-five percent (35/37) of cases with pizza purchases on loyalty cards purchased Brand X. The case- control study confirmed a strong association between consumption of Brand X pizza and disease (OR: 116 [95%CI 27- 503]). Samples of Brand X pizza from case homes and from the manufacturer were positive for both outbreak strains.

CONCLUSIONS

Outbreak investigations confirmed frozen pizzas as the source of the largest STEC-HUS outbreak ever documented in France. On 18 March, Brand X voluntarily recalled and withdrew the incriminated pizzas. This outbreak is highly unusual, as typical baking temperatures and times for frozen pizzas should eliminate infection risk. Investigations continue to understand the origin of contamination and the persistence of STEC in baked pizzas.

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I must admit I was a bit suspect when I flew from Seattle to DC a few months ago to testify for 5 minutes before the Independent Expert Panel. Putting aside if they would pay attention to me, but would the panel take to heart the experience and thoughtfulness of all the panels and the panel members. From a read of the report, I think they did. Now the question is will Congress and the FDA Commissioner take the recommendations to heart?

Here are a few highlights cut from the final report:

Culture

Most FDA employees understand the immense responsibility of the Agency’s Human Foods Program, appreciate the importance of their work, and share a common value of striving to protect public health. However, the current culture, structure, and governance model detract from the Program’s effectiveness. 

There are several factors contributing to this culture, including the lack of a clear vision and mission; a disparate structure and a consensus governance model; competing priorities; and the lack of a strong, supportive leader and, when the situation requires, an ultimate decision-maker, who is responsible for the Human Foods Program. The lack of a clear overarching leader of the Human Foods Program has contributed to a culture of indecisiveness and inaction and created disincentives for collaboration. 

The lack of a single clearly identified person to lead the Human Foods Program has adversely impacted the organizational culture and led to overlapping roles and competing priorities that result in what is perceived as constant turmoil…. As senior leaders are considered for the Human Foods Program, an ideal leadership skill set should include: 

·       Expertise and knowledge in food safety and/or nutrition 

·       Ability to make decisions in a complex regulatory environment 

·       Ability to lead in a complex work environment 

·       Strong demonstrated management capability 

·       Superb communication skills 

·       Ability to identify and nurture talent 

·       Commitment to collaboration, not isolation 

·       Capable of breaking down silos 

·       Proven abilities to lead, support, and incent teamwork 

·       Ability to support initiatives that increase staff professionalism and performance 

·       Commitment to joint staff development and other activities by the collective parts of the Human Foods Program 

To move the Human Foods Program toward a more enabling and effective culture, the Panel recommends FDA leadership consider the following:

·       Identify, communicate, embrace, and promote a clear and compelling vision, mission, and value statement for the Human Foods Program.  

·       Establish an organizational structure with a clear leader and ensure that there is a clear articulation of roles and responsibilities within the Human Foods Program and a culture that is well-equipped to survive (inevitable) leadership transitions.

·       Develop and nurture a culture where regulatory decision-making is rooted in scientific evidence and FDA’s legal framework. 

·       Commit to transparency, timeliness, and predictability in decision-making, with a preference towards action. 

·       Commit to an on-going process of culture change from the highest levels of FDA leadership. 

·       Develop and implement a change management strategy that not only manages change, but also effectively improves and monitors the environment for cultural change. 

·       Build expectations and incentives into the system to embrace a positive, collaborative culture that expects, values, and rewards teamwork. 

·       Create a culture of feedback and authenticity where continuous, honest, and constructive feedback is given and received.

·       Nurture current staff and recruit, hire, and promote top quality staff, including strong managers. 

Structure

FDA should increase the visibility and prominence of the Human Foods Program. 

Given the economic impact that foodborne illness and diet-related chronic disease have on Americans and the federal budget, it is imperative that the Human Foods Program become more prominent. When compared to the medical products programs within FDA, the Human Foods Program continuously struggles for visibility and prominence. A component of this elevation of the Human Foods Program is strong advocacy to advance the Human Foods Program at all levels of the government, especially at the Department of Health and Human Services (HHS) and the White House, including the Office of Management and Budget. 

The Human Foods Program should have clear lines of authority. 

Within the Human Foods Program, the importance of nutrition should be elevated. 

The foods portfolio of ORA should be integrated directly with the other elements of FDA’s Human Foods Program.

The food-relevant work of CVM should be integrated with the overall FDA Human Foods Program. 

A new Foods Advisory Committee, at the Commissioner-level, should be established to strengthen external input to Human Foods Program activities.

Structure changes should be implemented with cultural transformation efforts.

Honestly, this is what I focused on. I am convinced if you get the structure right and the right leaders in place, the culture will develop and the resources will be available. The Panel had five structural option. My preference is the first one:

Resources

The expectations of the FDA Human Foods Program and its impact on public health and our nation’s economy are immense. However, relatively modest increases in federal budget authority, flat staffing levels, and lack of sustained and sufficient commitment to upgrading information technology (IT)— contrasting with a rapidly changing food industry– have constricted the ability of the Human Foods Program to carry out its mission efficiently and effectively. In addition to aforementioned cultural and structural changes, the FDA’s Human Foods Program urgently needs additional personnel, financial, and IT resources to perform its Congressional mandate more effectively.

Here is the full report: https://www.marlerblog.com/files/2022/12/Human-Foods-Program-Independent-Expert-Panel-Final-Report-120622.pdf

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The Independent Expert Panel, charged with generating the report by December 6th, is comprised of researchers, former regulators, and process improvement specialists with disciplinary expertise and experience in epidemiology, food science and safety, microbiology, nutrition, and regulatory operations.

  • Francisco Diez-Gonzalez, PhD, a food safety microbiologist, is Director of the Center for Food Safety and a Professor in the Department of Food Science and Technology at the University of Georgia’s College of Agricultural and Environmental Sciences. He conducts research aimed to control foodborne pathogens and is a member of the USDA’s National Advisory Committee on Microbiological Criteria for Foods.
  • James Jones is President of JJones Environmental, following a 30-year career at the U.S. Environmental Protection Agency. His posts at EPA included five years as the Assistant Administrator, and his accomplishments include leading the agency’s effort to significantly reduce pesticides in food and navigating a years-long backlog of pesticide registrations and tolerances as well as leading the Obama Administration’s efforts to reform the Toxic Substances Control Act.
  • Barbara Kowalcyk, PhD, directs the Center for Foodborne Illness Research and Prevention at The Ohio State University’s College of Food, Agricultural, and Environmental Sciences and is Associate Professor of Food Safety and Public Health in the Department of Food Science and Technology. She is a well-respected epidemiologist and biostatistician, and a nearly ten-year member of the FDA Science Board, which she currently chairs.
  • Shiriki Kumanyika, PhD, MS, MPH, is Research Professor in the Department of Community Health and Prevention at Drexel University’s Dornsife School of Public Health. She has applied her interdisciplinary background and extensive research experience in numerous roles, and currently chairs the National Academies Food and Nutrition Board. She is also Emeritus Professor of Epidemiology at the Perelman School of Medicine, University of Pennsylvania.
  • John Taylor, JD, is President and Principal, Compliance and Regulatory Affairs, at Greenleaf Health. He spent more than 20 years at FDA, holding posts that included Counselor to the Commissioner, Acting Deputy Principal Commissioner, Acting Deputy Commissioner for Global Regulatory Operations and Policy, and Associate Commissioner for Regulatory Affairs.

I testified before the panel. It will be interesting to see the reccomendations.

And, did I say the the FDA appears to have closed its investigation after nearly 400 reported illnesses?

Tara, you might remember that it is an ingredient in both Daily Harvest French Lentil and Leek Crumbles and in Revive Pineapple and Mango Smoothies. Tara, or Caesalpinia spinosa is a shrub or tree that can reach a height of 8 meters with spreading, grey-barked leafy branches. The leaves are compound, bipinnate, alternate and spirally organized and reach a length of 35 cm. The fruit is a flat oblong indehiscent reddish pod which contains 4 ~ 7 large round black seeds composed of endosperm (22% by weight), germ (40%) and hull (38%). The tara tree is native to the Cordillera region of Peru and Bolivia in South America, where the fruit grows from April to December. Tara trees grow at up to 3,000 meters above sea level and tolerate dry climates and poor soils including those high in sand and rocks. The tree is also resistant to most pathogens and pests. Mature pods are usually harvested by hand and typically sun dried before processing. 

Months ago, I announced that both Daily Harvest and Revive used tara in products that have been linked to acute liver failure in some of its customers. In the past week, during the course of litigation, we have learned that Daily Harvest and Revive share a common manufacturer and supplier of tara – Molinos.

Here is the Daily Harvest chain of distribution – Daily Harvest sold it, Stonegate manufactured it, Smirk’s imported it and Molinos manufactured it.

Here is the Revive chain of distribution – Revive manufactured it and sold it, Miski imported it and Molinos manufactured it.

FSIS continues to investigate an E. coli outbreak linked to beef that has sickened an unknown number of people. It does appear that FSIS closed another investigation linked to Salmonella and beef that also sickened an unknown number of people.

The FDA on the other hand has at least six active investigations with one that has sickened 270 with Salmonella being “Not Yet Identified.” Listeria linked to mushrooms, E. coli linked to falafels, Salmonella linked to Seafood, Listeria linked to cheeses and Cronobacter linked to infant formula are still on the “menu.”