Proving a Foodborne Illness Case with Bill MarlerBill Marler
In this 2011 presentation given at the University of Colorado Law School, foodborne illness attorney William Marler explains the intricacies involved in successfully litigating a food poisoning case.
Proving a Foodborne Illness Case with Bill MarlerBill Marler
In this 2011 presentation given at the University of Colorado Law School, foodborne illness attorney William Marler explains the intricacies involved in successfully litigating a food poisoning case.
2011 NCASM Conference: Separating the Wheat from the Chaff with Bill MarlerBill Marler
Marler Clark Managing Partner Bill Marler's presentation to the Northern California American Society for Microbiology about the process of food safety plaintiff litigation
The Impact of Global Commerce on Food Safety and Liability in 2009 with Bill ...Bill Marler
Marler Clark's Bill Marler speaks on the impact of global commerce on food safety and liability to the Canadian Institute of Public Health Inspectors in 2009
Chapter 11 DiscussionLearning ObjectivesBy the end.docxbartholomeocoombs
Chapter 11 Discussion
Learning Objectives
By the end of this chapter, the reader will be able to:
State three measures for preventing foodborne illnesses
Discuss 10 microbiological agents that are implicated in foodborne illness
Explain the significance of foodborne illness for the world’s population
List five categories of contaminants in the food supply
Describe one major regulation for protecting the safety of food from carcinogens
Foodborne Diseases/Infections
“illnesses acquired by consumption of contaminated food; they are frequently and inaccurately referred to as food poisoning”
An outbreak indicates “the occurrence of a similar illness among two or more people which an investigation linked to consumption of a common meal or food items, except for botulism (one case is an outbreak)”
Burden of Illness Pyramid
Risk Factors for Foodborne Illness – USA
63% Inadequate cooling and cold holding temperatures
29% Preparing food ahead of planned event
27% Inadequate hot holding temperatures
26% Poor personal hygiene/infected persons
25% Inadequate reheating
9% Inadequate cleaning of equipment
7% Use of leftovers
6% Cross-contamination
5% Inadequate cooking or heating process
… List goes on…
Risk Factors for Foodborne Illness
So what are some of the prevention measures we can take?
Clean, separate, cook, & chill
Hand hygiene
Irradiation of food (common for meats)
Risk Factors for Foodborne Illness
Investigating Foodborne Outbreaks
Detecting a possible outbreak
Defining and finding cases
Generating hypotheses about likely sources
Testing the hypotheses
Finding the point of contamination
Controlling an outbreak
Deciding an outbreak is over
Investigating Foodborne Outbreaks
Detecting a possible outbreak
Defining and finding cases
Generating hypotheses about likely sources
Testing the hypotheses
Finding the point of contamination
Controlling an outbreak
Deciding an outbreak is over
First step of process
Generally through public health surveillance (usually passive)
Nationally Notifiable Conditions
Establish a normal baseline incidence of a given disease
Detect an increase in the incidence, or a “cluster”
If the cluster has something in common, then it is considered an outbreak
Investigating Foodborne Outbreaks
Detecting a possible outbreak
Defining and finding cases
Generating hypotheses about likely sources
Testing the hypotheses
Finding the point of contamination
Controlling an outbreak
Deciding an outbreak is over
Usually the first cases identified are only a small part of the total outbreak
Develop a “case definition”, including:
Pathogen & symptoms
Time range & geographic area
Other criteria (common source or DNA/PFGE fingerprint)
May distinguish probable vs. confirmed
Using the case definition, active surveillance for additional cases
Surveying individuals
Looking through health records/laboratory reports
Reaching out to other health officials
Investigating Foodborne Outbreaks
Detecting a poss.
2011 Food Defense Summit: Legal Risks and Responsibilities for Producing Safe...Bill Marler
Bill Marler of Marler Clark, The Food Safety Law Firm gives a presentation at the 2011 Food Defense Summit in Denver about the legal aspects of food safety in food production and reducing foodborne illness.
2018 Royal Society for Public Health SpeechBill Marler
Later this month I will be giving a talk to the Royal Society for Public Health. The talk will be a bit of history of E. coli and the Jack in the Box case.
CDC Webinar: Foodborne illness Outbreaks and Law with Attorney Bill MarlerBill Marler
Attorney and food safety expert William Marler give a May 2012, Centers for Disease Control and Prevention webinar on foodborne illness litigation and the role of public health officials.
Acute hemolytic uremic syndrome (HUS).
Post-diarrheal hemolytic uremic syndrome (D+HUS) is a severe, life-threatening complication that occurs in about 10 percent of those infected with E. coli O157:H7 or other Shiga toxin-producing (Stx) E. coli (STEC).
The cascade of events leading to HUS begins with ingestion of Stx-producing E. coli (e.g., E. coli O157: H7) in contaminated food, beverages, animal to person, or person-to-person transmission. The bacteria rapidly multiply in the gut, causing inflammation and diarrhea (colitis) as they tightly bind to cells that line the large intestine. This snug attachment becomes a route for the toxin to travel from the gut into the bloodstream, where it attaches to weak receptors on white blood cells (WBCs). From there, WBCs carry the toxin to the kidneys and other organs.
To induce toxicity in target cells, Shiga toxins must first bind to specific receptors on their surface (Gb3 receptors). Organ injury is primarily a function of Gb3 receptor location and density. They are found on epithelial, endothelial, mesangial, and glomerular cells of the kidney, as well as microvascular endothelial cells of the brain and intestine. Because this attachment causes these organs to be susceptible to the toxicity of Shiga toxins, this distribution explains the involvement of the gut, kidney, and brain in STEC-associated hemolytic uremic syndrome (HUS).
Within the target organ, Shiga toxins disrupt the cellular machinery, resulting in cell injury and/or death. Within the intestine, infectious bacterial lesions cause derangements in the intestinal lining, disrupting the structure of the villi, affecting absorption in the gut, and eventually leading to watery diarrhea. Damage to the intestinal endothelium also causes mucosal/submucosal edema and, hemorrhage, introducing blood into the diarrhea.
Within the circulatory system, Shiga toxins are directly involved in platelet activation and aggregation (clot formation). The thrombotic microangiopathy that characterizes hemolytic uremic syndrome (HUS) occurs when platelet microthrombi (tiny clots) form in the walls of small blood vessels (arterioles and capillaries) causing platelet consumption. This pathologic reduction in platelets is called thrombocytopenia and is one of the hallmarks of HUS. Within the microvasculature of the kidney these clots disturb blood flow to the organ, causing acute kidney injury and kidney failure.
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Chapter 11 DiscussionLearning ObjectivesBy the end.docxbartholomeocoombs
Chapter 11 Discussion
Learning Objectives
By the end of this chapter, the reader will be able to:
State three measures for preventing foodborne illnesses
Discuss 10 microbiological agents that are implicated in foodborne illness
Explain the significance of foodborne illness for the world’s population
List five categories of contaminants in the food supply
Describe one major regulation for protecting the safety of food from carcinogens
Foodborne Diseases/Infections
“illnesses acquired by consumption of contaminated food; they are frequently and inaccurately referred to as food poisoning”
An outbreak indicates “the occurrence of a similar illness among two or more people which an investigation linked to consumption of a common meal or food items, except for botulism (one case is an outbreak)”
Burden of Illness Pyramid
Risk Factors for Foodborne Illness – USA
63% Inadequate cooling and cold holding temperatures
29% Preparing food ahead of planned event
27% Inadequate hot holding temperatures
26% Poor personal hygiene/infected persons
25% Inadequate reheating
9% Inadequate cleaning of equipment
7% Use of leftovers
6% Cross-contamination
5% Inadequate cooking or heating process
… List goes on…
Risk Factors for Foodborne Illness
So what are some of the prevention measures we can take?
Clean, separate, cook, & chill
Hand hygiene
Irradiation of food (common for meats)
Risk Factors for Foodborne Illness
Investigating Foodborne Outbreaks
Detecting a possible outbreak
Defining and finding cases
Generating hypotheses about likely sources
Testing the hypotheses
Finding the point of contamination
Controlling an outbreak
Deciding an outbreak is over
Investigating Foodborne Outbreaks
Detecting a possible outbreak
Defining and finding cases
Generating hypotheses about likely sources
Testing the hypotheses
Finding the point of contamination
Controlling an outbreak
Deciding an outbreak is over
First step of process
Generally through public health surveillance (usually passive)
Nationally Notifiable Conditions
Establish a normal baseline incidence of a given disease
Detect an increase in the incidence, or a “cluster”
If the cluster has something in common, then it is considered an outbreak
Investigating Foodborne Outbreaks
Detecting a possible outbreak
Defining and finding cases
Generating hypotheses about likely sources
Testing the hypotheses
Finding the point of contamination
Controlling an outbreak
Deciding an outbreak is over
Usually the first cases identified are only a small part of the total outbreak
Develop a “case definition”, including:
Pathogen & symptoms
Time range & geographic area
Other criteria (common source or DNA/PFGE fingerprint)
May distinguish probable vs. confirmed
Using the case definition, active surveillance for additional cases
Surveying individuals
Looking through health records/laboratory reports
Reaching out to other health officials
Investigating Foodborne Outbreaks
Detecting a poss.
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Acute hemolytic uremic syndrome (HUS).
Post-diarrheal hemolytic uremic syndrome (D+HUS) is a severe, life-threatening complication that occurs in about 10 percent of those infected with E. coli O157:H7 or other Shiga toxin-producing (Stx) E. coli (STEC).
The cascade of events leading to HUS begins with ingestion of Stx-producing E. coli (e.g., E. coli O157: H7) in contaminated food, beverages, animal to person, or person-to-person transmission. The bacteria rapidly multiply in the gut, causing inflammation and diarrhea (colitis) as they tightly bind to cells that line the large intestine. This snug attachment becomes a route for the toxin to travel from the gut into the bloodstream, where it attaches to weak receptors on white blood cells (WBCs). From there, WBCs carry the toxin to the kidneys and other organs.
To induce toxicity in target cells, Shiga toxins must first bind to specific receptors on their surface (Gb3 receptors). Organ injury is primarily a function of Gb3 receptor location and density. They are found on epithelial, endothelial, mesangial, and glomerular cells of the kidney, as well as microvascular endothelial cells of the brain and intestine. Because this attachment causes these organs to be susceptible to the toxicity of Shiga toxins, this distribution explains the involvement of the gut, kidney, and brain in STEC-associated hemolytic uremic syndrome (HUS).
Within the target organ, Shiga toxins disrupt the cellular machinery, resulting in cell injury and/or death. Within the intestine, infectious bacterial lesions cause derangements in the intestinal lining, disrupting the structure of the villi, affecting absorption in the gut, and eventually leading to watery diarrhea. Damage to the intestinal endothelium also causes mucosal/submucosal edema and, hemorrhage, introducing blood into the diarrhea.
Within the circulatory system, Shiga toxins are directly involved in platelet activation and aggregation (clot formation). The thrombotic microangiopathy that characterizes hemolytic uremic syndrome (HUS) occurs when platelet microthrombi (tiny clots) form in the walls of small blood vessels (arterioles and capillaries) causing platelet consumption. This pathologic reduction in platelets is called thrombocytopenia and is one of the hallmarks of HUS. Within the microvasculature of the kidney these clots disturb blood flow to the organ, causing acute kidney injury and kidney failure.
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Acute hemolytic uremic syndrome (HUS).
Post-diarrheal hemolytic uremic syndrome (D+HUS) is a severe, life-threatening complication that occurs in about 10 percent of those infected with E. coli O157:H7 or other Shiga toxin-producing (Stx) E. coli (STEC).
The cascade of events leading to HUS begins with ingestion of Stx-producing E. coli (e.g., E. coli O157: H7) in contaminated food, beverages, animal to person, or person-to-person transmission. The bacteria rapidly multiply in the gut, causing inflammation and diarrhea (colitis) as they tightly bind to cells that line the large intestine. This snug attachment becomes a route for the toxin to travel from the gut into the bloodstream, where it attaches to weak receptors on white blood cells (WBCs). From there, WBCs carry the toxin to the kidneys and other organs.
To induce toxicity in target cells, Shiga toxins must first bind to specific receptors on their surface (Gb3 receptors). Organ injury is primarily a function of Gb3 receptor location and density. They are found on epithelial, endothelial, mesangial, and glomerular cells of the kidney, as well as microvascular endothelial cells of the brain and intestine. Because this attachment causes these organs to be susceptible to the toxicity of Shiga toxins, this distribution explains the involvement of the gut, kidney, and brain in STEC-associated hemolytic uremic syndrome (HUS).
Within the target organ, Shiga toxins disrupt the cellular machinery, resulting in cell injury and/or death. Within the intestine, infectious bacterial lesions cause derangements in the intestinal lining, disrupting the structure of the villi, affecting absorption in the gut, and eventually leading to watery diarrhea. Damage to the intestinal endothelium also causes mucosal/submucosal edema and, hemorrhage, introducing blood into the diarrhea.
Within the circulatory system, Shiga toxins are directly involved in platelet activation and aggregation (clot formation). The thrombotic microangiopathy that characterizes hemolytic uremic syndrome (HUS) occurs when platelet microthrombi (tiny clots) form in the walls of small blood vessels (arterioles and capillaries) causing platelet consumption. This pathologic reduction in platelets is called thrombocytopenia and is one of the hallmarks of HUS. Within the microvasculature of the kidney these clots disturb blood flow to the organ, causing acute kidney injury and kidney failure.
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Foodborne Illness Litigation: The Courtroom and the Science with Bill Marler
1.
2. Marler Clark, LLP PS
Since 1993 Marler Clark has
represented thousands of
legitimate food illness victims
in over 30 States. Settlements
and Verdicts – total nearly
$300,000,000.
Only a fraction of the victims
who contact our office end
up being represented.
Who do we turn away?
3. There is a Worm in my Freezer!
“I recently found a whole,
2-cm long worm packaged
inside a Lean Cuisine frozen
dinner.
I have the worm in my freezer.
I'm interested in discussing my
rights in this matter. Could you
please contact me, or refer me
to a firm that may be able to
give me assistance? ”
4. “Christening” the Carpet
“I opened a box of Tyson
Buffalo wings and saw an
unusually shaped piece of
chicken and I picked it up.
When I saw that the ‘piece’
had a beak, I got sick to my
stomach. My lunch and diet
coke came up and I
managed to christen my
carpet, bedding and clothing.
I want them to at least pay for
cleaning my carpet etc.”
5. Lending a Helping Hand
“My husband recently
opened a bottle of salsa
and smelled an unusual
odor but chose to eat it
regardless, thinking that it
was just his nose. He found
what appeared to be a
rather large piece of animal
or human flesh. He became
very nauseated and I feel
the manufacturer should be
held responsible.
6. The Chaff
Just like health departments we need
to quickly and reliably recognize
unsupportable claims
How Do We Do It?
7. Basic Tools of the Trade
Symptoms
Incubation
Duration
Food History
Medical Attention
Suspected source
Others Ill
Health Department Involvement
8. Matching Incubation Periods
Incubation Periods Of Common Pathogens
PATHOGEN INCUBATION PERIOD
Staphylococcus aureus 1 to 8 hours, typically 2 to 4 hours.
Campylobacter 2 to 7 days, typically 3 to 5 days.
E. coli O157:H7 1 to 10 days, typically 2 to 5 days.
Salmonella 6 to 72 hours, typically 18-36 hours.
Shigella 12 hours to 7 days, typically 1-3 days.
Hepatitis A 15 to 50 days, typically 25-30 days.
Listeria 3 to 70 days, typically 21 days
Norovirus 24 to 72 hours, typically 36 hours.
9. Matching Symptoms with Specific
Characteristics of Pathogens
E. coli O157:H7
Hepatitis A
Salmonella
Shigella
Campylobacter
Vibrio
16. Traceback Records
POS APOS A
POS BPOS B
POS CPOS C
POS DPOS D
FIRM AFIRM A
FIRM BFIRM B
FIRM CFIRM C
FIRM DFIRM D
FIRM EFIRM E
FIRM GFIRM G
FIRM HFIRM H
FIRM FFIRM F
FIRM IFIRM I
FIRM JFIRM J
FIRM KFIRM K
FIRM LFIRM L
FIRM MFIRM M
FIRM NFIRM N
FIRM OFIRM O
GROWER
A
GROWER
A
GROWER
B
GROWER
B
GROWER
D
GROWER
D
GROWER
C
GROWER
C
Firm Name
Firms A,C,D,G,
H,I,L,M,N
Growers A&C
Firms B,E,F,J,K
Firm O, Grower D
Grower B
No. of outbreaks
Assoc. with firm/
Total no. of outbreaks
1/4
1/4
2/4
3/4
4/4
17. Prior Health Department Inspections
Improper Cooking
Procedures
Improper Refrigeration
Improper Storage
and Cooking Procedures
Improper Sanitation
18. Improper Cooking Procedures
Hamburger buns are toasted on the grill
immediately adjacent to the cooking patties,
and it is conceivable that, early in the cooking
process, prior to pasteurization, meat juices and
blood containing active pathogens might possibly
splash onto a nearby bun.
Hamburger buns are toasted on the grill
immediately adjacent to the cooking patties,
and it is conceivable that, early in the cooking
process, prior to pasteurization, meat juices and
blood containing active pathogens might possibly
splash onto a nearby bun.
A young girl suffered HUS after eating a
hamburger from a midsized southern
California fast-food chain.
Her illness was not culture-confirmed.
No food on site tested positive
for E. coli O157:H7.
Review of health inspections revealed flaws
in cooking methods.
19. Improper Refrigeration
A Chinese buffet-restaurant in Ohio was
the suspected source of an E. coli
O157:H7 outbreak.
No contaminated leftover food was
found.
A number of ill patrons were children.
Jell-O was suspected as the vehicle of
transmission.
Health Department report noted “raw
meat stored above the Jell-O in the
refrigerator.”
The likely source of E. coli O157:H7 in the Jell-O was from
raw meat juices dripping on the Jell-O while it was
solidifying in the refrigerator.
20. Improper Storage and Cooking
Banquet-goers in southeastern
Washington tested positive for
Salmonella.
Leftover food items had been
discarded or tested negative.
Restaurant had “pooled”
dozens, if not hundreds, of raw
eggs in a single bucket for
storage overnight, then used
them as a “wash” on a
specialty dessert that was not
cooked thoroughly.
21.
22. Civil Litigation – A Tort – How it Really Works
Strict liability
It is their fault – Period!
Negligence
Did they act reasonably?
Punitive damages
Did they act with conscious disregard
of a known safety risk?
23. Strict Liability for Food – a Bit(e) of History
“…“… a manufacturer of a food product under
modern conditions impliedly warrants his
goods… and that warranty is available to all who
may be damaged by reason of its use in the
legitimate channels of trade…”
Mazetti v. Armour & Co.,
75 Wash. 622 (1913)
24. Who is a Manufacturer?
A “manufacturer” is
defined as a “product
seller who designs,
produces, makes,
fabricates, constructs,
or remanufactures the
relevant product or
component part of a
product before its sale to
a user or consumer….”
RCW 7.72.010(2); see also Washburn v. Beatt
Equipment Co., 120 Wn.2d 246 (1992)
25. The Legal Standard: Strict Liability
STRICT LIABILITY IS LIABILITY WITHOUT REGARD TO FAULT.
The focus is on the product; not the conduct
They are liable if:
The product was unsafe
The product caused the injury
26. It’s called STRICT Liability for a Reason
The only defense is prevention
Wishful thinking does not help
If they manufacture a product
that causes someone to be sick
they are going to pay IF they
get caught
27. Why Strict Liability?
Puts pressure on those
(manufacturers) that
most likely could
correct the problem
in the first place
Puts the cost of
settlements and
verdicts directly onto
those (manufacturers)
that profit from the
product
Creates incentive not
to let it happen again
29. The reason for excluding non-
manufacturing retailers from strict
liability is to distinguish between
those who have actual control
over the product and those who
act as mere conduits in the chain
of distribution.
Negligence Is The Legal Standard Applied
To Non-Manufacturers
See Butello v. S.A. Woods-Yates Am. Mach. Co.,
72 Wn. App. 397, 404 (1993).
30. But, Litigation Can Work – A History Lesson
Jack in the Box - 1993
Odwalla - 1996
31.
32.
33.
34. Punitive (or Exemplary) Damages:
Punish the defendant
for its conduct;
Deter others from
similar conduct.
Historically, such damages were awarded toHistorically, such damages were awarded to
discourage intentional wrongdoing, wanton anddiscourage intentional wrongdoing, wanton and
reckless misconduct, and outrageous behavior.reckless misconduct, and outrageous behavior.
35. William D. Marler
6600 Columbia Tower
701 Fifth Avenue
Seattle, Washington 98104
(206) 346-1890
bmarler@marlerclark.com
Questions?
36. The Legal Arsenal
Interrogatories
Requests for
production
Requests for
inspection
Request for
admission
Third-party
subpoenas
Depositions
Motions to compel
37. A Real Life Example
Benton Franklin
Health District
OCTOBER 1998
Call from Kennewick
General Hospital infection
control nurse
Call from elementary school principal
38. Preliminary Interviews
Kennewick General
Hospital
Kennewick Family
Medicine
Interview tool
– Knowledge of
community
– Asked questions
from answers
39. Case Finding
Established communication with area
laboratories, hospitals and physicians
Notified the Washington State Department
of Health Epidemiology office
Established case definition early and
narrowed later
40. Finley Schools
Finley School District
– K-5
– Middle School
– High School
Rural area
– Water supply
– Irrigation water
– Septic system
– Buses
41. Epidemiologic Investigation
Classroom schedules
Bus schedules
Lunch schedules
Recess schedules
Case-Control Study
Cohort Study of Staff
Cohort Study of Meals
Purchased
46. Results
Ill students in grades K-5
All but one ill child
at a taco meal
No other common
exposures detected
No ill staff members
47. Results
Food handling errors
were noted in the
kitchen
There was evidence
of undercooked taco
meat
No pathogen found
in food samples
48. Conclusions
Point source outbreak
related to exposure at
Finley Elementary School
A source of infection
could not be determined
The most probable cause
was consuming the
ground beef taco
49. The Lawsuit
Eleven minor plaintiffs:
10 primary cases, 1 secondary case
Parents also party to the lawsuit, individually
and as guardians ad litem
Two defendants: Finley School District and
Northern States Beef
50. The Basic Allegations
Students at Finley Elementary
School were infected with E. coli
O157:H7 as a result of eating
contaminated taco meat
The E. coli O157:H7 was present
in the taco meat because it was
undercooked
The resulting outbreak seriously
injured the plaintiffs, almost
killing one of them
51. At Trial: The Plaintiff’s Case
The State and the BFHD conducted
a fair and thorough investigation
Final report issued by the WDOH
concluded the taco meat was the
most likely cause of the outbreak
The conclusion reached as a result
of the investigation was the correct
one
52. More of The Plaintiff’s Case
There were serious deficiencies in the District’s
foodservice operation
There were reasons to doubt the District’s
explanation of how the taco meat was
prepared
The law only requires a 51% probability to
prove the outbreak’s cause-in-fact
53. The School District’s Defense
The taco meat was
safe to eat because:
– We love children
– We are always
careful to cook it
a lot
54. The Taco Meal Recipe Card
It’s not our fault, someone sold us
contaminated beef
55. More of the School District’s Defense
• We’ve never poisoned
anyone before
• The health departments
botched the investigation
and jumped to a hasty
conclusion
• Something else caused
the outbreak
57. What Did This Jury Think?
The investigation was fair
and thorough
More probably than not,
undercooked taco meat
caused the children to
become ill
The School District was
ultimately responsible for
ensuring the safety of the
food it sold to its students
58. In The End
After a six week trial,
plaintiffs were awarded
$4,750,000
The District appealed the
verdict on grounds that
product liability law did
not apply
September 2003 the WA
State Supreme Court
dismissed the District’s
case
Final award - $6,068,612.85
59. Real Events Happening Daily to Real People
1
Mead PS, et al., Food-related illness and death in the United States,
Emerg Infect Dis. 5:607-614. 1999.
2
Buzby, et al. Product Liability and Microbial Foodborne Illness
(2001)ERS Agricultural Economic Report No. 799.
76 million cases of foodborne
illness annually1
325,000 hospitalizations
5,000 deaths
Medical costs, productivity
losses, costs of premature
death costs 6.9 billion dollars
a year2
60. 6600 Bank of America Tower
701 Fifth Avenue
Seattle, Washington 98104
1-800-884-9840
www.marlerclark.com
Questions?