[GOOD]

Hello and welcome  to

“Recognition of  Chemical  Associated  Gastrointestinal  Foodborne Illness”.

 

I'm Cynthia Good,

your moderator for  this program which is  originating from the  studios of the  Centers for Disease  Control and  Prevention in  Atlanta, Georgia.

 

This program is  sponsored by the  National Center for  Environmental  Health, 

Agency for Toxic  Substances and  Disease Registry  and CDC’s Public  Health Training  Network.

 

The goal of this  program is to  enhance early  recognition,  reporting,

and clinical  management of  chemical associated  gastrointestinal  foodborne illness by  clinicians and  healthcare providers.

 

Upon successful  completion of the  program,

participants will be  able to:

 

* Distinguish features  of chemical  associated  foodborne illness

 

* Describe  epidemiologic clues  of a covert chemical  associated  foodborne illness

 

* Describe a  structured approach  to guide the  generation of a  differential diagnosis  targeting various  chemical etiologies

 

* Describe  appropriate reporting  strategies for  suspected covert  chemical associated  foodborne illness,  and...

 

* Discuss the clinical  course and general  management of  poisoning from  various chemicals

 

So, now that we’ve  gotten the business  part of the program  behind us,

let’s meet our  program guests.

 

I’d like to welcome  Dr. Helen

Schurz Rogers,

Research Scientist  with the National  Center for  Environmental  Health at CDC ... 

...and Lieutenant  Commander

Joshua Schier of the  United States Public  Health Service,  Medical Toxicologist  with the National  Center for  Environmental   Health at the CDC.

 

Welcome to the  program. 

Let’s begin with you,  Dr. Rogers.

 

 

[ROGERS]

Thank you, Cynthia.

 

The etiologies of a  large majority of  foodborne  gastrointestinal

illness, or

GI illness outbreaks  are never identified  or confirmed by the  laboratory. 

GI illness refers to  the presence of

GI signs and  symptoms including  nausea,

vomiting,

abdominal  discomfort and  diarrhea.

 

Chemicals are  seldom considered  early in the  differential diagnosis  of foodborne

GI illness since the  majority of these  illnesses in which an  etiology is identified  are caused by  biological organisms,  such as bacteria,  viruses or parasites.

 

Since the most  commonly identified  etiologies of

GI foodborne  illnesses are due to  biological organisms,  these are much more  commonly  considered early in  an outbreak. 

The wide variety of  possible chemicals  that can induce

GI illness hinders  accurate recognition  and diagnosis.

When chemicals are  finally considered,  biologic specimens  such as urine and  blood often have to  be re-collected and  may not show  evidence of the  chemical due to the  body’s normal  elimination  mechanisms.   Furthermore,

stool samples,

which are commonly  used for analysis of  infectious foodborne  illness are often not  the ideal specimen to  identify chemical  etiologies.

 

Chemical agents  have been used in  the deliberate  contamination of  food with the  intention of causing  illness in the past.   We will discuss  several examples  during the course of  this webcast. 

Since the terrorist  attacks of 2001,  concern has grown  about the use of  chemical agents in  future attacks.  Contamination of the  nation’s food supply  is one major area of  concern.

 

This webcast has  been structured to  assist clinicians and  public health officials  in the recognition of  chemical associated  GI foodborne

illness. 

It is also intended to  raise awareness and  recognition of how  many commonly  available chemicals  could be used in a  covert chemical  terrorism event.   Most chemicals tend  to produce

GI symptoms within  a short time frame,  less than 12 hours,  after ingestion.

 

Chemicals that do  not produce

GI symptoms within  that time frame or  those agents that do  not produce

GI symptoms at all  after ingestion will  NOT be discussed.

 

No etiologic agent  was identified in

62 percent of the  1073 foodborne  disease outbreaks  reported to the

CDC in 2003. 

Many of these  outbreaks had illness  characterized by the  onset of

GI symptoms such  as nausea,

vomiting,

diarrhea and  abdominal  discomfort of less  than 12 hours,  classifying them as  short incubation  outbreaks.

 

Possible etiologic  agents in these short  incubation outbreaks  include industrial  chemicals,

drugs,

pesticides,

and plant toxins -  most of which could  be identified and  quantified in  specialized  laboratories if  specimens were  collected and stored  correctly until  analysis was able to  be completed.   Detection of these  agents,

however,

requires

agent-dependent  specific biologic  specimen collection,

prompt collection  methods,

and testing  techniques that are  not routinely included  in the investigation of  many foodborne  outbreaks.

 

 

[GOOD]

Thank you,

Dr. Rogers. 

Allow me to interject  some information  concerning the  background for this  program.

 

This webcast will  provide clinicians  and public health  officials with the  following information  related to chemical  etiologies of  unintentional and  intentional covert  chemical associated  foodborne GI illness:

 

* background  information on  chemical poisoning

 

* the general  differences between  biological and  chemical foodborne  illnesses

 

* epidemiologic clues  of chemical  foodborne illnesses

 

* how to recognize a  possible covert  chemical terrorism  foodborne poisoning  event

 

* a structured  approach to guide  the generation of a  differential diagnosis  targeting chemical  etiologies

 

* discussion of  possible chemical  etiologies and their  management

 

AND, how to report  chemical associated  GI foodborne

illness.

 

To continue with this  background  information,

let’s go to Dr. Schier.

 

 

[SCHIER]

Thanks, Cynthia.

 

The rapid and  accurate  identification of a  chemical etiology in  foodborne illness  outbreaks is  necessary for many  reasons.

These includeing  proper patient  management,

risk assessment for  long-term adverse  health effects and  outbreak control.

In a true chemical  terrorism event this  is even more  important. 

Accurate  identification of a  chemical etiology in  a foodborne illness  outbreak is done  through good  investigative work,  early consideration  of a possible  chemical etiology  and prompt  collection of biologic  samples.

 

Historically,

most chemical  associated  foodborne

GI illnesses have  been unintentional.   However,

there have been  several notable  cases of intentional  poisoning through  food contamination.   When an intentional  poisoning occurs,

it may be overt or  covert.

 

In an overt  foodborne illness,  the contamination of  food is often obvious,  that is,

it may have been  announced in some  way such as by the  discovery of an  overturned chemical  container into  foodstuffs prior to  processing. 

In a covert foodborne  illness;

however,

it may not be  immediately  apparent that a food  or meal is  responsible for the  illness.

 

An example of a  covert event would  be the intentional or  inadvertent  contamination of  food in a restaurant  with a harmful agent  that is unknown to  the restaurant  patrons and not  immediately  identifiable. 

The presence of ill  persons at an  emergency  department,

or even at the  restaurant,

may be the first  indication of a  common source of  exposure. 

If there is a highly  suspected or known  exposure,

or a concurrent  credible threat of  poisoning,

then a clinical  diagnosis can be  much more easily  made. 

However,

if illness is occurring  as a result of a  covert event,

clinical diagnosis will  be much more  difficult.

 

 

[GOOD]

That’s very  interesting. 

Could you discuss  some historical  examples of  chemical foodborne  GI illness . . .  examples that would  differ in scope,  etiology of  contamination and  severity . . .

perhaps to illustrate  the various ways  chemical  contamination of  foodstuffs may  occur?

 

 

[SCHIER]

Sure. 

In March 2002,

a man and woman in  NJ became ill after  eating a meal of  pufferfish they had  prepared at home. 

A relative had caught  the fish in Florida  and shared part of  the catch with family.

 

Shortly after eating  the fish,

they both began to  feel tingling in the  mouth and around  the lips. 

During the next two  hours,

the woman began  vomiting and  experiencing chest  pain. 

The local poison  control center was  contacted and they  were both advised to  proceed to the  closest hospital.

At the hospital,

the woman had a  mild tachycardia,

an elevated blood  pressure and began  to develop an  ascending paralysis.

 

A test of her  respiratory function  indicated she had  less than 20 percent  of a normal vital  capacity for a woman  her age.

She was electively  intubated and placed  on a mechanical  ventilator.

Over the next  several days she  recovered and was  able to be  successfully  extubated 72 hours  later.

 

The examination of  Florida state poison  control center  records and the  national poison  center reporting  database back to  January of 2002  indicated that these  pufferfish poisoning  cases were not the  first.

From January to  July, a total of 23  cases of pufferfish  poisoning  sporadically occurred  in four states  including,

New Jersey,

New York,

Virginia and

Florida,

although all of the  fish had been  harvested in Florida.   Only one case was  from store-bought  fish;

all others were from  recreational fishers.

 

Fish tissue  specimens and urine  samples from  patients were  collected for  laboratory analysis.

Tetrodotoxin was  initially considered as  the etiologic agent  due to its known  presence in  pufferfish.   Tetrodotoxin was not  identified in the fish  tissue samples;  however,

additional analysis  confirmed the  presence of  saxitoxin.

 

Saxitoxin is a similar  toxin that is found in  certain types of  shellfish.

In these cases of  illness,

presumptive  diagnosis of  pufferfish poisoning  was made based on  the neurologic  symptoms the  patients  experienced,

the latency of the  symptoms and the  type of food  consumed.

What was important  in these events,  however,

was the rapid  consideration and  identification of the  type of  toxin most  consistent with their  symptoms. 

This greatly assisted  in the management  and treatment of  their clinical findings.  Helen….

 

 

[ROGERS]

Thanks Josh. 

In July 2004,

ten people reported  that they became ill  at a restaurant.   They were not part of  a large group that ate  together at the  restaurant,

and local hospitals  did not report any  rise in community  illness.

Some of the people  who became ill had  consumed food,  while others had only  consumed fountain  drinks. 

Nausea and vomiting  were the most  common symptoms,  and,

the average  incubation period  was 10 minutes.

Two people also  developed diarrhea  the following day.  

A health inspection  of the restaurant did  not indicate any  obvious etiologies or  health code  violations.

 

Further investigation,  however, 

found that seven out  of the 10 cases had  consumed fountain  drinks. 

Ice,

water and  carbonated  beverages from the  fountain machine  were collected for  testing.

 

Test results indicated  that copper was  almost seven times  higher in the fountain  drinks than the  acceptable limit for  human consumption.  This was ultimately  determined to be the  etiology of the  illnesses.

Copper may leach  out into the water  when acidic solutions  enter copper pipes.

 

In a post-dispensing  soda machine,

like those found in  fast-food  restaurants,  carbonation of the  water occurs after  the water leaves the  copper piping.   Regulations require  a functional

back-flow prevention  valve at the end of  the copper-pipe.   This valve prevents  the carbonated water  or carbonic acid from  back flowing back  into the copper pipe.   A faulty valve canwill  allow the carbonated  water to enter the  copper-pipe.  

Leaching of the  copper from the pipe  may occur after  prolonged contact  with carbonic acid. 

Most often,

the leaching occurs  overnight when the  dispenser is not  operated;

the first users in the  morning,

typically the  restaurant workers,  are the ones who  become ill -

hence copper  poisoning has been  called the

“restaurant worker  syndrome”.

Luckily all individuals  that were affected by  this contamination  recovered. 

Josh….

 

 

[SCHIER]

In April of 2003,

27 people stayed  after church services  for a council  meeting. 

During the meeting,  refreshments,  including pastries  and beverages,

were served.  Approximately 16  people became ill  with nausea,  vomiting and  diarrhea after  consuming

bitter-tasting coffee.

 

The ill parishioners  were taken to an  area hospital where  they were evaluated.   An infectious etiology  was initially  suspected;

however, as the  clinical course of  several of the ill  parishioners  worsened,

a possible chemical  etiology was  considered.

 

The rapid  progression of illness  and the failure to  respond to basic  supportive care  prompted  consultation with the  New England Poison  Control Center as  well as the local and  state health  departments.

 

Sixteen people were  ultimately  hospitalized and  some were seriously  ill. 

Even with prompt  recognition and  treatment of this  illness,

tragically,

one person died.

The collaboration  between clinicians,  local and state public  health officials and  the poison control  center targeted  several likely  etiologies,

including arsenic. 

 

The identification of  a clinical course  which was atypical  for most infectious  foodborne illness  and subsequent  laboratory analysis  for chemical agents  led to the rapid  identification of  arsenic as the  etiologic agent.   Antidotal chelation  therapy was then  initiated in  conjunction with  continued supportive  care.

 

 

[ROGERS]

GI illnesses can be  broken down into two  categories based on  GI tract symptoms.   These include upper  GI illnesses and  lower GI illnesses.

 

Upper GI illnesses  usually include  nausea and  vomiting.

 

Lower GI illnesses  usually include  abdominal cramps  and diarrhea.

 

The latency and  presence of upper

GI and/or lower

GI symptoms as well  as which ones occur  first or predominate,  are important clues  in determining if a  biological or  chemical foodborne  illness is occurring.

 

Although poisoning  without GI symptoms  may occur after  consumption of  some contaminated  foodstuffs,

most chemicals do  cause GI symptoms  if significant amounts  are ingested,

and only those  agents will be  discussed in this  presentation.

 

In general,

infectious foodborne  illnesses have mean  incubation periods  that are at least

12 hours long  although shorter  incubation periods  are the norm for  illness resulting from  the ingestion of  certain pre-formed  toxins from  Staphyloccus aureus  and Bacillus cereus.

 

The incubation  period,

however,

may not be  definitively known  until an investigation  pinpoints the actual  source.

 

Depending on the  agent, upper GI or  lower GI symptoms  may predominate.

 

In chemical  foodborne illnesses,  symptoms may be  similar to some  aspects of the flu,  namely the GI ones.   Upper GI symptoms  are more likely to  predominate.

 

The most important  indicator of chemical  contamination is the  latency of the illness  onset,

which is often very  short. 

Indeed,

symptoms from  many agents such as  metals,

detergents and  pesticides

can start within  minutes of ingestion.   Others such as ricin  poisoning may take  several hours.

 

Chemicals should be  strongly considered  in the differential  diagnosis of

GI foodborne illness  when:

 

* The latency period  is very short. 

Most GI  manifestations of  chemical illnesses  will occur within

30 to 60 minutes of  ingestion. 

There are some  exceptions,

however,

such as Amanita  mushroom poisoning  or ricin which may  take several hours  before they begin to  cause symptoms...

 

* Symptoms do not  resolve over time  with standard  supportive therapy,  or they rapidly  worsen over the next  12 to 24 hours  despite this therapy...

 

* There are reports  that the food had a  metallic taste, or  unusual odor or  appearance...

 

* The predominant  GI symptom is often  vomiting;

however,

case-patients may  have other  symptoms such as  neurologic findings,  depending on the  type of toxin.

 

 

[GOOD]

Thank you Dr.  Rogers.  

Those were some of  the symptom clues. 

Dr. Schier,

what are some  examples of clinical  manifestations that  go along with  chemical poisining?

 

 

[SCHIER]

Chemical poisoning  may result in a rapid  progression of illness  and cause a variety  of clinical  manifestations and  laboratory  abnormalities. 

Some examples  include:

 

* Metabolic acidosis

 

* Hypoglycemia

 

* Tachycardia

 

* Hypotension

and...

 

* Tachypnea

 

When present,

these  manifestations may  occur in conjunction  with multiple system  organ dysfunction  and rapid  progression of illness  that may be  unresponsive to  traditional therapies.

 

Neurologic  symptoms are more  indicative of a  chemical or  biological toxin  exposure than a  bacterial one. 

These symptoms  may include  parasthesias,  numbness,  weakness in  extremities,

visual disturbances  or dizziness.

 

Flushing,

diaphoresis or a  burning sensation  may occur.

 

The presence of  symptoms like these  can be an important  clue that a chemical  exposure has  occurred.

 

Similarly,  organoleptic  comments,

or comments that  describe a quality of  the food having to do  with taste,

smell or visual  appearance,

can be important  clues.

For example:

 

* Did the food have  an odd taste? 

Was it metallic,  acidic,

burning,

alcoholic or bitter?   Was there an  excessive amount of  flavor,

such as sweet,

salty or sour?

 

* Were there any  strange odors  associated with the  food,

such as a chemical  or metallic odor?

 

* Did the food look  different,

was there a strange  color or texture,

was it oily or  viscous?

 

Another factor which  complicates the  accurate  identification of a  chemical etiology is  possible exposure to  multiple agents. 

This may result in  clinical findings that  do not make up an  easily recognizable  pattern.

 

Healthcare providers  are generally less  familiar with clinical  presentations of  chemical poisonings  than they are with  signs and symptoms  resulting from  infectious  gastroenteritis.

 

The severity and  duration of  symptoms depends  on the type and  amount of exposure  to a given chemical  or toxin.

 

Depending on the  toxin,

specific antidotal  therapy,

supportive treatment  and hospital  observation may be  necessary to ensure  a good outcome.    Helen…

 

 

[ROGERS]

Once a chemical  exposure is  suspected,

it’s vitally important  to collect proper  samples so that the  agent can be  identified. 

This may mean that  several types of  samples need to be  collected initially.

 

Laboratory analysis  for a particular agent  usually involves  measuring the agent  itself,

a metabolite or a  surrogate marker.

 

If a chemical  foodborne illness is  suspected,

it is best to collect  appropriate biological  specimens as soon  as possible and  preferably within the  first 24 hours. 

If chemical analysis  is not immediately  available or the  differential diagnosis  is too broad to  enable efficient  analysis,

samples can usually  be stored in a  freezer.

 

In the laboratory  workup of chemical  foodborne illness,  the emphasis is often  placed on prompt  collection of a urine  specimen,

whereas in most  biologic foodborne  illnesses,

emphasis is placed  on the collection of  stool samples.

 

An early or first  vomitus sample may  sometimes be very  helpful in identifying  the chemical. 

Some agents are  also identifiable in  blood samples.

 

Stool samples are  generally not useful  for identification of  chemical etiologies.

 

Many chemicals  have a short-half life,  which refers to the  amount of time it  takes for half of a  dose to be  eliminated.  If too  much time passes  before a urine  sample is collected,

there won’t be  enough of the agent  left for identification.

 

It’s also important to  collect urine samples  from

non-symptomatic  people that shared in  the meal or food  item.

The reason for this is  that these individuals  provide an important  control sample that is  helpful when  evaluating laboratory  results.

 

Whenever possible,  samples of the  implicated food or  beverage should  also be obtained for  analysis. 

 

Sometimes,

if a method does not  exist for the  laboratory  confirmation of a  chemical in a  biological specimen,  like urine,

there may be a  method available that  can be utilized for  food samples.

 

Unused collection  containers,  preferably from the  same lot, should also  be stored. 

These containers are  used to help the  laboratory evaluate  for any background  contamination.

 

It is important to also  mention that  collection procedures  and guidelines are  similar for chemical  agents that do not  cause early onset

GI symptoms.

 

A useful resource for  the proper collection  of biological  materials is located  on the CDC website.

 

Details about proper  sample collection  techniques and  storage are also  given.

 

A vital part of the  investigative process  in a foodborne  outbreak is a  standardized food  history questionnaire.  One of the goals of  such a questionnaire  is to seek  commonalities  among the ill. 

These questions  may be essential to  implicate a particular  foodstuff. 

Once a food or meal  has been implicated,  pertinent questions  to ask include:

 

* What were the  predominant  symptoms?

 

* What was the  latency of illness?

 

* What food items  were available to the  patient,

which ones were  consumed and how  was the food  prepared?

 

For chemical  foodborne illnesses,  it is helpful to keep in  mind the following  questions,

and then include  these in the final  questionnaire: