[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:
* Were there neurologic symptoms in addition to GI complaints?
* Were there other types of symptoms not commonly
associated with foodborne
illness, such as sore throat?
* Did the food have a bitter or metallic taste,
was there an abnormal smell,
an unusual appearance?
And...
* What does the patient think made them ill?
[GOOD]
Those are good questions to ask,
but are there any conditions or
circumstances that may make it
difficult to recognize contamination?
[SCHIER]
Yes.
In fact,
an intentional or unintentional
contamination of foodstuffs is
likely to be covert or an unrecognized
incident in which the presence of
sick persons might be the first sign of an exposure.
There are four reasons why such an event may not be easily recognized. These include the following:
* Initial symptoms of illness resulting from chemical exposure may mimic those of more common
non-chemical etiologies such as an infectious
gastroenteritis...
* Exposure to contaminated
foodstuffs and/or water may
occur over a broad geographical area and time course.
For example,
a large-scale event may not be rapidly identified if patients present to different health care facilities in multiple states over the course of several weeks...
* Exposures to two or more chemical agents may result in symptoms of illness from both agents and therefore complicate identification...
* Finally,
infectious gastroenteritidies are seen much more commonly by health care workers than chemical induced
GI illness;
therefore, chemicals may not be high on a
provider's differential
diagnoses.
This may delay identification of the actual etiologic agent in a chemical
release.
There are certain epidemiologic clues the health care worker and public health official can use to assist in identifying a possible chemical release. These guidelines may be especially helpful in a covert chemical terrorism foodborne event.
These include:
* An unusual increase in the number of patients seeking care for potential chemical associated illness...
* Unexplained deaths among young or healthy persons
*Emission of unexplained odors by patients from their clothing or skin
* Clusters of illness in persons who have common
characteristics,
such as drinking water or eating foodstuffs from the same source
* Rapid onset of symptoms after an exposure to a
potentially contaminated medium.
An example would be the rapid
development of parasthesias
and vomiting following the consumption of a meal.
The following discussion is
presented in what is hoped to be
a more useable format for the health care provider and public health official in developing a
chemical based differential
diagnosis in the undifferentiated patient.
We will discuss differential diagnosis based on the clinical presentation of the individual patient.
This discussion is not meant to be
all-inclusive and should not be used as a restrictive flow diagram.
Significant overlap
of signs and symptoms may occur
depending on the route of
exposure, concentration of agent,
exposure to more than one agent, certain individual differences such as age and
ultimately the severity of toxicity. The following format is to be used as a guide in formulating a differential diagnosis and
applying a logical approach
toward identification of chemical associated GI foodborne illness.
CDC has developed the following
suggested clinical
presentation-based approach to
identify the etiologic agent in a suspected
chemical-associated GI foodborne
illness event.
Classification is based on the
primary presence or
absence of certain clinical manifestations in conjunction with expected GI signs and symptoms
such as nausea,
vomiting and abdominal
discomfort.
The major categories of agents that we will be talking about include those agents with GI signs and symptoms AND:
* Neurologic findings
* Cardiotoxic findings
* Multi-system Organ Failure
And...
* Localized GI Effects
Health care workers and public health officials should initially determine the presence or absence of neurologic signs and symptoms.
* Are cholinergic signs present?
* Does the patient have any
type of parasthesias and
weakness?
* Is there a history
of a rapid onset of severe agitation, seizures or status epilpeticus?
Cholinergic signs and symptoms result from the
overstimulation of cholinergic receptors.
This may occur due to:
* Excessive or increased synaptic concentrations of acetylcholine,
OR...
* A separate agent which has acetylcholine-like activity.
These latter compounds can be referred to as cholinergic agonists.
There are two types of cholinergic receptors:
nicotinic and muscarinic.
There are a variety of agents which may interact with one or both receptors. Clinical effects vary depending on which type of cholinergic receptor is
stimulated.
Organic phosphorous
compounds and carbamates are
most commonly used as insecticides.
These agents inhibit the enzyme which normally degrades the neurotransmitter, acetylcholine.
If enough of this enzyme is inhibited, an enormous
increase in synaptic
acetylcholine can occur which
results in overstimulation of cholinergic
receptors.
These agents differ in that organic phosphorous
compounds can bind irreversibly
to acetylcholinesterase; however,
carbamates spontaneously disassociate,
usually within
24 hours.
Clinical findings may include both nicotinic and muscarinic effects such as toxicity resulting from numerous types of organic phosphorous insecticides. However,
other agents may produce
predominantly either nicotinic
OR muscarinic symptoms. We will discuss these signs and symptoms
separately, with the
understanding that a mix of both
may occur, depending on the agent.
Agents which may cause muscarinic symptoms include toxins and toxicants such as:
* Organic phosphorous
compounds
* Carbamates
* Muscarine-
containing mushrooms
Toxicity from organic phosphorous and carbamate
compounds results from an excess
of acetylcholine since these agents inhibit the enzyme
acetylcholinesterase, which
breaks down acetylcholine. Muscarine is a natural ligand for the muscarinic receptor and can stimulate the receptor directly.
The stimulation of muscarinic receptors results in the expected GI
manifestations of vomiting and diarrhea as well as several other clinical findings.
They can be remembered by the pneumonic,
“DUMBELS”.
This stands for:
Diarrhea,
Urination,
Miosis,
Bradycardia, Bronchorrhea,
Bronchospasm, Emesis,
Lacrimation, Salivation,
Secretion and Sweating.
The onset of symptoms usually follows exposure very rapidly,
and medical treatment should be sought immediately. Supportive care such as assisted
ventilation, intravenous
fluids and antidotal therapy should be given as needed.
The antidotes for
this type of poisoning include atropine, which is a
competitive muscarinic
receptor antagonist,
and pralidoxime, which regenerates inactivated
acetylcholinesterase.
Muscarine- containing mushrooms may
also produce a similar
clinical picture.
Examples include numerous members of the
Clitocybe and
Inocybe genus. The mushroom Amanita muscaria also
contains muscarine,
but in much smaller amounts.
Treatment is usually supportive,
as toxicity is
usually limited.
In cases of severe toxicity,
small amounts of atropine may be considered
depending on the situation.
Pralidoxime is not used in muscarinic toxicity, resulting from muscarine, since there is no acetylcholinesterase inhibition.
Stimulation of nicotinic receptors results in different clinical findings.
These include:
* Mydriasis, Tachycardia,
Weakness, Hypertension and Hyperglycemia
and...
Fasciculations
They can be remembered by
taking the first letter of each
day of the week except for Thursday,
in which you remember the H instead of the T.
Agents that are able to cause
nicotinic-type signs and symptoms after exposure include:
*Organic phosphorous
compounds and carbamates
* Certain plants that contain nicotine, such as those from the genus Nicotiana, or the tobacco plant
* Tobacco-containing products
* And other plants with compounds that possess nicotinic-like activity,
such as those listed on the screen.
Treatment for
toxicity resulting from nicotine or nicotine- like compounds is generally supportive in nature.
Atropine only functions at
muscarinic receptors and is
therefore not helpful in selective
nicotinic-type
toxicity. Nicotinic symptoms resulting from agents such as organic phosphorous
compounds CAN be treated
with preladoxine to regenerate
inactivated acetylcholinesterase.
Benzodiazepines can be used as
anti-anxiety,
anti-agitation and anti-convulsive medications if needed.
[ROGERS]
The next
sub-category I would like to talk about includes those agents that cause the relatively rapid onset of
parasthesias and weakness,
in addition to GI manifestations. Cardiac
dysrhythmias such as
bradycardia, although not frequent,
may also occur.
These include the seafood toxins:
* Ciguatoxin
* Tetrodotoxin
* Saxitoxin
and...
* Brevetoxin
Treatment for these marine toxins are primarily supportive and symptomatic in nature.
There are no known antidotes.
Illness from these agents usually results from the consumption of seafood that
contains the toxins. A thorough
history from the patient or the patient’s family and/or friends will often elucidate a history of recent suspicious seafood consumption.
Ciguatoxin is a
heat-stable,
lipid-soluble, odorless and
tasteless toxin.
It is produced by bacteria within certain
dinoflagellates such as
Gambierdiscus toxicus.
These dinoflagellates serve as the major food source for small fish.
As these fish are eaten by larger, carnivorous species, bioaccumulation of the toxin occurs.
Ciguatera poisoning most often occurs after consumption of warm-water,
bottom-dwelling shore reef fish
such as barracuda,
sea bass,
amber jack,
kingfish and
red snapper.
Most poisoning in the United States occurs in Hawaii and
Florida.
Ciguatoxin causes its effects through binding to the sodium channel and
interfering with normal ion conduction
across the cell. Poisoning
usually occurs several hours after ingestion and includes an abrupt onset of:
* Nausea
* Vomiting
* Watery diarrhea
and...
* Neurologic symptoms
The neurologic symptoms can
include:
* Paresthesias
* A reversal of hot and cold sensation such that hot objects feel cold and cold objects are
perceived as hot
and...
* Headaches
In severe toxicity, ciguatoxin may interfere with ion conduction in
myocardial cells. Cardiac dysrhythmias such as bradycardia and orthostatic
hypotension may occur.
Other manifestations of poisoning include vertigo,
diaphoresis and seizures.
GI symptoms typically resolve in one-to-two days but neurologic and cardiac toxicity may last longer.
Tetrodotoxin is also a heat-stable,
water-soluble compound.
This toxin is
primarily found in puffer fish and puffer-like fish such as the
globefish, balloonfish,
blowfish and toadfish.
It is also found in
the blue-ringed Octopus, horseshoe crab eggs and the gastropod mollusk.
A specific variety of pufferfish known as fugu is considered a delicacy
but can cause tetrodotoxin
poisoning,
especially if improperly prepared.
Tetrodotoxin also interferes with normal sodium ion conductance in cells and in
neuromuscular transmission.
Signs of poisoning appear within
minutes of ingestion. Neurologic
signs and symptoms predominate and include:
* Headache
* Diaphoresis
and...
* Parasthesias – especially in the perioral area.
GI symptoms such as nausea,
vomiting and diarrhea often rapidly follow.
Patients are at risk
of developing an ascending paralysis within several hours of consumption of tetrodotoxin
containing foodstuffs.
Death by respiratory paralysis or cardiac dysfunction may occur.
Another type of marine toxin
poisoning...
Saxitoxin
poisoning... usually occurs after consumption of certain shellfish, including clams, oysters,
mussels and scallops.
It has also recently been identified in some species of pufferfish in waters off the coasts of Japan and Florida.
Neurologic symptoms such as perioral and
extremity parasthesias predominate.
Patients may also exhibit a
sensation of floating,
weakness,
paralysis and
cranial nerve dysfunction
including:
* Dysphagia
* Dysarthria
and...
* Dysphonia
GI symptoms such as nausea,
abdominal pain, vomiting and diarrhea are less common but can still occur.
Respiratory failure may occur in severe toxicity.
Lastly,
Brevetoxin can cause Neurotoxic Shellfish Poisoning which is
characterized by
GI and neurologic symptoms similar to those mentioned previously,
except it usually does not cause paralysis.
Its mechanism of action is also similar to tetrodotoxin and saxitoxin.
The GI and neurologic symptoms usually occur
simultaneously and within a few
hours of ingestion.
Cardiac effects such as bradycardia may also be seen.
Brevetoxin toxicity has tends to have more pronounced
GI effects than saxitoxin,
and a reversal of hot and cold temperature sensation may also be occasionally seen.
[GOOD]
That’s fascinating, Dr. SchierRogers. You’ve talked about a lot of different marine toxins, perhaps Dr Schier, you could discuss other environmental toxins, such as plant toxins, that present a potential hazard?
[SCHIER]
Of course.
The third
sub-category of agents with
neurologic effects,
in addition to
GI signs and symptoms,
consists of those agents that produce agitation,
confusion and/or seizures.
Examples include:
* Gyromitra mushrooms
* Tetramine-type compounds
* Organochlorine compounds
And...
* Camphor
The gyromitrin group of mushrooms
includes Gyromitra esculenta,
or the false morel,
as well as several others.
The false morel is often mistaken for the true morel,
or Morchella esculenta,
by amateur mushroom hunters because it is very similar in
appearance.
Toxicity from consumption of the false morel typically begins about five hours after
consumption. GI symptoms such as nausea,
vomiting,
abdominal pain and diarrhea are
common,
and patients may complain of
headaches and myalgias.
Most patients recover;
however,
severe toxicity may result in confusion, refractory seizures and coma.
Tetramine has been traditionally used as a rodenticide, particularly in China. Although it was banned by the
Chinese government,
it may still be found and imported or manufactured
elsewhere. Tetramine has been implicated in several mass poisonings in China and cases of poisoning exist in the United States, although they are rare.
Although tetramine ingestion may cause traditional GI symptoms such as nausea,
vomiting,
diarrhea and abdominal pain,
...its most
concerning toxicity is its propensity to cause seizures.
Patients may present with seizures and progress to status epilepticus after ingestion of very small amounts.
Treatment is primarily supportive in nature.
If seizures and/or status epilepticus is present as a result of tetramine poisoning, treatment should include anti-seizure medications and drug-induced status epilepticus protocols. The benzodiazepine and barbiturate classes of
anti-convulsant drugs are better agents for control of seizures resulting from chemical
poisoning.
There is no known specific antidote.
Treatment for Gyromitra poisoning is primarily
supportive and symptomatic; however,
it is important to
note that refractory seizures or status epilepticus should be rapidly treated with pyridoxine in
conjunction with typical
anti-convulsant drugs such as
benzodiazepines. This is
because gyromitrin,
found within some Gyromitra species such as the false morel,
interferes with the pyridoxine- dependent metabolism of GABA or gamma
amino-butyric acid. GABA is the major inhibitory
neurotransmitter of the central
nervous system.
Other examples of agents that may also cause central
nervous system hyperstimulation, altered mental status and even seizures include camphor and the organochlorine pesticides.
Both of these agents are likely to cause a rapid onset of concurrent
GI symptoms such as nausea,
vomiting and abdominal pain
after ingestion. Camphor-induced seizures are often brief and self-limited. Organochlorine ingestion may also cause recurring seizures and even status epilepticus depending on the class and overall dose.
Benzodiazepines and barbiturates should be used to control seizures if needed.
Supportive and symptomatic
treatment should be instituted
and
GI decontamination considered.
The second major category of agents which can cause rapid onset of
GI symptoms and also present with severe symptoms from another organ system are the cardioactive
glycosides.
The prescription medication Digoxin, is an example of a purified cardioactive glycoside,
but similar compounds exist throughout nature.
Examples of plants in which cardioactive glycosides can be extracted include:
* Oleander
* Lily of the Valley
* Foxglove
* Red Squill
* Dogbane
and...
* Siberian ginseng
The ingestion of
toxic amounts of these compounds may
result in nausea, vomiting and abdominal pain.
The patient may also be somewhat drowsy or confused.
The cardioactive glycosides are aptly named since they interfere with the normal electrolyte flux in and out of myocardial cells. This can result in myocardial ectopy and dysrhythmias.
Just about any kind of dysrthymia,
from bradydysrhythmias to tachydysrhythmias, can be seen in cardioactive
glycoside poisoning. These
patients also tend to have evidence of
myocardial conduction
delays, such as an
atrio-ventricular conduction block, due to their
pronounced effects on the vagus
nerve.
Toxicity is dependent on dose and type of compound,
as severity of
illness varies with the particular agent. Although a serum digoxin level may be helpful in the identification of poisoning,
the absence of a detectable digoxin level or a low but non-toxic level does not exclude
cardioactive glycoside toxicity
in the appropriate clinical setting. Cross-reactivity may occur between the digoxin assay and the various
cardioactive glycosides,
however,
the assay is designed to look for digoxin.
Therefore the absence of a
detectable digoxin level or a
non-toxic digoxin level does not necessarily indicate a
non-exposure.
In fact,
cardioactive glycoside poisoning should be highly suspected if a patient has a clinical picture consistent with Digoxin poisoning, and a low but
detectable digoxin level is
found,
and the patient does not have access to the medication Digoxin.
Definitive treatment is through the administration of Digoxin-specific antibodies.
Treatment should also
include supportive care as needed.
Calcium is
contra-indicated for cardioactive
glycoside-induced hyperkalemia
due to an inherent risk of worsening
cardiotoxicity.
[GOOD]
How serious can some of these
agents be?
[ROGERS]
Actually,
the third major category of agents is known for its ability to cause multisystem organ dysfunction and ultimately organ failure.
Sometimes only very small amounts of these agents are needed to cause poisoning.
Some well known examples of these agents include:
* the Amanita Phalloides
mushroom
* Ricin toxin from Ricinus communis, or castor bean plant
* Abrin toxin from Abrus precatorius,
or the jequirty pea
And...
* multiple forms of inorganic metals.
Poisoning from select Amanita species such as
Amanita Phalloides does not
occur until five or six hours
after ingestion. Severe watery diarrhea and other GI symptoms such as nausea are
common.
Initial iImprovement usually occurs with supportive care such as replacement fluid therapy.
However, approximately
24 to 36 hours after consumption,
the patient’s condition can worsen considerably as manifested by
hepatic and renal toxicity.
Death is common after severe
poisoning.
Treatment should include supportive and symptomatic therapies.
Multiple doses of activated charcoal should be
considered in conjunction with a clinical toxicologist and/or the local poison center.
If amanita poisoning is confirmed and presentation to a health care facility is within four hours, charcoal
hemoperfusion should be
strongly considered.
There are various other suggested but unproven treatments which may also be considered.
Ricin is one of several types of toxalbumins which exert their toxicity by inhibiting protein synthesis in
eukaryotic cells and therefore
can cause cell death.
It is a compound derived from Ricinus communis,
or the castor bean plant.
All of the
information available on oral ricin poisoning comes from people who have eaten castor beans.
There are no reports of anyone who has ingested purified ricin.
The information that follows is based on ricin consumed in the form of masticated castor beans and may vary somewhat if purified ricin is used.
Signs and symptoms are likely to be the same, however.
There are hundreds of reported cases of toxicity,
and several
fatalities, from castor bean mastication and ingestion.
If enough ricin is ingested,
the potential for significant morbidity and mortality exists.
Symptoms of mild toxicity include: nausea,
vomiting,
diarrhea,
and/or
abdominal cramping.
These symptoms are invariably present in people who chew and swallow a
significant amount of castor
beans. Oropharyngeal irritation may also follow ingestion.
Bloody diarrhea and systemic effects, such as hypotension, hemolysis and renal failure,
are NOT present and symptoms typically resolve within
24 hours.
Onset of
GI symptoms typically occurs in less than 10 hours. Delayed presentation of GI symptoms, beyond ten hours after ingestion,
is unlikely to occur.
Moderate to severe toxicity may include: GI symptoms such as persistent
vomiting and voluminous
diarrhea . . . bloody or
non-bloody . . .
which typically leads to significant fluid losses.
This may result in dehydration and hypovolemic shock, which would
manifest as tachycardia, hypotension,
decreased urine output,
and possibly altered mental status,
such as confusion or disorientation.
In severe poisoning, hepatic and renal failure and even death are possible within 36 to 72 hours of exposure.
Treatment is primarily
symptomatic and supportive in
nature.
Abrin is a closely related type of toxalbumin that is derived from Abrus precatorius,
or the jequirty pea. The seeds of this plant are commonly used in jewelry and in ornaments due to their colorful appearance.
Abrin poisoning can result from
mastication and ingestion of
Abrus precatorious seeds and from ingestion of purified abrin. Toxicity,
symptoms of poisoning and
treatment are similar to ricin
poisoning.
Other agents often implicated in
chemical-associated multisystem
organ failure include metals.
There are numerous metals that may cause GI illness once ingested. These include the inorganic salts of:
* Arsenic
* Mercury
* Iron
* Lead
* Copper
* Cadmium,
and...
* Numerous others
Patients who ingest metal salts in foodstuffs or
beverages may complain that the food had a bitter or metallic taste. Symptoms of
inorganic metal poisoning
often begin within 30 to 60 minutes of ingestion and can rapidly progress over the next several hours.
The ingestion of significant amounts of inorganic metal salts is usually rapidly followed by GI symptoms such as nausea,
vomiting,
abdominal pain and diarrhea.
The severity is directly dependent on the amount and form ingested.
An important clue to metal toxicity in the clinical course is a rapid progression, over 12 to 36 hours, of symptoms that include multiple organs and organ systems,
depending on the agent.
This may include renal failure, hepatotoxicity and pulmonary toxicity. The widespread damage done by metals is usually due to their nonspecific binding of functional groups,
such as sulfhydryl moieties,
on numerous enzymes and
proteins.
Binding can cause irreparable damage to the protein and cell to which it is attached.
Another clue to metal poisoning is severe GI fluid loss due to widespread damage to the GI tract.
This fluid loss may require large
amounts of intravenous fluid replacement and even intravenous vasopressor
therapies to maintain adequate
blood pressure.
This is not likely to happen with a typical viral or bacterial gastroenteritis other than cholera.
Metal salt poisoning may,
however,
be hard to distinguish clinically from ricin or abrin poisoning.
Laboratory testing is needed to definitively confirm metal
poisoning.
Blood and urine testing is available for most metals. This is dependent, however,
on the individual agent.
It is important to
note that many metals, such as arsenic and mercury,
can exist in nature and in the body in organic and
inorganic forms. Often,
interpretation of laboratory
results needs to take into account the amount in each form with the patient’s clinical presentation.
The ingestion of seafood can
substantially increase total
blood arsenic and mercury levels.
When certain metals such as these are analytically
measured in biologic specimens
like blood and urine,
the results often represent a
summation of the levels of
both inorganic and organic forms.
Therefore, interpretation of the results must take into account whether these different forms were measured,
or speciated,
during the analysis. Ideally,
and in non-acute cases,
patients should abstain from eating any kind of seafood for at least
three-to-five days prior to testing for some metals,
especially arsenic and mercury,
since this could affect the results.
In acutely ill
patients, this delay is unacceptable and specialized testing may be needed.
[GOOD]
That’s good advice Dr. Rogers.
Dr. Schier,
I believe you have something to add concerning localized GI illness.
[SCHIER]
Yes I do, Cynthia. Many agents may simply cause a limited clinical picture consistent with a severe
gastroenteritis. Chemicals
and biological toxins that may cause this include:
* Hydrocarbons
* Detergents
* Caustics
* Certain mushrooms
And...
* some pre-formed toxins from
Staphylococcus aureus,
Clostridium perfringens,
and Bacillus cereus
Hydrocarbons,
if ingested,
generally produce
GI symptoms but little else.
Their biggest risk is
if the patient aspirates after vomiting,
which can result in a hydrocarbon-induced pneumonitis.
Treatment is supportive and symptomatic in nature with a careful evaluation for aspiration.
Some hydrocarbons may have a
significantly greater risk of
additional toxicity and are commonly
remembered by the pneumonic,
CHAMP. This stands for:
* Camphor
* Halogenated hydrocarbons
* Aromatic hydrocarbons
* Hydrocarbons associated with metals
and...
* Hydrocarbons associated with pesticides
Treatment and management may
vary considerably for patients
who ingest these compounds.
Caustics include compounds with extreme pHs such as acids or alkalis. Common household products include toilet bowl cleaner, commercial drain blockage removal formulations and other products. Caustics may also include agents corrosive by nature of their oxidative state such as
chlorates, permanganates and chromates.
These agents are extremely irritating to the GI tract and can cause severe
damage,
including perforation and scarring.
Generally,
acute toxicity is limited to the GI tract, however,
airway burns may sometimes occur, necessitating
emergent airway control.
Ingested acids may cause a resultant metabolic acidosis due to systemic absorption in severe cases.
Endoscopy is often used to assess damage resulting from symptomatic caustic ingestion. Charcoal should NOT be given in caustic ingestions since the damage is usually done within minutes of the ingestion and may obscure visualization on endoscopy later.
As with any poison, the dose ingested determines severity.
The ingestion of detergents and soaps generally cause limited
GI signs and symptoms.
This usually resolves with time,
although supportive therapy and fluid replacement may be needed in severe cases.
However,
some detergents, such as powdered dishwasher
detergent,
are inherently caustic,
and closer evaluation along with
endoscopy may be needed.
A large variety of mushrooms from multiple genera can cause nausea,
vomiting and diarrhea after ingestion.
Symptoms are due to a wide
variety of poorly understood GI toxins with limited toxicity.
Patients poisoned by mushrooms from these groups
manifest symptoms within three hours
of ingestion.
This distinguishes the toxin class from the much more
deadly Amanita phalloides toxin, which does not induce symptoms until five-to-six hours after ingestion. Treatment is
supportive,
and symptoms generally resolve within 12-24 hours.
A small number of bacterial species may cause
GI foodborne illness by consumption of pre-formed toxin. These species primarily include Staphylococcus aureus,
Bacillus cereus,
and Clostridium perfringens.
Clinical illness includes nausea, vomiting,
abdominal pain, diarrhea,
and occasionally fever.
The presence of some of these
symptoms depends heavily on
which organism is present and which toxins are being produced. Treatment is with supportive care and fluid replacement when indicated.
Numerous other agents may cause GI symptoms if
ingested.
A few are worth briefly mentioning due to historical use, ease of availability or inherent toxicity. These include syrup of ipecac and various pharmaceuticals.
Syrup of ipecac can cause nausea and vomiting within half an hour of ingestion. Symptoms
commonly resolve after
two-to-three hours.
Ipecac has been historically used as an emetic in the treatment of
poisoning,
as well as abused in those trying to lose weight.
There are numerous drugs that can cause a clinical picture similar to those agents already described.
The sheer number of agents precludes their comprehensive review in this webcast;
however,
clinicians and public health officials are advised to at least consider the
possibility. The identification
of foodstuffs contaminated with pharmaceuticals in a foodborne illness event is unlikely to be unintentional.
If enough of any drug is ingested,
some degree of GI irritation may be expected.
Some examples of drugs which tend to cause more GI signs and symptoms
include:
* Acetaminophen, salicylates and nonsteroidal
anti-inflammatory drugs
* Theophylline
* Lithium
* Digoxin
* Colchicine
and...
* Podophyllum resin
..Helen...
[ROGERS]
Thank you for your attention during this webcast.
We have attempted to provide you with an organized
template from which you can
develop a differential diagnosis of possible chemical etiologies based on a patient’s clinical presentation.
The classification scheme includes many of the more common
GI presentations that may occur with chemical agents. The list of agents discussed is not comprehensive,
but rather includes many examples of the aforementioned categories.
We have also tried to emphasize certain clues in the patient’s history and clinical presentation,
as well as epidemiologic clues that may alert the astute clinician or public health official that a foodborne illness event may have a chemical etiology.
The regional poison control center should always be contacted in any case of suspected or known chemical associated
foodborne illness by calling
1-800-222-1222.
This will
automatically connect the caller
to the closest poison center.
Clinicians and health care workers should also contact their local and state departments of health for assistance.
Local and state health officials are also encouraged to call the Rapid Onset of Gastroenteritis with Unknown
Etiology,
or R.O.G.U.E., hotline to obtain epidemiological assistance.
In addition, CDC may be able to provide specialized
laboratory capabilities if needed and the
circumstances require it.
We hope that this
presentation will help clinicians and public health officials understand,
diagnose and manage chemical-associated GI foodborne illness.
[GOOD]
Thank you,
Dr. Rogers.
The many questions that we have
received concerning today’s
program will be posted,
with their answers, on our website at
w-w-w-
dot-
p-h-p-p-o-
dot-
c-d-c-
dot-
g-o-v-
slash-
p-h-t-n-
slash-
g-a-s-t-r-o-
hyphen-
zero-
five.
You can also view the archived version of this program at the same website.
In addition, videotapes and
CD-ROMs of this program will soon be available for
purchase through the Public
Health Foundation.
To order,
you can call
1-877-252-1200
or visit their online bookstore at
www
dot
p-h-f
dot
org.
Finally, I’d like to thank our guests . . . Doctors
Helen
Schurz Rogers
and
Joshua Schier,
...and I’d also like to thank our
viewing audience for submitting your thoughtful questions concerning today’s program.
And so,
that brings us to the close of
“Recognition of Chemical
Associated Gastrointestinal Foodborne Illness”.
I’m Cynthia Good, and it has been my pleasure to be your moderator today.
Good-bye.
#######
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