Foodborne Illness: Common Biological Contaminants and Pathogens
Authors: Jonathan I. Singer, MD, FAAP, FACEP, Associate Program Director for Emergency Medicine, Professor of Emergency Medicine and Pediatrics, Boonshoft School of Medicine, Wright State University, Dayton, OH; Jason Pickett, MD, Resident Physician, Emergency Medicine Residency, Boonshoft School of Medicine, Wright State University, Dayton, OH; Pat Chhuon, MD, Resident Physician, Emergency Medicine Residency, Boonshoft School of Medicine, Wright State University, Dayton, OH.
Peer Reviewer: Robert A. Felter, MD, FAAP, CPE, FACPE, Medical Director, Pediatric Emergency and Inpatient Services, Inova Loudon Hospital, Leesburg, VA.
Patients frequently present to the emergency department with gastrointestinal complaints such as vomiting, abdominal pain, and diarrhea. Identification of a foodborne illness may be very challenging. Foodborne illness (FBI) may cause atypical neurologic symptoms; rapid identification and treatment of those symptoms may decrease patient morbidity and mortality risk. Early identification of an FBI also may help find the source of the disease and prevent further dissemination. The authors comprehensively review foodborne illness, highlighting characteristics that may be utilized to recognize and diagnose this disease process.
— The Editor
Introduction
Foodborne illness (FBI) is a symptom or constellation of symptoms that are largely gastrointestinal. The clinical picture may vary widely from patients who suffer a minor inconvenience to those with life-threatening presentations. FBI results from ingestion of food or consumption of water that is contaminated. Various food groups can be vehicles for transmission of FBI. (See Table 1.)
A wide net must be cast to identify causative agents in patients who become symptomatic from ingestion of contaminated food or water. Some agents of foodborne illness rapidly cause symptoms, whereas other agents may take days or even weeks to be evident. This confounds attempts to identify the source of the illness. A single patient with symptoms that are suggestive of FBI is unlikely to be recognized unless the treating physician applies considerable skill and judgment. Identification of the source of illness is important for the individual patient and accurate identification of a source of illness may prevent illness in other patients. This article raises awareness for biological contaminants and pathogens that are common in transmission of FBI.
Epidemiology
In 2004, 76 million people in the United States suffered from, 325,000 were hospitalized for, and 5000 individuals died as a result of foodborne disease.2-5 It is projected that only 1-10% of foodborne illnesses are reported.6 Hence, FBI may be an underreported contributor to 200,000 annual pediatric hospital admissions and 1.5 million emergency department (ED) visits for "acute gastroenteritis."1,7 After microbiological diagnosis of several foodborne agents of disease, the hospital admission rate is 14%.8
Identification of Foodborne Illness (FBI)
The medical community can facilitate recognition of FBI. This can be globally accomplished by active surveillance of clusters of symptoms, and unusual spikes of similar complaints in the patient population. In the process of determining which disease process is at play for an individual patient with gastrointestinal complaints, physicians should ask specific questions while obtaining the history of the present illness.
Diet. Eating habits modify the patient's vulnerability to foodborne illnesses. Those who prepare their own foods, practice safe food handling techniques, and drink from treated community water systems are less likely to become ill. Those who lack food preparation skills (cross contaminate raw and cooked foods, inadequately heat foods), exhibit poor personal hygiene (fail to wash hands after handling food products), and ingest untreated water are more vulnerable to illness.9 Those who dine in licensed restaurants, cafeterias, or delicatessens are at increased risk for foodborne illness compared to eating at home. Licensing does not assure that food safety practices are enforced. Nearly 94% of foodborne outbreaks in the United States from 1993 to 1997 occurred in licensed establishments. Foodstuff purchased from unlicensed food services or street vendors magnifies the risk for FBI.10,11
The food industry has impacted FBI. Poultry and ground beef have high rates of bacterial contamination.10 The bacteria are often antibiotic-resistant strains due to the food industries use of antimicrobial agents in feed.12,13 Agricultural production adjacent to livestock has led to contamination. A 2006 spinach contamination with E. coli was attributed to adjacent livestock.14 When perishable foods are contaminated and widely distributed, as in the 2006 E. coli O157:H7 Taco Bell outbreak, there is nationwide exposure to these pathogens in the areas of ultimate distribution.
Parental eating habits influence the pediatric population. In recent years, parents have sought organic or healthy alternatives to processed or mass-produced foodstuffs. Small-batch food products from local farms have been brought with increased frequency into the home. Children have joined their parents in drinking unpasteurized milk or juice, and consumption of cheeses from unpasteurized milk. They have consumed raw shellfish and undercooked meats.
Asking patients with potential FBI the following focused questions may be enlightening:
1. What food and liquids have you consumed recently?
2. Has anyone else consumed the same food or drinks?
3. Has a co-consumer developed any symptoms?
4. Have any of the foods been:
a. Home canned?
b. From street vendors?
c. From restaurants?
d. Prepared by anyone you know to be ill?
e. Left out for long periods at room temperature?
f. Served beyond a perishable date of expiration?
5. Have any of the foods been:
a. Honey?
b. Unwashed fruits or vegetables?
c. Raw or undercooked?
d. Prepared from a wild animal?
e. Unpasteurized juices, milk, or cheese from species including cow, sheep, or goat?
Travel. Exposure to contaminated food or water may be increased with "unsafe" travel. "Unsafe" travel is defined as housing in unfavorable conditions and consumption of foods and liquids with unpredictable standards for cleanliness. Recreational activity during travel can intensify risk. Those who camp, visit a petting zoo, aquarium, or farm where there is handling of reptiles or amphibians are at increased risk for FBI. Those who swim in lakes and rivers are at increased risk for water-borne pathogens.15,16 Children taken to regions that are endemic for cholera, typhoid, and hepatitis also are at risk for FBI. International travel, particularly to resource-poor countries, intensifies risk.17,18
Questions directed to uncover patient travel and recreational exposure include:
1. Have you traveled recently?
2. Have you camped out?
3. Have you consumed lake or stream water?
4. Have you been exposed to reptiles, amphibians, or fowl?
Other Predispositions to FBI. Beyond food, travel, and play, other variables may change the vulnerability of a pediatric patient to FBI. Age has an impact. Those younger than age 5 are at increased risk for illness from pathogenic E. coli, including the development of hemolytic uremic syndrome. Small children and infants, who attend daycare, are in proximity to others with fecal incontinence. This predisposes them to specific pathogens associated with diarrheal illness.
In your questioning, pursue recent environmental changes and underlying medical conditions. They predispose patients to two specific pathogens associated with FBI. (See Table 2.)
Pathophysiology
The gastrointestinal tract possesses several nonimmunologic barriers that prevent illness from tainted food or water. Potential foodborne pathogens are largely eradicated in the environment of high gastric acidity. Indigenous intestinal flora compete for nutrients of potential pathogens. Nonpathogenic bacteria also lower intestinal pH and produce fatty acids, which inhibit the growth of pathogens. Mucin secreted by the intestine decreases the likelihood of bacterial adherence to the epithelial cells of the gut. Peristalsis minimizes the contact between the mucosal surface and a potential pathogen. It aids to expel pathogenic organisms that are nonadherent to epithelial cells. Further, peristalsis prevents retrograde migration of organisms from the colon to the small intestine.19
The gastrointestinal tract is further protected by immunologic defense. Secretary IgA is locally produced when an antigen is exposed to the intestinal surface. Toxins are bound and bacterial growth is inhibited.20
Systemic and local defense mechanisms can be overcome to produce foodborne illness. The manifestations result from a toxin or an infection, or a combination of invasion and elaboration of toxin may occur.
Preformed Toxins. Preformed toxin-related FBI results from one of three ways: 1) the toxin is produced by bacteria; 2) the toxin is a natural chemical in a foodstuff; or 3) the toxin is acquired in the course of the food chain.
In the preformed bacterial toxin-mediated illness, a food is contaminated during poor hygienic practice. The food then sits inadequately refrigerated, and the toxin is produced. The ingestion of the preformed toxin leads to symptoms.21 Common examples include staphylococcal toxin mediated illness in which ingestion of a contaminated high protein content food, such as mayonnaise-containing salad or custard pastry, causes illness, and B. cereus emetic toxin from contaminated rice and potato mix. Another circumstance is "classic" botulism food poisoning, where a home preserved and canned fruit or vegetable is not heated adequately in a pressure cooker.22 The food is contaminated with spores and toxins are elaborated. Ingestion of the toxin leads to a wide range of illness severity.
Natural chemical constituents are found in various vegetables that are not safe or appropriate for human consumption. Examples include green potatoes, unripe akee fruit, bitter cassava, and various mushrooms of the Amanita spp. Inadequate refrigeration of fish permits bacterial growth on the fish flesh. This leads to transformation of histidine to histamine, and no method of food preparation can make it safe to eat (scombroid poisoning).
Consumption of some marine fish or mollusks leads to preformed toxin exposure. Toxins produced by reef algae may get incorporated into large tropical and semitropical fish (ciguatera poisoning) or into filter-feeding shellfish.23
Toxins Produced In Vivo. Toxins can be produced within the patient.24 In the case of certain bacteria, a vegetative cell can be ingested and germinate in the patient's gut. The circumstances surrounding this typically involve a delay between food preparation and the eating of a meal. An example would be meat contaminated with Clostridium perfringens that slowly cooled or was left to sit on steam tables that permitted sporulation. Similarly, inadequate refrigeration of meat, dairy, poultry, or boiled rice contaminated with Bacillus cereus permits intestinal elaboration of a diarrheal toxin.25 Ingested Clostridium botulinum spores can germinate in the patient's gut, releasing toxin (infantile botulism).26
Host Invasion. FBI may be caused by an infectious invasion of the intestine by bacteria, viruses, or protozoa. These agents are transmitted by direct contact with humans or animals that harbor these organisms. They are transmitted by the fecal-oral route, or by contaminated food or water. The mode of transmission is dependent on the particular pathogen and the host immunity. Bacteria that gain entry to the gut have fimbria or pili that allow them to adhere to the mucosa. Adherence causes destruction of the microvilli brush border in underlying cell cytoplasm.27 Viruses damage the absorptive cells of the microvilli of the small bowel, thereby decreasing the available surface area for absorption of fluid and electrolytes. Shortening and blunting of these villi cause transient malabsorption until the microvilli are repaired. Protozoans attach to the mucosa of the small intestine where they cause blunting of the villi. There is variable invasion of colonic glands, and in some circumstances protozoa may enter the lamina propria layer of the colon. Examples of host invasion causing FBI are enteroinvasive E. coli and Salmonella food poisoning. Examples of common viral and protozoan agents include rotavirus, norovirus, Giardia spp., and Entamoeba spp.28
Host Invasion and Enterotoxin. Some agents that produce FBI can invade mucosal cells, creating cellular damage or death as well as elaborate toxins. The toxins can stimulate intestinal secretion of fluid and electrolytes, alter smooth muscle activity in the intestine, cause release of neurotransmitters, and produce systemic effects. Examples of dual toxicity are Vibrio parahaemolyticus (from ingestion of raw or uncooked crab, oysters, shrimp, or lobster) and enteroaggrative Escherichia coli (contaminated water, dairy, or meat products).
Clinical Features
Clues to FBI may come when a prominent symptom or constellation of symptoms occur with a suggestive travel history, dietary history, family contacts, or zoonotic exposure. The chief complaint or pattern and evolution of symptoms may help discriminate the likely cause of FBI.
Chief Complaint. Most patients with FBI present with an isolated or a combination of gastrointestinal complaints.28 Common symptoms include anorexia; nausea; non-bilious vomiting; non-foul-smelling, watery diarrhea, with or without passage of mucus and/or blood; tenesmus; and abdominal pain. Less common symptoms include constitutional symptoms such as malaise, fever, chills, or prostration. Uncommon symptoms include aches (back, joints, muscles), paresthesia, visual impairment (inability to focus, "wandering eyes," diplopia), difficulty speaking, difficulty ambulating, paralysis, or seizures. Some symptoms, such as increased thirst, weakness, blunted affect, and decreased urine output, result from dehydration.
History of Present Illness. FBI presents in one of four patterns: acute gastrointestinal (GI), chronic gastrointestinal, acute neurologic, or histamine syndrome.
Acute GI. The most common pattern of FBI is an acute syndrome with a duration of 1-2 days. The caretaker and patient are cognizant of the time that illness begins. In hyperacute cases of FBI (within 6 hours of exposures) and in acute cases (6-24 hours), the first manifestations are dramatic and typically are gastrointestinal. (See Table 3 and Table 4.) The illness may be heralded by one of three symptoms of varying frequency, depending upon the underlying cause. Most often, there is a constellation of gastrointestinal symptoms.
Vomiting occasionally may be concurrent with or follow abdominal pain, but most often vomiting precedes abdominal pain. The vomitus is first of undigested food. No matter how protracted, emesis remains nonbilious. Anorexia and nausea are prominent associated symptoms.
Abdominal pain is of variable intensity ranging from mild to severe. It often is generalized or periumbilical. The pain is crampy in nature. Occasionally, stool passage is a painful, aggravating factor. Generally, pain is alleviated somewhat by assuming a left lateral decubitus, curled-up posture and by passage of flatus or stool.
Diarrhea is an uncommon, isolated gastrointestinal symptom with FBI. Increased stool water and increased frequency of stooling generally follow abdominal pain and/or vomiting. The stools are non-foul smelling and contain no visible mucus or blood, especially if caused by a foodborne agent or viral pathogen. Mucoid or bloody diarrhea can follow infection with invasive pathogens that damage the lining of the bowel.
Chronic GI. Less commonly, there is a more gradual onset of not-so-severe manifestations and a duration of 2-4 days. Patients and their caretakers rarely recall the time of day that their illness began. The insidious manifestations can be tied to FBI with a careful history that reveals exposure in the last 1-2 days. (See Table 5.) Occasionally, a FBI will take from 2 to 14 days to create symptoms. (See Table 6.) The duration of symptoms in chronic FBI may be protracted.
Neurologic. If verbal, the pediatric patient may be able to express abnormal sensations. The sensation of weakness is prominent with botulism, ciguatera, paralytic shellfish, and mercury intoxication. Numbness and tingling of the lips, tongue and throat are seen in paralytic shellfish, pufferfish, and ciguatera. Reversal of hot or cold is seen with ciguatera and neurologic shellfish poisoning.29,30
Histamine Syndrome. Within 10 minutes to an hour after ingestion of a contaminated fish, patients with scombroid develop itching or a burning sensation of the skin associated with skin blotches, blisters, or hives.31,32
Physical Examination. It is more likely that uncovering the agent causing the FBI will come from the patient's history rather than the physical examination. Several effects of FBI on physical examination findings are discriminatory.
General Appearance. The general appearance will be significantly altered by a patient's pain, and a poor perfusion state. Excessive and distracting pain emanate from head, muscles, joints, or abdomen. Extra abdominal pain is prominent with FBI from Shigella spp., Vibrio parahaemolyticus, and rotavirus. Patients with FBI from Yersinia spp., Campylobacter spp., Clostridium perfringens, and B. cereus diarrheal toxin have heightened abdominal complaints that alter general appearance. Excessive fluid loss through hyperemesis or profusely watery stools blunts the patient's affect, skin turgor, and capillary refilling time. A dehydrated state is far more common with FBI from staphylococcal food poisoning, Vibrio cholerae, and Vibrio parahaemolyticus.
Vital Signs. Modest increases in heart rate, respiratory rate, or increased depth of respiration reflect acidosis and dehydration that may accompany foodborne illnesses. These vital sign changes are rarely discriminatory. Decreasing respiratory drive, respiratory distress, and/or apnea are discriminatory. These events may occur in the course of botulism or paralytic shellfish poisoning. Hyperpyrexia (> 40°C) in the context of FBI suggests Shigella spp. enteritis or Salmonella spp. enteritis with occult bacteremia. Extreme tachycardia and/or hypotension suggests septic shock or Vibrio cholerae.
Skin. Foodborne hepatitis A is generally nonicteric, but on occasion may cause jaundice. Facial and upper thoracic petechiae are common following forceful vomiting and are nondiscriminating. Diffuse petechiae in the context of FBI suggest hemolytic uremic syndrome. Hives or flushing suggest scombroid poisoning. Typically, flushing is most prominent on the face and upper body, sometimes with sharp demarcation between reddened and unaffected skin. Diaphoresis suggests ciguatera or mushroom poisoning.
HEENT (head, ears, eyes, nose, throat). There can be conjunctival suffusion (increased blood supply and redness from the conjunctival vessels) with scombroid. Decreased salivation and dry mouth occur in botulism. Increased salivation occurs with mushrooms and cadmium poisoning.
Abdomen. Distention and hyperactive bowel sounds are prominent with many causes of FBI. Hepatic percussion tenderness suggests hepatitis A or Entamoeba spp. liver invasion. Right upper quadrant pain and mass may accompany Salmonella infection as a result of hydrops of the gallbladder. Abdominal voluntary guarding with or without rebound tenderness may be seen in the right lower quadrant with Campylobacter spp. or Yersinia spp.
Neurologic. Absent or a persistently high-pitched cry, inability to console, poor eye contact, and decreased interaction with the environment are constituents of toxicity. Toxicity is seen with Vibrio parahaemolyticus, Vibrio cholerae, Shigella spp., Listeria monocytogenes, botulism, and staphylococcal food poisoning. Decreased motor activity, weakness, and hypotonia suggest ciguatera fish poisoning or botulism. Cranial nerve abnormalities, manifested by difficulty with swallowing and vision, with fixed and dilated pupils, are seen with severe botulism. Paralysis of respiratory muscles suggests paralytic shellfish poisoning or severe ciguatera. Ascending paralysis suggests pufferfish poisoning. Descending paralysis suggests botulism.
Diagnostic Studies
In the majority of cases of suspected foodborne illness, diagnostic testing is of limited utility. Laboratory assessments have value in several circumstances.33
Dehydration. When there is a history of > 10% acute weight loss, poor oral intake, reduced urine output, significant tachycardia, decreased capillary refilling time or decreased skin turgor and dry mucous membranes, CBC (complete blood count) and BMP (basic metabolic profile) are useful to bolster clinical suspicion of moderate to severe dehydration. The presence of hemoconcentration or electrolyte abnormalities may modify fluid treatment and disposition. Findings of thrombocytopenia or azotemia would require further evaluation for hemolytic uremic syndrome, such as coagulation studies and enzyme immunoassay to detect serum antibodies to E. coli 0157:H7 lipopolysaccharide.
Bloody Diarrhea. Patients with frank bloody diarrhea or positive Hemoccult test would benefit from a CBC and stool culture. The presence of leukocytosis does not discriminate likely pathogens, but the presence of a normal total white blood cell count with many immature forms suggests Shigella spp., Salmonella spp., or Yersinia spp. Rectal swab should be submitted for stool culture. The laboratory must be informed that you are trying to isolate Campylobacter spp., Yersinia spp., Salmonella spp., Shigella spp., E. coli 0157:H7, and Vibrio spp.
Acute Abdomen. The presence of shuffling gait, inability to climb onto the examining table, involuntary guarding, rebound tenderness, absent bowel sounds, positive psoas or obturator sign, or abdominal mass constitute manifestations of the "acute abdomen." With the presence of an acute abdomen, the evaluation should be as per the physician's routine for a similar clinical circumstance.34,35 These typically include submission of urine and appropriate consultation.
Toxic, Hyperpyrexic. Ill appearance should induce the clinician to search for systemic infection. The exact laboratory tests vary by practitioner routine and the patient's clinical state. Young age, immunosuppression, and illness following exposure to an invasive pathogen should be associated with a more aggressive search for invasive disease.
Suspicion for Catastrophic Cause. When there has been a clinical course that is highly suggestive of a particular catastrophic cause for FBI, the diagnosis should be pursued. Examples of diseases include botulism, where botulism toxin should be searched for in the stool. Fluorescent antibody techniques for cholera and E. coli 0157:H7 should be pursued in the appropriate clinical context.
Prolonged Course. When a patient has been symptomatic longer than a 3-5 day period and supportive care has not led to resolution of symptoms, the emergency physician should pursue a definitive diagnosis. Laboratory examination should include submission of several sets of stool specimens for culture, and ova and parasite examination.
Public Health. In a case of isolated illness, laboratory evaluation is not particularly cost effective. When an outbreak in the community has occurred, testing benefits the public. Acquire tests of stool for viral, bacterial, and protozoan infection; and serology for hepatitis profiling. The projected contaminated food, if retrieved, can be cultured.
Differential Diagnosis
Patients with FBI present with diverse gastrointestinal complaints. They may present to the ED hours to days after an abrupt onset, or delayed after insidious complaints have not resolved with self treatment. Patients may seek care at a time of escalating symptoms, at a time of plateau, or during a period of resolving complaints. As a result, the appearance and physical findings are highly variable. Given the wide constellation of symptoms, the differential diagnosis is wide ranging. The differential is narrowed when focus is placed on specific elements of the patient's history.
The differential diagnosis for the patient with non-foodborne anorexia, nausea, and abdominal pain who has a prominence of diarrhea includes infectious, inflammatory, structural, and metabolic conditions. These conditions can be divided by the presence or absence of blood in the stool, by either visual or Hemoccult examination. (See Table 7.)
The differential diagnosis for non-foodborne gastrointestinal complaints with a prominence of vomiting includes extraintestinal infection, intraabdominal infection, obstructive disease states, endocrine disorders, and toxic and traumatic conditions. (See Table 8.)
The differential diagnosis for non-foodborne gastrointestinal complaints with diffuse neurologic symptoms including visual impairment; increased oral secretions or contrasting, dry mouth; headache; numbness; abnormal sensations including altered heat and cold detection; weakness to paralysis; or seizures are limited to several infectious diseases, intoxicants, or inflammatory or autoimmune diseases. (See Table 9.)
Management
Initial Stabilization. In limited circumstances of foodborne illness (i.e., botulism, pufferfish, ciguatera, scombroid, shellfish neurotoxin, bacterial enteropathogens), a life-threatening presentation demands a primary survey directed toward the vital areas of airway, breathing, circulation, and neurologic instability. Perform endotracheal intubation for airway protection in FBI with hypovolemic shock, septic shock, decreased level of consciousness, loss of gag reflex, or prolonged seizure activity. Provide ventilatory support for those with fatigued muscles of respiration or impending respiratory failure. Administer epinephrine and corticosteroids for angioedema. Treat bronchospasm with inhaled beta2 agonists. Infuse intravenous normal saline at 20 mL/kg as rapidly as possible to treat a tenuous perfusion state. With reassessments in between infusions, provide up to 60 mL/kg. If the circulatory status is unresponsive, treat with pressors.
Refined Fluid Therapy. In the majority of patients with FBI, fluid and electrolyte status are the only management concerns. The therapeutic principle for those with dehydration from FBI is to restore perfusion and cellular functioning by providing rehydrating fluids while monitoring the patient's progress. The type of fluid given, route of fluid administration, and speed of administration rests with the initial assessment of the degree of dehydration. Oral glucose-electrolyte rehydration solutions are highly effective in the treatment of mild and moderate dehydration.36-39 A rapid rate of early repair is provided by giving from 40 to 90 mL/kg of a 75 or 90 mmol Na/L solution over 4-6 hours. This bolus is followed by maintenance solutions with concentrations from 40 to 50 mmol/L. Total daily volumes range from 150 to 250 mL/kg.
Intravenous fluids are given to patients who are unable to tolerate oral rehydration therapy.40 Intravenous fluids are provided routinely for those with severe dehydration who need rapid restoration of intravascular volume. Intravenous fluids also are suitable for lesser degrees of dehydration. Following bolus therapy of normal saline, 5% dextrose with one-half normal saline is the ideal maintenance fluid beyond the stabilization phase. The rate of fluid administration and the specific content of potassium supplementation should be tempered by serum electrolyte measurements and assessment of urine output. Renal perfusion is assumed to be adequate with the passage of urine at a rate of 1-2 mL/kg/hr.
Other Pharmacotherapy. Various pharmacologic agents may be of utility, whereas others are of marginal benefit or are overtly harmful.
Antiemetics. There are no studies of ondansetron or dexamethasone with FBI. However, patients with repeated vomiting may benefit from either drug.41,42 In a study of vomiting children with acute gastroenteritis, ondansetron given by mouth or intravenously (0.15 mg/kg to a maximum of 8 mg) prior to oral challenge reduced intravenous fluid rates and hospital admissions.43 The positive impact of ondansetron with acute gastroenteritis is likely to be more pronounced with patients who have mild to moderate dehydration as defined as a serum CO2 > 15 mEq/L.41 In acute pediatric gastroenteritis, there is an improved tolerance of oral fluids but no reduction in hospital admissions with the use of dexamethasone.44
Opioid Agonists. In adults, paregoric, diphenoxylate/ atropine (Lomotil), and loperamide (Imodium) have been shown to diminish fecal urgency, frequency, and volume of diarrheal stools. In children, a scant amount of evidence exists regarding the efficacy of loperamide.45 In vitro, opioid agonists predispose to ileus and increase the likelihood of intestinal perforation. In uncontrolled studies, paregoric and diphenoxylate/atropine have been noted to prolong fever and duration of diarrhea. Diphenoxylate/atropine has been associated with iatrogenic and accidental death in the pediatric population.46 Toxic megacolon has been reported with loperamide. Because of the deficiency of evidence for the benefit of these drugs and the potential for harm, none of the opioid agonists are recommended in children.17,47,48
Non-opioid Compounds. Kaolin and pectin (Kaopectate) use is without harm but does not reduce the frequency and water content of stools. Bismuth subsalicylate (Pepto-Bismol) decreases intestinal secretions and has some antibacterial effects. Bismuth subsalicylate has shown positive in vitro effects with several organisms including Salmonella spp., Campylobacter spp., C. difficile, and norovirus.49 Bismuth subsalicylate has been shown to be effective with patients with enteritis secondary to enterotoxigenic E. coli.
Antihistamines. Intravenous diphenhydramine and/or cimetidine may shorten the course and ameliorate the symptoms of scombroid poisoning.50
Osmotic Agents. Intravenous mannitol (1 g/kg infused over 0.5-4 hours), if provided within the first 24 hours of the onset of ciguatera poisoning, may improve neurologic manifestations caused by cigua toxin.23
Antitoxin. An equine-derived antitoxin is available from the CDC to treat patients with foodborne botulism. The trivalent toxin can prevent the progression of neurologic dysfunction if administered early in the course of the illness.28 No antitoxins are available for any of the shellfish toxins, tetrodotoxicity of pufferfish poisoning, Shiga toxin, or non-botulism food poisonings. Antitoxin is of no benefit in infantile botulism.
Antibiotics. Antimicrobials may be of theoretical, but unproven benefit, supported by clinical experience, or contraindicated by clinical outcomes. Antimicrobials are theoretically indicated in the management of infantile botulism, as there is an active infection from C. botulinum. However, it is difficult to measure the clinical impact of intravenous penicillin, the drug of choice. Response as measured clinically (reduction in fever, abdominal discomfort, or diarrhea) and bacteriologically (reduce stool shedding or eradication of organisms from the bloodstream) is seen with antibiotic treatment of Campylobacter spp., enterotoxigenic E. coli, C. difficile, V. cholerae, and amebic dysentery. Positive clinical and bacteriologic response is less clear with Yersinia spp. Antibiotic treatment fails to hasten clinical recovery and may prolong the period to resolution with Salmonella spp.51,52
Disposition
The majority of patients with FBI evaluated in the ED are suitable for immediate discharge or discharge home after assessment and/or management of fluid depletion. There are occasions, however, when admission to the hospital is advisable. They include toxic appearance; expectant antibiotic therapy for occult bacteremia or documented extraintestinal focus of infection; severe dehydration; laboratory abnormalities that include electrolyte imbalance, azotemia, hypoglycemia, thrombocytopenia, hemolysis, neutropenia; failed oral challenge in the ED; concern for acute abdomen; neurologic impairment; past medical history, such as immunocompromise; psychosocial, such as chronic poor parenting, acute parental illness, long distance to hospital, and inadequate transportation or follow-up; and need for continued healthcare observation.
Surveillance and Reporting
Foodborne disease surveillance and reporting are important public actions. The ED is a participant in the process. When an outbreak is suspected, the ED staff should contact by phone or e-mail the local or county health department in the jurisdiction of the event. The regional health department will investigate and forward a written case report to the state health department.
Should a diagnosis of FBI be confirmed in the ED, the state health department requests notification. Reporting requirements are mandated by individual state regulation. Details on specific state reporting requirements are available from state health departments. Additional information is available electronically at www.cste.org/nndss/reportingrequirements.htm and www.cdc.gov/epo/dphsi/phs/infdis2003.htm.
Members in the state health department implement disease control measures. They will conduct a more thorough epidemiologic investigation. The state coordinates laboratory testing that is unavailable locally. They may enact closure of local food establishments or alter central distribution of foodstuffs. The outcome is a curtailment of the outbreak. The state will collaborate with the Centers for Disease Control and Prevention (CDC). The CDC acts as a common agent for collecting information and reporting of nationally notifiable diseases. Reports of these diseases are transmitted to the CDC each week and provisional data are published in the Morbidity and Mortality Weekly Report.
Summary
Foodborne diseases frequently occur and are associated with multiple pathogens. The affected patient may present with a wide array of signs and symptoms. It is often unclear if a patient has foodborne illness based on history, physical, and readily available diagnostic tests. Supportive care reduces morbidity. The emergency physician should report potential FBI to local health authorities when two or more patients present with an illness that may have resulted from ingestion of a common food or fluid. Public health authorities may be able to curtail further outbreak of foodborne illness.
References
1. AAP. 1997 Red Book. Report of the committee on infectious disease. Elk Grove Village, IL: American Academy of Pediatrics, 1997.
2. Acheson DW, Fiore AE. Preventing foodborne disease—what clinicians can do. N Engl J Med 2004;350:437-440.
3. Mead PS, Slutsker L, Dietz V, et al. Food-related illness and death in the United States. Emerg Infect Dis 1999;5:607-625.
4. Glass RI, Lew JF, Gangarosa RE, et al. Estimates of morbidity and mortality rates for diarrheal diseases in American children. J Pediatr 1991;118:S27-33.
5. Kennedy M, Angulo FJ, Group FW. Incidence of foodborne illnesses: 1999 data from FoodNet. Irish Journal of Agricultural and Food Research 2000;39:295-300.
6. Motarjemi Y, Kaferstein FK. Global estimation of foodborne diseases. World Health Stat Q 1997;50:5-11.
7. Herikstad H, Yang S, Van Gilder TJ, et al. A population-based estimate of the burden of diarrheal illness in the United States: FoodNet, 1996-7. Epidemiol Infect 2002;129:9-17.
8. Helms M, Simonsen J, Molbak K. Foodborne bacterial infection and hospitalization: a registry-based study. Clin Infect Dis 2006;42:498-506.
9. Collins JE. Impact of changing consumer lifestyles on the emergence/reemergence of foodborne pathogens. Emerg Infect Dis 1997;3:471-479.
10. Lynch M, Painter J, Woodruff R, et al. Surveillance for foodborne-disease outbreaks—United States, 1998-2002. MMWR Surveill Summ 2006;55:1-42.
11. Olsen SJ, MacKinnon LC, Goulding JS, et al. Surveillance for foodborne-disease outbreaks—United States, 1993-1997. MMWR CDC Surveill Summ 2000;49:1-62.
12. Report on Infectious Diseases. Overcoming antimicrobial resistance. Geneva: World Health Organization, 2000.
13. White DG, Zhao S, Sudler R, et al. The isolation of antibiotic-resistant salmonella from retail ground meats. N Engl J Med 2001;345:1147-1154.
14. Centers for Disease Control and Prevention. Ongoing multistate outbreak of Escherichia coli serotype O157:H7 infections associated with consumption of fresh spinach—United States, September 2006. MMWR Morb Mortal Wkly Rep 2006;55:1045-1046.
15. Dziuban EJ, Liang JL, Craun GF, et al. Surveillance for waterborne disease and outbreaks associated with recreational water—United States, 2003-2004. MMWR Surveill Summ 2006;55:1-30.
16. Guerrant RL, Hughes JM, Lima NL, et al. Diarrhea in developed and developing countries: magnitude, special settings, and etiologies. Rev Infect Dis 1990;12 Suppl 1:S41-50.
17. Juarez J, Abramo TJ. Diarrhea in the recent traveler. Pediatr Emerg Care 2006;22:602-609; quiz 610-601.
18. Shepherd SM, Talbot-Stern JK. Evaluation of the traveler. An introduction to emporiatrics for the emergency physician. Emerg Med Clin North Am 1991;9:273-301.
19. Acheson DW, Luccioli S. Microbial-gut interactions in health and disease. Mucosal immune responses. Best Pract Res Clin Gastroenterol 2004;18:387-404.
20. Mowat AM. Anatomical basis of tolerance and immunity to intestinal antigens. Nat Rev Immunol 2003;3:331-341.
21. Le Loir Y, Baron F, Gautier M. Staphylococcus aureus and food poisoning. Genet Mol Res 2003;2:63-76.
22. Cengiz M, Yilmaz M, Dosemeci L, et al. A botulism outbreak from roasted canned mushrooms. Hum Exp Toxicol 2006;25:273-278.
23. Mines D, Stahmer S, Shepherd SM. Poisonings: food, fish, shellfish. Emerg Med Clin North Am 1997;15:157-177.
24. Cohen MB. Etiology and mechanisms of acute infectious diarrhea in infants in the United States. J Pediatr 1991;118:S34-39.
25. Ehling-Schulz M, Fricker M, Scherer S. Bacillus cereus, the causative agent of an emetic type of food-borne illness. Mol Nutr Food Res 2004;48:479-487.
26. Bartram U, Singer D. [Infant botulism and sudden infant death syndrome]. Klin Padiatr 2004;216:26-30.
27. Knutton S, Lloyd DR, McNeish AS. Adhesion of enteropathogenic Escherichia coli to human intestinal enterocytes and cultured human intestinal mucosa. Infect Immun 1987;55:69-77.
28. Diagnosis and management of foodborne illnesses: a primer for physicians and other health care professionals. MMWR Recomm Rep 2004;53:1-33.
29. Centers for Disease Control and Prevention. Ciguatera fish poisoning—Texas, 1998, and South Carolina, 2004. MMWR Morb Mortal Wkly Rep 2006;55:935-937.
30. Barton ED, Tanner P, Turchen SG, et al. Ciguatera fish poisoning. A southern California epidemic. West J Med 1995;163:31-35.
31. Wu ML, Yang CC, Yang GY, et al. Scombroid fish poisoning: an overlooked marine food poisoning. Vet Hum Toxicol 1997;39:236-241.
32. Morrow JD, Margolies GR, Rowland J, et al. Evidence that histamine is the causative toxin of scombroid-fish poisoning. N Engl J Med 1991;324:716-720.
33. Liu LJ, Yang YJ, Kuo PH, et al. Diagnostic value of bacterial stool cultures and viral antigen tests based on clinical manifestations of acute gastroenteritis in pediatric patients. Eur J Clin Microbiol Infect Dis 2005;24:559-561.
34. Gupta H, Dupuy DE. Advances in imaging of the acute abdomen. Surg Clin North Am 1997;77:1245-1263.
35. Weinberger E, Winters WD. Abdominal pain & vomiting in infants & children: imaging evaluation. Compr Ther 1997;23:679-686.
36. Alhashimi D, Alhashimi H, Fedorowicz Z. Antiemetics for reducing vomiting related to acute gastroenteritis in children and adolescents. Cochrane Database Syst Rev 2006:CD005506.
37. Spandorfer PR, Alessandrini EA, Joffe MD, et al. Oral versus intravenous rehydration of moderately dehydrated children: a randomized, controlled trial. Pediatrics 2005;115:295-301.
38. Hartling L, Bellemare S, Wiebe N, et al. Oral versus intravenous rehydration for treating dehydration due to gastroenteritis in children. Cochrane Database Syst Rev 2006;3:CD004390.
39. Phin SJ, McCaskill ME, Browne GJ, et al. Clinical pathway using rapid rehydration for children with gastroenteritis. J Paediatr Child Health 2003;39:343-348.
40. Bellemare S, Hartling L, Wiebe N, et al. Oral rehydration versus intravenous therapy for treating dehydration due to gastroenteritis in children: a meta-analysis of randomised controlled trials. BMC Med 2004;2:11.
41. Reeves JJ, Shannon MW, Fleisher GR. Ondansetron decreases vomiting associated with acute gastroenteritis: a randomized, controlled trial. Pediatrics 2002;109:e62.
42. Stork CM, Brown KM, Reilly TH, et al. Emergency department treatment of viral gastritis using intravenous ondansetron or dexamethasone in children. Acad Emerg Med 2006;13:1027-1033.
43. Ramsook C, Sahagun-Carreon I, Kozinetz CA, et al. A randomized clinical trial comparing oral ondansetron with placebo in children with vomiting from acute gastroenteritis. Ann Emerg Med 2002;39:397-403.
44. Stork CM, Reilly TH, Brown KM. Dexamethasone vs. ondansetron in children with refractory vomiting from acute viral gastritis. Acad Emerg Med 2005;12:19-20.
45. Kaplan MA, Prior MJ, McKonly KI, et al. A multicenter randomized controlled trial of a liquid loperamide product versus placebo in the treatment of acute diarrhea in children. Clin Pediatr (Phila) 1999;38:579-591.
46. Michael JB, Sztajnkrycer MD. Deadly pediatric poisons: nine common agents that kill at low doses. Emerg Med Clin North Am 2004;22:1019-1050.
47. Armon K, Stephenson T, MacFaul R, et al. An evidence and consensus based guideline for acute diarrhea management. Arch Dis Child 2001;85:132-142.
48. Practice parameter: the management of acute gastroenteritis in young children. American Academy of Pediatrics, Provisional Committee on Quality Improvement, Subcommittee on Acute Gastroenteritis. Pediatrics 1996;97:424-435.
49. Manhart MD. In vitro antimicrobial activity of bismuth subsalicylate and other bismuth salts. Rev Infect Dis 1990;12 Suppl 1:S11-15.
50. Blakesley ML. Scombroid poisoning: prompt resolution of symptoms with cimetidine. Ann Emerg Med 1983;12:104-106.
51. Johnson JE, Sullivan PB. The management of acute diarrhea. Current Paediatrics 2003;13:95-100.
52. Phavichitr N, Catto-Smith A. Acute gastroenteritis in children : what role for antibacterials? Paediatr Drugs 2003;5:279-290.
Patients frequently present to the emergency department with gastrointestinal complaints such as vomiting, abdominal pain, and diarrhea. Identification of a foodborne illness may be very challenging.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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