44: Food Poisoning

Each year in the United States there are approximately 9.4 million illnesses, 55,961 hospitalizations, and 1351 deaths from known foodborne agents, and 38.4 million gastroenteritis illnesses, 71,878 hospitalizations, and 1686 deaths from unspecified agents.³⁹ Worldwide food distribution, large-scale national food preparation and distribution networks, limited food regulatory practices, and corporate greed place everyone at risk. Food poisoning causes morbidity and mortality by one or more of the following mechanisms: Infectious agents (bacteria, viruses, parasites) can be transmitted in food; toxins, produced by organisms, can be consumed in food; toxins or chemicals can be inadvertently or purposefully used to contaminate food and be ingested.

This chapter is organized into four major types of food poisoning: foodborne poisoning with neurologic effects, food poisoning with gastrointestinal symptoms, foodborne poisoning with anaphylaxislike effects, and food poisoning used for bioterrorism.

In recent years in the United States, Salmonella spp and Escherichia coli have become the major causes of food poisoning responsible for epidemics that afflict millions, hospitalize hundreds, and kill many unsuspecting people.

The most common causes of foodborne disease include bacteria—Salmonella spp, Campylobacter spp, Shigella spp, and E. coli⁶⁶ (Table 44–1). In the last decade, large numbers of people have also suffered from food poisoning due to purposeful placement of chemicals in food,⁴¹ and staphylococcal toxin.¹⁵⁴

The differential diagnosis of patients with foodborne poisoning presenting with neurologic symptoms is vast (Tables 44–2 and 44–3). The sources of many of these cases are ichthyosarcotoxic, involving toxins from the muscles, viscera, skin, gonads, and mucous surfaces of the fish; rarely, toxicity follows consumption of the fish blood or skeleton. Shellfish poisoning also must be considered. Most episodes of poisoning are not species specific, although particular forms of toxicity from Tetraodontiformes (puffer fish), Gymnothoraces (moray eel), and newts (Taricha and other species) are recognized.

In cases of ciguatera poisoning, the major symptoms usually are neurotoxic, and the gastrointestinal (GI) symptoms are minor. Scombroid poisoning, which is exceptionally common, is not associated with focal neurologic manifestations, but facial flushing, headache, and dysphagia are its major signs and symptoms.

Knowing where the fish was caught often helps establish a diagnosis, but refrigerated transport of foods and rapid worldwide travel can complicate that assessment. Travelers to Caribbean and Pacific islands, as well as those traveling within the United States, have experienced ciguatera poisoning.⁹⁶ In geographically disparate regions of Canada,¹³⁰ individuals have experienced domoic acid poisoning due to ingestion of cultivated mussels from Prince Edward Island.

In the differential diagnosis of foodborne poisons presenting with neurologic findings, activities other than eating must always be considered. In particular, sport divers often perform their activities in high-risk areas such as Florida, California, and Hawaii, and often during the high-risk periods from May through August. In the process, they may sustain a sting from a stingray tail, or laceration (from a deltoid or pectoral fin spine of a lionfish or stonefish) that can cause consequential marine toxicity (Chap. 119).

Ciguatera Poisoning

Ciguatera poisoning is one of the most commonly reported forms of vertebrate fishborne poisonings in the United States accounting for almost one-half of the reported cases.⁶⁶ Ciguatera poisoning is endemic to warm water, bottom dwelling reef fish living around the globe between 35° north and 35° south latitude, which includes tropical areas such as the Indian Ocean, the South Pacific, and the Caribbean. Hawaii and Florida report 90% of all cases occurring in the United States, most commonly from May through August.⁹⁸

More than 500 fish species have caused human cases of ciguatera poisoning, with the barracuda, sea bass, parrot fish, red snapper, grouper, amber jack, kingfish, and sturgeon the most common sources. The common factor is the comparably large size of the fish involved.

Large fish (4–6 lb or more) become vectors of ciguatera poisoning in accordance with complex feeding patterns inherent in aquatic life. Ciguatoxin can be found in blue-green algae, protozoa, and the free algae dinoflagellates. These plankton members of the phylum Protozoa are single-celled, motile, flagellated, pigmented organisms thriving through photosynthesis. Photosynthetic dinoflagellates such as Gambierdiscus toxicus and bacteria within the dinoflagellates are the origins of ciguatoxin.^51,77,104 Dinoflagellates are the main nutritional source for small herbivorous fish, which, in turn, are the major food source for larger carnivorous fish, thereby increasing the ciguatoxin concentrations in the flesh, adipose tissue, and viscera of larger and larger fish.¹¹

Ciguatoxin is heat stable, lipid soluble, acid stable, odorless, and tasteless. When purified, the toxin is a large (molecular weight: 1100 Da) complex ester that does not harm the fish but is stored in its tissues.^100,105 The molecule binds to voltage-sensitive sodium channels in diverse tissues and increases the sodium permeability of the channel.^10,159 The ciguatoxins cause hyperpolarization and a shift in the voltage dependence of channel activation, which opens the sodium channels. Ciguatoxins bind selectively to a particular binding site on the neuron’s voltage-sensitive sodium channel protein.¹⁰³

Multiple ciguatoxins are identified in the same fish, perhaps explaining the variability of symptoms and differing severity.¹⁰⁴ People can be afflicted after eating fresh or frozen fish that was prepared by all common methods: boiling, baking, frying, stewing, or broiling. The appearance, taste, and smell of the ciguatoxic fish are usually unremarkable. The majority of symptomatic episodes begin 2 to 6 hours after ingestion, 75% within 12 hours, and 96% within 24 hours.¹¹ Symptoms include acute onset of diaphoresis; headaches, abdominal pain with cramps, nausea, vomiting; profuse watery diarrhea; and a constellation of dramatic neurologic symptoms.¹⁷⁵ A sensation of loose or painful teeth may occur. Typically, peripheral dysesthesias and paresthesias predominate. Watery eyes, tingling, and numbness of the tongue, lips, throat, and perioral area occur. A strange metallic taste is frequently reported as is a reversal of temperature discrimination, the pathophysiology of which remains to be elucidated.²⁸ Myalgias, most often in the lower extremities, arthralgias, ataxia, and weakness are commonly experienced.¹¹

Dysuria⁶⁴ and symptoms of dyspareunia and vaginal and pelvic ­discomfort may occur in women after sexual intercourse with men who are ciguatoxic and whose semen contains the toxin.⁹⁵ Vertigo, seizures, and visual disturbances such as blurred vision, scotomata, and transient blindness) are reported.

Bradycardia and orthostatic hypotension are described.⁶⁰ The GI symptoms usually subside within 24 to 48 hours; however, cardiovascular and neurologic symptoms may persist for several days to weeks, depending on the amount of toxin ingested. Delayed effects may include protracted itching and hiccoughs. Although deaths are reported, internationally none have been documented in the United States.⁶⁶ When it occurs, mortality is a result of respiratory paralysis and seizures not managed with adequate life support. Ciguatoxin may be transmitted in breast milk²⁰ and can cross the placenta.¹²⁸

Laboratory analysis using an enzyme-linked immunosorbent assay (ELISA) test for ciguatera toxin can be performed; alternatively, high-­pressure liquid chromatography (HPLC) is accurate. A dipstick immunobead assay test being developed for field use will allow testing of fish without laboratory processing of the toxin-containing tissues.^10,75,127 A useful approach to diagnosis and management includes laboratory testing to exclude other diagnostic possibilities and determine the need for, or extent of, specific therapeutic interventions.

Initial treatment for victims of ciguatoxin poisoning includes standard supportive care for a toxic ingestion.¹⁷⁵ In most patients, elimination of the toxin is accelerated if vomiting (40%) and diarrhea (70%) have occurred. Administration of activated charcoal may be of some benefit. In patients with significant GI fluid loss through vomiting, diarrhea, or both, intravenous fluid and electrolyte repletion are essential. The orthostatic hypotension may respond to intravenous fluids and α-adrenergic agonists. Bradycardia may be treated with atropine.⁵⁷

Intravenous mannitol may alleviate neurologic and muscular dysfunctional symptoms associated with ciguatera; however, GI symptoms are not ameliorated.^126,129 In one randomized controlled trial, mannitol failed to produce any greater improvement in symptoms than did intravenous 0.9% sodium chloride solution.¹⁴⁷ Mannitol should be used with caution because it may cause hypotension. Vascular reexpansion and cardiovascular stability should be initial treatment priorities. Mannitol may work by inhibiting the ciguatoxin-induced opening of sodium channels on the neuron membranes or reducing the neural edema via an osmotic gradient.

Admission to the hospital for cautious supportive care is essential when the diagnosis is uncertain or when volume depletion or any consequential manifestations are present (Tables 44–2 and 44–3). The etiology of the symptoms must be rapidly identified to provide specific therapy, if available. Diaphoresis is a common clinical finding and an important factor in the differential diagnosis. Late in the course of ciguatera poisoning, amitriptyline 25 mg orally twice daily may alleviate symptoms,²³ which may persist up to 1 year. Victims recovering from ciguatera should avoid alcohol and nuts for 3 to 6 months if exposure exacerbates symptoms.

Ciguateralike Poisoning

Moray, conger, and anguillid eels carry a ciguatoxinlike neurotoxin in their viscera, muscles, and gonads that does not affect the eel itself. The toxin is a complex ester that may be structurally very similar to ciguatoxin and is heat stable.¹²³ Individuals who eat these eels may manifest neurotoxic symptoms similar to ciguatoxin or may show signs of cholinergic toxicity, such as hypersalivation, nausea, vomiting, and diarrhea. Shortness of breath, mucosal erythema, and cutaneous eruptions may also occur. These findings may be present in addition to the neurotoxic symptoms.⁷¹ Management is supportive. Mortality is related to the complications of neurotoxicity, such as seizures and respiratory paralysis.

Shellfish Poisoning

Healthy mollusks living between 30° North and 30° South latitude ingest and filter large quantities of dinoflagellates. These dinoflagellates are the major source of available ocean food during the “non-R” months (May through August) in the northern hemisphere. During this time, these dinoflagellates are responsible for the “red tides” that may be seen from California to Alaska, from New England to the St. Lawrence, and across the west coast of Europe.¹¹⁰ The number of toxic dinoflagellates may be so overwhelming that birds and fish die, and humans who walk along the beach may experience respiratory symptoms caused by aerosolized toxin.¹¹²

Ingestion of shellfish, including oysters, clams, mussels, and scallops, contaminated by dinoflagellates or algae may cause neurotoxic, paralytic, and amnestic syndromes. The dinoflagellates most frequently implicated are Karenia brevis (originally named Gymnodinium breve in 1948, renamed Ptychodiscus brevis in 1979, and reclassified again to the current nomenclature in 2000). The diatoms causing neurotoxic shellfish poisoning include Protogonyaulax catanella and Protogonyaulax tamarensis, which cause paralytic shellfish poisoning; and Nitzschia pungens, the diatom implicated in amnestic shellfish poisoning. Proliferation of these diatoms may cause a red tide, but shellfish poisoning may occur even in the absence of this extreme proliferation.

Paralytic shellfish poisoning is caused by saxitoxin. Saxitoxin blocks the voltage-sensitive sodium channel in a manner identical to tetrodotoxin (TTX; see later). The shellfish implicated usually are clams, oysters, mussels, and scallops, but poisoning has occurred through consumption of crustaceans, gastropods, and fish.

The higher the number of shellfish consumed, the more severe the symptoms. Symptoms usually occur within 30 minutes of ingestion. Neurologic effects predominate and include paresthesias and numbness of the mouth and extremities, a sensation of floating, headache, ataxia, vertigo, muscle weakness, paralysis, and cranial nerve dysfunction manifested by dysphagia, dysarthria, dysphonia, and transient blindness. GI symptoms are less common and include nausea, vomiting, abdominal pain, and diarrhea. Fatalities may occur as a result of respiratory failure, usually within the first 12 hours after symptom onset. Muscle weakness may persist for weeks.

Treatment is supportive. Early intervention for respiratory failure is indicated. Orogastric lavage and cathartics were used to remove unabsorbed toxin from the GI tract but probably are not necessary or efficacious.^{26,101,116,152} Activated charcoal may be given. Antibodies against saxitoxin have reversed cardiorespiratory failure in animals,¹⁴ but this therapy is not yet available for humans. Assays for saxitoxin include a mouse bioassay, ELISA, and HPLC. High-pressure liquid chromatography has good interlaboratory accuracy,¹⁷⁰ but the differences in saxitoxin derivatives make standardization of an analytic test difficult.^9,97

Neurotoxic shellfish poisoning (NSP) is caused by brevetoxin. Brevetoxin, which is produced by Karenia brevis (previously Gymnodium brevis, and subsequently Ptychodiscus brevis), is a lipid-soluble, heat-stable polyether toxin similar to ciguatoxin. It acts by stimulating sodium flux through the sodium channels of both nerve and muscle.^6,29 NSP is characterized by gastroenteritis with associated neurologic symptoms. GI symptoms include abdominal pain, nausea, vomiting, diarrhea, and rectal burning. Neurologic features include paresthesias, reversal of hot and cold temperature sensation, myalgias, vertigo, and ataxia. Other effects may include headache, malaise, tremor, dysphagia, bradycardia, decreased reflexes, and dilated pupils. Paralysis does not occur. The combination of bradycardia and mydriasis is unusual. The incubation period is 3 hours (range 15 minutes to 18 hours). GI and neurologic symptoms appear simultaneously. Other manifestations of brevetoxin poisoning include mucosal irritation, cough, and bronchospasm, which occur when P. brevis is aerosolized by wave action during red tides. The duration of effects averages 17 hours (range 1–72 hours).¹¹⁶

Brevetoxins can be assayed using mouse bioassay, ELISA, and, more recently, antibody radioimmunoassay and reconstituted sodium channels.^132,167 Treatment is supportive, and severe respiratory depression is very uncommon. Therapy includes removal of the patient from the environment and the administration of bronchodilators. Neurotoxic shellfish poisoning is not fatal.

Amnestic shellfish poisoning is caused by domoic acid, a structural analogue of glutamic and kainic acids produced by the diatom N. pungens. The most extensively documented human outbreak occurred in Canada in 1987, when 107 individuals who had consumed mussels harvested from cultivated river estuaries on Prince Edward Island were affected.¹³⁰ Other human outbreaks may have occurred due to a similar diatom—Pseudonitzschia australis—which has been isolated in shellfish from other areas.⁵⁸ Pelican deaths caused by domoic acid–laden anchovies were reported in 1991 and Canada instituted monitoring for domoic acid after this outbreak.¹⁶⁴ The death of 400 sea lions in California in 1998 was linked to domoic acid from the same diatom.¹⁴⁸

Amnestic shellfish poisoning is characterized by GI symptoms of nausea, vomiting, abdominal cramps, diarrhea, and by neurologic symptoms of memory loss and, less frequently, coma, seizures, hemiparesis, ophthalmoplegia, purposeless chewing, and grimacing. Other signs and symptoms include hemodynamic instability and cardiac dysrhythmias. Symptoms typically begin 5 hours (range 15 minutes to 38 hours) after ingestion of mussels. The mortality rate is 2%, with death most frequently occurring in older patients, who experience more severe neurologic symptoms. Ten percent of victims may have long-term antegrade memory deficits, as well as motor and sensory neuropathy. Postmortem examinations have revealed neuronal damage in the hippocampus and amygdala.¹⁶³

Tetrodotoxin Poisoning

This type of fish poisoning involves only the order Tetraodontiformes. Although this order of fish is not restricted geographically, it is eaten most frequently in Japan, California, Africa, South America, and Australia.⁷¹ Cases have also occurred in Florida and New Jersey, as well as Europe, the Mediterranean, and Bangladesh. Approximately 100 freshwater and saltwater species exist in this order, including a number of pufferlike fish such as the globe fish, balloon fish, blowfish, and toad fish.¹¹⁸ TTX found in these fish is also isolated from the blue-ringed octopus⁵⁵ and the gastropod mollusk,¹⁷⁷ and has also been responsible for fatalities from ingestion of horseshoe crab eggs.⁸¹ Certain TTX containing newts (Taricha, notophthalmus, triturus, and cynops), particularly Taricha granulosa, found in Oregon, California, and southern Alaska, can be fatal when ingested. Most newts and salamanders with bright colors and rough skins contain toxins.²⁴ In Japan, fugu (a local variety of puffer fish) is considered a delicacy, but special licensing is required to prepare this exceedingly toxic fish. In 1989, the US Food and Drug Administration (FDA) legalized the importation of puffer fish. However, prior to exportation from Japan, the fish must be laboratory tested and certified by two Japanese organizations to be free of TTX.

TTX is a heat-stable (except in alkaline milieu), water-soluble nonprotein, found mainly in the fish skin, liver, ovary, intestine, and possibly muscle.^71,143 The ovary has a high concentration of the toxin and is most poisonous if eaten during the spawning season. TTX is detected by mouse bioassay. It is unstable when heated to 212°F (100°C) in acid, distinguishing it from saxitoxin. TTX from fish can be detected using fluorescent spectrometry⁹ or from the urine of poisoned patients using a combination of immunoaffinity chromatography and fluorometric HPLC.⁸²

TTX and saxitoxin are produced by marine bacteria and likely accumulate in animals higher on the food chain that consume these bacteria.¹²² Accumulation of toxins, primarily in the skin, of two species of Asian puffer fish has been documented. Whether this accumulation of toxin is simply an evolutionary adaptation, to remove a toxic substance, or one that has evolutionary advantages of protection is unclear.¹²¹

Neurotoxicity is produced by inhibition of sodium channels and blockade of neuromuscular transmission.^119,120 The sodium channel is blocked from the external surface of the neuron by the TTX molecule, which contains a guanidinium group that fits into the external orifice of sodium channel. This causes external “plugging” of the sodium channel, although the gating mechanism is functional.^119,120

Effects of tetrodotoxin poisoning typically occur within minutes of ingestion. Headache, diaphoresis, dysesthesias, and paresthesias of the lips, tongue, mouth, face, fingers, and toes evolve rapidly. Buccal bullae and salivation may develop. Dysphagia, dysarthria, nausea, vomiting, and abdominal pain may ensue. Generalized malaise, loss of coordination, weakness, fasciculations, and an ascending paralysis (with risk of respiratory paralysis) occur in 4 to 24 hours. Other cranial nerves may be involved. In more severe toxicity, hypotension is present. In some studies, mortality has approached 50%.¹⁵⁵

Therapy is supportive. Removal of the toxin and prevention of absorption are the essential measures. Supportive respiratory care emphasizing airway protection, including intubation, if necessary, is extremely important.

Less Common Poisonings: Echinoderms

The sea urchin usually causes toxicity by contact with its spinous processes, but this Caribbean delicacy also is toxic upon ingestion. When the sea urchin is prepared as food, the venom containing gonads should be removed because they contain an acetylcholinelike substance that causes the cholinergic syndrome of profuse salivation, abdominal pain, nausea, vomiting, and diarrhea. The sea star is considered edible by some individuals, although an asteriotoxin with saponinlike activity that produces nausea and vomiting is reported.

Careful evaluation of the symptoms and meticulous reporting to local and state health departments, as well as to the US Centers for Disease Control and Prevention (CDC), will allow for more precise analysis of epidemics of poisoning from contaminated or poisonous food or fish. Many states and countries have developed rigorous health codes with regard to harvesting certain species of fish in certain areas at certain times.

Some examples of actions taken by state and foreign health agencies in controlling epidemics of seafood-borne food poisoning are the following: A 3230-km stretch of Massachusetts coastline was noted to be unsafe for shellfish harvesting due to a red tide bloom. The state declared a health emergency and confiscated shellfish harvested in this area, and prohibited the marketing, export, and serving of shellfish.¹⁰⁹ The health code of Miami, Florida, prohibits the sale of barracuda and warns against eating fillets from large and potentially toxic fish containing ciguatoxin. The Japanese closely regulate preparation and selling of the puffer fish (fugu), requiring that preparers receive special training and licensing. The sale of fugu is now also permitted under strict control in the United States as well. The Canadian government marks the location and time of harvesting of mussels, and mussels are tested for the presence of domoic acid.^58,130

The initial differential diagnosis for acute diarrhea involves several etiologies: infectious (bacterial, viral, parasitic, and fungal), structural (including surgical), metabolic, functional, inflammatory, toxin induced, and food induced. The differential diagnosis is described in greater detail in Chap. 20.

An elevated temperature may be caused by invasive organisms, including Salmonella spp, Shigella spp, Campylobacter spp, invasive E. coli, Vibrio parahaemolyticus, and Yersinia spp, as well as some viruses. Episodes of acute gastroenteritis not associated with fever can be caused by organisms producing toxins, including Staphylococcus aureus, Bacillus cereus, Clostridium perfringens, enterotoxigenic E. coli, and viruses.³

Fecal leukocytes typically are found in patients with invasive shigellosis, salmonellosis, Campylobacter enteritis, typhoid fever, invasive E. coli colitis, V. parahaemolyticus, Yersinia enterocolitica, and inflammatory bowel disease. In all of these conditions, except typhoid fever, the leukocytes are primarily polymorphonuclear; in typhoid fever, they are mononuclear. No stool leukocytes are noted in cholera, viral diarrhea, noninvasive E. coli diarrhea, or nonspecific diarrhea.⁷⁴

The timing of diarrhea onset after exposure or the incubation period can be useful in differentiating the cause. Extremely short incubation periods of less than 6 hours are typical for Staphylococcus, B. cereus (type I), enterotoxigenic E. coli,^3,107,162 and preformed enterotoxins, as well as roundworm larvae ingestions. Intermediate incubation periods of 8 to 24 hours are found with C. perfringens, B. cereus (type II enterotoxin), enteroinvasive E. coli,^49,114 and salmonella. Longer incubation periods occur in other bacterial causes of acute gastroenteritis (Table 44–4).

The three most likely etiologies of diarrhea are infectious, xenobiotics (chemicals found in an organism, not normally present, frequently a pollutant or contaminant), and foodborne. These three etiologies are not mutually exclusive. The differential diagnosis must be made among these groups. When the time from exposure to onset of symptoms is brief, all of the nonbacterial infectious etiologies (viral, parasitic, fungal, and algal) except for upper GI invasion by roundworm larvae can be eliminated. The possibility of a bacterial etiology with enterotoxin production should be considered (Table 44–4).^3,21

Epidemiologic analysis is of immediate importance, particularly when GI diseases strike more than one person in a group. The questions raised in Table 44–5 must be answered.¹⁴² If available, an infectious disease consultant or infection control officer should be called for assistance. Alternatively, assistance from state and local health departments should be sought. Often, only the CDC or state health department has the resources to investigate and confirm a presumptive diagnosis in an outbreak. Sophisticated techniques such as toxin detection, matching the organism in the food by phage type with a food handler, matching an organism by phage type with other persons, isolating 10 or more organisms per gram of implicated food,^49,52 or polymerase chain reaction (PCR) identification of bacterial or plasmid DNA are potentially useful, although generally not possible using the laboratory and personnel available in most hospitals.^27,32,65 Structural, metabolic, and functional causes often can be eliminated. As in these diseases, neither a significant grouping of cases nor a limited clinical history is characteristic. Foodborne parasites such as Trichinella spiralis (trichinosis), Toxoplasma gondii (toxoplasmosis), and G. lamblia (giardiasis) must be considered, although acute GI symptoms are not usually prominent.

Salmonella Species

Salmonella enteritidis infections are of great concern in the United States. Two particular outbreaks define very special problems. In the 1980s, recurrent outbreaks associated with grade A eggs or food containing such eggs occurred. In the past, such outbreaks of salmonella enteritis were attributed to infection of the egg with salmonella (from the chicken’s GI tract) through cracks in the shell. More recently, outbreaks have involved noncracked, nonsoiled eggs.¹¹⁵ In these cases, presumably the salmonella has infected the eggs before the shell was formed. In either case, people who consume raw or undercooked eggs are at most risk for salmonella enteritis. Raw eggs can be found as ingredients of chocolate mousse, hollandaise sauce, eggnog, Caesar salads, and homemade ice cream. Whole, partially cooked eggs are problematic when eaten sunny side up or poached.³⁷ The second group of outbreaks was associated with raw milk,¹³³ which has become very popular in certain communities. Inadequate microwave cooking may cause small outbreaks.⁵³ These outbreaks are of great concern because they frequently involve multiple drug resistant salmonella infections.⁴⁵ Drinking pasteurized milk may not be protective. An outbreak of salmonellosis resulting in more than 16,000 culture-proven cases was traced to one Illinois dairy. The probable cause of the outbreak was a transfer line connecting raw and pasteurized milk containment tanks.¹³⁹

The contamination of food that is widely distributed places thousands at risk. An outbreak of salmonella food poisoning from peanut butter caused 529 confirmed illnesses in 48 states and Canada, 116 hospitalizations, and possibly eight deaths.⁴⁰ The CDC estimates that the proportion of salmonella infections that are confirmed by laboratory testing is 3% of the total, so the estimated number of infected people affected by this contamination incident may be more than 15,000. News reports state that the peanut butter contamination with salmonella was known, and that the peanut butter was retested for contamination, until no salmonella was reported. The peanut butter was then nationally distributed.⁷³

Additional concern has developed over the widespread use of anti-biotics in animal feed, responsible for meats, poultry, and manure-fertilized vegetables now frequently containing resistant bacterial strains to which virtually the entire population may be exposed.^45,139“Household” pets such as chicks, turtles, and iguanas host salmonella and frequently transmit the organism to household contacts, including infants, who are at particular risk for invasive diseases, as well as other family members.¹

The hemolytic uremic syndrome (HUS) is frequently caused by a bacterial gastroenteritis. The most commonly responsible organism is E. coli O157:H7.⁶⁸ Other bacteria and xenobiotics cause the same findings.

Typical laboratory findings in HUS include microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury.

HUS begins with a prodrome of diarrhea 90% of the time. The diarrhea lasts for 3 to 4 days and frequently becomes bloody. Abdominal pain due to colitis is common, and vomiting, altered mental status (irritability or lethargy), pallor, and low-grade fever frequently occur. At presentation, many have oliguria or anuria, and 10% of children have a generalized seizure at HUS onset.¹⁵¹

HUS is frequently associated with enterohemorrhagic E. coli (EHEC) or E. coli O157:H7 with postdiarrheal HUS.^{25,109,124,125,137,172} Food products from cattle (ground beef, milk, yogurt, cheese) and water contaminated with fecal material are EHEC sources.^48,111 Contaminated water used in gardens and unpasteurized apple cider have caused bloody diarrhea and HUS as a result of EHEC.^16,44

EHEC, including E. coli O157:H7, produces a toxin similar to the toxin produced by Shigella dysenteriae type I, referred to as Shigalike toxin (SLT) or verotoxin.²¹ The proposed mechanism for SLT damage is intestinal absorption, bloodstream access to renal glomerular endothelium, intracellular adsorption via glycolipid receptors, ribosomal inactivation, and cell death.¹⁶¹ In animal models, organ damage is more severe if endothelial cells have high concentrations of globotriaosylceramide receptors, which have a high binding affinity for Shiga toxin. Other organs with these receptors include the kidney, GI, and central nervous systems, which may explain the pattern of organ damage in children with HUS. Endothelial cell damage and other pathologic processes, including platelet and leukocyte activation, triggering of the coagulation cascade, and the production of cytokines, occur.^83,169 More than one type of SLT exists; SLT-1, SLT-2, and variants of SLT-2 structure are identified.¹⁷

Detection of E. coli O157:H7 through stool culture early in the course of disease is useful. The recovery decreases after the first week of illness.¹⁶¹E. coli O157:H7 almost always produces SLT; therefore, if stool cultures are negative, enzyme immunoassay (EIA) and PCR tests can be used to detect SLT in the stool when E. coli can no longer be identified by culture.²⁷

Treatment of HUS should focus on meticulous supportive care, with fluid and electrolyte balance the priority. Dialysis should be instituted early for azotemia, hyperkalemia, acidosis, and fluid overload. Red blood cells and platelet transfusions may be required. Hypertension should be treated with short-acting calcium channel blockers (nifedipine 0.25–0.5 mg/kg/dose orally) and seizures with benzodiazepines. Plasmapheresis has been used in nondiarrheal HUS and in recurrent HUS after renal transplants. Anti–SLT-2 antibodies have protected mice from SLT-2 toxicity, but intravenous immunoglobulin with SLT-2 activity has not improved outcome in children with HUS. A double-blind, placebo-controlled study on the use of synthetic SLT receptors attached to an oral carrier found that mortality or serious morbidity of HUS syndrome did not change as a result.¹⁶⁶

The mortality from HUS with good supportive care is approximately 5%; another 5% of victims suffer end-stage kidney disease or cerebral ischemic events and chronic neurologic impairment. Prolonged anuria (>1 week), oliguria (>2 weeks), or severe extrarenal disease may serve as markers for higher mortality and morbidity.¹³¹

There is some evidence that early treatment with antibiotics increases the risk of development HUS in children with E. coli O157:H7 infections.¹⁵⁶ An earlier meta analysis and randomized trial did not find this association.^134,140 Due to this concern, many experts recommend not treating patients with clinical or epidemiologic presentations consistent with E. coli O157:H7 infections (crampy abdominal pain, bloody diarrhea, regional outbreak) until a definitive pathogen can be identified.

Strategies to prevent the spread of E. coli O157:H7 and subsequent HUS include public education on the importance of thorough cooking of beef to a “well-done” temperature of 170°F (77°C), pasteurization of milk and apple cider, and thorough cleaning of vegetables. Public health measures include education of clinicians to consider E. coli O157:H7 in patients with bloody diarrhea and insuring the routine capability of microbiology laboratories to culture E. coli O157:H7 and provide for EIA or PCR determination of SLT. Public health departments should provide active surveillance systems to identify early outbreaks of E. coli O157:H7 infection.

Staphylococcus Species

In cases of suspected food poisoning with a short incubation period, the physician should first assess the risk for staphylococcal causes. The usual foods associated with staphylococcal toxin production include milk products and other proteinaceous foods, cream-filled baked goods, potato and chicken salads, sausages, ham, tongue, and gravy. Pie crust can act as an insulator, maintaining the temperature of the cream filling and occasionally permitting toxin production even during refrigeration.⁴ A routine assessment must be made for the presence of lesions on the hands or nose of any food handlers involved. Unfortunately, carriers of enterotoxigenic staphylococci are difficult to recognize because they usually lack lesions and appear healthy.⁷⁶ A fixed association between a particular food and an illness would be most helpful epidemiologically but rarely occurs clinically. Factors such as environment, host resistance, nature of the agent, and dose make the results surprisingly variable.

Although patients with staphylococcal food poisoning rarely have significant temperature elevations, 16% of 2992 documented cases in a published review had a subjective sense of fever.⁷⁶ Abdominal pain, nausea followed by vomiting, and diarrhea dominate the clinical findings. Diarrhea does not occur in the absence of nausea and vomiting. The mean incubation period is 4.4 hours with a mean duration of illness of 20 hours. Two staphylococcal enterotoxin food poisoning incidents involving large numbers of people have been reported. At a public event in Brazil in 1998, one-half of the 8000 people who attended had nausea, emesis, diarrhea, abdominal pain, and dizziness within hours of consuming food. Of the ill patients, 2000 overwhelmed the capacity of local emergency departments, 396 (20%) were admitted including 81 to intensive care units, and 16 young children and elderly participants died.¹⁵⁴ In another report, 328 individuals became ill with symptoms of diarrhea, vomiting, dizziness, chills, and headache after eating cheese or milk.¹⁵³ In both reports, staphylococcus enterotoxin was found in the food consumed.

Most enterotoxins are produced by S. aureus coagulase–positive species. The enterotoxins initiate an inflammatory response in GI mucosal cells and lead to cell destruction. The enterotoxins also may exert a sudden explosive effect on the emesis center in the brain and diverse other organ systems. Discrimination of unique S. aureus isolates from those found in foodborne outbreaks can be made using restriction fragment length polymorphism analysis by pulsed-field gel electrophoresis and PCR techniques.¹⁷³

Bacillus cereus

Another foodborne toxin with GI symptoms is associated with eating reheated fried rice. Bacillus cereus type I is the causative organism, and bacterial overgrowth and toxin production causes consequential early onset nausea and vomiting.² Infrequently this toxin causes liver failure.¹⁰⁸ Bacillus cereus type II has a delayed onset of similar GI symptoms, including diarrhea.⁵⁹

Campylobacter jejuni

Campylobacter jejuni is a major cause of bacterial enteritis. The organism is most commonly isolated in children younger than 5 years and in adults 20 to 40 years of age. Campylobacter enteritis outbreaks are more common in the summer months in temperate climates. Although most cases of Campylobacter enteritis are sporadic, outbreaks are associated with contaminated food and water. The most frequent sources of Campylobacter in food are raw or undercooked poultry products⁵⁴ and unpasteurized milk.¹⁵⁷ Birds are a common reservoir, and small outbreaks are associated with contamination of milk by birds pecking on milk-container tops.¹⁵⁷ Contaminated water supplies are also frequent sources of Campylobacter enteritis involving large numbers of individuals.¹⁹C. jejuni is heat labile; cooking of food, pasteurization of milk, and chlorination of water will prevent human transmission.

The incubation period for Campylobacter enteritis varies from 1 to 7 days (mean 3 days). Typical symptoms include diarrhea, abdominal cramps, and fever. Other symptoms may include headache, vomiting, excessive gas, and malaise. The diarrhea may contain gross blood, and leukocytes are frequently present on microscopic examination.⁷⁴ Illness usually lasts 5 to 6 days (range 1–8 days). Rarely, symptoms last for several weeks. Severely affected individuals present with lower GI hemorrhage, abdominal pain mimicking appendicitis, a typhoidlike syndrome, reactive polyarthritis (Reiter syndrome), or meningitis. The organism may be detected using PCR identification techniques.⁶² Treatment is supportive, and consists of volume resuscitation, and possibly antibiotics for the more severe cases.³

Group A Streptococcus

Bacterial infections not usually associated with food or food handling are nevertheless occasionally transmitted by food or food handling. Transmission of streptococcal pharyngitis in food prepared by an individual with streptococcal pharyngitis has been demonstrated.⁴⁶ A Swedish food handler caused 153 people to become ill with streptococcal pharyngitis when his infected finger wound contaminated a layer cake served at a birthday party.⁷

Clostridium botulinum

In the last 3 decades, a median of four cases of foodborne botulism, three cases of wound botulism, and 71 cases of infant botulism have been reported annually to the CDC.¹⁵⁰ Home-canned fruits and vegetables, as well as commercial fish products, are among the common foods causing botulism. The incubation period usually is 12 to 36 hours; typical symptoms include some initial GI symptoms, followed by malaise, fatigue, diplopia, dysphagia, and rapid development of small muscle incoordination.⁹⁸ In botulism, the toxin is irreversibly bound to the neuromuscular junction, where it impairs the presynaptic release of acetylcholine.⁹² A patient’s survival depends on rapidly diagnosing botulism and immediate initiation of aggressive respiratory therapy. Establishing the diagnosis early may make it possible to treat the “sentinel” or index patient and also others who consumed the contaminated food with antitoxin prior to their developing signs and symptoms (Chap. 41 and Antidotes in Depth: A6). The differential diagnosis of botulism includes myasthenia gravis, atypical Guillain-Barré syndrome, tick-induced paralysis, and certain chemical ingestions (Tables 41–1 and 41–2).

Yersinia enterocolitica

Yersinia enterocolitica causes enteritis most frequently in children and young adults. Typical clinical features include fever, abdominal pain, and diarrhea, which usually contains mucus and blood.^8,160,171 Other associated symptoms include nausea, vomiting, anorexia, and weight loss. The incubation period may be 1 to 7 days or more. Less common features include prolonged enteritis, reactive polyarthritis, pharyngeal and hepatic involvement, and rash. Yersinia is a common pathogen in many animals, including dogs and pigs. Sources of human infection include milk products, raw pork products, infected household pets, and person-to-person transmission.^22,70,99 The diagnosis may be based on cultures of food, stool, blood, and, less frequently, skin abscesses, pharyngeal cultures, or cultures from other organ tissues (mesenteric lymph nodes, liver). Yersinia may be identified by PCR.⁸⁴ Patients receiving the chelator deferoxamine (Antidotes in Depth: A7) may acquire yersinia infections due to the patients’ increased susceptibility. The deferoxamine-iron complex acts as a siderophore for organism growth. Therapy is usually supportive, but patients with invasive disease (eg, bacteremia, bacterial arthritis) should be treated with intravenous antibiotics. Fluoroquinolones and third-generation cephalosporins are highly bacteriocidal against Yersinia spp.

Listeria monocytogenes

Listeriosis transmitted by food usually occurs in pregnant women and their fetuses, the elderly, and immunocompromised individuals using corticosteroids or with malignancies, diabetes mellitus, kidney disease, or HIV infection.^15,34,36,146 Typical food sources include unpasteurized milk, soft cheeses such as feta, and undercooked chicken. Individuals at risk should avoid the usual sources and should be evaluated for listeriosis if typical symptoms of fever, severe headache, muscle ache, and pharyngitis develop. Treatment with intravenous ampicillin and aminoglycoside, or trimethoprim/­sulfamethoxazole is indicated for systemic Listeria infections.

Xenobiotic-Induced Diseases

In addition to the aforementioned saxitoxin TTX, domoic acid, and ciguatoxin, many other xenobiotics contaminate our food sources. Careful assessment for possible foodborne pesticide poisoning is essential. For example, aldicarb contamination has occurred in hydroponically grown vegetables and watermelons contaminated with pesticides.⁶⁷ Eating malathion-­contaminated chapatti and wheat flour resulted in 60 poisonings including a death in one outbreak⁴² (Chap. 113). Insecticides, rodenticides, arsenic, lead, or fluoride preparations can be mistaken for a food ingredient. These poisonings usually have a rapid onset of signs and symptoms after exposure.

The possibility of unintentional acute metal salt ingestion must also be considered. This type of poisoning most typically occurs when very acidic fruit punch is served in metal-lined containers. Antimony, zinc, copper, tin, or cadmium in a container may be dissolved in an acidic food or juice medium.

Mushroom-Induced Disease

Some species produce major GI effects. Amanita phalloides, the most poisonous mushroom, usually causes GI symptoms as well as hepatotoxic effects with a delay to clinical manifestations. The rapid onset of symptoms suggests some of the gastroenterotoxic mushrooms (Chap. 120).

Intestinal Parasitic Infections

The popularity of eating raw fish, or sushi, has led to an increase in reported intestinal parasitic infections. Etiologic agents are roundworms (Eustrongyloides anisakis) and fish tapeworms (Diphyllobothrium spp). Symptoms of anisakiasis may be upper intestinal (occur 1–12 hours after eating) or lower intestinal (delayed for days or weeks). Typical symptoms include nausea, vomiting, and severe crampy abdominal pain; with intestinal perforation severe pain, rebound, and guarding occur. A dietary history of eating raw fish is needed to establish diagnosis and therapy. Visual inspection of the larvae (on endoscopy, laparotomy, or pathologic examination) is useful. Treatment of intestinal infection involves surgical or laparoscopic removal. Anisakis simplex and Pseudoterranova decipiens are Anisakidae that may be found in several types of consumed raw fish, including mackerel, cod, herring, rockfish, salmon, yellow fin tuna, and squid. Reliable methods of preventing ingestion of live anisakid larvae are freezing at –4°F (–20°C) for 60 hours or cooking at 140°F (60°C) for 5 minutes.^{31,89,106,138,144,176}

Diphyllobothriasis (fish tapeworm disease) is caused by eating uncooked fish that harbor the parasite, including herring, salmon, pike, and whitefish. The symptoms are less acute than with intestinal roundworm ingestions and usually begin 1–2 weeks after ingestion.³⁰ Signs and symptoms include nausea, vomiting, abdominal cramping, flatulence, abdominal distension, diarrhea, and megaloblastic anemia. The diagnosis is based on a history of ingesting raw fish and on identification of the tapeworm proglottids in stool. Treatment with niclosamide, praziquantel, or paromomycin usually is effective.³⁵

Monosodium Glutamate

This clinical presentation is misnamed “Chinese restaurant syndrome” since it results from the ingestion of monosodium glutamate (MSG), which has multicultural use in the preparation of many foods. Affected individuals present with a burning sensation of the upper torso, facial pressure, headache, flushing, chest pain, nausea and vomiting, and, infrequently, life-threatening bronchospasm,³ and angioedema.^1,58 Intensity and duration of symptoms are generally dose related but with significant variation in individual responses to the amount ingested.^145,178 MSG causes “shudder attacks” or a seizurelike syndrome in young children. Absorption is more rapid following fasting, and the typical burning symptoms rapidly spread over the back, neck, shoulders, abdomen, and occasionally the thighs. GI symptoms are rarely prominent and symptoms can usually be prevented by prior ingestion of food. When symptoms do occur, they tend to last approximately one hour. The syndrome is a reaction to MSG, which had been commonly used in Chinese and many other restaurants. MSG is also marketed as an effective flavor enhancer.¹³ Many sausages and canned soups contain large doses of MSG.

MSG (regarded as “safe” by the FDA) can cause other acute and bizarre neurologic symptoms. There is evidence that humans have a unique taste receptor for glutamate.⁹¹ This explains its ability to act as a flavor enhancer for foods. Glutamate is also an excitatory neurotransmitter that can stimulate central nervous system neurons through activation of glutamate receptors, and may be the explanation for some of the neurologic symptoms described with ingestion.¹⁷⁹

Anaphylaxis and Anaphylactoid Presentations

Some foods and foodborne toxins may cause allergic or anaphylacticlike manifestations,⁸⁵ also sometimes referred to as “restaurant syndromes”¹⁴⁹ (Table 44–6). The similarity of these syndromes complicates a patient’s future approach to safe eating. Isolating the precipitant is essential so that the risk can be effectively assessed. Manufacturers of processed foods should provide an unambiguous listing of ingredients on package labels. Sensitive individuals (or in the cases of children their parents) must be rigorously attentive.^141,180 Those who experience severe reactions should make sure that epinephrine and antihistamines are always available immediately. Attempts to prevent allergic reactions to dairy products by avoiding dairy-containing foods may fail. Nondairy foods may still be processed in equipment used for dairy products or contain flavor enhancers of a dairy origin (eg, partially hydrolyzed sodium caseinate), both of which can cause morbidity and death in allergic individuals.⁶¹ Individuals with known food allergies do not always carry prescribed autoinjectable spring-injected epinephrine syringes, in some cases from a belief that the allergen is easily identifiable and avoidable.⁸⁵ Food additives that can cause anaphylaxis include ­antibiotics, aspartame, butylated hydroxyanisole, butylated hydroxytoluene, nitrates or nitrites, sulfites, and paraben esters.¹⁰² Regulation of these preservatives is limited, and xenobiotics such as sulfites are so ubiquitous that predicting which guacamole, cider, vinegar, fresh or dried fruits, wines, or beers contain these sensitizing agents may be impossible.

Scombroid Poisoning

Scombroid poisoning originally was described with the Scombroidae fish (including the large dark-meat marine tuna, albacore, bonito, mackerel, and skipjack). However, the most commonly ingested vectors identified by the CDC are nonscombroid fish, such as mahi mahi and amber jack.³³ All of the implicated fish species live in temperate or tropical waters. Ingestion of bluefish in New Hampshire was the probable cause of scombroid poisoning in five people,⁵² and in a large outbreak, tuna was the offender in 71 cases reported from a military outpost.⁴⁷ The incidence of this disease is probably far greater than was originally perceived. This type of poisoning differs from other fishborne causes of illness in that it is entirely preventable if the fish is properly stored following removal from the water.

Scombroid poisoning results from eating cooked, smoked, canned, or raw fish. The implicated fish all have a high concentration of histidine in their dark meat. Morganella morganii, E. coli, and Klebsiella ­pneumoniae, commonly found on the surface of the fish, contain a histidine decarboxylase enzyme that acts on a warm (not refrigerated), freshly killed fish, ­converting histidine to histamine, saurine, and other heat-stable ­substances. Although saurine has been suggested as the causative toxin, chromatographic analysis demonstrates that histamine is found as histamine phosphate and saurine is merely histamine hydrochloride.^56,117 The term saurine originated from saury, a Japanese dried fish delicacy often associated with scombroid poisoning. The extent of spoilage usually correlates with histamine concentrations. Histamine concentrations in healthy fish are less than 0.1 mg/100 g fish meat. In fish left at room temperature, the concentration rapidly increases, reaching toxic concentrations of 100 mg/100 g fish within 12 hours.

The appearance, taste, and smell of the fish are usually unremarkable.⁵ Rarely, the skin has an abnormal “honeycombing” character or a pungent, peppery taste that may be a clue to its toxicity. Within minutes to hours after eating the fish, the individual experiences numbness, tingling, or a burning sensation of the mouth, dysphagia, headache, and, of particular significance for scombroid poisoning, a unique flush characterized by an intense diffuse erythema of the face, neck, and upper torso.⁸⁶ Rarely, pruritus, urticaria, angioedema, or bronchospasm ensues. Nausea, vomiting, dizziness, palpitations, abdominal pain, diarrhea, and prostration may develop.^43,63,86,113

The prognosis is good with appropriate supportive care and parenteral antihistamines such as diphenhydramine. H₂-receptor antagonists such as cimetidine or ranitidine may also be useful in alleviating gastrointestinal symptoms.¹⁸ The toxic substance should be removed or absorbed from the gut. Inhaled β₂-adrenergic agonists and epinephrine may be necessary if bronchospasm is prominent. Patients usually show significant improvement within a few hours.

Elevated serum or urine histamine concentrations can confirm the diagnosis, but are usually unnecessary. If any uncooked fish remains, isolation of causative bacteria from the flesh is suggestive, but not diagnostic. A capillary electrophoretic assay makes rapid histamine detection possible.⁷⁹ Histamine concentrations greater than 50 mg/100 g fish meat are considered hazardous by the FDA; in Europe the concentrations are 100 to 200 mg/100 g.⁷⁹ Isoniazid may increase the severity of the reaction to scombroid fish by inhibiting enzymes that break down histamine.^78,168

Patients may be reassured that they are not allergic to fish if other individuals experience a similar reaction to eating the same fish at the same time, or if any remaining fish can be preserved and tested for elevated histamine concentrations. If this information is not available, then an anaphylactic reaction to the fish must be considered. Table 44–6 lists the differential diagnosis of flushing, bronchospasm, and headache. Because many people often consume alcohol with fish, alcohol must be considered an independent variable.

The differential diagnosis of the scombrotoxic flush apart from a disulfiramlike reaction includes ingestion of niacin or nicotinic acid, and pheochromocytoma. The history and clinical evolution usually establish the diagnosis quickly.

Global Food Distribution, Illegal Food Additives

Xenobiotics are given to animals to increase their health and growth. ­Clenbuterol, a β₂ agonist, has been administered to cattle raised for human consumption. The substance can cause toxicity in humans who eat contaminated animal meat. Tachycardia, tremors, nausea, epigastric pain, headache, muscle pain, and diarrhea were present in 50 poisoned patients. Other findings included hypertension and leukocytosis.¹³⁶ No deaths have been reported. The use of antibiotics, β₂ agonists, and other growth enhancers continues, despite safety concerns and laws against their use, because these practices increase yield and profit.

The globalization of food supplies and international agricultural trade has created a new global threat, the apparent purposeful contamination of food for profit. In 2008, almost 300,000 children in China were affected by melamine contamination of milk. Of these, 50,000 were hospitalized and 6 reported deaths occurred.

The melamine-contaminated milk was sold in China as powdered infant formula, with more than 22 brands containing melamine. The contamination was not limited to China, as melamine has been found in candy, chocolate, cookies, and biscuits sold in the United States, likely due to the adulteration of milk used in preparation of these products.

Melamine is a non-nutritious, nitrogen-containing compound, usually used in glues, plastics, and fertilizers. To increase profits, milk sold in China had previously been diluted, causing protein malnutrition in children. Because the nitrogen content of milk (a surrogate measure for protein content) is now carefully monitored to detect dilution and to prevent another episode of malnutrition, melamine was added to increase the measured nitrogen content and hide the dilution. This purposeful addition of melamine is suspected to be the cause of the melamine contamination of powdered milk in China.

Melamine and its metabolite cyanuric acid are excreted in the kidneys. Kidney stones containing melamine and uric acid were found in 13 children with acute kidney injury, who had consumed melamine containing milk formula.⁶⁹ Both melamine and cyanuric acid appear necessary to cause kidney stones in animals. The combination alone caused renal crystals in cats.¹³⁵ Melamine found in wheat gluten was added to pet food in 2007 resulted in thousands of complaints, and dozens of suspected animal deaths in the United States.

The melamine milk contamination is one of the largest reported deliberate food adulteration incidents. It affected about 300,000 Chinese infants and young children and caused six deaths.^41,80

Food products from all over the world find their way into our foods. Increased vigilance by the agencies responsible for food safety, both in countries where the food originates and in countries that import the food, is needed to prevent other events such as the melamine contaminations.

Vegetables and Plants

Plants, vegetables, and their diverse presentations often are involved in food poisonings.^{72,87,88,93,94} Edible plants and plant products may be poorly cooked or prepared, or they may be contaminated. Extensive discussion of this may be found in Chap. 121.

The threat of terrorist assaults has received increased attention and is discussed in Chaps. 132 and 133. The use of food as a vehicle for intentional contamination with the intent of causing mass suffering or death has already occurred in the United States.^38,90,165 In the first report, 12 laboratory workers had GI symptoms, primarily severe diarrhea, after consuming food purposefully contaminated with Shigella dysenteriae type II served in a staff break room.⁹⁰ Four workers were hospitalized; none had reported long-term sequelae. This Shigella strain rarely causes endemic disease. Nevertheless an identical strain, identified by pulsed-field gel electrophoresis, was found in eight of the 12 symptomatic workers, as well as in the pastries served in the break room, and in the laboratory stock culture of S. dysenteriae. This finding suggests purposeful poisoning of food eaten by laboratory personnel. The person responsible and the motive remain unknown.

The second case series describes a large community outbreak of food poisoning caused by Salmonella typhimurium.¹⁶⁵ The outbreak occurred in the Dalles, Oregon, area during the fall of 1984; a total of 751 people suffered salmonella gastroenteritis. The outbreak was traced to the intentional contamination of restaurant salad bars and coffee creamer by members of a religious commune using a culture of S. typhimurium purchased before the outbreak of food poisoning. A criminal investigation found a Salmonella culture on the religious commune grounds that contained S. typhimurium identical to the salmonella strain found in the food poisoning victims. It was identified by using antibiotic sensitivity, biochemical testing, and DNA restriction endonuclease digestion of plasmid DNA. Only after more than one year of investigation was this salmonella outbreak linked to terrorist activity. Reasons for the delay in identifying the outbreak as a purposeful food poisoning included (1) no apparent motive, (2) no claim of responsibility, (3) no pattern of unusual behavior in the restaurants, (4) no disgruntled restaurant employees identified, (5) multiple time points for contamination indicated by epidemic exposure curves, suggesting a sustained source of contamination and not a single act, (6) no previous event of similar nature as a reference, (7) the likeliness of other possibilities (eg, repeated unintentional contamination by restaurant workers), and (8) fear that the publicity necessary to aid the investigation might generate copycat criminal activity.

Publication of the event was delayed by almost 10 years out of fear of unintentionally encouraging copycat activity. On the other hand, use of biological weapons by the Japanese cult Aum Shinrikyo appears to have motivated authorities to release this publication in the hopes of quickly identifying similar deliberate food poisoning patters in the future.

A third report describes a disgruntled employee who contaminated 200 lb of meat at a supermarket with a nicotine-containing insecticide.³⁸ Ninety-two people became ill, and four sought medical care. Symptoms included vomiting, abdominal pain, rectal bleeding, and one case of atrial tachycardia.

In another case of human greed, a Chinese restaurant owner poisoned the food in his neighbor’s restaurant with tetramine. Tetramine or tetramethylenedisulfotetramine is a highly lethal neurotoxic rodenticide, once used worldwide, now illegal in the United States. The snack shop owner caused hundreds to become ill and 38 deaths by spiking his competitors breakfast offerings (fried dough sticks, sesame cakes, and sticky rice balls). Tetramethylenedisulfotetramine is an odorless and tasteless white crystal that is water-soluble. The mechanism of action is noncompetitive irreversible binding to the chloride channel on the γ-aminobutyric acid receptor complex, which blocks the influx of chloride and alters the neurons potential. It is referred to as a “cage convulsant” because of its globular structure. Severe toxicity presents with tachycardia, dysrhythmias, agitation as well as status epilepticus and coma. Immediate or early treatment with sodium-(RS)-2,3-dimercaptopropane-1-sulfonate (DMPS) and pyridoxine (vitamin B6) appears to be effective in a mouse model.^12,50,174

The capacity of foodborne xenobiotics that are easy to obtain and disburse to infect large numbers of people is clearly exemplified by two specific outbreaks: (1) the purposeful salmonella outbreak in Oregon, (2) the apparently unintentional salmonella outbreak that resulted in more than 16,000 culture-proven cases traced to contamination in an Illinois dairy. The probable cause of the outbreak was a contaminated transfer pipe connecting the raw and pasteurized milk containment tanks.¹³⁹ These events emphasize the vulnerability of our food supply and the importance of ensuring its safety and security.

• The diverse etiologies of food poisoning involve almost all aspects of toxicology.

• Our concerns center around the natural toxicity of plants or animals, the contamination of which can occur in the field, during factory processing, subsequent transport and distribution, or during home preparation or storage.

• Whether these events are intentional or unintentional, they alter our approaches to general nutrition and society.

• Issues in food safety include the governmental role in food preparation and protection, bacteria such as Salmonella and E. coli0157:H7, prions in Creutzfeldt-Jacob disease (bovine encephalopathy), and genetically altered materials such as corn.

• Future discussions of food poisonings and interpretations of the importance of these problems may dramatically alter our food sources and their preparation and monitoring.

References