Food-Borne Illness: Differential Diagnosis and Targeted Management
Authors: Charles M. Seamens, MD, FACEP, Assistant Professor of Emergency Medicine, Vanderbilt University, Nashville, TN.
Gary Schwartz, MD, FAAP, Assistant Professor of Emergency Medicine, Vanderbilt University, Nashville, TN.
Editor: Gideon Bosker, MD, Assistant Clinical Professor, Section of Emergency Services, Yale University School of Medicine, Associate Clinical Professor, Oregon Health Sciences University, Portland.
Peer Reviewer: Steven M. Winograd, MD, FACEP, Attending Physician, Department of Emergency Medicine, Lakeland Regional Health System, St. Joseph, MI.
Editor's Note-When patients seek advice about whether they may have contracted a food-borne illness, it is important that the physician is able to determine what is and is not a foodborne illness, treat the problem, and counsel the patient appropriately. When the index of suspicion for a food-borne illness is high, this information should be reported to the local health department authorities for definitive diagnosis and epidemiological management.
More than 250 different diseases and syndromes have been associated with contaminated food or drink.1 Estimates of the number of cases of food-borne disease in the United States range from 6.5 to 81 million cases per year, with from 525 to more than 7000 associated deaths.1 More precise estimates are lacking for two reasons: 1) Patients with food-borne disease often do not seek medical care because the symptoms are mild and self-limited; and 2) oftentimes, the patient or clinician does not recognize the link between food and the illness.1 In fact, it is estimated that fewer than 5% of food poisoning cases are recognized and reported.2
The risk of food-borne illness depends on the type of food, its source of production, how it is prepared and handled, and the consuming host's resistance to the infectious agent.1 The great majority of food items that cause these diseases are raw or undercooked foods of animal origin, such as meat, milk, eggs, cheese, fish, or shellfish.3
Background
The number of food poisoning cases in the United States are increasing, in large part because the eating habits of many Americans have changed over the years. In this regard, Americans have increased consumption of food prepared by commercial service establishments, where food service workers and handlers may be hired with inadequate training or attention to proper sanitation and hygiene. In addition, fresh fruit, vegetables, and other cold food items are now mass produced and sold through large and complex distribution networks, where sanitation quality assurance standards are suboptimal. Imported foods comprise an increasing proportion of the diet and, oftentimes, are shipped from developing countries where food hygiene and basic sanitation measures and protocols are poorly monitored.3 The size and complexity of these operations can magnify the public health significance of food-borne contamination.1
The most common foodborne diseases are infections caused by such bacteria as Salmonella and Campylobacter, or by viruses, such as Norwalk or hepatitis A.3 Food poisoning caused by bacteria comprises about two-thirds of U.S. poisoning outbreaks linked to a known etiology.4 Specifically, about 75% of reported cases of bacterial food poisoning in the United States can be traced to Campylobacter, Salmonella, Staphylococcus, and Clostridium perfringens. The pathogenesis of diarrhea associated with foodborne illness involves either a) the production of enterotoxin causing secretory diarrhea; b) inflammation from a cytotoxin; or c) direct invasion of intestinal mucosa by the organism.5 Toxin-mediated gastroenteritis is caused by ingestion of performed toxin or by toxin produced after ingestion and is characterized by watery diarrhea and the absence of fever, vomiting, or bloody diarrhea.5 Syndromes caused by ingestion of performed toxins are characterized by a shorter incubation period of 1-6 hours and a shorter duration of illness, usually less than 12 hours.5 In contrast, syndromes caused by in vivo production of toxin or by direct mucosal invasion are characterized by a longer incubation period (6-72 h) and a longer duration of illness (1-10 d).5 (See Table 1.) One clinical feature that suggests a toxin or chemical etiology rather than an infectious cause is the simultaneous occurrence of gastrointestinal and neurologic signs and symptoms.6
Spectrum of Food-Borne Syndromes
Campylobacter. Campylobacter has surpassed salmonella to become the most common cause of bacterial food poisoning.7 This is somewhat surprising since the organism was not considered a human pathogen until the 1970s; currently more than 2 million cases of human Campylobacter infections are reported in the United States each year.8 Interestingly, one factor that has been cited to explain the increased incidence of Campylobacter infections, is the change in food consumption, away from red meat in favor of poultry in a cholesterol-conscious socitey.
Campylobacter, which infects more than half of the chickens in the United States,9 requires a body temperature of approximately 40°C for incubation, making poultry an ideal source host.10 Also contributing to the high rate of infection are the methods by which chickens are raised. Most chickens sold in the United States are produced by the broiler method, which involves raising large number of chickens in enclosed areas with unlimited food and water. These chickens frequently become infected within the first two or three weeks of life and remain infected until they are harvested at 6-7 weeks of life. In addition to becoming infected in the chicken houses, chicken meat can also be cross-contaminated when infected chicken meat is mixed with non-infected meat at the processing plant. Water, unpasteurized milk, and red meat are less common sources of Campylobacter infection. Sick pets, such as dogs and cats, may also be a source of infection.11 Campylobacter is rarely spread person-to-person. If this does occur, it is usually spread among young children.
Campylobacter is derived from a greek word meaning "curved rod." There are multiple species of Campylobacter but only four that are pathogenic in humans-C. jejuni, C. coli, C. lari, and C. upsaliensis. Most important of these species is C. jejuni, which causes 90% of human infections.12 From an epidemiological perspective, infections tend to occur in children younger than 4 years and in adults 15-44 years of age. The peak time of the year for Campylobacter infections is May-June, although, most cases of food poisoning caused by campylobacter are sporadic, making it more difficult to identify the exact source.
Campylobacter has an incubation period of 1-7 days, with most patients developing symptoms within 24-72 hours. The organism can cause a range of symptoms from mild diarrhea of brief duration to severe diarrhea, cramps, and gastrointestinal bleeding. In most cases the disease is self limiting, lasting 3-5 days. Malaise may follow for a period of 1-2 weeks. In addition to the gastrointestinal complaints, patients may present with influenza-like symptoms and may have a fever as high as 39-40°C.
Complications from Campylobacter are rare and include bacteremia, which is seen in approximately 1% of infected patients and, for the most part, is generally limited to neonates, the elderly, and immunocompromised patients.13 Of special note is the fact that bacteremic patients are at risk for developing meningitis, cholecystitis, and urinary tract infections. Late complications include Guillain Barré Syndrome (GBS) and reactive arthritis.14 In fact, it is estimated that up to 40% of GBS may be caused by Campylobacter infection; this complication typically occurs anywhere from one to three weeks after the initial infection.14 Fortunately, death from Campylobacter is a rare complication.
Treatment measures beyond supportive care are required only for high-risk patients, such as neonates, the elderly, and immunocompromised patients. Treatment for neonates consists of erythromycin and, for adults, is either erythromycin (500 mg twice a day for 5 days) or a fluoroquinolone. Local resistance patterns should also be considered since there is increasing resistance to fluoroquinolones. Although the disease is self limited, about 10% of infected patients will require hospitalization.7 Patients may return to work at any time, unless they are involved in catering or health care-related activities, in which case they should return to work only after symptoms have resolved. There is no need to reculture infected patients who have improved clinically.
Salmonella. Salmonella is the second most common cause of food poisoning.7 Although Salmonella is ubiquitous, its primary reservoir is in the intestinal tracts of infected or colonized animals, such as chicken, cattle, and pigs, which are sources that commonly infect humans. While fresh fruit and vegetables are less likely to carry Salmonella, Salmonella can be spread though consumption of eggs. In the past, fecal contamination through small cracks in the egg shell lead to infected eggs. This method of contamination is much less likely due to improved sanitary conditions. Presently, most eggs become contaminated through transovarian spread with an intact shell. Still, it is estimated that each year one in every 50 egg consumers will be exposed to Salmonella-contaminated eggs; overall, about three-quarters of all Salmonella enteritis outbreaks being traced back to infected eggs.15 In the past, pet turtles spread Salmonella to children, but these turtles have been banned from sale since 1975.
Interestingly, Salmonella food poisoning is more common in industrialized countries than it is in less developed, emerging countries where good sanitation is less common. It has been suggested that less developed countries tend to grow food locally and process it on a smaller scale, which minimizes cross contamination. Additional reasons for higher infection rates among industrialized countries include the practice of feeding animals meat packing byproducts, which may be infected, and overcrowding on farms and in slaughter houses.
Salmonella is a gram-negative rod that causes infection through ingestion of the organism. There are several thousand subtypes of Salmonella, but fewer than 200 of these infect humans. Approximately one-half of Salmonella infections are caused by S. typhimurium and S. enteriditis.16 Salmonella species are sensitive to heat and acid and, therefore, are frequently killed by cooking or by gastric acids in the stomach. For this reason, a large inoculum is typically required to cause infection. Organisms that survive passage through the stomach will attempt to invade the intestinal mucosa of the distal ileum or proximal colon and replicate. Although the precise manner by which salmonella causes symptoms is not yet known, it is thought to be due to inflammatory mediators.
Infections most commonly occur in the warmer months, with a peak incidence in August and September. Most infections occur in children younger than 5 years, with a higher incidence in children younger then 1 year, and in adults older than 60 years. Patients at highest risk for infection include those who are immunocompromised, have low gastric pH ( patients on H2 blockers, post gastrectomy, etc.), have altered gastrointestinal motility, have altered intestinal flora (on antibiotics), or have diabetes.
Table 1. Food-Borne Syndromes5,43
ORGANISM |
INCUBATION |
DURATION |
FEVER |
VOMITING |
DIARRHEA |
S. aureus |
1-6 hr |
< 24 hr |
- |
+ |
+ |
B. cereus (emetic) |
1-6 hr |
< 24 hr |
- |
+ |
- |
B. cereus (diarrheal) |
6-24 hr |
< 24 hr |
- |
- |
+ |
C. perfringens |
6-24 hr |
< 24 hr |
± |
± |
+ |
Heavy metal |
5-120 min |
< 24 hr |
- |
+ |
- |
Norwalk virus |
24-48 hr |
24-48 hr |
+ |
+ |
+ |
ETEC |
16-72 hr |
5-10 d |
± |
- |
+ |
EIEC |
16-48 hr |
+ |
|
+ | |
EHEC |
1-8 d |
5-10 d |
- |
+ |
+ |
Nontyphoidal Salmonella |
6-48 hr |
< 7 d |
+ |
± |
+ |
Typhoidal Salmonella |
1-3 wk |
3-4 wk |
+ |
+ |
+ |
Shigella |
16-72 hr |
1d-1 mo |
+ |
+ |
+ |
Campylobacter |
16-48 hr |
3-5 d |
+ |
+ |
+ |
V. parahemolyticus |
5-24 hr |
1-3 d |
+ |
+ |
+ |
Ciguatera |
1-30 hr |
wks-mos |
- |
+ |
+ |
Scombroid |
10-180 min |
4-6 hr |
- |
- |
+ |
Paralytic shellfish |
5 min-4 hr |
hrs-days |
- |
± |
± |
C. botulinum |
12-36 hr |
wks-mos |
- |
- |
- |
MSG |
< 1 hr |
1-6 hr |
- |
- |
- |
Gastroenteritis is the most common presentation of Salmonella infection. Typically, symptoms occur 6-48 hours after ingestion but can have a shorter onset with larger inoculum sizes.17 The illness usually begins with nausea, vomiting, myalgias, headache, and diarrhea. The diarrhea may be mild or severe and may present with gross blood per rectum. Abdominal cramps are present in three-quarters of patients.18 Temperature elevation to 38-39°C is common and usually lasts less than two days, unless the patient is infected with S. typhi, in which case the fever can persist for weeks. Unfortunately, the presentation in the elderly, who are at high risk of complications, may be varied. Laboratory testing is nonspecific and usually includes a normal peripheral white blood cell count and moderate number of white cells and red cells on microscopic examination of stool.
Most patients with Salmonella enteritis will have a self limiting disease and should do well with supportive care measures such as good fluid intake. More aggressive treatment, including antibiotics, is warranted in neonates, the elderly, and in other immunocompromised patients who are at risk for systemic illness. The systemic complications of Salmonella infection typically begin with bacteremia, which is observed in 5-10% of high-risk patients.18 The antibiotic of choice for adults is a fluoroquinolone.19 For neonates, the preferred agents are ampicillin, trimethoprim-sulfamethoxazole, and ceftriaxone.20 Treatment should begin within 48 hours from the onset of illness in order to be maximally effective.21 Immunocompetent patients usually are not treated since the disease is self limited and antibiotics may prolong the excretion of the organism.23-25 Furthermore, resistance to the antibiotic can occur with unnecessary treatment.18
In addition to bacteremia, reactive arthritis occurs in approximately 5% of infected patients and can last for years.25 This disability has been correlated with radiographic evidence of joint damage. A clinical risk factor for arthritis is prolonged diarrhea during the acute illness. Another complication is prolonged excretion of the organism because of a chronic carrier state. Osteomyelitis, which can result from Salmonella bacteremia, is a complication most often encountered in patients with sickle cell anemia.
Prevention primarily involves limiting cross contamination in processing plants and food preparation areas. This should include preventing cross contamination by kitchen utensils and thorough hand washing. Fortunately, the organism can be killed from thorough cooking. Eggs cooked at 140°F and maintained at this temperature for 26 seconds, or at 160° for only 10 seconds, should be free of salmonella.26 Food heated to the appropriate temperature in a microwave oven may not be free of contamination because of uneven heating.27
Escherichia coli O157:47. This cause of food poisoning has received much attention in the past several years due to a number of outbreaks in fast food restaurants and meat packing plants. First isolated only 16 years ago in Michigan and Oregon, E. coli O157:47 is now known to be present throughout the world.28 Most cases are reported in the United States and Canada. Ground beef is the primary source of E. coli infections in humans. Infection can result either directly from infected cattle or from cross contamination when large amounts of ground beef are mixed together. Infected meat can cause significant numbers of ill people since only a small number of bacteria are needed to cause illness. E. coli is not known to cause disease in cattle. Therefore, even healthy animals may transmit the organism. Other possible sources include unchlorinated water supplies, swimming in fecally contaminated lakes, or person-to-person transmission. The latter is a significant problem affecting young children in daycare and the elderly in nursing homes.29,30
E.coli O157:H7 is a gram-negative, noninvasive pathogen that attaches to the gastrointestinal mucosa. It is the third leading cause of diarrhea in regions of the United States. In patients with bloody diarrhea, E. coli can be isolated in much higher percentage of stool cultures. The disease caused by this pathogen is thought to be mediated by two cytoxins. These cytoxins are similar to those produced by shigella, and are called shigella-like toxins (SLT) 1 and 2.
Infections most commonly occur during the warm months-June through September-with an incidence as high as 6.1 infections per 100,000 per year in children younger than 5 years old.31 The incubation period is as short as one day, or as long as eight, and averages between three and four days. After the incubation period, infected patients can present with a spectrum of clinical manifestations that may include bloody diarrhea, hemolytic uremic syndrome (HUS), or death. The illness typically begins with severe cramps and non-bloody diarrhea that turns bloody by the second or third day of illness. The cramps can be severe enough to mimic an acute abdomen. Bloody diarrhea is present in 90% of patients and can be of variable severity.32 Diarrhea typically lasts 3-7 days, with 10-11 stools on the worst day. Nausea and vomiting are common complaints, affecting one-half of these patients.32 An elevated temperature may or may not be present.
Typically, the disease lasts about one week without treatment, although approximately one-fourth of infected patients will require hospitalization.7 Most hospitalized patients will require only supportive therapy such as intravenous fluids, but some patients will develop HUS (6% of infected patients) and a small percentage (5%) of these patients will die.33-35
HUS is the most worrisome complication of E. coli O157:47 infection and is a common cause of acute renal failure in children. It usually occurs 5-10 days after the onset of diarrhea and is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. Of patients who develop HUS, the mortality is about 5%, with one-third of survivors sustaining a persistent disability.31 Exactly how the pathogen causes HUS is unknown, but is thought to be mediated by the shigella-like toxins. Central nervous system complications such as irritability, lethargy, seizure, or coma are seen in approximately 30% of patients with HUS.35 Risk factors for the development of HUS include age younger than 2 years, severe gastrointestinal prodrome, fever, and a leukocytosis (> 12,000 WBCs/mm3).34-36 HUS is rarely seen in the absence of bloody diarrhea.
There is controversy as to how this disease is best treated. There is some consensus for a treatment plan that includes supportive care measures without antibiotics, since there is speculation that antibiotics may increase toxin release as bacteria are lysed. However, there are no good studies to support this approach, and some authorities use antibiotics at the outset. Antimotility agents are also thought to potentially worsen the condition, and, therefore, are not recommended.36 Treatment is primarily supportive, with attention to fluid and electrolyte balance and monitoring for the development of complications.
Ciguatera. Ciguatera fish poisoning is the most commonly reported food-borne disease associated with eating fish in the United States; this condition is even more common in the tropics and subtropics.37,38 The Pacific Islands and Caribbean region are considered endemic areas.39 In the United States, 90% of cases occur in Hawaii and southern Florida, but even fish caught in North Carolina waters have been implicated in ciguatera poisonings.37 Due to travel and importation of ciguatoxic fish, outbreaks have the potential to occur anywhere.37 Disease may occur in nonendemic areas in individuals who have consumed fish caught in endemic areas that have been transported into nonendemic areas, and in individuals consuming infected fish in endemic areas and then flying home to nonendemic areas shortly thereafter.37,38,40 Hence, cases of ciguatera poisoning have been diagnosed in nonendemic states, among them Texas, Louisiana, New York, Massachusetts, and Maryland. The incidence is probably underestimated because the disease is not always recognized, it is misdiagnosed, or it goes unreported.37,41
Ciguatera outbreaks have been reported in association with the ingestion of more than 400 species of fish.6 Grouper, red snapper, amberjack, and barracuda are the most common species of fish implicated.6,41 Species known to be toxic in a significant percentage of cases are often barred from sale because of the fear of ciguatera poisoning (e.g., barracuda in southern Florida). Interestingly, ciguatoxic fish look, smell, and taste normal.42,43
Ciguatoxin is a naturally occurring toxin found in algae-associated microorganisms that live in coral reefs.37,41 The ciguatoxins become concentrated in larger fish, making them more toxic.37,40 Ciguatera does not appear to harm the sea creatures and produces toxicity only in birds and mammals that feed upon them.42 Fish merely transport the toxin up the food chain.41 Because the toxin appears to be concentrated in the head, viscera, and roe, these parts of the fish should never be eaten.41
The ciguatera syndrome may actually be caused by eight or nine ciguatoxins.44 The toxins, which act as sodium channel agonists in nerve, muscle, and cardiac cells, are odorless, colorless, tasteless, and both heat and acid stable.37 Moreover, these toxins are unaffected by normal cooking procedures and they cannot be eliminated by salting, drying, smoking, or marinating.37,38
People of all ages can be affected. Symptoms are highly variable and frequently subjective.44 The same fish may produce mild symptoms in some patients, while other persons may exhibit a more severe illness.40 Geographic and seasonal differences in the number of ciguatoxic fish, the mixture of toxins, and patient susceptibility account for variability in clinical symptomatology of symptoms.44 Not surprisingly, children seem to be more sensitive. A history of multiple ciguatoxin exposures has been linked to progressively more severe symptoms with each exposure.38 Death may occur in patients who have eaten parts of the fish that contain higher levels of the toxin.38
Clinical manifestations appear 2-30 hours (mean, 5 hours) after eating a toxic fish.6,40 Duration, severity, order, and occurrence of symptoms may vary considerably. Gastrointestinal symptoms lasting 1-2 days are often the first manifestations of poisoning and include abdominal pain, nausea, vomiting, painful defecation, and diarrhea.37,40
Neurologic symptoms are the most bothersome and persistent complaints.37 Paresthesias and sensory reversal of hot and cold sensation has been considered the symptomatic hallmark of ciguatera poisoning; these symptoms may occur within three hours of ingestion of contaminated fish.43,44 Pruritis and paresthesias, described as uncomfortable tingling sensations, most often develop in the extremities, oral cavity, and pharynx.37,40 Perceptions of loose teeth and ataxia can occur.38,42 Pupillary size, reflexes, and body temperature are normal.37 Neurological symptoms usually resolve after 1-2 weeks.38 Pain, paresthesias, pruritis, and weakness may persist for several weeks, followed by an increase in symptoms following ingestion of animal proteins.40 Chronic symptoms have been reported and may be the result of permanent nerve damage.44
Cardiovascular symptoms often occur within 2-5 days after ingestion.37 Bradycardia, hypotension, and T wave abnormalities have been reported.37,40,41 Bradycardia has been associated with the amount of fish eaten and the size of the fish and is more common in older victims.41 Ciguatoxin causes an increase in parasympathetic tone and impairs sympathetic reflexes.38 Pulmonary edema also has been reported.44 Cardiovascular symptoms usually resolve within five days after onset.38 Other symptoms include dysuria, chills, sweating, vertigo, neck stiffness, rash, a metallic taste, and polymyositis.40
Breast-fed infants may also be at risk because mothers with ciguatera poisoning who breast feed have reported excessive nipple pain and diarrhea in their infants.37,38,40 It may also be possible to transmit ciguatera through sexual intercourse. Because ciguatoxin is concentrated in the gonads of fish, the same has been suggested of humans.38
Symptoms, which may vary in severity, tend to disappear in a few days; however, they may become chronic and last for months or even years.40,41,44 Patients may become sensitized to the toxin, with symptoms initially disappearing, only to return at a later date following ingestion of alcohol or animal protein.37,44
Treatment of ciguatera remains symptomatic and supportive.38,40 Successful management of neurologic symptoms has been accomplished with IV mannitol (1 g/kg),44 which is most effective if given within the first 48 hours of symptoms, but may still be moderately effective if administered after that time. Mannitol may provide some relief even after several months.37,44 Mannitol does not seem to affect cardiovascular or gastrointestinal symptoms, but it does reduce the severity and duration of neurological symptoms.38 The mechanism of mannitol's effect is obscure.40 It should be used with caution in patients with severe dehydration caused by vomiting.38 Amitriptyline, tocainide, and mexilitene have been shown to be of some symptomatic benefit.37,41,43 Some experts recommend that steroids, opiates, and barbiturates be avoided in this disease.37
Ciguatera is rarely fatal, but morbidity is high and symptoms may be debilitating and prolonged.37,40 It is difficult to diagnose ciguatera with any degree of confidence because reliable methods for detecting ciguatoxins in humans are not widely available.40,43,44 However, ciguatoxin can be detected by commercially available test kits, using a stick-enzyme immunoassay.42 Rapid immunoassays for identification of ciguatoxic fish are currently being developed.37
Scombroid. In contrast to ciguatera, in which the fish are toxic when caught, fish responsible for causing scombroid become toxic after they are caught.6 Scombroid is caused by improper refrigeration of fish, which encourages bacterial growth and degradation of the fish flesh, resulting in the conversion of histidine to histamine.42 Bacterial growth also produces a histamine-like toxin, saurine.6 Both of these substances are unaffected by normal cooking temperatures.37 Fish of the scombroid family, including bluefin and yellowfin tuna, skipjack, and mackeral, are usually responsible for this condition. Such non-scombroid fish as dolphin fish (mahimahi) or marlin may also produce this syndrome.6,42,44 These fish often have a bitter, peppery, or metallic taste. Unfortunely, they may also taste, smell, and appear perfectly normal.6,42,43
Symptoms consist of a histamine-like reaction, which occurrs 10-30 minutes after ingestion. These include flushing, rash, hot sensations of the skin (especially of the head and face), headache, dizziness, burning sensation on the mouth and throat, diarrhea, and, rarely, bronchospasm.37,42,44,63 Symptoms are usually self limited and resolve after 3-6 hours. Antihistamines such as diphenhydramine are effective.44
Paralytic Shellfish Poisoning. The symptoms of paralytic shellfish poisoning begin shortly after ingestion. A gastrointestinal prodrome is seen during the first 30 minutes to several hours, followed by sensory disturbances of the face and limbs.6,42,43 Saxitoxin, the principal offender, blocks sodium channels and inhibits peripheral nerve conduction.42,43,45 Disturbances include paresthesias of the mouth, lips, face, and fingertips. This is followed by dysphagia, dysphoria, and weakness.45 Paralytic features predominate during the next few hours.42 Most deaths associated with paralytic shellfish poisoning are caused by saxitoxins and occur within the first 12 hours of ingestion; the deaths result from diaphragmatic paralysis and respiratory depression.43,45,46
The diagnosis is suggested by a recent history of mussel or scallop consumption, appearance of typical symptoms, and detection of toxin in the uneaten shellfish.44,45,46 There are no antitoxins available, and treatment is supportive. Ingestion of alcohol increases absorption of the toxin.46 Lavage may help remove unabsorbed toxin.46 Cooking does not destroy the toxin.45
Other seafood toxins and syndromes. Poisonous seafood produces a number of different toxins that are capable of producing a variety of syndromes. Diarrhetic shellfish poisons, such as okadic acid, pectenotoxins, and dinophysistoxins, produce gastrointestinal disorders such as diarrhea.44 Domoic acid, which is found in mussels and dungeness crab, causes the syndrome of amnesic shellfish poisoning.42-44
Neurologic shellfish poisoning is caused by the brevitoxins, a heat stable neurotoxin that can be aerosolized by the surf and produces transient respiratory and mucous membrane irritation.43,44 Brevitoxins also cause neurological dysfunction, such as paresthesias, reversal of hot and cold sensations, ataxia, depression of cardiovascular and respiratory function, and such GI symptoms as nausea, vomiting, and diarrhea.44-45 Palytoxin-induced symptoms consist of severe headache and paresthesia followed by paralysis.44 Palytoxin is a coronary vasoconstrictor. Ischemia is widespread, causing anoxia in major organs.44 Palytoxin may cause symptoms similar to ciguatera, as well as intense muscle contractions and rhabdomyolysis.37
Table 2. Toxins and Syndromes
TOXIN |
SYNDROME |
Ciguatoxin |
Ciguatera |
Histamine, saurine |
Scombroid |
Saxitoxin |
Paralytic shellfish poisoning |
Domoic acid |
Amnesic shellfish poisoning |
Tetrodotoxin |
Pufferfish poisoning |
Brevitoxin |
Neurologic shellfish poisoning |
Okadaic acid |
Diarrhetic shellfish poisoning |
Puffer fish poisoning from tetrodotoxin causes symptoms within 30 minutes of ingestion and begins with parasthesias, usually tingling of the tongue and mouth; this progresses to vomiting, diarrhea, abdominal pain, and ultimately, ascending motor paralysis, hypotension, respiratory failure, and death.47-49
Nonparalytic shellfish poisoning is a relatively mild form of seafood poisoning.42 Symptoms typically occur within three hours of ingestion and consists of a syndrome of gastrointestinal and sensory disturbances of face and limbs, including paradoxical sensory disturbances with reversal of hot and cold sensation.42 Motor, respiratory, and bulbar musculature are not affected.42 (See Table 2.)
Staphylococcus aureus Intoxication. S. aureus is the most common cause of toxin-related food poisoning in the United States.5 Because its symptoms are frequently self-limited, the true incidence of this syndrome is likely much higher.43 Intoxication occurs from preformed toxins, which accumulate in foods that have been inadequately refrigerated.43 Food that typically causes S. aureus poisoning has previously been cooked and contains a large proportion of protein, salt, and sugar.43,51,52 Staphylococci thrive in high concentrations of salt and sugar that other organisms cannot tolerate.53 Meat and meat products, especially ham and chicken, are most commonly implicated. Other implicated foods include fish and shellfish, milk and milk products, cream filled cakes, and potato and macaroni salads.43,52,54 Since toxigenic staph are ubiquitous, most foods are contaminated with small numbers of viable organisms at some point before consumption.51 Even foods from cans and jars have been implicated.53
Improper storage of previously cooked food is most often implicated as a cause, but contaminated equipment and poor personal hygiene may also account for transmission of disease.52 In most instances, it is the food handler who contaminates the food.54 However, only about one-third of implicated food handlers had lesions on their hands or nose indicative of staphyloccal infection (e.g., furuncles).52 Between 30% and 50% of the general population carry S.aureus, and one-third to one-half of these carry enterotoxigenic strains.54
Five Staphylococcal enterotoxins have been identified: A, B, C, D, and E.55 Staphylococci that produce A or A and D together account for the majority of cases of food poisoning.52,55 Temperatures normally used for cooking will not destroy these heat-resistant toxins. Since staphylococci enterotoxin are colorless, odorless, and tasteless, foods containing the toxins usually look and taste normal.42,51,53,55
Staphylococcal food poisoning occurs rapidly after ingestion of the contaminated food.43 The incubation period may vary in relation to individual susceptibility, the amount of toxin in the food, and the amount of food ingested.53 Sudden onset of nausea, vomiting, abdominal pain, and watery diarrhea usually occurs 30 minutes to eight hours after eating contaminated food.5,52,53 Fever is rare, and symptoms usually last less than 12-24 hours.5,43,52
Treatment is supportive; attempts to eradicate staphylococcus with antibiotics are not recommended since this disease is toxin-mediated.43 Definitive diagnosis can be made by culturing the implicated food, the vomitus, or the stools of the patient.43 Because the illness is mediated by toxins and not infection, secondary transmission does not occur.43 Although the duration of illness is short and almost always self-limited, the hospitalization rate may be as high as 14%, and a few deaths have occurred.52,53
Bacillus cereus Intoxication. Bacillus cereus is a ubiquitous aerobic, spore forming, gram-positive rod that produces gastrointestinal illness. As with other food-borne illnesses, the incidence is under-reported because the illness is self-limiting and, usually, is not severe.56 If the illness is reported, it still may go undetected because not all state public health laboratories make B. cereus testing routinely available.56
Although the spore is not particularly heat stable, spores of some strains are able to withstand relatively high temperatures, particularly if the food has a high fat content, which seems to have a protective effect.57 Meat has been identified as a vehicle of transmission in multiple outbreaks of B. cereus, but the illness is most commonly associated with fried rice.58 B. cereus is frequently present in uncooked rice.56 If the cooked rice is maintained at room temperature while it drains, spores can germinate and a heat stable enterotoxin is produced that can survive brief heating such as stir frying.5,43,56,57 Toxin production is enhanced by the addition of protein in the form of egg or meat.57 Consequently, the enterotoxin may be preformed in the food, or it may be produced within the small intestine.57
B. cereus not only produces gastrointestinal illness, but it is also responsible for nongastrointestinal infections including wound infections, infections of lines and shunts, ocular infections, primary cutaneous infections, endocarditis, CNS infections, and respiratory infections.
B. cereus causes two distinct gastrointestinal syndromes: an acute emetic syndrome within 1-6 hours of consumption and a diarrheal syndrome 8-16 hours after ingestion.43 In the emetic syndrome, low numbers of contaminating organisms produce a heat stable enterotoxin that is consumed.43 The preformed toxin is stable to trypsin, pepsin, and pH extremes.43,56,58 The clinical presentation of the emetic syndrome caused by B. cereus food poisoning is characterized by the acute onset of nausea, vomiting, and abdominal pain, which usually resolve within about 10 hours.5,43 Diarrhea occurs in one-third of patients.57 In particular, the emetic syndrome is strongly associated with ingestion of fried rice obtained from Chinese restaurants.43,57 The emetic syndrome is more common than the diarrheal syndrome, which is associated with ingestion of a variety of prepared foods that have been inadequately refrigerated.43 The diarrheal syndrome is mediated by a heat-labile enterotoxin that is produced in vivo after ingestion of the organism.5
This enterotoxin is sensitive to heating, proteolytic enzymes, and acids.56,58 Abdominal cramps and profuse watery diarrhea develop 6-24 hours after ingestion and lasts 24 hours.5,56,57 Vomiting is unusual and fever is uncommon.12,25,56,58 The diarrheal syndrome resembles C. perfringens food poisoning.25
Supportive therapy is usually not needed, and the patient recovers within 24 hours.57 There is no role for antimicrobial therapy.57 Diagnosis is complicated by natural contamination of many foodstuffs with spores, and the detection of B. cereus in the absence of clinical symptoms may not always signify food-borne disease.57 Stool cultures are not generally useful in B. cereus intoxication.58 In most cases, expensive reference laboratory biological tests are needed to conclusively prove the presence of toxigenic strains and to establish an association between foodstuffs and symptoms.57
Clostridium perfringens. Clostridium perfringens is an anaerobic, spore-forming, gram-positive bacillus.43 It is present in human (95% of normal adults harbor C. perfringens in their stool) and animal feces, soil, water, and air, and is a contaminant of most commercially available meat and poultry products.51,52 Five types of C. perfringens are recognized, and most cases of self-limited diarrheal disease are caused by Type A strains.55 The 24-hour illness caused by type A organisms is found almost exclusively in meat and poultry products when there has been a delay between cooking and consumption of the meat products.43 Type C strains can cause severe hemorrhagic necrotizing jejunitis accompanied by bloody diarrhea, severe abdominal pain, and shock; these strains are uncommon in developed countries.55
Clostridial spores germinate and multiply rapidly after cooking in foods that have been allowed to sit for 2-3 hours or longer.43,55 The contaminated food is ingested and a heat sensitive enterotoxin is produced.43 Ingestion of spores does not produce the illness; the toxin must be produced within the GI tract to cause the illness.43 The attack rate is approximately 50% in individuals who are exposed to contaminated food.43
After an incubation period of 6-24 hours, patients experience epigastric pain, abdominal cramps, and watery diarrhea.5 Fever, nausea, and vomiting occur less commonly.5 Symptoms resolve within 12-24 hours.5,43
The diagnosis is confirmed by: a) identifying the organism in suspected food; b) a high spore count in the patient's stool; or c) by isolating organisms with the same serotype from stool and suspected food.43 The CDC criteria for diagnosis rely on organism and spore counts in food and feces. Serotyping of the isolates can be helpful.52
Listeria. The identification of food as the major vector for human listeriosis was made in the early 1980s in an outbreak caused by coleslaw contaminated with Listeria from vegetables that had been fertilized with sheep manure.59 An estimated 1850 persons become seriously ill with listeriosis in the United States each year.60
Listeria monocytogenes is a motile, gram-positive rod.12 It is found in the stools and the female genital tract of 1% of normal individuals.43,59 Listeria has also been found in dish cloths, kitchen and bathroom drains, refrigerator vegetable compartments, and toothbrushes.61 The bacterium also has been found in a variety of raw foods, such as uncooked meats and vegetables.59,60 Vegetables can become contaminated from soil or manure.60 Chicken seems particularly susceptible to listeria contamination.62 Foodborne outbreaks of listeriosis associated with lettuce, cabbage, milk, cheese, shellfish, raw vegetables, and turkey frankfurters have been identified.1,43 When Listeria is isolated from processed foods, it is usually not the result of inadequate heating or refrigeration. Rather, food is usually contaminated after processing.60 Listeria is killed by pasteurization, but is unique in its ability to grow at refrigerated temperatures.4,61 Little is known of the pathogenesis of adult listeriosis. Despite its widespread occurrence, only a minority of people acquire the disease after ingesting contaminated food. Its virulence may depend on the immune status of the individual and the particular strain ingested.59,62
Diagnosis is made difficult by a prolonged incubation period. The time between eating the food and the onset of symptoms varies from several days to five weeks. Listeria produces a self-limited febrile gastroenteritis, as well as myalgias, arthralgias, and headache.4 It is not detected by routine stool cultures.4,59
Two major types of human listeriosis occur: materno-fetal and adult. Pregnant women are about 20 times more likely than other healthy adults to get listeriosis.60 Pregnant women develop a self-limiting flu-like illness that may lead to birth complications. The infant may become infected either by transplacental passage of listeria following maternal bacteremia or by contact with infected maternal vaginal secretions. In adults, as well as neonates, listeriosis may present as a meningitis and, sometimes, as a septicemic illness. The adult disease is thought to occur predominately in immunocompromised individuals. Healthy adults and children can occasionally get infected with Listeria, but they rarely become seriously ill.60 The mortality rate of immunocompromised individuals with listeriosis is about 25-30%.59
Vibrio Infections. Vibrio are curved, gram-negative, flagellated rods so named because they are so motile that they appear to vibrate.51 In the United States, Vibrio infections are most common in states bordering the Gulf of Mexico.63 Most food-borne illness in the United States caused by Vibrio is caused by two species, V. vulnificus and V. parahemolyticus. Vibrio bacteria are natural inhabitants of marine environments and can cause gastroenteritis, wound infections, and septicemia.63 V. vulnificus is commonly found in U.S. coastal waters and, presumably, in all species of coastal shellfish.64
V. vulnificus infection more often follows eating raw or undercooked oysters, and V. parahemolyticus infection is more likely to be associated with eating shrimp or crabs.45 Vibrio infections may occur in persons who live some distance from the Gulf Coast, but have recently consumed raw shellfish while visiting the Gulf of Mexico.63 Outbreaks typically occur during the summer and fall when the water is warmer and the Vibrio can multiply quickly.41 The majority of patients with Vibrio gastroenteritis have ingested seafood, especially raw oysters, within 37 days before the onset of illness.63 Consumption of raw clams and other seafood is a less common cause.63 Vibrio contamination does not alter the appearance, taste, or odor of oysters.65
V. vulnificus may both invade the mucosa and produce a enterotoxin.55 Therefore, not unexpectedly, fever, chills, and headache in addition to gastrointestinal symptoms, are common manifestations of this infection.55 GI symptoms include watery or bloody diarrhea, abdominal cramping, nausea, and vomiting.55,63 The mean duration of illness is about eight days.63 In the case of V. parahaemolyticus, a similar syndrome occurs after an incubation period of 12-24 hours. The duration of illness is about 1-3 days.45 No treatment is required for V. parahaemolyticus as the disease does not seem to be altered by antibiotics.66,67 Treatment of V. vulnificus consists of doxycycline, a third generation cephalosporin, and an aminoglycoside.68 Patients with liver disease, impaired immune systems, and diabetes should be warned against eating raw or partially cooked molluscan shellfish because of the increased risk of fulminant infections.64,65
Hepatitis A Shellfish Infections. Unlike bacteria, viruses do not multiply or produce toxins in food; food items merely act as vehicles for their transfer.69 Most infections associated with consumption of oysters, clams, cockles, and mussels are viral in origin.69 Clams, oysters, and mussels harvested from waters contaminated by raw sewage are the most frequent cause of food-borne viral hepatitis A.43 Soft fruits, such as strawberries and raspberries, have also been implicated.69 Other foods also have been implicated, but the true source is usually contaminated water.43 It is difficult to associate a specific food item with the illness because of the long incubation period, which may be as long as 2-8 weeks.64 Cases of gastroenteritis reported 24 hours after eating shellfish, which is then followed by hepatitis A 3-4 weeks later have been recorded.69 Symptoms include fever, malaise, jaundice, nausea, and abdominal pain.43 Diarrhea is rare.43 There is no carrier state and no chronic state associated with HAV infection.70 Treatment is supportive.43 Infection with hepatitis A in chronic carriers of hepatitis B and C is associated with high morbidity and mortality.71
Norwalk Virus Infection. Foods most commonly associated with the Norwalk virus include poorly cooked or raw shellfish, especially oysters and clams. Contamination often occurs when these shellfish filter untreated infectious sewage.72 Contaminated drinking water has also been implicated.43,73 Steaming shellfish until the shells open does not adequately destroy the virus.45,74 Outbreaks occur year round and affect older children and adults, but not infants or young children.75 The infectious virus may be excreted in the feces of food handlers for at least 48 hours after they recover from infections.75
Symptoms typically appear 24-48 hours after ingestion of contaminated food products,43,64 and include the rapid onset of nausea, vomiting, nonbloody diarrhea, cramps, headache, and malaise. These symptoms resolve over a 24-48 hour period.43 The abdominal symptoms are frequently associated with fever and leukocytosis.76 Gastroenteritis caused by Norwalk virus is unusual in young children.39 Older children and adolescents are likely to experience vomiting more frequently than diarrhea, while adults experience diarrhea more than vomiting.39 Complications are rare, and patients usually recover fully.45
Treatment with bismuth subsalicylate has been shown to decrease the duration of symptoms.43 The diagnosis is made by documenting a rise in antibody titer or by identifying the virus in the stool. These tests are not widely available.43
Heavy Metal Poisoning. Heavy metal poisoning is a rare cause of gastroenteritis and results from gastric irritation caused by copper, zinc, iron, tin, or cadmium.6,43,77 These illnesses are uaually associated with acidic or carbonated beverages that have been stored in, or allowed to come in contact with, metal containers or tubing, such as soft drink dispensers or metal containers.6,43,78,79 Common symptoms of acute heavy metal ingestion caused by copper and tin include bloating, nausea, vomiting, cramps, diarrhea, and a metallic taste that usually occur 5-60 minutes after ingestion.6,43,79,80 Copper poisoning is suggested by vomitus that is blue or green in color.81 Cadmium may be found in seafoods such as oysters, clams, and lobsters, as well as grains and peanuts. Cadmium and zinc cause myalgias, nausea, vomiting, abdominal pain, diarrhea, and weakness. Cadmium is also associated with increased salivation.43,81 Symptoms are usually self limited and abate gradually over hours.43 The best, although expensive, method to make the diagnosis is to assay for individual heavy metals in the beverage fluid.43
Infant botulism. Botulism is caused by ingestion of C. botulinum, an anaerobic, gram-positive, spore producing organism that is both heat and cold tolerant. The organism is found in contaminated foods and is ubuiquitous in the environment. Home-canned asparagus, green beans, peppers, and other vegetables are frequent sources of infection. Jams and jellies are rarely a cause of botulism because their high sugar content prevents growth of C. botulinum.82 In other parts of the world, garlic, fish, and meats are leading causes, but these foods rarely cause botulism in the United States.83,84 Infants may contract the disease through ingestion of Clostridial spores. Contaminated honey is a classic but uncommon source of spores.85 More frequently, spores are contracted from some other environmental source.86 After ingestion of spores, the Clostrdial toxin must be produced in vivo for symptoms to occur. Most environmental exposures of infant botulism have been described in California, Utah, and Pennsylvania, where the levels of spores are high.
Infant botulism is the most common form of botulism, and affects children between 2 and 6 months of age.86 The incubation period can range from three to 30 days. Infant botulism frequently presents as nonspecific symptoms that may include lethargy, weakness, poor feeding, and constipation. On exam, the child will have poor head control and hypotonia, as well as cranial nerve abnormalities such as ptosis and impaired gag and suck reflexes. These symptoms can be difficult to distinguish from those seen in a septic child.
Whereas infants usually ingest the spores, adults typically become infected after ingesting the preformed neurotoxin.The Clostridial neurotoxin binds to peripheral nerve endings, where it interferes with the release of neurotransmitters and causes a flaccid paralysis. There are seven different neurotoxin subtypes labelled A-G, but only A, B, and E cause illness in humans.87
The presentation of botulism in adults is different than in children. Typically, the incubation period is 12-36 hours, but may take up to 10 days for symptoms to develop.88 Adults also present with impaired cranial nerve function, which is more easily detected than it is in infants. Other common complaints include difficulty with speech and swallowing, and visual complaints such as blurrred vision and diplopia. As the disease progresses, a descending weakness develops; this is associated with autonomic dysfunction, including dry mouth, urinary retention, and hypotension. Sensation usually remains intact; there is no CNS involvement and sensorium is unaffected.
Triavalent botulism antitoxin is the treatment of choice for botulism and must be administered as soon as possible after symptoms develop. The antitoxin neutralizes only unbound toxin, so patients may not improve immediately after administration, although they should not worsen either. The antitoxin is derived from an equine source, and up to 9% of patients may develop a hypersensitivity reaction or serum sickness.89 Antibiotic use is controversial, but if antimicrobials are used, penicillin is the drug of choice. Treatment, otherwise, is supportive. Mechanical ventilation may be necessary until the neurotoxin's effects diminish. In adults and children who do not require immediate intubation, respiratory status should still be observed in an intensive care setting. Approximately 80% of affected children will have some degree of respiratory compromise.90
Monosodium glutamate. Monosodium glutamate is a powdered food additive used as a flavor enhancer.43 Symptoms include a burning sensation, facial pain, chest tightness, headache, nausea, abdominal pain, diaphoresis, and palpitations.91,92 The association between monosodium glutamate and the classic symptoms of the Chinese Restaurant Syndrome is tenuous. These symptoms may be due to monosodium glutamate or they may be due to a variety of other ingredients such as allergenic proteins (nuts, seafood), preservatives (sulfites, nitrites, etc.), food dyes, or histamine.92,93 The symptoms are self-limited.
Another, yet uncommon, cause of food-borne illness is parasitic infections. These include Cryptosporidium, Entamoeba histolytica, and Giardia lamblia. Each of these organisms is spread via the fecal/oral route, but can contaminate food and water. The contaminated water can be from a lake, stream, or municipal water supply, since chemical decontamination of drinking water may not kill cryptosporium. Filtration will remove the parasite, but it is not used by all communities treating their water supply. The presenting complaints of a symptomatic patient with parasitic intestinal infection are non-specific, including diarrhea, abdominal cramping, and low-grade fever. In order to diagnose these types of infection, evidence of parasites should be found on microscopic examination of a fresh stool specimen. Often, multiple stool specimens (3 or more) are needed to make a diagnosis. Mucosa biopsy can also be helpful in making the diagnosis. Treatment for Giardia is metronidazole, while E. histolytica is treated with a combination of metronidazole followed by iodoquinol. Cryposporidium has no effective treatment, but is a self limited disease in immunocompetent patients. Unfortunately, immunocompromised patients can have a prolonged problem if they become infected, and, therefore, should be knowledgeable on how Cryptosporidium is spread in order to avoid possible exposure.
Evaluation of Diarrhea
Most diarrheal disease is mild and self-limited, does not require hospitalization, and does not require laboratory evaluation, unless there is evidence of significant dehydration or systemic toxicity.94,95 Routine bacteriologic testing is not cost-effective and usually does not alter treatment.96 However, patients who are sick enough to require hospitalization should have a complete blood count with differential and electrolyte studies performed.95 Enterocolitis with fever, cramping abdominal pain, and blood and mucus in the stools also requires laboratory evaluation.94
The practice of dividing diarrheal infections into inflammatory vs. noninflammatory presentations is based on the supposition that a patient with bloody stools, tenesmus, fever, persistent abdominal cramping, and the presence of fecal leukocytes is infected with an invasive bacterial pathogen such as Shigella and will require antimicrobial therapy.96 However, because there is significant overlap among the syndromes caused by bacterial pathogens (i.e., some invasive bacteria cause watery diarrhea without fever, blood, or abdominal pain, as would be typical in cases of noninflammatory diarrhea), the utility of this classification is somewhat limited.96
To avoid the unnecessary cost associated with culturing every patient with diarrhea, stool cultures should be reserved for patients with blood, mucus, and WBCs in the stool, for those with significant toxicity or dehydration, or for patients with an underlying immunocompromising illness.95 The most simple and helpful test for identifying patients who may need antibiotics is the stool WBC examination.94 Fecal leukocytes usually are not present in diarrhea caused by viruses and toxins.75,97 The yield of positive cultures increases for patients in whom fecal leukocytes are detected.96 One study found that bloody and watery diarrhea with leukocytes resulted from Shigella, Salmonellae, or Campylobacter in about 83% of cases.98 The positive and negative predictive values of the fecal leukocyte test are approximately 45% and 93%, respectively.96 The absolute fecal leukocyte count is not predictive of a specific infection and their absence does not preclude bacterial diarrhea.98 For diarrheal disease caused by Shigella, the sensitivity of the fecal leukocyte test is about 73%. For other pathogens, the sensitivity is about 50%.96 It has yet to be proven that patients with fecal leukocytes benefit more from antimicrobial therapy than those without fecal leukocytes.96
Stool cultures are indicated to help identify cases in which antimicrobial therapy should be given in order to shorten the course of illness and to prevent spread to contacts.94 The clinician should be familiar with the capabilities of their hospital's laboratory. Most laboratories are able to test for Salmonella, Shigella, and Campylobacter. The laboratory should be notified of suspicion of less common organisms such as V. parahemolyticus or E. coli O157:H7.96
Collection of stool is optimally performed within 30 minutes of passage.98 Consequently, although the practice of giving a specimen kit to the patient to take home may be more convenient for the clinician, this approach will likely decrease diagnostic yields. Refrigeration of specimens also may decrease yields inasmuch as cold temperatures decrease viability of Shigella and Salmonella to some extent.98 Stool cultures should not be taken with a swab.98 Two stool cultures will yield a detection rate of 99%, and this appears to be the standard for routine workups.96
Salmonella is easily isolated and serotyped.66 Campylobacter must be cultured on selective media and usually must be requested specifically because it is not cultured routinely. Enteropathic E. coli (EPEC) testing is complex and expensive.98 The rate of recovery of E. coli O157:H7 is highest during the first few days after the onset of diarrhea and drops off significantly after seven days.96 A latex agglutination test is available to identify E. coli O157:H7.66 There is no specific culture medium that differentiates Enterohemorrhagic E. coli (EHEC) from other pathogenic types of E. coli, but sorbitol-MacConkey agar is a good screening media in combination with serotyping.67 Serologic tests are available, but are not routinely useful.66 V. parahaemolyticus is easily identified by culture.66 Diagnosis of V. vulfinicus infections is made by stool, wound, or blood cultures on special media.68 (See Table 3.)
Table 3. Diagnosis of Food-Borne Illness100
ORGANISM |
DIAGNOSIS |
S. aureus |
Culture organism in vomitus or food |
B. cereus |
Culture organism in stool and food |
C. perfringens |
Culture organism in stool and food |
C.botulinum |
Demonstrate toxin in stool or food, culture organism in stool |
S. enteritidis |
Culture organism in stool |
C. jejuni |
Culture organism in stool |
Viral gastroenteritides |
Demonstrate virus in stool and antibody in blood |
E. coli |
Culture organism in stool |
Because many different microorganisms may cause diarrhea, a variety of tests, in addition to bacterial cultures may be needed to establish an etiology.94 The gram stain can easily demonstrate C. jejuni, a gram-negative rod, with sensitivities as high as 94%, and specificities greater than 99%. Unfortunately, the gram stain has no value for detecting any other common pathogen, since these cannot be differentiated from normal stool flora.96,98
Laboratory confirmation of the cause of viral food-borne gastroenteritis requires either detection of the virus in the stool or a rise in virus-specific antibody.39 Identification of viruses that cause gastroenteritis depends largely upon examination of stool specimens by electron microscopy.69,70 Specimens should be stored without freezing, and should be examined within 48-72 hours after onset of symptoms, after which the virus concentration in stool declines below levels detectable by electron microscopy.4 Antibody to Norwalk virus begins to develop within five days after onset of illness, peaks within three weeks, and begins to decline by week 6.39 Enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay tests may be used to detect the Norwalk virus, but they are not widely used.39,75,95 Polymerase chain reaction (PCR) has shown promise in detection of Norwalk viruses not only in feces and vomitus but also in the shellfish itself.73 Unless PCR is available, it is not practical to examine food remnants because the number of virus particles will be much too low for other currently available detection methods.69
Since HAV is excreted mainly before infection is apparent, stool specimens are inappropriate. Laboratory diagnosis of infection depends on detection of specific anti-HAV IgM in serum.69
The diagnosis of botulism can be made by detection of the toxin in the serum or stool, or by culturing the organism from stool or gastric samples. Obtaining a stool specimen for analysis may be problematic since constipation is often a problem with botulism. Enema fluid can be cultured as an alternative. Toxin isolation is best done within three days of ingestion, but it is positive in only 50% of cases. To distinguish botulism from other paralytic disorders, electromyography may be necessary.
For some cases, antibiotic therapy may be required to minimize the duration of illness, reduce morbidity, or reduce the contagiousness.95 Several studies have shown that empirical therapy for acute diarrheal disease with fluoroquinolones, regardless of the infecting organism, reduces the number of stools, as well as other signs and symptoms.96,99 However, ciprofloxacin is no more effective than placebo in reducing the duration of diarrhea in patients with positive bacteriology.99 Consequently, it seems the precise role of fluoroquinolones in gastroenteritis needs to be further delineated.
Summary
The use of new technologies, such as irradiation of food stuffs, may play a critical role in ensuring the microbial safety of the food supply in the future.1 In the meantime, people should be counseled to cook their meat thoroughly, and to be sure that juices or drippings from raw meat or poultry do not contaminate other foods.3
As the safety of foodstuffs receives more media scrutiny, more patients with concerns about food-borne illness will present to their primary care physician, who will will be called upon to make these diagnoses and provide treatment. In this regard, the physician must recognize these syndromes, be aware the difficulty in making the diagnosis, but not be tempted to waste resources trying to confirm the precise etiology of all patients who present with food-borne illness. Surveillance summaries on foodborne illnesses can be obtained by writing:
Public Inquiries, Office of Public Affairs, Centers for Disease Control and Prevention, 1600 Clifton Road, Atlanta, Georgia, 30333.71
The authors greatly appreciate the assistance of Keith Wrenn, MD, in the preparation of this manuscript.
References
1. Hedberg CW, MacDonald KL, Osterholm MT. Changing Epidemiology of Food-Borne Disease: A Minnesota Perspective. Clin Infect Dis 1994;18:671-678.
2. Chicken: What you don't know can hurt you. Consumer Reports 1998;63:12-18.
3. Food and Water Borne Bacterial Diseases @http://www.cdc.gov/ ncidod/disease/bacter/foodborn.htm
4. Food poisoning, listeriosis, and febrile gastroenteritis. Nutr Rev 55:57-60.
5. Afghani B, Stutman HR. Toxin-related diarrheas. Ped Ann 1994;3:549-555.
6. Hughes JM, Horwitz MA, Merson MH, et al. Foodborne disease outbreaks of chemical etiology in the United States, 1970-1974. Am J Epidem 1977;105:233-244.
7. Foodborne Diseases Active Surveillance Network. 1996. Morb Mortal Wkly Rep MMWR 1997;46:258-261.
8. Allos BM, Blaser MJ. Campylobacter jejuni and the expanding spectrum of related infections. Clin Infect Dis 1995;20:1092-2101.
9. Humphrey TJ, Henley A, Lanning DG. The colonization of broiler chickens with Campylobacter jejuni: Some epidemiological investigations. Epidemiol Infect 1993;110:601-607.
10. Wood RC, MacDonald KL, Osterholm MT. Campylobacter Enteritis outbreaks associated with drinking raw milk during youth activities. JAMA 1992;268:3228-3230.
11. Blaser MJ, Laforce FM, Wang WL. Reservoirs for Human Campylobacteriosis. Clinic Res 1979;27:40A.
12. Tauxe RV, Gargrett-Bean N, Patton CM, et al. Campylobacter isolates in the United States, 1982-1986. Morb Mortal Wkly Rep MMWR 1988;37:1-12.
13. Skirrow MB, Sutcliffe E, Benjamin J. Campylobacter bacteremia in England and Wales, 1981-91. Epidemiol Infect 1993;110: 567-573.
14. Allos BM. Association between Campylobacter infection and Guillain-Barrré Syndrome. J Infect Dis 1997;176:(S)125-128.
15. Salmonella enteiditidis infection. CDC website at http:/www.cdc. gov/ncidod/publications/brochures/salmon.htm
16. Hargrett-Bean NT, Pavia AT, Tauxe RV. Salmonella isolates from humans in the United States, 1984-1986. Morb Mortal Wkly Rep MMWR 37;(SS-2)25-31.
17. Mintz ED, Cartter ML, Hadler JL, et al. Dose response effects in an outbreak of Salmonella enteritidis. Epidemiol Infect 1994;112: 13-23.
18. Lee LA, Puhr ND, Maloney EK, et al. Increase in antimicrobial resistant Salmonella infections in the United States, 1989-1990. J Infect Dis 1994;170;128-134.
19. Stanford JP, Gibert DN, Moellering RC, et al. The Sanford Guide to Antimicrobiol Therapy, 27 Ed. 1997.
20. Report of the Committee on Infectious Diseases 1997. American Academy of Pediatrics. Elk Grove, IL
21. Wistrom J, Norrby SR. Fluoroquinolones and bacterial enteritis, when and for whom? J Antimicrob Chemother 1995;36:23-39.
22. Smith ER, Badley WD. Treatment of Salmonella enteritis and its effect on the carrier state. CMA Journal 1971;104:1004-1006.
23. Antibiotics prolong Salmonella excretion. BMJ 1969:699-700.
24. Aserroff B, Bennett JV. Effect of antibiotic therapy in acute Salmonellosis on the fecal excretion of salmonella. N Engl J Med 1969; 281:636-640.
25. Thompson GT, DeRubeis DA, Hodge MA, et al. Post Salmonella reactive arthritis: Late clinical sequelae in a point source cohort. Am J Med 1995;98:13-21.
26. Doyle MP. Questions and answers. JAMA 1994;272:895.
27. Evans MR, Parry SM, Ribeiro CD. Salmonella outbreak from microwave cooked food. Epidemiol Infect 1995;115:227-230.
28. Riley LE, Remis RS, Helgerson SD, et al. Hemorrhagic colitis associated with a rare Escherichia Coli serotype. N Engl J Med 1983;308:681-685.
29. Carter AO, Borczyk AA, Carlson JAK, et al. A severe outbreak of Escherichia coli O157:47 associated hemorrhagic colitis in a nursing home. N Engl J Med 1987;317:1496-1500.
30. Spika JSA, Parsons JE, Nordenberg D, et al. Hemolytic uremic syndrome and diarrhea associated with Escherichia coli O157:47 in a day care center. J Pediatr 1986;109;287-291.
31. Ostroff SM, Kobayashi JM, Lweis JH. Infections with Escherichia coli O157:47 in Washington State. JAMA 1989;262:355-359
32. Bell BP, Goldoft M, Griffin PM, et al. A Multistate outbreak of Escherichia coli O157:47 associated bloddy diarrhea and hemolytic uremic syndrome from hamburgers. JAMA 1994;272:1349-1353.
33. Escherichia coli O157:47 outbreak at a summer camp-Virginia 1994. MMWR Morb Mortal Wkly Rep 1995;44:419-421.
34. Martin DL, MacDonald KL, White K, et al. The epidemiology and clinical aspects of the Hemolytic Uremic Syndrome in Minnesota. N Eng J Med 1990;323:1161-1167.
35. Siegler RL, Pavia AT, Christofferson RD, et al. A 20-year population based study of postdiarrheal hemolytic uremic syndrome in Utah. Pediatrics 1994;94:35-40.
36. Cimolai N, Carter JE, Morrison BJ, et al. Risk factors for the progression of Escherichia coli 1057:H7 enteritis to hemolytic uremic syndrome. J Peds 1990;116:589-592.
37. Swift AEB, Swift TR. Ciguetera. Clin Tox 1993;31:1-29.
38. Beadle A. Ciguatera Fish Poisoning. Military Med 1997;162: 319-322.
39. Hedberg CA, Osterholm MT. Outbreaks of food-borne and waterborne viral gastroenteritis. Clin Micro Rev 1993;6:199-210.
40. Glaziou P, Legrand A. The epidemiology of Ciguatera fish poisoning. Toxicon 1994;8:863-873.
41. oone J. A case of Ciguatera fish poisoning. J Emerg Nurs 1996; 22:101-104.
42. Watters MR. Organic neurotoxins in seafoods. Clin Neuro Neurosurg 1995;97:119-124.
43 Bishai WR, Sears CL. Food poisoning syndromes. Gastroenterol Clin NA 1993;22:579-608.
44. Tosteson TR. The diversity and origins of toxins in Ciguetera fish poisoning. PRHSJ 1995;14:117-129.
45. oble RC. Death on the half-shell: The health hazards of eating shellfish. Perspect Bio Med 1990;33:313-322.
46. Food and Water Borne Bacterial Diseases@ http://www.cdc.gov /ncidod/disease/bacter/shelfish.htm
47. Sun K, Wat J, So P. Puffer Fish Poisoning. Anaesth Intens Care 1994;22:307-308.
48. LangeWR. Puffer fish poisoning. Am Fam Phys 1990;42: 1029-1033.
49. Tetrodotoxin poisoning associated with eating puffer fish transported from Japan-California, 1996. JAMA 1996;275:163.
50. Sun KO. Management of puffer fish poisoning. Br J Anaesth 1995; 75:500.
51. Grady GF, Keusch GT. Pathogenesis of bacterial diarrheas. N Eng J Med 1971;285:831-841.
52. Holmberg SD, Blake PA. Staphylococcal food poisoning, New facts and old misconceptions. JAMA 1984;251:487-489.
53. Outbreak of staphyloccal food poisoning associated with precooked ham-Florida, 1997. Morb Mortal Wkly Rep MMWR 1997;46: 1189-1191.
54. Wieneke AA, Roberts D, Gilbert RJ. Staphylococcal food poisoning in the United Kingdom, 1969-90. Epidemiol Infect 1993;110: 519-531.
55. Plotkin GR, Kluge RM, Waldman RH. Gastroenteritis: Etiology, pathophysiology and clinical manifestations. Medicine 1979;58: 95-114.
56. Bacillus cereus food poisoning associated with fried rice at two child day care centers-Virginia, 1993. Morb Mortal Wkly Rep MMWR 1994;43:177-178.
57. Drobniewski FA. Bacillus cereus and related species. Clin Microbiol Rev 1993;6:324-338.
58. Luby S, Jones J, Dowda H, et al. A large outbreak of gastroenteritis caused by diarrheal toxin-producing Bacillus cereus. JID 1993; 167:1452-1455.
59. Lacey RW. Food-borne bacterial infections. Parasitology 1993; 107(S):S75-S93.
60. Preventing Foodborne Illness: Listeriosis@ http://www.cdc.gov/ ncidod/disease/bacter/foodborn/lister.htm
61. Brumer RR, Giffel MC, Spoorenberg E, et al. Listeria species in domestic environments. Epidemiol Infect 1996;117:437-442.
62. Wilson IG. Occurrence of Listeria species in ready to eat foods. Epidemiol Infect 1995;115:519-526.
63. Hlady WG, Klontz KC. The epidemiology of Vibrio infections in Florida, 1981-1993. J Infect Dis 1996;173:1176-1183.
64. Rippey SR. Infectious diseases associated with Molluscan shellfish consumption. Clin Microbiol Rev. 1994;7:419-425.
65. Warning about Vibrio infections and raw Molluscan shellfish consumption. JAMA 1993;269:1361.
66. Qadri SMH. Infectious diarrhea. Postgrad Med 1990;88:169-184.
67. Cheney CP, Wong RKH. Acute infectious diarrhea. Med Clin NA 1993;77:1169-1196.
68. Questions and answers about Vibrio vulnificus@http://www. cdc.gov/ncidod/disease/bacter/foodborn/vibriovu.htm
69. Appleton H. Foodborne viruses. Lancet 1990;336:1362-1364.
70. Alcoff J. Viral hepatitis. J Fam Pract 1982;15:141-162.
71. Morse DL, Guzewich JJ, Hanrahan JP, et al. Widespread outbreak of clam and oyster gastroenteritis: Role of Norwalk virus. NEJM 1986;314:678-681.
72. Kohn MA, Farley TA, Ando T, et al. An outbreak of Norwalk virus gastroenteritis associated with eating raw oysters. JAMA 1995;272: 466-471.
73. Sugieda M, Nakajima K, Nakajima S. Outbreaks of Norwalk-like virus-associated gastroenteritis traced to shellfish: Coexistence of two genotypes in one specimen. Epidemiol Infect 1996;116: 339-346.
74. Kirkland KB, Meriwether RA, Leiss JK, et al. Steaming oysters does not prevent Norwalk-like gastroenteritis. Pub Health Rep 1996;111:527-530.
75. Blacklow NR, Greenberg HB. Viral gastroenteritis. N Engl J Med 1991;325:252-264.
76. Taterka JA, Cuff CF, Rubin DH. Viral gastrointestinal infections. GI Clin NA 1992;21:303-330.
77. Benoy CJ, Hooper PA, Schneider R. The toxicity of tin in canned fruit juices and solid foods. Fd Cosmet Toxicol 1971;9:645-656.
78. Spitalny KC, Brondum J, Vogt RL, et al. Drinking-water-induced copper intoxication in a Vermont family. Pediatrics 1984;74: 1103-1106.
79. Barker WH, Runte V. Tomato juice-associated gastroenteritis, Washington and Oregon, 1969. Am J Epidemiol 1972;96:219-226.
80. Taylor A. Detection and monitoring of disorders of essential trace elements. Ann Clin Biochem 1996;33:486-510.
81. Louria DB, Joselow MM, Browder AA. The human toxicity of certain trace elements. Ann Int Med 1972;76:307-319.
82. CDC. Foodborne Botulism-Oklahoma, 1994. Morb Mortal Wkly Rep MMWR 1995;44:200-202.
83. St. Louis ME, Peck Sh, Bowering D, et al. Botulism from chopped garlic: Delayed recognition of a major outbreak. Ann Int Med 1988; 108:363-368.
84. Centers for Disease Control. Fish Botulism-Hawaii, 1990. Morb Mortal Wkly Rep MMWR 1991;40:412-414.
85. Arnon SS, Midura TF, Damus K, et al. Honey and other environmental risk factors for infant botulism. J Pediatr 1979;94;331-336.
86. Long SS. Botulism in infancy. Pediatr Infect Dis 1984;84:266-271.
87. Woodruff BA, Grufflin JF, McCroskey LM, et al. Clinical and laboratory comparison of botulism from toxin types A, B, and E in the United States, 1975-1988. J Infect Dis 1992;166:1281-1286.
88. Shapiro BE, Soto O, Shafqat S, et al. Adult botulism. Muscle Nerve 1997;20:100-102.
89. Black RD, Gunn RA. Hypersensitivity reactions associated with botulinum antitoxin. Am J Med 1980;69:567-570.
90. Schreiner MS, Firel EM, Ruddy R. Infant botulism: A review of 12 years' experience at The Children's Hospital of Philadelphia. Pediatrics 1991;87:159-165.
91. Zautcke JL, Schwartz JA, Mueller EJ. Chinese restaurant syndrome: A review. Ann Emerg Med 1986;15:1210-1213.
92. Pulce C, Vial T, Verdier F, et al. The Chinese restaurant syndrome: A reappraisal of monosodium glutamate's causative role. Adv Drug Tox Rev 1992;11:19-39.
93. Tarasoff L, Kelly MF. Monosodium L-Glutamate: A double-blind study and review. Fd Chem Tox 1993;31:1019-1035.
94. Overall JC. Is it bacterial or viral? Laboratory differentiation. Ped Rev 1993;14:251-261.
95. Leung AKC, Robeson WLM. Acute diarrhea in children. Postgrad Med 1989;86:161-173.
96. Hines J, Nachamkin I. Effective use of the clinical microbiology laboratory for diagnosing diarrheal diseases. Clin Infect Dis 1996;23:1292-1301.
97. Sabol VK, Diarrhea. AACN Clin 1997;8:425-436.
98. Adler PM. Stool examination: Culture versus gram stain. Ann Emerg Med 1986;15:337-340.
99. Welsby PD. Infectious diseases. Postgrad Med J 1994;70:74-85.
100. Katelaris PH, Farthing MJG. Traveler's diarrhea: Clinical presentation and prognosis. Chemother 1995;41:40-47.
You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content