Laboratory Studies

Obtain the following laboratory studies in cases of suspected food poisoning:

Gram staining and Loeffler methylene blue staining of the stool for WBCs help to differentiate invasive disease from noninvasive disease.
Perform microscopic examination of the stool for ova and parasites.
Bacterial culture for enteric pathogens, such as Salmonella, Shigella, and Campylobacter organisms, becomes mandatory if a stool sample shows positive results for WBCs or blood or if patients have fever or symptoms persisting for longer than 3-4 days.
Perform blood culture if the patient is notably febrile.
CBC with differential, serum electrolyte assessment, and BUN and creatinine levels help to assess the inflammatory response and the degree of dehydration.
Assay for C difficile to help rule out antibiotic-associated diarrhea in patients receiving antibiotics or in those with a history of recent antibiotic use.

Histamine food poisoning from gram-negative bacteria in fin-fish products is also common, and Morganella morganii and M psychrotolerans are particularly strong histamine producers. The development of real-time quantitative polymerase chain reaction (RTiqPCR) techniques in conjunction with the use of selective primers and a quantitative enrichment step appear to have the potential to identify and quantify these two species in fish products.^[15]

Imaging Studies

Flat and upright abdominal radiographs should be obtained if the patient experiences bloating, severe pain, or obstructive symptoms or if perforation is suggested.

Procedures

When a stool examination is nondiagnostic, performing sigmoidoscopy/colonoscopy with biopsy and esophagogastroduodenoscopy (EGD) with duodenal aspirate and biopsy may be beneficial. This is especially important in patients who are immunocompromised.

Consider sigmoidoscopy in patients with bloody diarrhea. It can be useful in diagnosing inflammatory bowel disease, antibiotic-associated diarrhea, shigellosis, and amebic dysentery.

Treatment & Management

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Table 1.Causes of Food Poisoning.

Table 1.Causes of Food Poisoning.

Causative Agents		Source and Clinical Features	Pathogenesis	Diagnosis and Treatment
Staphylococci		Improperly stored foods with high salt or sugar content favors growth of staphylococci. Intense vomiting and watery diarrhea start 1-4 h after ingestion and last as long as 24-48 h	Enterotoxin acts on receptors in the gut that transmit impulses to the medullary centers	Symptomatic treatment
B cereus		Contaminated fried rice (emetic) Meatballs (diarrheal) Emetic: Duration is 9 h, vomiting and cramps Diarrheal: Lasts for 24 h Mainly vomiting after 1-6 h and mainly diarrhea after 8-16 h after ingestion; lasts as long as 1 d	Emetic enterotoxin (short incubation and duration) - Poorly understood Diarrheal enterotoxin (long incubation and duration) - Increasing intestinal secretion by activation of adenylate cyclase in intestinal epithelium	Symptomatic treatment
C perfringens	Inadequately cooked meat, poultry, or legumes Acute onset of abdominal cramps with diarrhea starts 8-24 h after ingestion. Vomiting is rare. It lasts less than 1 d. Enteritis necroticans associated with C perfringens type C in improperly cooked pork (40% mortality)		Enterotoxin produced in the gut, and food causes hypersecretion in the small intestine	Culture of clostridia in food and stool Symptomatic treatment
C botulinum		Canned foods (eg, smoked fish, mushrooms, vegetables, honey) Descending weakness and paralysis start 1-4 d after ingestion, followed by constipation. Mortality is high	Toxin absorbed from the gut blocks the release of acetylcholine in the neuromuscular junction	Toxin present in food, serum, and stool. Respiratory support Intravenous trivalent antitoxin from CDC
Listeria monocytogenes		Raw and pasteurized milk, soft cheeses, raw vegetables, shrimp Systemic disease associated with bacteremia Intestinal symptoms precede systemic disease Can seed meninges, heart valves, and other organs Highest mortality among bacterial food poisonings	Highly motile, heat-resistant, gram-positive organism	CSF or blood culture Must treat with antibiotics if bacteremic
Enterotoxic E coli (eg, traveler's diarrhea)		Contaminated water and food (eg, salad, cheese, meat) Acute-onset watery diarrhea starts 24-48 h after ingestion Concomitant vomiting and abdominal cramps may be present. It lasts for 1-2 d	Enterotoxin causes hypersecretion in small and large intestine via guanylate cyclase activation	Supportive treatment No antibiotics
Enterohemorrhagic E coli (eg, E coli O157:H7)		Improperly cooked hamburger meat and previously spinach Most common isolate pathogen in bloody diarrhea starts 3-4 d after ingestion Usually progresses from watery to bloody diarrhea. It lasts for 3-8 d May be complicated by hemolytic-uremic syndrome or thrombotic thrombocytopenic purpura	Cytotoxin results in endothelial damage and leads to platelet aggregation and microvascular fibrin thrombi	Diagnosis with stool culture Supportive treatment No antibiotics
Enteroinvasive E coli		Contaminated imported cheese Usually watery diarrhea (some may present with dysentery)	Enterotoxin produces secretion Shigalike toxin facilitates invasion	Supportive treatment No antibiotics
Enteroaggregative E coli		Implicated in traveler's diarrhea in developing countries Can cause bloody diarrhea	Bacteria clump on the cell surfaces	Ciprofloxacin may shorten duration and eradicate the organism
V cholera		Contaminated water and food Large amount of nonbloody diarrhea starts 8-24 h after ingestion. It lasts for 3-5 d	Enterotoxin causes hypersecretion in small intestine Infective dose usually is 10⁷ -10⁹ organisms	Positive stool culture finding Prompt replacement of fluids and electrolytes (oral rehydration solution) Tetracycline (or fluoroquinolones) shortens the duration of symptoms and excretion of Vibrio
V parahaemolyticus		Raw and improperly cooked seafood (ie, mollusks and crustaceans) Explosive watery diarrhea starts 8-24 h after ingestion It lasts for 3-5 d	Enterotoxin causes hypersecretion in small intestine Hemolytic toxin is lethal Infective dose is usually 10⁷ -10⁹ organisms	Positive stool culture Prompt replacement of fluids and electrolytes Sensitive to tetracycline, but unclear role for antibiotics
V vulnificus		Wound infection in salt water or consumption of raw oysters Can be lethal in patients with liver disease (50% mortality)	Polysaccharide capsule Growth correlates with availability of iron (especially transferrin saturation >70%)	Culture of characteristic bullous lesions or blood Immediate antibiotics if suspected (eg, doxycycline and ceftriaxone)
C jejuni		Domestic animals, cattle, chickens Fecal-oral transmission in humans Foul-smelling watery diarrhea followed by bloody diarrhea Abdominal pain and fever also may be present; it starts 1-3 d after exposure and recovery is in 5-8 d	Uncertain about endotoxin production and invasion	Culture in special media at 42°C Erythromycin for invasive disease (fever)
Shigella		Potato, egg salad, lettuce, vegetables, milk, ice cream, and water Abrupt onset of bloody diarrhea, cramps, tenesmus, and fever starts 12-30 h after ingestion. Usually self-limited in 3-7 d	Organisms invade epithelial cells and produce toxins Infective dose is 10² -10³ organisms Enterotoxin-mediated diarrhea followed by invasion (dysentery/colitis)	Polymorphonuclear leukocytes (PMNs), blood, and mucus in stool Positive stool culture Oral rehydration is mainstay Trimethoprim-sulfamethoxazole (TMP-SMX) or ampicillin for severe cases No opiates
Salmonella		Beef, poultry, eggs, and dairy products Abrupt onset of moderate-to-large amount of diarrhea with low-grade fever; in some cases, bloody diarrhea Abdominal pain and vomiting also present, beginning 6-48 h after exposure and lasts 7-12 d	Invasion but no toxin production	Positive stool culture finding Antibiotic for systemic infection
Yersinia		Pets; transmission in humans by fecal-oral route or contaminated milk or ice cream Acute abdominal pain, diarrhea, and fever (enterocolitis) Incubation period not known Polyarthritis and erythema nodosum in children May mimic appendicitis	Gastroenteritis and mesenteric adenitis Direct invasion and enterotoxin	Polymorphonuclear leukocytes and blood in stool Positive stool culture finding No evidence that antibiotics alter the course but may be used in severe infections
Aeromonas		Untreated well or spring water Diarrhea may be bloody May be chronic up to 42 d in the United States	Enterotoxin, hemolysin, and cytotoxin	Positive stool culture Fluoroquinolones or TMP/SMX for chronic diarrhea
Parasitic Food Poisoning		Source and Clinical Features	Pathogenesis	Diagnosis and Treatment
E histolytica		Contaminated food and water 90% asymptomatic 10% dysentery Minority may develop liver abscesses	Invasion of the mucosa by the parasites	Criterion standard is colonoscopy with biopsy Ova and parasites may be seen in the stool but has low sensitivity Luminal amebicides (eg, paromomycin) Tissue amebicides (eg, metronidazole)
G lamblia		Contaminated ground water Fecal-oral transmission in humans Mild diarrhea with nausea and abdominal cramps starts 2-3 d after ingestion; lasts for 1 wk May become chronic	Unknown Highest concentration in the distal duodenum and proximal jejunum	Initial diagnostic test is stool enzyme-linked immunosorbent assay Duodenal aspiration or small bowel biopsy Cyst in the stool Metronidazole
Seafood/Shellfish Poisoning		Source and Clinical Features	Pathogenesis	Diagnosis and Treatment
Paralytic shellfish poisoning		Temperate coastal areas Source - Bivalve mollusks Onset usually is 30-60 min Initial symptoms include perioral and intraoral paresthesia Other symptoms include paresthesia of the extremities, headache, ataxia, vertigo, cranial nerve palsies, and paralysis of respiratory muscles, resulting in respiratory arrest	Fish acquires toxin-producing dinoflagellates	General observation for 4-6 h Maintain patent airway. Administer oxygen, and assist ventilation if necessary For recent ingestion, charcoal 50-60 g may be helpful
Neurotoxic shellfish poisoning		Coastal Florida Source - Mollusks Illness is milder than in paralytic shellfish poisoning	Fish acquires toxin-producing dinoflagellates	Symptomatic
Ciguatera		Hawaii, Florida, and Caribbean Source - Carnivorous reef fish Vomiting, diarrhea, and cramps start 1-6 h after ingestion and last from days to months Diarrhea may be accompanied by a variety of neurologic symptoms including paresthesia, reversal of hot and cold sensation, vertigo, headache, and autonomic disturbances such as hypotension and bradycardia Chronic symptoms (eg, fatigue, headache) may be aggravated by caffeine or alcohol	Fish acquires toxin-producing dinoflagellates Toxin increases intestinal secretion by changing intracellular calcium concentration	Symptomatic Anecdotal reports of successful treatment of neurologic symptoms with mannitol 1 g/kg IV
Tetrodotoxin poisoning		Japan Source - Puffer fish Onset of symptoms usually is 30-40 min but may be as short as 10 min; it includes lethargy, paresthesia, emesis, ataxia, weakness, and dysphagia; ascending paralysis occurs in severe cases; mortality is high.	Neurotoxin is concentrated in the skin and viscera of puffer fish.	Symptomatic
Scombroid		Source - Tuna, mahi-mahi, kingfish Allergic symptoms such as skin flush, urticaria, bronchospasm, and hypotension usually start within 15-90 min	Improper preservation of large fish results in bacterial degradation of histidine to histamine	Antihistamines (diphenhydramine 25-50 mg IV) H2 blockers (cimetidine 300 mg IV) Severe reactions may require subcutaneous epinephrine (0.3-0.5 mL of 1:1000 solution)
Heavy Metal Poisoning		Source	Symptoms	Treatment
Mercury		Ingestion of inorganic mercuric salts	Causes metallic taste, salivation, thirst, discoloration and edema of oral mucous membranes, abdominal pain, vomiting, bloody diarrhea, and acute renal failure	Consult a toxicologist Remove ingested salts by emesis and lavage, and administer activated charcoal and a cathartic Dimercaprol is useful in acute ingestion
Lead		Toxicity results from chronic repeated exposure It is rare after single ingestion	Common symptoms include colicky abdominal pain, constipation, headache, and irritability Diagnosis is based on lead level (>10 mcg/dL)	Other than activated charcoal and cathartic, severe toxicity should be treated with antidotes (edetate calcium disodium [EDTA] and dimercaprol).
Arsenic		Ingestion of pesticide and industrial chemicals	Symptoms usually appear within 1 h after ingestion but may be delayed as long as 12 h Abdominal pain, watery diarrhea, vomiting, skeletal muscle cramps, profound dehydration, and shock may occur	Gastric lavage and activated charcoal Dimercaprol injection 10% solution in oil (3-5 mg/kg IM q4-6h for 2 d) and oral penicillamine (100 mg/kg/d divided qid for 1 wk)

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Author

Roberto M Gamarra, MD Consulting Gastroenterologist, Digestive Health Associates, PLC

Roberto M Gamarra, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Crohn's and Colitis Foundation of America

Disclosure: Nothing to disclose.

Coauthor(s)

David Manuel, MD Affiliate Faculty, Department of Medicine, Loyola University Health System; Gastroenterologist, Digestive Health Center

David Manuel, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Crohn's and Colitis Foundation of America

Disclosure: Nothing to disclose.

Michael H Piper, MD Clinical Assistant Professor, Department of Internal Medicine, Division of Gastroenterology, Wayne State University School of Medicine; Consulting Staff, Digestive Health Associates, PLC

Michael H Piper, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American College of Physicians, Michigan State Medical Society

Disclosure: Nothing to disclose.

Senthil Nachimuthu, MD, FACP Interventional Cardiologist, SSM Health

Senthil Nachimuthu, MD, FACP is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Priyankha Balasundaram, MD Director, Kovai Heart Foundation, India; Resident, Department of Surgery, Tulane University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Chief Editor

Praveen K Roy, MD, MSc Clinical Assistant Professor of Medicine, University of New Mexico School of Medicine

Praveen K Roy, MD, MSc is a member of the following medical societies: Alaska State Medical Association, American Gastroenterological Association

Disclosure: Nothing to disclose.

Additional Contributors

Jose A Perez, Jr, MD, MBA, MSEd Residency Director, Internal Medicine Residency Program, Vice Chair of Education, Department of Medicine, Methodist Hospital; Associate Professor of Clinical Medicine, Weill Cornell Medical College

Jose A Perez, Jr, MD, MBA, MSEd is a member of the following medical societies: American Association for Physician Leadership, American College of Physicians, Society of General Internal Medicine, Society of Hospital Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Simmy Bank, MD Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.