Diarrhea is defined as a stool volume of greater than 10 g/kg/day in infants and toddlers and greater than 200 g/day in older children. Functionally, diarrhea should be considered if a patient is passing 3 or more unusually loose stools in a 24-hour period or is passing stools more frequently than usual, with a consistency looser than what is considered normal for that individual. Diarrhea is classified broadly by the duration of symptoms. Acute diarrhea is usually a self-limited illness that lasts for 2 weeks or less. Chronic diarrhea persists for more than 2 weeks. The etiologies of acute and chronic diarrhea differ by age ( Table 11.1 ).
| Infants | Children | Adolescents |
|---|---|---|
| Acute | ||
| Common |
|
|
| ||
| Rare | ||
| ||
| Chronic | ||
Disorders of Absorption and Transport of Nutrients and Electrolytes
Defects in Enterocyte Structure
Neuro-Enteroendocrine Diarrhea
Defects in Intestinal Immune-Related Homeostasis
Pancreatic Insufficiency
| Disorders of Absorption and Transport of Nutrients and Electrolytes
Disorders of Intestinal Motility
Infectious Etiologies
Defects in Enterocyte Structure Trichohepatoenteric syndrome (syndromic diarrhea) Neuro-Enteroendocrine Diarrhea
Defects in Intestinal Immune-Related Homeostasis
Pancreatic Insufficiency
| Disorders of Absorption and Transport of Nutrients and Electrolytes
Disorders of Intestinal Motility
Infectious Etiologies
Neuro-Enteroendocrine Diarrhea Primary adrenal insufficiency Defects in Intestinal Immune-Related Homeostasis
Pancreatic Insufficiency Chronic pancreatitis |
Diarrhea is further classified by pathophysiology, which typically involves 1 or more of the following mechanisms: (1) osmotic diarrhea , characterized by the presence of an increased intraluminal osmotic load leading to passive diffusion of fluid into the gastrointestinal lumen; (2) secretory diarrhea , characterized by increased secretion of fluid into the gastrointestinal lumen beyond the capacity to be reabsorbed; and (3) altered gastrointestinal tract motility. Differentiating osmotic from secretory diarrhea allows for a more directed diagnostic evaluation ( Table 11.2 ). Osmotic diarrhea may be related to the malabsorption of carbohydrate, fat, or protein or to the presence of nonabsorbable substances in the gastrointestinal lumen. The characteristics of the stool may provide information that allows for the identification of the malabsorbed substance, particularly for isolated carbohydrate and fat malabsorption ( Table 11.3 ). Secretory diarrhea is characterized by an excess of crypt cell fluid and electrolyte secretion that exceeds the absorptive capabilities of the villi and is classified by the presence or absence of normal villi. Inflammatory diarrhea of both infectious and noninfectious etiologies usually involves both osmotic and secretory components. Finally, surgical bowel resection may decrease the surface area available for the resorption of both fluid and solutes, leading to both a secretory and osmotic diarrhea. The causes of diarrhea based on pathophysiology are presented in Table 11.4 .
| Osmotic | Secretory | |
|---|---|---|
| Stool volume | Small (<200 mL/24 hr) | Large (>200 mL/24 hr) |
| Response to fasting | Diarrhea improves | Diarrhea continues |
| Stool sodium | <70 | >70 |
| Stool osmotic gap * | >50 | <50 |
| Stool pH | <5 | >6 |
| Isolated Carbohydrate Malabsorption | Isolated Fat Malabsorption | |
|---|---|---|
| Stool character | Loose and watery, non–foul-smelling | Bulky large stool, foul-smelling, oil droplets visible |
| Perianal rash/skin erosion | Present | Present |
| Signs of fat-soluble vitamin deficiency | Variable | Present |
| Stool pH | Acidic (usually <6) | Alkaline |
| Stool reducing/non-reducing substances | Present | Absent |
Osmotic Diarrhea
|
Secretory Diarrhea
Autoimmune polyglandular syndrome type 1 Neuroendocrine tumors |
Inflammatory (Combination of Secretory and Osmotic)
|
Decreased Surface Area for Absorption
|
Acute Diarrhea
History
Acute diarrhea in children is most often infectious ( Table 11.5 ), although it may be secondary to noninfectious inflammatory processes, toxins, or medications. The etiology of acute diarrhea is suggested by both the history and characteristics of the stool. Fever or blood in the stool suggests an infectious cause. Watery diarrhea is typical of viral gastroenteritis, as well as some bacterial and parasitic infections. Dysentery , characterized by severe diarrhea and the presence of blood and mucus in the stool, suggests bacterial colitis. Vomiting and diarrhea developing within hours of ingesting food suggests exposure to preformed toxins in the food, rather than the acquisition of an enteric pathogen from the food, which is characterized by a predominantly diarrheal illness developing within days of exposure ( Fig. 11.1 ). A recent history of travel suggests traveler’s diarrhea , more than 80% of which is caused by bacterial species that are endemic to the area of travel, to which the patient has not been previously exposed. Recent travel may also suggest parasitic or helminthic infection. Exposure to health care settings suggests nosocomial diarrhea . Patients with a history of immunodeficiency or malnourishment may be more likely to have an infection with atypical or opportunistic organisms or to have a more protracted and severe course. Hematuria or oliguria may suggest hemolytic uremic syndrome as a complication of infection with Escherichia coli 0157 : H7 or Shigella.
Viruses
|
Bacteria
|
Protozoa
|
Helminths
|
Physical Examination
Physical examination should focus on assessing the level of hydration and the need for fluid resuscitation ( Table 11.6 ). The general examination may reveal nonenteric infections that could present with diarrhea, such as otitis media, pneumonia, or sepsis. Abdominal tenderness or masses suggest appendicitis, intussusception, or less commonly, toxic megacolon. Generalized toxicity or shock may occur with hemolytic uremic syndrome or with sepsis, such as from invasive Salmonella or staphylococcal toxic shock syndrome.
| Signs and Symptoms General Appearance | Mild | Moderate | Severe |
|---|---|---|---|
| Infants/young children | Thirsty; alert; restless | Thirsty; restless or listless | Drowsy or lethargic; limp, cold, sweaty, cyanotic |
| Older children | Thirsty; alert; restless | Thirsty; alert (usually) | Usually conscious (but at reduced level), apprehensive; cold, sweaty, cyanotic extremities; wrinkled skin on fingers/toes; muscle cramps |
| Tachycardia | Absent | Present | Present |
| Palpable pulses | Present | Present (weak) | Decreased |
| Blood pressure | Normal | Orthostatic hypotension | Hypotension |
| Cutaneous perfusion | Normal | Normal | Reduced/mottled |
| Skin turgor | Normal | Slight reduction | Reduced |
| Fontanel | Normal | Slightly depressed | Sunken |
| Mucous membranes | Moist | Dry | Very dry |
| Tears | Present | Present/absent | Absent |
| Respirations | Normal | Deep, may be rapid | Deep and rapid |
| Urine output | Normal | Oliguria | Anuria/severe oliguria |
Viral Diarrhea
Rotavirus infection.
Rotavirus is the leading cause of severe diarrhea in infants and young children. The introduction of an effective vaccine has decreased the incidence, with most infections occurring in unvaccinated children under 3 years of age. Transmission is by the fecal-oral route and the incubation period ranges from 1 to 3 days. Patients typically present with the acute onset of fever and vomiting followed 1-2 days later by watery diarrhea. Symptoms generally persist for 3-8 days. In moderate to severe cases, dehydration, electrolyte abnormalities, and acidosis may occur. In immunocompromised children, persistent infection and chronic diarrhea can develop, with persistently positive diagnostic assays. Chronic infection is to be differentiated from postinfectious malabsorption seen in some immunocompetent children, in whom the small intestinal mucosa may require 3-8 weeks to recover its absorptive ability. Diagnosis is confirmed by nucleic acid amplification assays, enzyme immunoassay (EIA), immunochromatography, or latex agglutination assay for group A rotavirus antigen detection in the stool.
Norovirus infection.
Norovirus is a single-stranded RNA virus of the Calciviridae family and is the leading cause of epidemic outbreaks of acute gastroenteritis, as well as the most common cause of foodborne illness and foodborne disease outbreaks in the United States. Young children have the highest incidence of infection. Transmission is via the fecal-oral route or through contaminated food or water. Norovirus gastroenteritis typically presents with the abrupt onset of vomiting accompanied by watery diarrhea, abdominal cramps, nausea, and vomiting. Systemic manifestations, including myalgia, fatigue, and headache may accompany gastrointestinal symptoms. Diagnosis is confirmed by nucleic acid amplification assays that detect viral RNA from the stool.
Bacterial Diarrhea
Most bacterial diarrheal illnesses are foodborne and affect infants and young children more frequently than adults. Bacterial infections of the intestine cause diarrhea via direct invasion of the intestinal mucosa, followed by intraepithelial cell multiplication or invasion of the lamina propria. Cellular invasion may be followed by the production of cytotoxin, which disrupts cell function, and/or the production of enterotoxin, which alters cellular electrolyte and water balance. Bacterial adherence to the mucosal surface may result in flattening of the microvilli and disruption of normal cell functioning. Symptomatic differentiation from viral causes of diarrhea may be difficult, and sequelae of infections are varied ( Table 11.7 ).
| Complication | Important Bacterial Agents | Clinical Considerations |
|---|---|---|
| Dehydration | Vibrio cholerae , any bacterial enteropathogen | Complication of all forms of acute watery diarrhea; should prompt aggressive fluid and electrolyte replacement |
| Bacteremia | Salmonella , Campylobacter fetus | Organisms that deeply penetrate the intestinal mucosa are prone to cause bacteremia; certain high-risk conditions predispose to systemic Salmonella infection |
| Hemolytic uremic syndrome | Shiga toxin–producing Escherichia coli, Campylobacter jejuni | Shiga toxin is absorbed, causing injury to endothelial cells of the glomerular capillaries with intravascular coagulation |
| Guillain-Barré syndrome | Campylobacter , Salmonella , Shigella flexneri , Yersinia | Most cases occur as a result of molecular mimicry, with antibodies directed to Campylobacter lipooligosaccharides and peripheral nerve gangliosides; probability of development of Guillain-Barré syndrome within 2 mo after Campylobacter infection estimated at <2/10,000 cases |
| Reactive arthritis and iritis | Inflammatory bacterial pathogens (e.g., Campylobacter ) are most important, but most bacterial pathogens can produce the syndrome | Occurs in 2.1/100,000 cases of Campylobacter infection and 1.4/100,000 cases of Salmonella infection; affected persons may be HLA-B27–positive or HLA-B27–negative |
| Postinfectious irritable bowel syndrome | Vibrio cholerae , any bacterial enteropathogen | Enteric bacterial infection with intestinal inflammation in a susceptible host leads to altered intestinal findings and postinfectious irritable bowel syndrome; duration is ≥5 yr |
Salmonella infection.
Nontyphoidal Salmonella organisms are estimated to cause 1 million annual gastrointestinal infections in the United States. The attack rate is highest in infancy; the incidence of symptomatic infections is lower in patients older than 6 years. Salmonella infection may cause an asymptomatic intestinal carrier state (rare in children), enterocolitis with diarrhea, or bacteremia without gastrointestinal manifestations but with subsequent local infections, such as meningitis or osteomyelitis. Salmonella infection is usually spread through contaminated water supplies or food (e.g., meat, chicken, eggs, raw milk, and fresh produce). Most infections in the United States are sporadic rather than epidemic. Although an infected food handler may contaminate food sources, farm animals or pets are often the vector. Cats, turtles, lizards, snakes, and iguanas may also harbor Salmonella organisms. Outbreaks may occur among institutionalized children; outbreaks in daycare centers are rare.
After a 12- to 72-hour incubation period, gastroenteritis develops and is characterized by the sudden onset of diarrhea, abdominal cramps and tenderness, and fever. The diarrhea is watery, with stools containing polymorphonuclear leukocytes and, on occasion, blood. The peripheral blood white blood cell count is usually normal. Symptoms slowly resolve within 3-5 days, although excretion of the organism may persist for several weeks. The organism is readily isolated from culture of the stool or a rectal swab, or may be identified via multiplex polymerase chain reaction (PCR) assays that detect multiple bacterial, viral, and parasitic enteric pathogens.
Shigella infection.
Most Shigella infections in the United States occur in young children 1-4 years of age, with a peak seasonal incidence in late summer and early autumn. It may also be the most common bacterial cause of diarrhea outbreaks in daycare settings. The organism is transmitted via the fecal-oral route, most often by the hands. During a 12- to 72-hour incubation period, patients may develop a nonspecific prodrome characterized by fever, chills, nausea, and vomiting. A predominantly rectosigmoid colitis develops and results in abdominal cramps and watery diarrhea. In more severe infections ( bacillary dysentery ), blood and mucus are passed in small, very frequent stools. High fever in young infants may induce febrile seizures, and some patients may develop hemolytic uremic syndrome. Bacterial culture of the stool or a rectal swab, or the use of multiplex PCR assays, allows for differentiating this organism from other pathogens. If positive, antibiotic treatment is usually indicated.
Campylobacter infection.
Many animal species, including poultry, farm animals, and household pets, serve as reservoirs for Campylobacter jejuni . Transmission occurs through ingestion of contaminated food, especially undercooked food, and through person-to-person spread via the fecal-oral route. The disease is common in infants and adolescents, and both daycare and college outbreaks have been reported. Asymptomatic carriage is uncommon. Campylobacter infection causes disease that may range from mild diarrhea to frank dysentery. The organism causes diffuse, invasive enteritis that involves the ileum and colon. Fever, cramping, abdominal pain, and bloody diarrhea are characteristic and may mimic symptoms of acute appendicitis or inflammatory bowel disease. Fever and diarrhea usually resolve after 5-7 days; prolonged illness or relapse occasionally occurs. Campylobacter infection is also known to cause meningitis, abscesses, pancreatitis, and pneumonia. Guillain-Barré syndrome has been reported after Campylobacter infection. Identification is via stool or rectal swab bacterial culture, or via multiplex PCR assay. If positive, antibiotic treatment is indicated.
Yersinia infection.
Infection with either Yersinia enterocolitica or Y. pseudotuberculosis may cause various clinical syndromes, including gastroenteritis, mesenteric adenitis, pseudoappendicitis, and postinfectious reactive arthritis. The organism is present in animals and may be spread to humans by consumption of undercooked meat (especially pork), unpasteurized milk, and other contaminated foods. Person-to-person spread also occurs. Young children are particularly susceptible to disease, and the frequency of infections increases during the summer months.
The organisms may be identified via multiplex PCR assay or may be cultured from rectal swab or stool specimens, but selective media are required, and the organism may not be identified via culture for several weeks. The microbiology laboratory should be notified if Yersinia infection is suspected. Antibiotics are not effective in alleviating symptoms of Yersinia enteritis or in shortening the period of bacterial excretion. Patients with extraintestinal infection should receive therapy.
Escherichia coli infection.
Although E. coli comprise the predominant normal flora in the colon, some strains are pathogenic. Diarrhea caused by E. coli can be watery, inflammatory, or bloody, depending on the strain involved. These diarrheogenic E. coli strains are classified into 5 major groups on the basis of serogrouping or pathogenic mechanisms: (1) enteropathogenic E. coli (EPEC), an important cause of diarrhea in infants; (2) enterotoxigenic E. coli (ETEC), a cause of diarrhea in infants and a cause of traveler’s diarrhea; (3) enteroinvasive E. coli , a cause of watery ETEC-like illness or, less commonly, a dysentery-like illness; (4) enterohemorrhagic E. coli , a cause of hemorrhagic colitis and hemolytic uremic syndrome (HUS); and (5) enteroaggregative E. coli , a cause of persistent diarrhea.
Enteric infections with E. coli are acquired via the fecal-oral route. Enterohemorrhagic strains are the only diarrhea-producing E. coli strains common in the United States and have been associated with foodborne epidemic outbreaks transmitted in some cases by undercooked meat.
EPEC is a well-established cause of infantile diarrhea, especially in developing countries. Asymptomatic carriage is common. At least 2 separate mechanisms are responsible for diarrhea: adherence to intestinal epithelial cells leading to villous injury and mucosal inflammation, and production of a toxin similar to that of Shigella organisms. Chronic infection resulting in failure to thrive may also occur.
ETEC is the major cause of traveler’s diarrhea; occasional nosocomial outbreaks have also occurred in hospitalized infants. At least 3 different types of E. coli enterotoxins (heat-labile, heat-stable toxin A, and heat-stable toxin B) have been identified. Definitive diagnosis requires enterotoxin identification, and this method is not widely available.
Enterohemorrhagic E. coli produces a Shiga-like cytotoxin and causes diarrhea, hemorrhagic colitis, and, in about 20% of infected persons, hemolytic uremic syndrome (HUS) . Both epidemic and sporadic cases have been recognized. Infection is more common in the summer and fall. A particular serotype, E. coli 0157 : H7, has been linked to the development of HUS in young children. The most common manifestations of enterohemorrhagic E. coli infection begin with severe abdominal cramps and watery diarrhea, followed by grossly bloody stools and emesis. Fever is uncommon. Fecal leukocytes are absent or few. Other manifestations include asymptomatic infection and watery diarrhea without progression to hemorrhagic colitis. E. coli 0157 : H7 is cleared from the stool in 5-12 days. If HUS develops, symptoms become noticeable in the week after the onset of diarrhea and consist of renal failure, microangiopathic hemolytic anemia, thrombocytopenia, and diarrhea. There is no role for antimicrobial therapy in enterohemorrhagic E. coli disease. Antibiotics neither shorten the duration of disease nor prevent progression to HUS; they may predispose to HUS.
Clostridium difficile infection.
Clostridium difficile causes acute and chronic diarrhea in children when the normal colonic flora is disrupted. Pseudomembranous colitis is the most severe form of this infection, occurring as a result of a severe inflammatory response to the C. difficile toxins. Transmission occurs through person-to-person contact and through environmental contamination via the spores formed by C. difficile , which retain viability for up to 1 week on dry surfaces.
The prevalence of carrier status for C. difficile in healthy, asymptomatic outpatients is as high as 50% in healthy infants, but is usually less than 5% in patients over 5 years of age. C. difficile and its toxin have been identified in the feces of healthy infants in concentrations similar to those found in adults with pseudomembranous colitis. The apparent resistance of infants to C. difficile and its toxin is related to the developmental absence of the toxin-binding site in the immature intestine. Asymptomatic carriage rates in hospitalized patients may be as high as 20%. Infection is highly associated with recent antibiotic exposure, particularly to broad-spectrum antibiotics, which disrupt the endogenous colonic flora that inhibits the growth of C. difficile . Other risk factors for C. difficile diarrhea include inflammatory bowel disease, gastrointestinal surgery or procedures, and immunocompromised status.
C. difficile infection should be considered in patients in whom diarrhea develops during or within several weeks of antibiotic therapy. Illness associated with this organism varies from a mild, self-limited, nonbloody diarrhea to severe hemorrhagic colitis, protein-losing enteropathy, toxic megacolon, colonic or cecal perforation, peritonitis, sepsis, shock, and death. In rare cases, manifestations of C. difficile infection include fever or abdominal pain without diarrhea.
The colitis is caused by potent toxins produced by the organism: toxin A , a lethal enterotoxin that causes hemorrhage and fluid secretion in the intestines; and toxin B , a cytotoxin detectable by its cytopathic effects in tissue culture. Both toxins play a role in disease production, although toxin A may be more important.
C. difficile infection is currently diagnosed either by enzyme immunoassay for toxins in stool or by nucleic acid amplification tests that identify the microbial toxin genes in unformed stool. Sigmoidoscopy or colonoscopy reveals pseudomembranes in 30-50% of cases, typically in association with more severe disease. Treatment is indicated for severe disease.
Aeromonas infection.
Aeromonas species are gram-negative bacilli that are found in a variety of freshwater sources and that are capable of causing a wide array of disease, including a mild, self-limited diarrheal illness in children. Occasionally, Aeromonas may cause dysentery or a protracted diarrheal illness. The most common manifestation is a watery, nonbloody, nonmucoid diarrhea seen during the late spring, summer, and early fall. More severe infections may resemble ulcerative colitis, with chronic bloody diarrhea and abdominal pain.
Plesiomonas infection.
Plesiomonas shigelloides is a Vibrio -like organism found in soil and water that is sometimes implicated in childhood diarrhea. It has been linked to consumption of raw shellfish or contaminated water, exposure to reptiles and tropical fish, and travel to Mexico and Asia. After an incubation period of 1-2 days, patients typically develop watery diarrhea and vomiting, although some may develop dysentery. Diagnosis is via stool culture. Symptoms may last up to 2 weeks, although the disease is typically self-limited in immunocompetent individuals.
Parasitic Diarrhea
Giardiasis.
Giardia intestinalis is a flagellated protozoan that can cause diarrhea, malabsorption, abdominal pain, and weight loss. It spreads through contaminated food and water, as well as through person-to-person contact via the fecal-oral route. The latter mode of transmission is responsible for outbreaks of diarrhea in daycare centers and residential facilities. Infection is often asymptomatic. Symptomatic illness usually develops 1-3 weeks after exposure and may mimic acute gastroenteritis with low grade or no fever, nausea, vomiting, and watery diarrhea. In some patients, a chronic illness develops, characterized by intermittent, foul-smelling diarrhea, abdominal bloating, nausea, abdominal pain, and weight loss. Up to 40% of patients may develop secondary lactase deficiency following infection. Diagnosis is via EIA or direct fluorescent antibody (DFA) tests, which offer superior sensitivity and specificity compared to microscopy. If microscopy is performed, three separate samples of fresh stool should be examined for cysts or trophozoites, because excretion of the organism is only intermittent. Treatment is typically indicated in the presence of symptoms, to prevent institutional outbreaks, or to prevent spread to immunocompromised individuals.
Entamoeba histolytica infection.
Entamoeba histolytica is acquired in warm climates via the ingestion of cysts in fecally contaminated food or water. Infected individuals are often asymptomatic. Amebic dysentery may occur, but hepatic abscess and other remote infections are uncommon. Because cysts are shed in the stool on an intermittent basis, examination of several fecal specimens may be required for identification. Stool antigen detection assays allow for differentiation between E. histolytica and the more prevalent though less pathogenic E. dispar , which may also be detected on microscopy. Treatment is indicated to prevent the development of extraintestinal manifestations or spread to other individuals.
Cryptosporidium infection.
This intracellular protozoan causes watery diarrhea in both immunocompetent and immunocompromised hosts and is an important cause of severe diarrhea in individuals infected with the human immunodeficiency virus. Cryptosporidium has also been recognized as an occasional cause of self-limited diarrhea in travelers, as well as in children in daycare centers and persons in residential institutions. The mechanisms by which these organisms cause diarrhea are unknown. Nucleic acid amplification assays and EIA tests are available for diagnosis. Identification via microscopy requires specialized staining techniques that should be requested if Cryptosporidium infestation is suspected.
Other Causes of Acute Diarrhea
Parenteral secondary diarrhea.
Acute diarrhea that accompanies infections outside of the gastrointestinal tract is termed parenteral diarrhea . Upper respiratory tract and urinary tract infections may be associated with increased bowel movement frequency or stool water. The mechanism is unclear but may involve alterations in bowel motility, changes in diet, or the effects of antibiotic treatment.
Medications.
Various nonlaxative prescription and over-the-counter medications may cause acute diarrhea ( Table 11.8 ). The most commonly implicated agents are antibiotics, acting through mechanisms other than C. difficile .
| Agent | Mechanism |
|---|---|
| Stimulant laxatives (e.g., senna, bisacodyl) | Increased intestinal secretion (phenolphthalein, bisacodyl) |
| Antacids | Osmotic effect (Mg 2+ ) |
| Prokinetic agents | Increased peristalsis (metoclopramide, bethanechol, cisapride) |
| Measles-mumps-rubella vaccine | Unknown |
| Thyroid hormone | Increased peristalsis |
| Chemotherapeutics | Intestinal mucosal injury |
| Heavy metals | Toxic effect |
| Organophosphates | Cholinergic effects |
| Diuretics | Unknown |
| Digitalis | Unknown |
| Colchicine | Unknown |
| Indomethacin | Prostaglandin synthesis inhibition |
| Theophylline | Increased peristalsis |
Food poisoning ( Table 11.9 ; see Fig. 11.1 ).
Staphylococcal food poisoning results from ingestion of preformed enterotoxin, produced in contaminated food that has incubated at or above room temperature for a suitable period. Staphylococcal food poisoning is suggested by the sudden onset of vomiting that is followed by explosive diarrhea, usually within 4-6 hours after ingestion of the contaminated food. The illness is self-limited and usually resolves within 12-24 hours. The diagnosis is based on the typical historical presentation. Treatment is supportive; antibiotics are not indicated.
| Cause | Incubation Period | Clinical Clues | Common Vehicle | Diagnosis |
|---|---|---|---|---|
| Monosodium glutamate | Minutes to 2 hr | Burning in abdomen, chest, extremities, and neck; lightheadedness; chest pain | Found in some Asian cuisines | Large amount of monosodium glutamate in implicated food |
| Heavy metals (copper, zinc, cadmium, tin) | Minutes to 2 hr | Metallic taste, diarrhea, prominent vomiting, no fever | Carbonated or acidic beverages in metal containers | Chemical study of implicated beverage |
| Mushroom poisoning * | Minutes to 2 hr | Altered mental status with visual disturbance (encephalopathy) | Noncommercially obtained mushrooms | Identify mushroom and/or toxic chemical (e.g., muscarine, psilocybin) |
| Fish/Shellfish-Related Toxins * | ||||
| Scombrotoxin poisoning | Minutes to 2 hr | Histamine reaction: flushing, headache, dizziness, burning of throat and mouth | Scombridae fish (includes tuna, mackerel, and bonito species), mahi-mahi | Identify fish and/or chemical toxin (ciguatoxin, tetrodotoxin, histamine, etc.) |
| Paralytic shellfish poisoning | Minutes to 2 hr | Paresthesia, dizziness, sometimes paralysis | Mussels, clams, oysters, scallops contaminated with toxins, typically from dinoflagellate algae species | |
| Tetrodotoxin poisoning | Minutes to 2 hr | Paresthesia | Various pufferfish and angelfish species. The toxin is produced by symbiotic or infecting bacteria in the fish species | |
| Ciguatoxin poisoning | 2-24 hr | Itching, arthralgias, metallic taste, Paresthesias, cramps, visual disturbances, “Loose” painful teeth | Barracuda, red snapper, grouper, amberjack | |
| Norovirus | 24-48 hr | Epidemic watery diarrhea | Contaminated ice machines, shellfish, ready-to-eat foods | Nucleic acid amplification assays |
| Staphylococcal enterotoxins | 2-8 hr | Prominent vomiting, no fever, duration less than 24 hr | Ham, poultry, pastries (cream-filled), mixed salads, egg salad | Identification of preformed toxin or isolation of 10 5 colony-forming-units of organism from food |
| Bacillus cereus | ||||
| Emetic form: short incubation | 2-8 hr | Prominent vomiting, no fever, duration less than 48 hr | Fried rice, macaroni-and-cheese, vegetables, other ready-to-eat foods left at room temperature. Symptoms and rapidity of onset are due to presence of preformed toxin | Identification of preformed toxin or isolation of 10 5 colony-forming-units of organism from food |
| Diarrheal form: longer incubation | 8-14 hr | Abdominal cramps, severe diarrhea, no fever, duration less than 48 hr | Fried rice, macaroni-and-cheese, vegetables, other ready-to-eat foods left at room temperature. Symptoms are due to in vivo toxin production | Identification of preformed toxin or isolation of 10 5 colony-forming-units of organism from food or stool |
| Clostridium perfringens | 8-14 hr | Abdominal cramps, severe diarrhea, no fever, duration less than 48 hr | Meat, poultry, gravy | Identification of preformed toxin or isolation of 10 5 colony-forming-units of organism from food or stool |
| Enterotoxigenic Escherichia coli (ETEC) | 12 hr to several days | Abdominal cramps, watery diarrhea may be prolonged up to 7 days | Incomplete data (rarely reported) | Identification of enterotoxin or isolation of organism from stool |
| Invasive Escherichia coli | 12 hr to days | Prolonged febrile diarrhea and/or dysentery | Incomplete data (rarely reported) | Isolation of organism from stool |
| Vibrio cholerae | 12 hr to days | Abdominal cramps, watery diarrhea (rice-water stools). May be prolonged up to 1 wk | Contaminated food and water (very rare in United states) | Isolation of organism from food or stool |
| Vibrio parahemolyticus | 12 hr to days | Prolonged febrile diarrhea and/or dysentery | Seafood | Stool culture (or food culture) |
| Shigella species | 12 hr to days | Prolonged febrile diarrhea and/or dysentery | Fish, mixed salads | Stool culture (or food culture) |
| Campylobacter species | 12 hr to days | Prolonged febrile diarrhea and/or dysentery | Unpasteurized milk, poultry or meat | Stool culture (or food culture) |
| Clostridium botulinum | 12 hr to days |
| Home-canned foods, fish, honey | Botulinum toxin in food, stool, and serum |
| Yersinia enterocolitica | Uncertain | Prolonged diarrhea and/or dysentery | Milk, pig intestine | Stool culture |
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
