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The specific causes of acute diarrhea differ between developing and developed countries. In the United States, viral and food-borne diarrhea] illnesses are common; however, in the majority of cases, the causes cannot be determined. In developing countries, poor sanitation and poor hygiene lead to infectious diarrhea caused by parasites, bacteria, and viruses. Bacterial causes are as common as viral infections in these countries. Table Common Infectious Diarrheas and Their Treatment highlights some of the common viral, bacterial, and protozoal diarrheas and their treatment.
Epidemiologic factors that increase the risk for particular infectious diarrhea] diseases or their spread include attendance or employment at day care centers, occupation as a food handler or caregiver, congregate living conditions (e.g., nursing homes, prisons, and multifamily dwellings), consumption of unsafe foods (e.g., raw meat, eggs, and shellfish), and presence of medical conditions, such as acquired immunodeficiency syndrome, that predispose to infectious diarrhea.
Acute diarrhea may also be caused by poisoning, medications, intolerance of certain foods, or various non-gastrointestinal (gastrointestinal) acute or chronic illnesses.
Viral Gastroenteritis
Norovinises are the most common viral pathogens, accounting for approximately 70% to 75% of viral gastroenteritis. The symptoms and clinical course are described in Table Common Infectious Diarrheas and Their Treatment. The virus is usually transmitted by contaminated water or food. Community-wide outbreaks may result when municipal water supplies become contaminated. Recent outbreaks of norovirus gastroenteritis on cruise ships have received attention, although 60% to 80% of all outbreaks occur on land.” Contaminated food is the most frequently identified vehicle of infection in this setting.” Person-to-person transmission may also be important, and it has been suggested that infected cruise ship crew members may serve as reservoirs of infection for passengers.
Rotaviruses account for about 12% of all acute gastroenteritis and up to 50% of infantile gastroenteritis. The incidence of rotavirus infection is highest among children between 3 to 24 months of age. The peak infectious period is during the winter months (November to February). Spread is by the fecal-oral route. Clinical features are presented in Table Common Infectious Diarrheas and Their Treatment. Treatment is usually restricted to fluid and electrolyte therapy. Severe dehydration and electrolyte disturbances, however, can occur and may result in death. In 2006, a live, oral vaccine to prevent rotavirus gastroenteritis was licensed by the Food and Drug Administration (FDA) for routine use in healthy infants. In clinical trials, this vaccine prevented 74% of all rotavirus gastroenteritis cases and 98% of the severe cases, and reduced the need for hospitalization attributable to rotavirus gastroenteritis by 96%.
Other, less frequent viral causes of gastroenteritis include adenoviruses, astroviruses, and hepatitis A virus.
Bacterial Gastroenteritis
Bacterial pathogens cause approximately 5 million episodes of acute gastroenteritis in the United States each year. Pathogens most commonly responsible for these cases, in order of decreasing incidence, are Cainpylobacicr sp.. Salmonella sp., Shigella sp., Eschcrichia coli (including 0157:H7, non-0157:H7 Shigatoxin-producing E. coli |STEC), enterotoxigenic E. coli, and other diarrheagenic strains), Siapliylococcus sp., Clostridium sp., Yersinia ciucrocoliliai, and Bacillus cereus. Aeromonas sp. are being increasingly recognized as enteropathogens. particularly in food-borne disease; Bacteroidesfiagilis, Klebsiella oxytoca, and Laribacter honkongensis are newly identified causes of acute diarrhea.Cainpylobacicr is identified as the etiologic agent two to seven times more frequently than Salmonella, Shigella, or E. coli.
Common Infectious Diarrheas and Their Treatment
| Type | Epidemiologic/
Etiologic Factors |
Symptoms | Treatment | Usual Prognosis | ||
| Viral | ||||||
| Rotaviruses | Infects infants; oral-fecal
spread |
Onset of 24-48 hours;
vomiting, fever, nausea, acute watery diarrhea |
Vigorous fluid and electrolyte replacement; no antibiotics | Self-limiting; usually lasts
5-8 days |
||
| Norovirus | Infects all ages; frequently spread person to person by the
fecal-oral route; causes “24-hour stomach flu” |
Onset of 24-48 hours;
sudden-onset vomiting, nausea, headache, myalgia, fever, watery diarrhea |
Fluid and electrolytes;
no antibiotics |
Self-limiting; usually lasts
12-60 hours |
||
| Bacterial | ||||||
| Campylobacter jejuni | Ingestion of contaminated food or water;
oral-fecal spread; immunocompromised host |
Onset of 24-72 hours; nausea, vomiting,
headache, malaise, fever, watery diarrhea |
Fluid and electrolytes; in
severe or persistent diarrhea, antibiotics may be required |
Self-limiting, usually
<7 days |
||
| Salmonella | Ingestion of improperly
cooked or refrigerated poultry and dairy products; immunocompromised host |
Onset of 12-24 hours; diarrhea, fever, and chills | Fluid and electrolytes for
mild cases; antibiotics reserved for complicated cases |
Self-limiting | ||
| Shigella | Ingestion of contaminated vegetables or
water; frequently spread person to person; immunocompro- mised host |
Onset of 24-48 hours; nausea, vomiting, diarrhea | Fluid and electrolytes;
antibiotics |
Self-limiting | ||
| Escherichia coli
Enterotoxigenic E. coli, Enteroaggregative E. coli |
Ingestion of contaminated food or water;
recent travel outside the United States or to a U.S. border area |
Onset of 8-72 hours;
watery diarrhea, fever, bdominal cramps, bloating, malaise, occasional vomiting |
Fluid and electrolytes;
antibiotics |
Self-limiting, usually
within 3-5 days |
||
| Shigatoxin-producing
E. coli (STEC) |
Ingestion of contami-
nated food or water, direct person-to-person spread |
Onset of 8-72 hours;
watery, often bloody, diarrhea, abdominal cramps, hemolytic uremic syndrome |
Fluid and electrolytes | Self-limiting, usually
within 5-10 days |
||
| Clostridium difficile | Antibiotic-associated diarrhea leading to pseudomembranous colitis | Onset during or up to
several weeks after antibiotic therapy; watery or mucoid diarrhea, high fever, cramping |
Fluid and electrolytes;
discontinuation of offending agent; antibiotics (metronidazole, vancomycin) |
Self-limiting | ||
| Closthdium perfringens | Ingestion of contami-
nated food, especially meat and poultry |
Onset of 8-14 hours;
watery diarrhea with- out vomiting, cramping, midepigastric pain |
Fluid and electrolytes;
no antibiotics |
Self-limiting, usually
resolves within 24 hours |
||
| Staphylococcus aureus | Ingestion of improperly
cooked or stored food |
Onset of 1-6 hours; nausea, vomiting, watery | Fluid and electrolytes;
no antibiotics |
Self-limiting | ||
| Yersinia enterocolitica | Ingestion of contaminated food | Onset within 16-48 hours;
fever, abdominal pain, diarrhea, vomiting |
Fluid and electrolytes;
antibiotics may be needed in severe cases |
Self-limiting, although
diarrhea may persist for up to 3 weeks |
||
| Vibrio cholera | Ingestion of contaminated food, including
undercooked or raw seafood; recent travel outside the United States |
Onset within 24-48 hours;
painless, watery, often voluminous, diarrhea, vomiting |
Fluid and electrolytes;
antibiotics needed in moderate-to-severe cases |
Self-limiting, although
V. cholera may cause severe, fatal illness |
||
| Bacillus cereus | Ingestion of contami-
nated food |
Onset within 10-12 hours;
abdominal pain, watery diarrhea, tenesmus, nausea, vomiting |
Fluid and electrolytes;
no antibiotics |
Self-limiting | ||
| Protozoal | ||||||
| Giardia lamblia | Ingestion of water contaminated with
human or animal feces; frequently spread person to person; immunocompro- mised host |
Onset of 1-3 weeks;
acute or chronic watery diarrhea, nausea, vomiting, anorexia, flatulence, abdominal bloating. epigastric pain |
Fluids and electrolytes;
antimicrobial therapy” |
Good, if treated | ||
| Cryptosporidium sp. | Frequently spread person to person; travel outside the United States; acquired immunodeficiency syndrome, immunocompromised
host |
Onset of 2-14 days; acute or chronic
watery diarrhea, abdominal pain, flatulence, malaise |
Fluid and electrolytes;
antimicrobial therapy |
Self-limiting, lasting up
to 3 weeks, except in patients with acquired immunodeficiency syndrome or other immunosup- pressive diseases |
||
| Entamoeba histolytica | Travel outside the
United States; fecal soiled food or water. Immunocompromised host |
Chronic watery diarrhea,
abdominal pain, cramps |
Fluid and electrolytes;
antibiotics |
Good, except for immunocompromised
host |
||
| Isospora belli | Ingestion of contaminated food or water;
immunocompromised host |
Onset of approximately
1 week; profuse watery diarrhea, malaise, anorexia, weight loss, abdominal cramps |
Fluid and electrolytes;
antibiotics |
Self-limited, remitting in
2-3 weeks |
||
Key: acquired immunodeficiency syndrome, acquired immunodeficiency syndrome.
Empirical therapy with prescription antibiotics (azithromycin, erythromycin) should be considered for patients with febrile diarrheal illness, especially if moderate-to-severe invasive disease is suspected, and for patients in whom supportive therapy fails to manage symptoms. Ciprofloxacin has been recommended, but it is no longer considered a first-line agent, because many Campylobacter strains are resistant to fluoroquinolones.
Antibiotics are not indicated routinely for Salmonella gastroenteritis; antibiotic therapy is used in young infants and children who fail to respond to supportive treatment, who do not spontaneously remit, or who are at increased risk of disseminated disease. Antibiotic therapy is also indicated for suspected bacteremia in patients at high risk for this complication. These include patients who appear to be toxic with high fever (>102.2°F [39°C]); infants (<3 months); older adult patients (>65 years); patients with cancer, immunodeficiency (e.g., acquired immunodeficiency syndrome), or hemoglobinopathy (e.g., sickle cell disease); patients receiving corticosteroids or on hemodialysis; and patients with vascular grafts or prosthetic joints. Duration of antimicrobial therapy is usually 7-10 days.
Antibiotic treatment with fluoroquinolones, azithromycin, or rifaximin (prescription antibiotics) is given for travelers’ diarrhea caused by E. coli. Trimethoprim/sulfamethoxazole is no longer an optimal choice because of increasing worldwide resistance. Antibiotic treatment is not recommended for gastroenteritis caused by E. coli 0157:H7, because the treatment is likely to enhance toxin release and may increase risk for hemolytic uremic syndrome.
Self-treatment of giardiasis is not appropriate; metronidazole, nitazoxanide, tinidazole, quinacrine, furazolidone, and paromomycin are effective prescription alternatives for treating giardiasis.
Self-treatment of cryptosporidiosis is not appropriate. Symptomatic relief of cryptosporidiosis may be achieved in acquired immunodeficiency syndrome patients by adding paromomycin and azithromycin (both prescription antimicrobial agents) to the patient’s antiretroviral therapy.
Self-treatment of amebiasis is not appropriate; prescription therapy with metronidazole followed by either paromomycin or iodoquinol is the preferred treatment.
Bacteria cause diarrhea through elaboration of an enterotoxin (e.g., toxigenic E, coli and Siapliylococcus aurcus) or by directly invading the mucosal epithelial cells (e.g., Shigella, Salmonella, Yersinia, Cainpylobacicr jejuni, and invasive E. coli). Patients with diarrhea caused by toxin-producing agents have a watery diarrhea, which primarily involves the small intestine. If the large intestine is the site of attack, invasive organisms produce a dysentery-like (bloody diarrhea) syndrome characterized by fever, abdominal cramps, tenesmus (straining), and the frequent passage of small-volume stools that may contain blood and mucus. Clinical features of common bacterial diarrheas are presented in Table Common Infectious Diarrheas and Their Treatment.
Food-borne transmission of pathogens accounts for 36% of acute gastroenteritis episodes in the United States; of these infections, 30% are due to bacteria, 67% to viruses, and 3% to protozoa. Recent surveillance statistics on the incidence of food-borne illnesses in the United States document that Salmonella and Cainpylobacicr, which caused 14.81 and 12.71 cases of illness per 10(1,000 population in 2006, respectively, are the most frequently diagnosed bacterial pathogens, followed by Shigella (6.09 cases per 100,000 population). Shigatoxin-producing coli 0157:H7 (1.31 cases per 100.000 population). Yersinia (0.35 cases per 100.000 population). Vibrio (0.34 cases per 100,000 population), and Lisieria (0.31 cases per 100.000 population).
Outbreaks of food-borne bacterial infection have been traced to poor sanitary conditions in meat-processing plants and various retail outlets (e.g.. grocery stores and restaurants). Outbreaks of infection have also been associated with specific foods, such as milk (Cainpylobacicr), raw eggs (Salmonella), chicken (Cainpylobacicr, Salmonella), melons (Lisieria). hummus (Lisieria), and raspberries (Cyclospora). Therefore, an attentive and thorough history regarding food intake before the onset of diarrhea is essential in identifying a probable cause. For example, toxin-producing S. aureus grows rapidly in food (especially salads, custard, sausage, ham, dairy products, and poultry). Upon ingestion the enterotoxin provokes nausea and vomiting with diarrhea within 6 hours. In contrast, the incubation period for Salmonella, which is harbored on raw foods and particularly on eggs, is 12 to 24 hours. These microbes invade the mucosal layer of the gastrointestinal tract and disrupt the normal absorptive-secretory mechanisms. Fever, malaise, muscle aches, and profound epigastric or peri-umbilical discomfort with severe anorexia suggest an infectious, inflammatory disease of the large intestine. Abdominal pain, vomiting, and diarrhea suggest viral gastroenteritis, and symptoms usually persist for 2 to 3 days before gradually subsiding.
A major public health issue is contamination of food, especially undercooked hamburger and unpasteurized apple cider with E. coli 0157:H7 and other STECs. Recently, outbreaks of STEC OI57 have been caused by consumption of contaminated spinach, lettuce, and raw milk. The toxins produced by these organisms cause an acute bloody diarrhea, but they may also be associated with serious, potentially fatal systemic complications such as hemolytic uremic syndrome or thrombotic thrombo-cytopenic purpura.
Other causes of food-borne gastroenteritis include Lisieria monocyiogeiics, (Cyclospora cayeiancnsis, and viruses. Noroviruses and rotavirus have also been implicated in food-borne disease.
Travelers’ diarrhea is a secretory diarrhea acquired, for the most part, through ingestion of contaminated food or water. This acute diarrhea is usually caused by bacterial enteropathogens. It affects millions of tourists visiting foreign countries or U.S. border areas with poor sanitation. Although Salmonella. Shigella, Cainpylobacicr, Eniamoeba hisiolylica, Ciardia, and rotavirus have all been implicated in the disease. E. coli is the most common infecting organism in travelers’ diarrhea. Two strains, enterotoxigenic E. coli (ETEC) and enteroaggregative E. coli (EAEC), are responsible for most cases. ETEC is found in up to 40% of travelers with diarrhea in various areas around the world; EAEC is almost as common, causing approximately 25% of cases. The causative organisms are found most often on foods such as fruits, vegetables, raw meat, seafood, and even hot sauces; less commonly, pathogens are found in the local water, including ice cubes. After ingestion, ETEC produces two plasmid-mediated enterotoxins that cause symptoms: one of these enterotoxins is Structurally, functionally, and immunologically closely related to cholera toxin. The pathogenic mechanisms underlying diarrhea caused by EAEC are not well understood these organisms may produce disease through elaboration of an enterotoxin, a cytotoxin, or some other means. The diarrheal disorder caused by these organisms is characterized in Table Common Infectious Diarrheas and Their Treatment. Patients may experience between three and eight (or more) watery stools per day, with symptoms usually subsiding over 3 to 5 days.
Bacterial pathogens not only cause acute illness, they can also cause functional bowel disorders, including postinfectious irritable bowel syndrome (irritable bowel syndrome), for 6 months or longer after a bout of acute gastroenteritis. In 10% to 30% of patients, bowel dysfunction persisted 6 months after infectious diarrhea caused by Cainpylobacicr, Shigella, Salmonella, and diarrheagenic coli (ETEC and EAEC). Irritable bowel syndrome is diagnosed in 4% to 10% of patients 1 to 2 years after an episode of acute bacterial gastroenteritis.
Protozoal Diarrhea
Diarrhea may also be caused by protozoa, including Ciardia lamblia, E. hisiolylica, Isospora belli, and Crypiosporidinm sp. (Table Common Infectious Diarrheas and Their Treatment). No nonprescription therapies are available to manage diarrhea caused by these pathogens and self-management is inappropriate.
Food-Induced Diarrhea
Food intolerance can provoke diarrhea and may result from a food allergy or ingestion of foods that are excessively fatty or spicy, or contain a high amount of roughage or many seeds. Carbohydrates in the diet commonly include the disaccharides lactose and sucrose, which are normally hydrolyzed to mono-saccharides by the enzyme lactase. When these disaccharides are not hydrolyzed. they pool in the lumen of the intestine, where they not only ferment but also produce an osmotic imbalance and pH change. The resulting hyperosmolarity draws fluid into the intestinal lumen, causing diarrhea. Lactase enzymatic activity may be reduced in intestinal disorders such as infectious diarrhea and gastrointestinal allergy. Acute viral diarrhea may cause temporary milk intolerance in patients of all ages. Lactase deficiency resulting from viral gastroenteritis is short-lived and is particularly problematic during the first few days of the disease. Infants bom with lactase deficiency and adults who develop lactase deficiency are intolerant of cow’s milk and milk-based products. Lactase enzyme products are effective treatments for some patients.
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