Browse the corpus

Acute diarrheal illness is a common yet potentially serious condition with a significant global health impact. While most cases are viral and self-limited, bacterial infections such as Salmonella infection, Shigellosis, and Clostridioides difficile infection can lead to severe complications, including sepsis, hemolytic uremic syndrome, and death. Clinical features such as fever, bloody stools, and severe abdominal pain help differentiate bacterial from viral etiologies. This activity reviews evidence-based approaches to diagnosis and management, emphasizing appropriate use of stool studies, oral rehydration therapy, and selective antibiotic treatment. Participants will learn to identify high-risk patients, avoid unnecessary antimicrobial use, and recognize situations where antibiotics may be harmful, such as in Shiga toxin–producing Escherichia coli infections. Emphasis is placed on optimizing clinical decision-making, preventing complications, and improving patient outcomes while addressing antibiotic stewardship and reducing healthcare burden. Objectives: Identify the common bacterial pathogens responsible for diarrhea, including Salmonella, Shigella, Campylobacter, and Escherichia coli. Apply infection control measures to prevent the spread of bacterial diarrhea in healthcare settings and the community. Select appropriate diagnostic tests, including stool cultures, polymerase chain reaction tests, and antigen detection assays, to confirm a bacterial etiology of diarrhea. Communicate effectively with the healthcare team, including nurses, pharmacists, and laboratory personnel, to ensure timely diagnosis, appropriate treatment, and comprehensive patient education for bacterial diarrhea management. Access free multiple choice questions on this topic.

The World Health Organization (WHO) defines diarrhea as loose or liquid stools occurring 3 or more times per day or more frequently than usual for an individual.[1][2][3] Dysentery is the invasive form of diarrhea, with visible blood or mucous often accompanied by fever and abdominal pain. Viruses are the main culprits of acute infectious diarrhea in adults and children. However, identifying clinical features consistent with bacterial infection is critical to prevent morbidity and mortality. A strategic assessment is essential to determine which patients require stool studies, empiric antibiotic therapy, and intravenous fluid (IVF) resuscitation. Distinguishing between viral and bacterial causes of gastroenteritis can be challenging, as their symptoms may overlap. However, findings like fever, bloody or mucoid stools, or a history of recent antibiotic use or hospitalization help alert clinicians to the possibility of a bacterial etiology. Salmonella, Shigella, Campylobacter jejuni, Yersinia enterocolitica, C difficile, and Escherichia coli are common bacterial causes of acute diarrhea that can lead to complications such as sepsis, seizures, hemolytic-uremic syndrome (HUS), Guillain-Barré syndrome (GBS), and death. Accurately identifying bacterial gastroenteritis and deciding when to investigate less common causes, such as sexually transmitted infections, is essential to avoid unnecessary testing and antibiotic use and to prevent potential complications. While the goal of antimicrobial treatment is to shorten symptom duration and prevent complications, many causes are self-limited and do not require treatment. Antimicrobials may cause more harm in some cases, as in Shiga toxin-producing E coli (STEC) infection, where antibiotics increase the risk of developing HUS.

Salmonella, Shigella, Campylobacter jejuni, Yersinia enterocolitica, C difficile, and Escherichia coli are common bacterial causes of acute diarrhea that can lead to complications such as sepsis, seizures, hemolytic-uremic syndrome (HUS), Guillain-Barré syndrome (GBS), and death. Accurately identifying bacterial gastroenteritis and deciding when to investigate less common causes, such as sexually transmitted infections, is essential to avoid unnecessary testing and antibiotic use and to prevent potential complications. While the goal of antimicrobial treatment is to shorten symptom duration and prevent complications, many causes are self-limited and do not require treatment. Antimicrobials may cause more harm in some cases, as in Shiga toxin-producing E coli (STEC) infection, where antibiotics increase the risk of developing HUS. Laboratory testing is not usually necessary. However, if available, clinicians should perform stool studies during an epidemic or when patients have severe illness, symptoms persisting for more than 7 days, or risk factors such as pregnancy, older age, or immunocompromised status. Stool studies are also indicated when blood or mucus is present along with fever.[4] Identifying the bacterial pathogen helps inform clinicians about potential complications and treatment decisions. A routine stool culture is the ideal test for identifying Salmonella, Campylobacter, and Shigella. E coli requires a different medium, but antigen testing or polymerase chain reaction (PCR) of stool is an alternative diagnostic option. Oral rehydration is the mainstay of therapy, with IVF reserved for individuals with severe hypovolemia. Clinicians reserve empiric antibiotic treatment for patients with severe illness, a high likelihood of C difficile, high-risk host features, and bloody mucoid stools.[5][6] A clear understanding of the guidelines regarding empiric antibiotic use will decrease antibiotic misuse and prevent antibiotic resistance.

Diarrhea is classified as acute if it lasts less than 2 weeks, chronic if it lasts more than a month, and persistent if it continues for 2 to 4 weeks. Most acute diarrhea is infectious and self-limited, with viral causes like norovirus, rotavirus, and adenoviruses as the primary offenders. Severe diarrhea increases the likelihood of bacterial etiology. While only 2% to 6% of stool cultures are generally positive, a recent study of patients with severe diarrhea found that 86% had positive bacterial culture results.[7][8] The following list includes potential bacterial causes of diarrhea and their associated sources or risk factors: C difficile: Antibiotic use, hospital stays, chemotherapy, gastric acid suppression, and inflammatory bowel disease Clostridium perfringens: Consumption of meat, poultry, and home-canned goods Enterotoxigenic E coli: Fecal contamination of food or water and travel to resource-limited areas Listeria monocytogenes: Eating processed deli meats, hot dogs, soft cheese, pâtés, and fruits, especially by patients who are pregnant, immunosuppressed, or at extremes of age. Nontyphoidal Salmonella: Consumption of poultry, eggs, meat, fish, unpasteurized milk or juice, nut butter, and spices; exposure to petting zoos, reptiles, and live poultry; travel to resource-limited settings Campylobacter spp: Eating poultry, meat, or unpasteurized milk; traveling to resource-limited settings; having contact with puppies and kittens Shigella spp: Eating raw vegetables, staying at daycare centers or crowded living conditions, engaging in sexual activity with men (in men), and traveling to resource-limited areas Enterohemorrhagic E coli: Consuming ground beef, fresh produce, and unpasteurized milk and juice; staying in daycare centers and nursing homes; being at an extreme age Yersinia spp: Consuming pork or untreated water; receiving blood transfusion; having abnormalities of iron metabolism like hemochromatosis, cirrhosis, or thalassemia Vibrio parahemolyticus: Eating raw seafood and shellfish; having cirrhosis Aeromonas hydrophila: Consuming seafood, meats, and vegetables like sprouts; receiving medicinal leech therapy Bacillus cereus: Eating rice, dairy products, spices, bean sprouts, and certain vegetables

Yersinia spp: Consuming pork or untreated water; receiving blood transfusion; having abnormalities of iron metabolism like hemochromatosis, cirrhosis, or thalassemia Vibrio parahemolyticus: Eating raw seafood and shellfish; having cirrhosis Aeromonas hydrophila: Consuming seafood, meats, and vegetables like sprouts; receiving medicinal leech therapy Bacillus cereus: Eating rice, dairy products, spices, bean sprouts, and certain vegetables Plesiomonas shigelloides: Consumption of raw shellfish, contaminated vegetables, or contaminated water; contact with freshwater aquariums or fish tanks; exposure to amphibians or reptiles Klebsiella oxytoca: Exposure to contaminated water or soil; in healthcare settings, contact with the contaminated hands of healthcare workers Chlamydia trachomatis, Neisseria gonorrhea, and Treponema pallidum: In men having sex with other men, diarrhea is a possible sign of proctitis. Salmonella spp: Ingestion of undercooked or raw animal products like poultry, eggs, meat, and unpasteurized milk; contact with infected animals like reptiles or pets with diarrhea Staphylococcus aureus: Consumption of processed meats, dairy products, and mayonnaise-based salads, cream-filled pastries; cross-contamination due to poor hand hygiene [9]

According to the United States Centers for Disease Control (CDC), 179 million cases of acute gastroenteritis occur in the United States annually. Experts estimate that 48 million cases are due to foodborne contamination, resulting in nearly 128,000 hospitalizations and 3,000 deaths. Globally, diarrhea is the 2nd leading cause of death among children younger than 5, accounting for 9% of fatalities in this age group—approximately 440,000 deaths annually—and 50,851 deaths among children 5 to 9.[10] The highest mortality rates occur in South Asia and sub-Saharan Africa. Diarrhea is a major contributor to the utilization of healthcare resources throughout the United States, accounting for nearly 5% of all office visits and 10% of hospitalizations in children younger than 5. Infectious diarrhea does not have a sex predilection. However, individuals who are at the extremes of age, pregnant, or immunocompromised are at the highest risk of contracting bacterial sources of diarrheal illnesses. Lack of access to safe and clean water supplies and poor hygiene and sanitation practices also increase the risk. According to the CDC, Campylobacter is the most common bacterial pathogen in the United States, with an estimated 1.5 million infections annually. Nontyphoidal salmonellosis is another major culprit.[11] Hospital-onset C difficile infections occur at a rate of 8.3 cases per 10,000 patient days.[12] In resource-limited areas, Shigella dysenteriae serotype 1 and Vibrio cholerae are the primary pathogens responsible for epidemics, with E coli O157:H7 being an additional contributor.[13] Among cases of invasive or bloody diarrhea, Shigella is the most common cause in children in these settings.[14] According to the CDC, enterotoxigenic E coli (ETEC) is the leading cause of diarrhea among travelers. Traveler’s diarrhea affects 30% to 70% of individuals during a 2-week trip, depending on the destination and travel season.

Acute infectious diarrhea occurs via fecal-oral transmission, person-to-person contact, and consumption of contaminated water or undercooked food. Under normal physiological conditions, water moves across the intestinal lining via osmosis, driven by the movement of sodium (Na+), chloride (Cl-), bicarbonate (HCO3-), potassium (K+), and glucose. The active transport of Na+ in parallel with the absorption of Cl- or HCO3- drives intestinal fluid absorption. The sodium/hydrogen exchanger 3 (NHE3), sodium/glucose cotransporter 1 (SGLT1), and chloride/bicarbonate exchangers (DRA and PAT1) facilitate fluid absorption in the small intestine. Cl- channels and transporters regulate intestinal fluid secretion. Patients with diarrhea have excessive fluid within the intestines due to increased secretion or reduced water absorption from the lumen. In both scenarios, the intestinal lumen has an increased concentration of osmotically active nutrients or electrolytes, thereby increasing its water content. Vibrio cholerae and ETEC stimulate fluid secretion by releasing enterotoxins that alter intracellular cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP), and calcium (Ca2+) levels. These signals affect the channels that regulate fluid absorption and secretion. Cholera toxin elevates cAMP, activating the Cl– channel cystic fibrosis transmembrane conductance regulator (CFTR) and inhibiting the Na+ exchanger NHE3, causing a rapid efflux of Cl– ions and a decreased influx of Na+ ions, leading to massive water efflux through the intestine and profuse, watery diarrhea.[15] Colonization with C difficile occurs by the fecal-oral route, most often during episodes of altered gut microbiome when taking antimicrobials. C difficile produces exotoxins, toxins A and B, that inactivate members of the ρ family of guanosine triphosphatases involved in cytoskeleton formation and signal transduction. The resulting tissue injury causes the death of colonocytes, loss of intestinal barrier function, and neutrophilic colitis.[16]

Colonization with C difficile occurs by the fecal-oral route, most often during episodes of altered gut microbiome when taking antimicrobials. C difficile produces exotoxins, toxins A and B, that inactivate members of the ρ family of guanosine triphosphatases involved in cytoskeleton formation and signal transduction. The resulting tissue injury causes the death of colonocytes, loss of intestinal barrier function, and neutrophilic colitis.[16] Additionally, bacteria can increase levels of humoral agonists, neurotransmitters, and neuropeptide receptors, such as 5-hydroxytryptamine, vasoactive intestinal peptides, and the galanin receptor type 1, thereby activating Cl- secretion and inhibiting Na+ absorption. The inflammatory responses caused by Salmonella and Shigella stimulate cytokine release via intracellular Ca2+ signaling. Patients with acute-onset diarrhea after an infectious episode may have residual mucosal damage and lactase deficiency.

The history and physical examination help clinicians delineate potential underlying causes of diarrhea and guide empiric treatment. Some causes of bacterial diarrhea present with characteristic features, while others have less reliable symptoms. Based on stool characteristics, healthcare professionals can determine whether the stool originated in the small or large intestine. Large-volume, watery stools with less than 5 white blood cells (WBCs) per high-power field (hpf) likely arise from the small bowel. These stools may test positive for guaiac but are rarely grossly bloody. Potential bacterial pathogens include Bacillus species, Staphylococcus aureus, E coli, Vibrio cholerae, Clostridium perfringens, Vibrio species, and Listeria monocytogenes. Small-volume stools with visible mucus or blood and possibly more than 10 WBCs/hpf likely originate from the large bowel. Possible culprits include E coli, Shigella, Salmonella, Campylobacter, Yersinia, Aeromonas, Plesiomonas species, and C difficile.[17][18] Additional key historical features are symptom onset and duration, a food diary, fever, abdominal pain, recent travel, exposure to ill contacts, recent hospital stay or antimicrobial use, and any comorbid conditions. Assessing the patient's volume status is critically important. Mild hypovolemia presents with increased thirst and slightly dry mucous membranes. Irritability, restlessness, sunken eyes, absence of tears, a dry mouth and tongue, and a heightened desire to drink mark moderate hypovolemia. Moderately dehydrated patients also exhibit reduced skin turgor and an elevated pulse. Patients with severe hypovolemia have profound lethargy, minimal thirst drive, absence of tears, severely sunken eyes, skin tenting, and a rapid, thready pulse. Aeromonas species

Additional key historical features are symptom onset and duration, a food diary, fever, abdominal pain, recent travel, exposure to ill contacts, recent hospital stay or antimicrobial use, and any comorbid conditions. Assessing the patient's volume status is critically important. Mild hypovolemia presents with increased thirst and slightly dry mucous membranes. Irritability, restlessness, sunken eyes, absence of tears, a dry mouth and tongue, and a heightened desire to drink mark moderate hypovolemia. Moderately dehydrated patients also exhibit reduced skin turgor and an elevated pulse. Patients with severe hypovolemia have profound lethargy, minimal thirst drive, absence of tears, severely sunken eyes, skin tenting, and a rapid, thready pulse. Aeromonas species Aeromonas spp live in freshwater and marine environments. Diarrheal disease associated with Aeromonas spp is most commonly recognized as traveler's diarrhea in the United States, manifesting as malaise, anorexia, and abdominal cramps, followed by self-limited watery diarrhea.[19] However, Aeromonas can present in many ways, including acute dysenteric diarrhea with blood and mucus, diarrhea mimicking cholera with "rice water" stools, chronic diarrhea, and HUS associated with Aeromonas hydrophila.[20] The incubation period associated with Aeromonas is negligible. The symptoms can persist for up to 2 weeks. Patients may or may not have associated nausea and vomiting. Accompanying abdominal pain is not a characteristic feature. Bacillus species An important cause of foodborne illness, the Bacillus cereus group involves 22 species, with most human infections caused by Bacillus cereus sensu stricto. Other well-known culprits are Bacillus anthracis (the cause of anthrax), Bacillus subtilis, and Bacillus licheniformis.

Aeromonas spp live in freshwater and marine environments. Diarrheal disease associated with Aeromonas spp is most commonly recognized as traveler's diarrhea in the United States, manifesting as malaise, anorexia, and abdominal cramps, followed by self-limited watery diarrhea.[19] However, Aeromonas can present in many ways, including acute dysenteric diarrhea with blood and mucus, diarrhea mimicking cholera with "rice water" stools, chronic diarrhea, and HUS associated with Aeromonas hydrophila.[20] The incubation period associated with Aeromonas is negligible. The symptoms can persist for up to 2 weeks. Patients may or may not have associated nausea and vomiting. Accompanying abdominal pain is not a characteristic feature. Bacillus species An important cause of foodborne illness, the Bacillus cereus group involves 22 species, with most human infections caused by Bacillus cereus sensu stricto. Other well-known culprits are Bacillus anthracis (the cause of anthrax), Bacillus subtilis, and Bacillus licheniformis. Researchers have isolated Bacillus cereus from foods like rice, dairy products, bean sprouts, vegetables, sauces, pasta, and desserts. Bacillus cereus forms spores in uncooked food that survive high temperatures, then germinate and multiply when refrigeration is inadequate. Holding cooked rice at ambient temperatures for a prolonged period, followed by quickly frying and serving it, is a frequent cause of Bacillus cereus infection. Affected patients can develop either emetic or diarrheal disease characterized by abdominal cramping and diarrhea 8 to 16 hours after ingesting the spores, followed by resolution within 24 hours. Individuals with emetic disease experience nausea, vomiting, and abdominal cramps, with a third also developing diarrhea.[21] Bacillus anthracis is an uncommon infection that typically affects the skin. However, anthrax can also affect the oropharynx or gastrointestinal tract through the consumption of undercooked meat. After 1 to 6 days, necrotic ulcers surrounded by edema form in the stomach, esophagus, and duodenum, potentially leading to gastrointestinal hemorrhage. Additional symptoms are asthenia, headache, low-grade fevers, facial flushing, and conjunctival injection, followed by abdominal pain, nausea, vomiting, and some diarrhea. As symptoms progress, patients can develop ascites and hypotension.[22] Campylobacter species

Bacillus anthracis is an uncommon infection that typically affects the skin. However, anthrax can also affect the oropharynx or gastrointestinal tract through the consumption of undercooked meat. After 1 to 6 days, necrotic ulcers surrounded by edema form in the stomach, esophagus, and duodenum, potentially leading to gastrointestinal hemorrhage. Additional symptoms are asthenia, headache, low-grade fevers, facial flushing, and conjunctival injection, followed by abdominal pain, nausea, vomiting, and some diarrhea. As symptoms progress, patients can develop ascites and hypotension.[22] Campylobacter species C jejuni and  Campylobacter coli are the likely causes of Campylobacter enteritis. Most commonly contracted due to contamination from the intestinal tracts of animals, especially poultry, Campylobacter can be a common source of foodborne illness. Patients may also become infected through waterborne outbreaks or through direct contact with animals or animal products. Symptom onset typically occurs within 3 days of exposure. Campylobacter infection may present asymptomatically in resource-limited areas. Adults often experience an abrupt onset of abdominal pain and diarrhea, but up to a third of affected individuals initially experience symptoms of high fever, rigors, generalized aches, dizziness, and delirium. Upwards of 10 bowel movements a day are common, and bloody stools may occur on the 2nd and 3rd days in nearly 15% of patients.[23][24] Diarrhea typically lasts 7 to 10 days, with the abdominal pain persisting longer. A subset of patients experience abdominal pain radiating to the right lower quadrant without diarrhea, raising the concern for acute appendicitis. Experts refer to this ileocecitis as "pseudoappendicitis." Campylobacter relapses in 5% to 10% of affected patients, who may excrete the bacteria in their stool for extended periods after their symptoms resolve. Children often present with fever, abdominal pain, and diarrhea. Nearly 50% also experience bloody stools. Children older than 1 usually have high fevers that may be associated with febrile seizures. Infants tend to experience vomiting and bloody stools with less fever and abdominal pain. Neonates may present with isolated fever or grossly bloody stools due to infection at the time of birth. Clostridioides difficile

Children often present with fever, abdominal pain, and diarrhea. Nearly 50% also experience bloody stools. Children older than 1 usually have high fevers that may be associated with febrile seizures. Infants tend to experience vomiting and bloody stools with less fever and abdominal pain. Neonates may present with isolated fever or grossly bloody stools due to infection at the time of birth. Clostridioides difficile C difficile infection is a leading cause of nosocomial infection and the primary cause of antibiotic-associated colitis. Symptoms may begin during or within 2 weeks of antibiotic therapy, though nearly 30% of patients have no history of recent antibiotic use.[25] Age older than 65, a recent hospital stay, and use of proton pump inhibitors like omeprazole also increase the risk of C difficile infection. Watery diarrhea is the primary symptom of C difficile infection, with lower abdominal cramping, low-grade fever, nausea, and loss of appetite as additional associated features. Some patients may have occult blood and mucus in their stool, but frank blood and melena are rare. Patients may have lower abdominal tenderness on examination, and endoscopy findings vary from friable mucosa to severe pseudomembranous colitis. Some patients are at risk of developing fulminant colitis, presenting with abdominal distention, fever, hypovolemia, lactic acidosis, hypotension, ileus, and megacolon. Abdominal rigidity, involuntary guarding, diminished bowel sounds, rebound tenderness, and severe localized tenderness in the left or right lower quadrants signify a bowel perforation due to megacolon. Clinicians must maintain a high index of suspicion for C difficile in the presence of these symptoms. Some patients may present with fever, leukocytosis, ileus, and minimal diarrhea due to colonic atony, which leads to intraluminal fluid pooling and dilation. Others may experience ascites and peripheral edema secondary to a protein-losing enteropathy due to the leakage of albumin into the lumen through the inflamed bowel wall. Nearly 25% of patients will experience recurrent disease within 30 days.[26] Clostridium perfringens

Some patients may present with fever, leukocytosis, ileus, and minimal diarrhea due to colonic atony, which leads to intraluminal fluid pooling and dilation. Others may experience ascites and peripheral edema secondary to a protein-losing enteropathy due to the leakage of albumin into the lumen through the inflamed bowel wall. Nearly 25% of patients will experience recurrent disease within 30 days.[26] Clostridium perfringens Clostridium perfringens causes foodborne, toxin-mediated, watery diarrhea, second only to Salmonella species in resource-rich settings. Like Bacillus species, the spores from type A strains can survive at standard cooking temperatures and thrive in improperly stored foods. Common sources are incorrectly reheated meats, gravies, and poultry. Watery diarrhea and abdominal cramping are the primary symptoms occurring within 6 to 24 hours, while fever and vomiting are uncommon. Symptoms generally resolve within 24 to 48 hours. Type C strains produce a β-toxin that causes pigbel, or hemorrhagic necrosis of the jejunum, also known as enteritis necroticans, most often encountered after pork consumption in resource-limited countries. Enterohemorrhagic Escherichia coli STEC strains are E coli strains that harbor genes encoding Shiga toxins 1 or 2. Ingestion of contaminated food and water, animal contact, and person-to-person spread are all potential modes of STEC transmission. Strains with genes encoding Shiga toxin 2 have a high propensity to cause HUS. The average incubation period is 3 days, with a range of 1 to 10. The initial symptoms are painful, nonbloody diarrhea that becomes bloody after 1 to 3 days. Fever is an uncommon finding and, if present, should raise suspicion of alternative causes such as Shigella, Campylobacter, or Salmonella. The diarrhea associated with STEC typically resolves after 7 days. Enterotoxigenic Escherichia coli ETEC is a common cause of epidemic diarrheal illnesses in resource-limited areas, as well as traveler's diarrhea, due to the ingestion of fecally contaminated food and water. Common symptoms are vomiting, stomach cramps, headache, and low-grade fever. Rapid dehydration can occur within a few hours. Listeria species

Enterotoxigenic Escherichia coli ETEC is a common cause of epidemic diarrheal illnesses in resource-limited areas, as well as traveler's diarrhea, due to the ingestion of fecally contaminated food and water. Common symptoms are vomiting, stomach cramps, headache, and low-grade fever. Rapid dehydration can occur within a few hours. Listeria species Listeria monocytogenes is the only member of the Listeria species that regularly infects humans. The organism most commonly thrives in soil and decaying vegetable matter and can survive and multiply at refrigerator temperatures. Infection is due to oral ingestion. Immunosuppression, pregnancy, and extremes of age increase the risk of disease from this infection, with pregnant patients accounting for a third of all cases.[27] Listeria can cross the placenta and infect the fetus during maternal bacteremia. Occasionally, a previously healthy patient will contract Listeria. Meningitis and bacteremia are the predominant manifestations of Listeria infection in individuals without comorbidities, though self-limited febrile gastroenteritis is also a possible manifestation in this group. Gastroenteritis due to Listeria monocytogenes is more common in the summer and linked to the consumption of processed delicatessen meats, hot dogs, soft cheeses, pâtés, and raw produce. Pasteurized dairy products, ready-to-eat meals, frozen foods, and ready-to-eat salads are increasingly common sources of infection. Plesiomonas species Plesiomonas shigelloides causes diarrhea associated with the ingestion of raw seafood, particularly in warmer climates. The incubation period is generally 24 to 48 hours long, after which watery diarrhea occurs. Infected patients may occasionally present with dysentery. The associated abdominal pain and cramping can be quite severe, and diarrhea can last up to 14 days. Immunocompromised hosts, neonates, and patients with hepatobiliary disease or hemochromatosis are at risk of extraintestinal manifestations like bacteremia, cellulitis, skin abscesses, peritonitis, pneumonia, and ocular infections.[28][29] Salmonella species

Plesiomonas shigelloides causes diarrhea associated with the ingestion of raw seafood, particularly in warmer climates. The incubation period is generally 24 to 48 hours long, after which watery diarrhea occurs. Infected patients may occasionally present with dysentery. The associated abdominal pain and cramping can be quite severe, and diarrhea can last up to 14 days. Immunocompromised hosts, neonates, and patients with hepatobiliary disease or hemochromatosis are at risk of extraintestinal manifestations like bacteremia, cellulitis, skin abscesses, peritonitis, pneumonia, and ocular infections.[28][29] Salmonella species Clinical symptoms of nontyphoidal Salmonella typically begin within 8 to 72 hours after ingesting contaminated food or water. The classic symptoms are diarrhea, nausea, vomiting, fevers, and abdominal cramps. The disease course is generally self-limited, with fever resolving over 48 to 72 hours and diarrhea after 4 to 10 days. The higher the ingested dose, the worse the symptoms. Bloody stools are uncommon but may be observed. Bacteremia is a potential complication leading to endocarditis, mycotic aneurysm, visceral abscesses, osteomyelitis, and meningitis. Enteric fever, caused by Salmonella enterica serotypes Typhi and Paratyphi A, B, and C, is a disease of humans only. The incubation period is 5 to 21 days after ingesting contaminated food or water. The 1st week of symptoms consists of a stepwise rise of fever and chills with an associated bradycardia or pulse-temperature dissociation. Patients develop salmon-colored macules or "rose spots" on the trunk and abdomen during the 2nd week, and abdominal pain. The 3rd week brings hepatosplenomegaly, intestinal bleeding, and possible intestinal perforation due to lymphatic hyperplasia of the Peyer patches in the ileocecal region. While 15% may develop septic shock, symptoms gradually resolve over weeks to months in the remaining patients.[30] Interestingly, constipation occurs in nearly 30% of infected individuals.[31][32] Shigella species

Enteric fever, caused by Salmonella enterica serotypes Typhi and Paratyphi A, B, and C, is a disease of humans only. The incubation period is 5 to 21 days after ingesting contaminated food or water. The 1st week of symptoms consists of a stepwise rise of fever and chills with an associated bradycardia or pulse-temperature dissociation. Patients develop salmon-colored macules or "rose spots" on the trunk and abdomen during the 2nd week, and abdominal pain. The 3rd week brings hepatosplenomegaly, intestinal bleeding, and possible intestinal perforation due to lymphatic hyperplasia of the Peyer patches in the ileocecal region. While 15% may develop septic shock, symptoms gradually resolve over weeks to months in the remaining patients.[30] Interestingly, constipation occurs in nearly 30% of infected individuals.[31][32] Shigella species Often linked to poverty and crowded living conditions, Shigella sonnei and Shigella flexneri are the 2 predominant forms of Shigella causing bacterial diarrhea, with Shigella dysenteriae less frequently isolated due to sanitation improvement. Humans transmit Shigella by the fecal-oral route and are the only natural reservoir of this organism. Transmission between household contacts and sexual partners is common. Ingestion of contaminated food and drinking water also contributes to the spread of disease. The exposure can be minimal, since the bacteria can survive stomach acid. Once exposed, the incubation period spans 1 to 3 days. Symptomatic patients start with fever, malaise, anorexia, and watery diarrhea. Eventually, blood and mucus may be present in the stool, and tenesmus is a common complaint. In contrast to other forms of bacterial gastroenteritis, nausea and vomiting are generally absent.[33] Shigella most often affects the colon. Consequently, significant fluid loss is uncommon, unlike other bacteria that infect the small bowel and produce profuse, watery diarrhea. Moreover, the infection is generally self-limited.

The exposure can be minimal, since the bacteria can survive stomach acid. Once exposed, the incubation period spans 1 to 3 days. Symptomatic patients start with fever, malaise, anorexia, and watery diarrhea. Eventually, blood and mucus may be present in the stool, and tenesmus is a common complaint. In contrast to other forms of bacterial gastroenteritis, nausea and vomiting are generally absent.[33] Shigella most often affects the colon. Consequently, significant fluid loss is uncommon, unlike other bacteria that infect the small bowel and produce profuse, watery diarrhea. Moreover, the infection is generally self-limited. Shigella sonnei commonly causes mild disease, whereas Shigella flexneri and Shigella dysenteriae 1 commonly cause dysenteric symptoms. Vaginitis and vulvovaginitis may be the presenting features in young patients, causing vaginal discharge that may be bloody in the presence or absence of diarrhea. Keratitis associated with diarrhea is an additional clue to the presence of Shigella. Likewise, Shigella flexneri may cause reactive arthritis in combination with urethritis and conjunctivitis. Among patients who develop reactive arthritis, 70% are HLA-B27-positive.[34] Shigella can cause severe inflammation of the rectum and colon, resulting in proctitis or rectal prolapse, toxic megacolon, intestinal obstruction, and perforation. Seizures and a leukemoid reaction (a white blood cell count of 50,000/mm³ or more) are additional potential findings associated with Shigella infection.[35] Staphylococcus aureus Patients who present with nausea and vomiting as their predominant symptoms have likely ingested a preformed enterotoxin like that generated by Staphylococcus aureus or Bacillus cereus. In addition, chemical irritants or viral gastroenteritis may present with nausea and vomiting as initial or predominant symptoms. Ingestion of the preformed toxin causes symptoms within 30 minutes to 8 hours of ingestion, which resolve within 24 hours. Foods not cooked after handling or stored at unsafe temperatures are at high risk for Staphylococcus aureus contamination. The primary source of contamination is food handlers who carry Staphylococcus aureus in their noses or hands or through respiratory secretions. Vibrio species

Patients who present with nausea and vomiting as their predominant symptoms have likely ingested a preformed enterotoxin like that generated by Staphylococcus aureus or Bacillus cereus. In addition, chemical irritants or viral gastroenteritis may present with nausea and vomiting as initial or predominant symptoms. Ingestion of the preformed toxin causes symptoms within 30 minutes to 8 hours of ingestion, which resolve within 24 hours. Foods not cooked after handling or stored at unsafe temperatures are at high risk for Staphylococcus aureus contamination. The primary source of contamination is food handlers who carry Staphylococcus aureus in their noses or hands or through respiratory secretions. Vibrio species Vibrio mimicus, Vibrio fluvialis, Vibrio furnissii, Grimontia hollisae (initially known as Vibrio hollisae), and Vibrio cholerae are the primary Vibrio species that cause diarrheal illnesses. Consumption of seafood is the leading risk factor for Vibrio mimicus gastrointestinal infection. In the United States, raw oysters and shellfish are the primary culprits. Typical symptoms are cholera-like illness with diarrhea, nausea, and vomiting. Vibrio fluvialis thrives in river and estuarine waters and does not produce a cholera toxin. However, this species has a high incidence of bloody diarrhea along with abdominal pain, vomiting, and fever. Researchers link illness due to Grimontia hollisae to the ingestion of seafood.[36] Yersinia species Transmission of Yersinia is typically foodborne or waterborne. Occasionally, transmission occurs from person to person through blood transfusions and from exposure to household pets. Y enterocolitica and Yersinia pseudotuberculosis both cause enteritis. Y enterocolitica colonizes vertebrate animals, most notably the tonsils and oropharynx of pigs, where it spreads to the gastrointestinal tract and contaminates other sites during slaughter. Eating raw or undercooked pork is a primary way to contract Yersinia. Consumption of contaminated lettuce, carrots, and milk has led to reports of Yersinia pseudotuberculosis infection. The incubation period is generally 4 to 6 days, followed by nausea, vomiting, fever, abdominal pain, and diarrhea. Bloody diarrhea is more common in children than in adults. Like Campylobacter, Yersinia can also cause pseudoappendicitis. Diarrhea From Other Infectious Agents

Transmission of Yersinia is typically foodborne or waterborne. Occasionally, transmission occurs from person to person through blood transfusions and from exposure to household pets. Y enterocolitica and Yersinia pseudotuberculosis both cause enteritis. Y enterocolitica colonizes vertebrate animals, most notably the tonsils and oropharynx of pigs, where it spreads to the gastrointestinal tract and contaminates other sites during slaughter. Eating raw or undercooked pork is a primary way to contract Yersinia. Consumption of contaminated lettuce, carrots, and milk has led to reports of Yersinia pseudotuberculosis infection. The incubation period is generally 4 to 6 days, followed by nausea, vomiting, fever, abdominal pain, and diarrhea. Bloody diarrhea is more common in children than in adults. Like Campylobacter, Yersinia can also cause pseudoappendicitis. Diarrhea From Other Infectious Agents Receptive anal intercourse or oral-anal intercourse can serve as a potential route of direct inoculation of pathogens. Acute diarrhea can be a manifestation of proctitis due to chlamydia, gonorrhea, and syphilis. Anoscopy may reveal anorectal discharge and friability of the rectal mucosa.[37][38]

The initial evaluation of adults and children with diarrhea involves a thorough history and physical examination, which help determine stool consistency, the presence of blood in the stool, and the patient's volume status. Obtaining a detailed food history can aid in diagnosing foodborne illnesses, as the timing of symptom onset after eating can help identify the most likely sources of contamination. A travel history can expand the range of potential diagnoses.[39] Questions about the patient’s occupation, hobbies, pets, and living conditions are also important. Documenting and reviewing medication use is crucial since many medications can cause diarrhea as an adverse effect, particularly when taken for the first time. Drugs commonly associated with diarrhea include antacids containing magnesium, laxatives, nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics, chemotherapy agents, and metformin. Antibiotic use, particularly in patients with C difficile, increases the risk of diarrhea associated with C difficile. Most patients with diarrhea do not require laboratory evaluations. However, determining the etiology is helpful during an epidemic. Serum electrolytes, creatinine, and blood glucose levels in the presence of significant hypovolemia are necessary to evaluate for hypokalemia, hypoglycemia, and acute kidney injury. A complete blood count (CBC) helps detect thrombocytopenia or anemia associated with HUS or a leukemoid reaction consistent with C difficile or Shigella. Patients may develop sepsis associated with diarrhea due to Salmonella species and toxigenic strains of Staphylococcus aureus. Profuse watery diarrhea is often the initial presenting feature of staphylococcal toxic shock syndrome. Clinicians should obtain blood cultures in patients with high fevers or who appear toxic. Individuals with suspected nontyphoidal Salmonella gastroenteritis who are younger than 12 months or older than 50 years, or who have comorbidities such as hemoglobinopathy, atherosclerosis, or immunosuppression, require blood cultures due to an increased risk of bacteremia and extraintestinal infections, such as endocarditis and endovascular infections. Patients at high risk, with evidence of inflammatory diarrhea or severe illness, should undergo stool studies. The following list includes indications for microbiologic stool testing: Hypovolemia Severe abdominal pain Bloody stools

Patients may develop sepsis associated with diarrhea due to Salmonella species and toxigenic strains of Staphylococcus aureus. Profuse watery diarrhea is often the initial presenting feature of staphylococcal toxic shock syndrome. Clinicians should obtain blood cultures in patients with high fevers or who appear toxic. Individuals with suspected nontyphoidal Salmonella gastroenteritis who are younger than 12 months or older than 50 years, or who have comorbidities such as hemoglobinopathy, atherosclerosis, or immunosuppression, require blood cultures due to an increased risk of bacteremia and extraintestinal infections, such as endocarditis and endovascular infections. Patients at high risk, with evidence of inflammatory diarrhea or severe illness, should undergo stool studies. The following list includes indications for microbiologic stool testing: Hypovolemia Severe abdominal pain Bloody stools Temperature of 38.5 ºC (101.3 ºF) or greater Age 70 or older Pregnancy Inflammatory bowel disease Symptoms for longer than 1 week Public health concerns like illness in food handlers Comorbid conditions exacerbated by hypovolemia Greater than 6 stools per day Fecal leukocytes and calprotectin are both markers of neutrophil activity and can help distinguish between inflammatory and noninflammatory causes of diarrhea, but do not differentiate between infectious and noninfectious etiologies.[40] Fecal leukocytes are more likely to be associated with bacterial than with viral gastroenteritis. Ideally, stool studies should be performed with fresh diarrheal stool. A rectal swab is a possible alternative when fresh stool is unavailable.[41] Routine stool cultures can identify Salmonella, Campylobacter, and Shigella. E coli O157:H7 requires an alternative medium, or the stool can undergo antigen or polymerase chain reaction testing. Clinicians should notify the laboratory of their specific concerns to ensure proper testing and identification. People typically excrete bacteria continuously in their stool, unlike ova and parasites, which patients excrete intermittently. Hence, a negative result is not typically a false negative when using the correct culture media.

Routine stool cultures can identify Salmonella, Campylobacter, and Shigella. E coli O157:H7 requires an alternative medium, or the stool can undergo antigen or polymerase chain reaction testing. Clinicians should notify the laboratory of their specific concerns to ensure proper testing and identification. People typically excrete bacteria continuously in their stool, unlike ova and parasites, which patients excrete intermittently. Hence, a negative result is not typically a false negative when using the correct culture media. Multiplex stool tests identify the genetic material of the organisms and test for bacterial, viral, and parasitic causes. However, confirmatory cultures are necessary since the detection of genetic material does not confirm infection with a viable organism.[42] In addition to stool cultures, bloody stools should be tested for Shiga toxin using immunoassays, molecular tests, or fecal leukocytes or lactoferrin. Patients with bloody diarrhea and no fecal leukocytes should undergo testing for amebiasis, as these organisms destroy leukocytes. Testing for C difficile in a patient hospitalized for 72 hours or more is likely more beneficial and cost-effective than routine stool cultures. C difficile infection is the primary concern in patients receiving antibiotics, particularly those who have undergone antibiotic therapy or been hospitalized in the past 3 months. Available tests include nucleic acid amplification testing (NAAT), glutamate dehydrogenase (GDH) tests on rectal swabs, enzyme immunoassay (EIA) toxin assays, and aerobic cultures. The sensitivity of C difficile cultures is relatively low, and the turnaround time is slow. For these reasons, this method is not routinely used to establish the diagnosis. Clinicians should only test liquid stool, and a 2-tiered approach is preferred to distinguish between infection and an asymptomatic carrier state. A standard protocol begins with NAAT and, if positive, proceeds with EIA for toxins A and B. A positive result on both tests confirms C difficile infection. A positive NAAT and negative EIA for toxins A and B indicate either a carrier state or an infection with low toxin production. Please see StatPearls' companion reference, "Clostridioides Difficile Infection," for additional information regarding establishing the diagnosis of C difficile infection.

Clinicians should only test liquid stool, and a 2-tiered approach is preferred to distinguish between infection and an asymptomatic carrier state. A standard protocol begins with NAAT and, if positive, proceeds with EIA for toxins A and B. A positive result on both tests confirms C difficile infection. A positive NAAT and negative EIA for toxins A and B indicate either a carrier state or an infection with low toxin production. Please see StatPearls' companion reference, "Clostridioides Difficile Infection," for additional information regarding establishing the diagnosis of C difficile infection. Given the high colonization rate of C difficile early in life, systematic testing is necessary for infants and children. Infants younger than 12 months who are not in the hospital or neonatal intensive care unit should only undergo testing for C difficile in the presence of Hirschsprung disease or other motility disorders. Those in the neonatal intensive care unit should only undergo testing in the presence of pseudomembranous colitis or when clinicians have excluded other potential causes of diarrhea. Children aged 1 to 3 should undergo testing only after other causes of diarrhea have been excluded, or if clinical suspicion is high based on risk factors. Children 3 years and older with clinical symptoms consistent with C difficile and concurrent associated conditions must be tested.[44] Imaging is generally unnecessary in patients with acute diarrhea without peritoneal signs or ileus. When warranted, imaging, such as computed tomography, evaluates for potential complications, including perforation, abscess, toxic megacolon, and intestinal obstruction. Children may need an ultrasound if they present with intermittent abdominal pain and bloody diarrhea to evaluate for intussusception or if appendicitis is suspected.

Most cases of acute diarrhea are self-limited and only require supportive care. Rehydration is the mainstay of treatment, preferably orally with a solution containing water, sugar, and salt. Commercially available or WHO-provided oral rehydration solutions are acceptable. Children can begin with 5 mL every 1 to 2 minutes to avoid too much liquid in the stomach at one time. Clinicians reserve IVF replacement for patients who cannot tolerate oral fluids or are moderately to severely dehydrated. The rate of fluid replacement depends on the level of volume depletion. Adults with severe hypovolemia should receive 1 to 2 liters quickly to help restore tissue perfusion. Once the signs and symptoms of hypovolemia improve or resolve, the rate of fluid infusion can decrease. All other patients should receive enough fluids to cover urine output, insensible losses, and any other fluid losses. Insensible losses are usually 30 to 50 mL/h in adults. Clinicians should calculate fluid requirements for children based on weight. Please see StatPearls' companion topic, "Pediatric Fluid Management," for an in-depth discussion regarding pediatric fluid administration. Most patients receive isotonic or one-half isotonic saline with or without potassium. However, the final choice of fluid depends on electrolyte levels. Children with severe hypovolemia receive an isotonic saline bolus of 20 mL/kg, followed by reassessment and repeat bolus if necessary. Children with less severe volume depletion can receive 10 mL/kg over 30 to 60 minutes with reassessment and a repeat bolus if necessary. All patients must be encouraged to eat nutrient-rich foods once adequately rehydrated to counter diarrhea. Dietary restrictions are unnecessary. Breastfed infants should continue their usual feedings if possible. Clinicians often suggest bananas, rice, applesauce, and toast (BRAT) or bland diets to improve the condition, as some individuals may tolerate these regimens better. However, reliable data or prospective studies confirming their effectiveness are lacking, with most assumptions based on limited studies or personal experiences.

All patients must be encouraged to eat nutrient-rich foods once adequately rehydrated to counter diarrhea. Dietary restrictions are unnecessary. Breastfed infants should continue their usual feedings if possible. Clinicians often suggest bananas, rice, applesauce, and toast (BRAT) or bland diets to improve the condition, as some individuals may tolerate these regimens better. However, reliable data or prospective studies confirming their effectiveness are lacking, with most assumptions based on limited studies or personal experiences. Similarly, research does not substantiate that certain foods, such as dairy products, should be excluded. However, dairy may be problematic to digest in patients with lactase enzyme deficiency. A systematic review suggests that evidence is insufficient to support or refute the benefits of dietary restrictions in diarrhea, and a typical diet may be resumed as tolerated. Antibiotics Empiric antibiotic therapy for diarrhea is typically initiated when a bacterial etiology is suspected, especially in cases of severe illness, high fever, or prolonged symptoms. The choice of antibiotics depends on the suspected pathogen, local resistance patterns, and the patient's underlying health conditions. In many cases, however, antibiotics are not recommended unless specific bacterial infections, such as C difficile or certain invasive organisms, are confirmed or strongly suspected. Empiric antibiotics The decision to treat with antibiotics is often made empirically while awaiting stool study results. Due to the increased risk of HUS associated with STEC, clinicians generally avoid antibiotics in adults unless the patient has severe symptoms such as hypovolemia, intense abdominal pain, and a fever of 38.5°C (101.3°F) or higher. Antibiotics may also be considered in high-risk individuals, including those aged 70 or older or with underlying conditions like cardiovascular disease or immunosuppression, which increase the risk of complications from acute diarrheal illness.

The decision to treat with antibiotics is often made empirically while awaiting stool study results. Due to the increased risk of HUS associated with STEC, clinicians generally avoid antibiotics in adults unless the patient has severe symptoms such as hypovolemia, intense abdominal pain, and a fever of 38.5°C (101.3°F) or higher. Antibiotics may also be considered in high-risk individuals, including those aged 70 or older or with underlying conditions like cardiovascular disease or immunosuppression, which increase the risk of complications from acute diarrheal illness. Adults with dysentery, fever, or a risk of fluoroquinolone-resistant infection should receive azithromycin. A single 1-gram dose is appropriate for patients without dysentery, and clinicians may use 500 mg daily for 3 days, regardless of dysentery status. Fluoroquinolones may also be prescribed as alternatives. Appropriate agents include ciprofloxacin, administered as a single dose of 750 mg or twice-daily dose of 500 mg for 3 to 5 days, as well as levofloxacin, given as a single dose of 500 mg or once-daily dose of 500 mg for 3 to 5 days. Empiric therapy for children should cover Shigella and include 3rd-generation cephalosporins. Parenteral therapy is necessary for children with an underlying immunodeficiency like HIV infection, suspected bacteremia, or inability to tolerate oral intake (see Table 1. Antibiotics and Their Corresponding Dosages for Bacterial Gastroenteritis in Children). Table Table 1. Antibiotics and Their Corresponding Dosages for Bacterial Gastroenteritis in Children. Clostroidies difficile Oral fidaxomicin or vancomycin may be used to treat C difficile infection, with fidaxomicin preferred due to its lower recurrence rate.[43] Metronidazole is a possible alternative, but it is less effective.[44] Treatment duration is 10 days, unless the clinician expects the patient to require a prolonged course of antibiotics due to an underlying condition. In that instance, treatment for C difficile continues throughout antibiotic therapy and for an additional 1 week after completion. Repeat stool studies are unnecessary in patients who have improved or recovered, as 50% will continue to have positive stool assays for up to 6 weeks after therapy cessation.

Oral fidaxomicin or vancomycin may be used to treat C difficile infection, with fidaxomicin preferred due to its lower recurrence rate.[43] Metronidazole is a possible alternative, but it is less effective.[44] Treatment duration is 10 days, unless the clinician expects the patient to require a prolonged course of antibiotics due to an underlying condition. In that instance, treatment for C difficile continues throughout antibiotic therapy and for an additional 1 week after completion. Repeat stool studies are unnecessary in patients who have improved or recovered, as 50% will continue to have positive stool assays for up to 6 weeks after therapy cessation. Oral vancomycin, fidaxomicin, and metronidazole are treatment options for children with C difficile infection. Children with mild-to-moderate disease should receive either oral vancomycin 40 mg/kg/day with a maximum of 125 mg per dose divided into 4 doses for 10 days, oral metronidazole 30 mg/kg/day with a maximum of 500 mg per dose divided into 4 doses for 10 days, or oral fidaxomicin dosed according to body weight. Oral vancomycin is the 1st-line therapy for children with severe C difficile infection. Fulminant disease warrants intravenous metronidazole and oral or rectal vancomycin. Listeria monocytogenes Pregnant patients with febrile Listeria gastroenteritis undergo hospital admission and receive ampicillin 2 g intravenously every 4 hours. Immunocompetent patients younger than 65 do not require antibiotics. For individuals older than 65 or immunocompromised, oral amoxicillin 500 mg 3 times daily or trimethoprim-sulfamethoxazole (TMP-SMX) 1 double-strength tablet twice daily for 7 days is appropriate. In children older than 3 months, the amoxicillin dose is 25 to 50 mg/kg/day divided every 8 hours with a maximum of 500 mg per dose. In children 2 months or older, the dosing of TMP-SMX is 6 to 12 mg/kg of the trimethoprim (TMP) component per day divided every 12 hours with a maximum single dose of 160 mg of TMP per dose. Shigella species Clinicians should prescribe a carbapenem like imipenem 500 mg intravenously every 6 hours for patients with severe illness and suspected shigellosis who are at risk of drug-resistant infections. High-risk groups include men who have sex with men, international travelers, individuals with HIV, and people experiencing homelessness. Vibrio cholerae

Clinicians should prescribe a carbapenem like imipenem 500 mg intravenously every 6 hours for patients with severe illness and suspected shigellosis who are at risk of drug-resistant infections. High-risk groups include men who have sex with men, international travelers, individuals with HIV, and people experiencing homelessness. Vibrio cholerae Patients with profuse, watery diarrhea from potential exposure to Vibrio cholerae should receive empiric treatment based on local resistance rates. Possible options are tetracyclines, fluoroquinolones, and macrolides. Resistance to tetracyclines is common, and fluoroquinolone resistance is becoming increasingly prevalent (see Table 2. Antibiotic Choices and Dosing for the Treatment of Cholera). Table Table 2. Antibiotic Choices and Dosing for the Treatment of Cholera. Additional Therapies The WHO recommends zinc supplementation for children with acute diarrhea in resource-limited settings. The suggested doses are 20 mg per day for children aged 6 months to 5 years and 10 mg per day for children younger than 6 months. Some experts prefer limiting supplementation to 10 mg per day for children aged 6 months to 5 years due to the association between zinc and vomiting, as well as recent studies showing no benefit in children younger than 6 months.[45] Studies indicate that zinc supplementation reduces the duration of diarrhea by half a day to one day.[46] Clinicians should also provide vitamin A supplements to children with signs of vitamin A deficiency, such as xerophthalmia, keratitis, keratoconjunctivitis, corneal ulceration, or Bitot spots. These spots result from keratin build-up caused by pathologic dryness of the conjunctiva and cornea.[47] Experts advise against prescribing antimotility agents and antiemetics for children. Antimotility agents can prolong some bacterial infections and, rarely, may cause a fatal paralytic ileus. Antiemetics can cause sedation, impede rehydration efforts, and induce extrapyramidal reactions and respiratory depression. For adults, loperamide may be used cautiously in patients without fever or bloody stool. Appropriate loperamide dosing is 2 tablets (4 mg) initially, followed by 2 mg after each unformed stool for up to 2 days, with a maximum of 16 mg/d. Bismuth salicylate, 30 mL or 2 tablets every 30 minutes for 8 doses, is an alternative to antimotility agents for patients with dysentery.

For adults, loperamide may be used cautiously in patients without fever or bloody stool. Appropriate loperamide dosing is 2 tablets (4 mg) initially, followed by 2 mg after each unformed stool for up to 2 days, with a maximum of 16 mg/d. Bismuth salicylate, 30 mL or 2 tablets every 30 minutes for 8 doses, is an alternative to antimotility agents for patients with dysentery. Some experts believe that antimotility agents may be used cautiously in patients with dysentery and that antibiotics should be started simultaneously. However, these agents must be avoided in patients with Shigella as they may prolong the illness. Patients must be aware that antimotility agents may cause fluid pooling in the intestine, potentially masking the amount of fluid lost. Patients must continue with diligent fluid replacement. Clinicians should keep in mind that bismuth salicylate is less effective and may cause salicylate toxicity. The Infectious Disease Society of America guidelines state clinicians may offer probiotics to adults and children with acute infectious gastroenteritis. However, the organization provides no specific recommendations regarding the strain or dosing. To date, studies have not shown a consistent, proven benefit from this treatment. Prevention Controlling the spread of organisms is the cornerstone of preventing diarrheal illnesses. Key measures include the following: Washing hands with soap Providing access to safe drinking water Breastfeeding infants and children Practicing proper sanitation and safe food handling Controlling flies Vaccinations, when available, are another valuable resource. Depending on their destination and country of origin, clinicians may recommend cholera and typhoid vaccines for travelers. The oral whole-cell killed cholera vaccine (Dukoral) has shown promise in reducing the incidence of traveler’s diarrhea caused by ETEC. The protective effect against ETEC is due to the antigenic similarity between the cholera toxin B subunit and the heat-labile enterotoxin of ETEC. The vaccine provides 85% protection against cholera and 43% to 67% against ETEC.[48] Dukoral is not available in the United States, but the live attenuated cholera vaccine CVD 103-HgR (Vaxchora), which protects against cholera caused by serotype O1, is available for travelers aged 2 to 64 at high risk of exposure.

Vaccinations, when available, are another valuable resource. Depending on their destination and country of origin, clinicians may recommend cholera and typhoid vaccines for travelers. The oral whole-cell killed cholera vaccine (Dukoral) has shown promise in reducing the incidence of traveler’s diarrhea caused by ETEC. The protective effect against ETEC is due to the antigenic similarity between the cholera toxin B subunit and the heat-labile enterotoxin of ETEC. The vaccine provides 85% protection against cholera and 43% to 67% against ETEC.[48] Dukoral is not available in the United States, but the live attenuated cholera vaccine CVD 103-HgR (Vaxchora), which protects against cholera caused by serotype O1, is available for travelers aged 2 to 64 at high risk of exposure. Clinicians should not routinely prescribe empiric antibiotics to prevent traveler's diarrhea unless the patient has an underlying condition that increases their risk of complications.[49][50] Rifaximin 200 mg 3 times a day for the duration of the trip would be indicated in patients with underlying severe cardiovascular disease, vascular or renal disorders, and inflammatory bowel disease.

Infectious agents account for most acute diarrhea cases, with viral infections being the most common. However, clinicians must consider all possibilities, as symptoms often overlap among viral, bacterial, and protozoal etiologies. Additional causes of diarrhea should also be excluded, including the following: Inflammatory bowel disease [51] Irritable bowel syndrome [52] Malabsorption syndromes like celiac or Whipple disease Cystic fibrosis Lactose intolerance Hyperthyroidism Antibiotic-induced diarrhea [53] Otitis media Urinary tract infection Food allergy [54] Starvation stools Functional diarrhea due to excess fructose or sorbitol intake Partial bowel obstruction Blind loop syndrome Intussusception Toxic megacolon Short gut syndrome Congenital secretory diarrhea Acrodermatitis enteropathica Congenital adrenal hyperplasia Hypoparathyroidism Neonatal drug withdrawal [55] Medication adverse effects Appendicitis Disaccharidase deficiency Neuroendocrine secretory tumors HIV infection Artificial sweeteners Radiation effects Autonomic neuropathy Dumping syndrome Accurate diagnosis requires thorough evaluation to distinguish infectious causes from other conditions that may mimic diarrhea. Clinicians should consider a broad differential to ensure appropriate management and treatment.

The prognosis of bacterial diarrhea is usually excellent in developed countries with appropriate support, hydration, and antibiotics. By comparison, morbidity and mortality increase in developing areas where access to care may limit opportunities for rehydration, particularly for vulnerable populations.

The most common complications of bacterial diarrhea are dehydration, malnutrition, and malabsorption syndromes. Additional complications are often specific to the underlying pathogen. C difficile Chronic diarrhea Toxic megacolon Ileus Shigella species Seizures HUS Bowel perforation Reiter syndrome Encephalopathy Vaginitis or vulvovaginitis [56] Keratitis [57] Myocarditis Proctitis or rectal prolapse in infants and young children [58] Toxic megacolon Intestinal obstruction Colonic perforation Bacteremia Listeria species Bacteremia Meningitis Meningoencephalitis Cholecystitis Peritonitis Enterohemorrhagic E coli O157:H7 HUS Salmonella species Enteric fever Endovascular infection Bacteremia Meningitis Osteomyelitis Myocarditis Reiter syndrome Septic arthritis Brain abscess Vibrio species Rapid dehydration Yersinia enterocolitica Appendicitis Bowel perforation Intussusception Peritonitis Toxic megacolon Cholangitis Bacteremia Reiter syndrome Campylobacter species Bacteremia Meningitis Cholecystitis Urinary tract infection Pancreatitis Reiter syndrome Peritonitis Rash [59] Osteomyelitis [60][61] Septic pseudoaneurysm [62] Pericarditis Myocarditis GBS Bacillus species Liver failure Rhabdomyolysis Aeromonas caviae Intussusception Sepsis HUS Clostridium perfringens Hemorrhagic necrosis of the jejunum or pigbel Recognizing and promptly managing the various complications of bacterial diarrhea can significantly improve patient outcomes and minimize the risk of severe consequences.

Viral pathogens cause most acute diarrheal illnesses, and supportive care with oral rehydration solutions and prompt resumption of a regular diet is typically sufficient. Educating patients about effective hydration strategies is crucial to preventing dehydration and its associated health risks. Patients should be encouraged to practice proper hand hygiene by thoroughly washing their hands with soap and water, particularly before eating, after using the restroom, and after handling raw foods to reduce the risk of bacterial gastroenteritis. Safe food handling is equally important, including cooking meats using safe internal temperatures, avoiding cross-contamination between raw and cooked foods, and promptly refrigerating perishable items. Clinicians should also emphasize the importance of drinking bottled or properly boiled water, especially when traveling to areas with inadequate sanitation. Additionally, international travelers should avoid high-risk foods, such as raw seafood, unpasteurized juice or dairy products, and uncooked produce that may have been washed with contaminated water. Clinicians play a key role in avoiding unnecessary diagnostic tests and preventing inappropriate antibiotic use. Most cases of bacterial enteritis resolve without specific treatment. However, identifying the bacterial cause is crucial when treating patients with severe symptoms, underlying health conditions, or prolonged illness lasting more than a week, as well as managing cases with potential public health implications. Patients should understand the risks associated with antibiotic misuse, including antibiotic resistance and disruption of the gut microbiota, and be discouraged from self-medicating. Healthcare professionals should prioritize patient hydration and adherence to prescribed treatment plans when managing bacterial gastroenteritis. Educating patients on recognizing severe symptoms, such as dehydration or prolonged illness, ensures timely medical intervention. Healthcare professionals and childcare providers must diligently work to prevent outbreaks by isolating symptomatic individuals and maintaining strict hygiene practices. By promoting awareness and proactive strategies, clinicians can help reduce the prevalence and impact of bacterial gastroenteritis in their communities.

As defined by the WHO, diarrhea involves loose or watery stools occurring 3 or more times daily, often accompanied by additional symptoms such as fever and abdominal pain, and may be accompanied by visible blood or mucus in the case of dysentery. While viruses are the primary cause of acute diarrhea, bacterial etiologies, including Salmonella, Shigella, Campylobacter, Y enterocolitica, C difficile, and E coli, are significant contributors and can lead to severe complications such as sepsis, HUS, and GBS. Diagnosing bacterial causes requires careful clinical assessment, with key indicators including fever and bloody or mucoid stools, as well as risk factors such as recent antibiotic use, hospitalization, and immunocompromised status. Clinicians reserve stool studies when evaluating at-risk patients with severe or persistent symptoms or during a pandemic. Treatment focuses on oral rehydration, with intravenous fluids for severe dehydration. The selective use of antibiotics balances the benefits with risks, such as the potential for HUS in Shiga toxin-producing E coli infections. Accurate diagnosis and appropriate management are critical to preventing morbidity, mortality, complications, and antibiotic resistance. Effective management of bacterial diarrhea requires a collaborative, interdisciplinary approach involving healthcare professionals, including physicians, advanced practitioners, nurses, pharmacists, and laboratory personnel, to enhance patient-centered care, improve outcomes, and ensure patient safety. Physicians and advanced practitioners are central to diagnosing the condition, determining its etiology, and developing evidence-based treatment plans, including the appropriate use of antibiotics. Nurses play a crucial role in educating patients, monitoring for signs of dehydration or worsening symptoms, administering treatments, and providing ongoing support. Pharmacists contribute by verifying medication appropriateness, counseling on antibiotic use, and addressing potential drug interactions to reduce adverse effects and antimicrobial resistance.

Effective management of bacterial diarrhea requires a collaborative, interdisciplinary approach involving healthcare professionals, including physicians, advanced practitioners, nurses, pharmacists, and laboratory personnel, to enhance patient-centered care, improve outcomes, and ensure patient safety. Physicians and advanced practitioners are central to diagnosing the condition, determining its etiology, and developing evidence-based treatment plans, including the appropriate use of antibiotics. Nurses play a crucial role in educating patients, monitoring for signs of dehydration or worsening symptoms, administering treatments, and providing ongoing support. Pharmacists contribute by verifying medication appropriateness, counseling on antibiotic use, and addressing potential drug interactions to reduce adverse effects and antimicrobial resistance. Ensuring all team members align with the care plan requires clear, effective interprofessional communication, including discussions of laboratory results, patient progress, and emerging complications. Effective care coordination involves ensuring timely referrals to specialists, such as gastroenterology or infectious disease experts, and integrating dietary and hydration recommendations from dietitians. This teamwork improves patient outcomes and promotes safety by reducing medication errors and ensuring adherence to treatment protocols. A collaborative, patient-centered strategy that leverages each professional's unique skills fosters trust, improves health literacy, and enhances overall team performance in managing bacterial diarrhea.