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Gastroenteritis

Gastroenteritis, often referred to as stomach flu, is an inflammation of the lining of the stomach and intestines that typically causes acute diarrhea and vomiting, along with abdominal cramps, nausea, and sometimes fever.^[1] Although commonly self-limiting in healthy individuals, it can lead to severe dehydration and electrolyte imbalances, particularly in vulnerable groups such as infants, young children, older adults, and immunocompromised people.^[2] The condition is distinct from influenza, as it does not involve respiratory viruses, and most cases resolve within a few days with supportive care.^[1] The primary causes of gastroenteritis are infectious agents, including viruses (such as norovirus and rotavirus, which account for the majority of cases), bacteria (like Salmonella, Escherichia coli, and Campylobacter), and parasites (such as Giardia and Cryptosporidium).^[2] Noninfectious triggers include ingestion of toxins, certain medications, or food intolerances, though these are less common.^[2] Transmission occurs mainly through the fecal-oral route via contaminated food or water, direct person-to-person contact, or contact with contaminated surfaces, making outbreaks frequent in settings like schools, cruise ships, and nursing homes.^[3] Globally, diarrhoeal diseases like gastroenteritis remain a major public health concern, causing approximately 1.7 billion episodes in children annually and contributing to approximately 340,000 deaths among children under 5 years old each year (as of 2021), primarily in low- and middle-income countries due to poor sanitation and lack of clean water.^[3]^[4] In the United States, it results in about 179 million illnesses yearly, with norovirus alone responsible for roughly 19 to 21 million cases.^[5] Diagnosis typically involves clinical evaluation and stool testing to identify pathogens when necessary, while treatment focuses on rehydration using oral rehydration solutions and, in specific bacterial or parasitic cases, targeted antimicrobials.^[2] Prevention strategies emphasize hand hygiene, safe food and water practices, and vaccination against rotavirus for infants.^[3]

Clinical Presentation

Signs and Symptoms

Gastroenteritis typically presents with an acute onset of gastrointestinal symptoms, most commonly watery diarrhea, vomiting, nausea, abdominal pain or cramping, fever, and headache.^[6] Diarrhea is often the predominant feature, characterized by loose or liquid stools occurring three or more times per day, while vomiting may be explosive and frequent, particularly in viral cases.^[3] Abdominal discomfort arises from cramping or bloating, and systemic symptoms like low-grade fever (usually below 102°F) and headache can accompany the illness, reflecting inflammation in the gastrointestinal tract.^[7] The duration of symptoms varies by etiology, with viral gastroenteritis generally resolving within 1 to 3 days, though it can extend up to 10 days in some instances.^[8] Bacterial and parasitic causes often lead to prolonged illness, lasting 5 to 7 days or longer, with more severe manifestations such as bloody diarrhea in infections like shigellosis.^[9] Specific symptom profiles differ; for example, viral infections such as norovirus or rotavirus typically cause profuse watery diarrhea without blood, whereas bacterial pathogens like Shigella produce dysentery-like symptoms including bloody, mucoid stools, tenesmus, and higher fever.^[10]^[11] Symptom presentation can vary by age group. In infants and young children, irritability, poor feeding, and dehydration signs such as sunken eyes or dry mucous membranes may predominate alongside diarrhea and vomiting.^[3] Adults more commonly report dehydration indicators like dry mouth, reduced urine output, and fatigue, in addition to the core gastrointestinal complaints.^[12] These manifestations can overlap with other conditions like food poisoning, but severe dehydration represents a key potential complication requiring prompt attention.^[13]

Complications

Gastroenteritis can lead to dehydration of varying severity due to fluid loss from vomiting and diarrhea. Mild dehydration, typically involving a 3-5% fluid deficit, manifests as increased thirst and slightly dry mucous membranes.^[14] Moderate dehydration, with a 6-9% fluid deficit, is characterized by sunken eyes, dry mucous membranes, and reduced urine output.^[14] Severe dehydration, exceeding 10% fluid loss, presents with lethargy, a rapid thready pulse, and can progress to shock and multi-organ failure if untreated.^[14] Electrolyte imbalances are common complications, particularly hyponatremia and hypokalemia resulting from gastrointestinal fluid losses.^[15] Hyponatremia involves serum sodium levels below 135 mmol/L and can exacerbate neurological symptoms in severe cases.^[16] Hypokalemia, with serum potassium below 3.5 mmol/L, may lead to cardiac arrhythmias, muscle weakness, and in extreme instances, paralysis or respiratory failure.^[17] A subset of patients may develop post-infectious irritable bowel syndrome (PI-IBS) following acute gastroenteritis, characterized by persistent abdominal pain and altered bowel habits meeting Rome criteria.^[18] This condition is linked to microbiome disruption, where alterations in gut bacterial composition contribute to ongoing symptoms.^[19] Additionally, small intestinal bacterial overgrowth (SIBO) can emerge, causing bloating and diarrhea due to excessive bacterial proliferation in the small bowel.^[20] Autoimmune mechanisms, including elevated anti-vinculin antibodies, have been implicated in the pathogenesis of PI-IBS and related disorders.^[21] Rare but serious complications include hemolytic uremic syndrome (HUS), primarily associated with Shiga toxin-producing Escherichia coli O157:H7 infections, which can cause microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury.^[22] Another infrequent sequela is Guillain-Barré syndrome, most commonly triggered by Campylobacter jejuni gastroenteritis, leading to acute inflammatory demyelinating polyneuropathy with potential for ascending paralysis.^[23] Long-term gastrointestinal issues mimicking gastroenteritis symptoms have been observed after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, including persistent diarrhea, bloating, and abdominal discomfort.^[24] These effects are attributed to gut dysbiosis, with sustained alterations in the intestinal microbiota contributing to chronic inflammation and motility disturbances.^[25]

Causes and Transmission

Viral Causes

Viral gastroenteritis is predominantly caused by norovirus, which accounts for the majority of cases worldwide and is responsible for an estimated 685 million episodes annually.^[26] Norovirus, a member of the Caliciviridae family, exists in multiple genotypes, with genogroup II genotype 4 (GII.4) historically dominant in outbreaks; however, in the 2024-2025 season, genogroup II genotype 17 (GII.17) emerged as the predominant strain, comprising 75% of reported U.S. outbreaks.^[27] The virus typically has an incubation period of 12 to 48 hours, leading to symptoms that are usually self-limiting in healthy adults but can cause significant morbidity in vulnerable populations.^[6] Rotavirus, a double-stranded RNA virus in the Reoviridae family, remains a primary cause of severe gastroenteritis in children under 5 years old, often resulting in dehydration requiring medical intervention.^[28] Prior to widespread vaccination, rotavirus was a leading cause of hospitalization for diarrhea in young children; vaccination programs have since reduced severe cases by approximately 80% in vaccinated populations.^[29] Other viruses contributing to gastroenteritis include enteric adenoviruses (types 40 and 41), astroviruses, and sapoviruses, which are less common than norovirus or rotavirus but play significant roles in outbreaks, particularly among children and in institutional settings.^[30] These pathogens, along with norovirus and rotavirus, exhibit seasonality, with outbreaks peaking during winter months in temperate climates.^[31] Recent trends indicate a post-2023 resurgence of norovirus activity, with 2024-2025 outbreak levels surpassing pre-COVID-19 peaks in some regions.^[32]

Bacterial Causes

Bacterial gastroenteritis is primarily caused by invasive or toxin-producing pathogens that infect the gastrointestinal tract, leading to inflammation, diarrhea, and often systemic symptoms. Common culprits include non-typhoidal Salmonella, Shigella, Campylobacter jejuni, and certain strains of Escherichia coli such as enterotoxigenic (ETEC), enteropathogenic (EPEC), and enterohemorrhagic (EHEC). These bacteria typically enter through contaminated food or water, with Salmonella often linked to undercooked poultry or eggs, causing symptoms like watery diarrhea, fever, and abdominal cramps after an incubation period of 12-72 hours. Shigella stands out for its low infectious dose of 10-100 organisms, which enables person-to-person spread and results in dysentery characterized by bloody, mucoid stools and tenesmus. Campylobacter jejuni, frequently associated with raw or undercooked poultry and unpasteurized milk, has an incubation of 2-5 days and produces inflammatory diarrhea that may include blood. ETEC primarily causes watery diarrhea via heat-labile and heat-stable toxins, common in traveler's diarrhea, while EPEC adheres to intestinal cells inducing attaching-effacing lesions in infants, and EHEC produces Shiga toxins leading to hemorrhagic colitis and potential hemolytic uremic syndrome (HUS) in vulnerable populations. Clostridium difficile represents a distinct bacterial cause, often secondary to antibiotic disruption of gut microbiota, resulting in pseudomembranous colitis with profuse, watery diarrhea and toxin-mediated inflammation. Unlike primary invaders, C. difficile spores thrive in healthcare settings, with broad-spectrum antibiotics like clindamycin or cephalosporins increasing risk by up to 10-fold. Vibrio cholerae, particularly serogroups O1 and O139, causes severe, toxin-mediated dehydration through cholera toxin that activates adenylate cyclase, producing massive volumes of "rice-water" stools—pale, watery diarrhea with mucus flecks—after a 12-hour to 5-day incubation, often via contaminated water in endemic areas. Antibiotic resistance complicates bacterial gastroenteritis management, with high rates observed in key pathogens since 2020. High resistance rates are observed globally, particularly in low- and middle-income countries, with rates exceeding 70% for tetracycline in Campylobacter and trimethoprim-sulfamethoxazole in Shigella in many regions; ampicillin resistance in non-typhoidal Salmonella averages 20-30% globally but can reach higher levels regionally.^[33] Multidrug resistance has risen, with over 40% of monitored pathogen-antibiotic combinations showing increased resistance from 2018-2023.^[33] As of 2025, WHO surveillance indicates ongoing increases, with roughly 1 in 6 bacterial infections involving resistant pathogens globally.^[33] Fluoroquinolone resistance in Salmonella reaches up to 50% in Asia and Africa. C. difficile strains like BI/NAP1/027 exhibit hypervirulence and resistance to multiple agents, while V. cholerae maintains low resistance but faces emerging threats to tetracyclines in outbreak regions. These patterns underscore the need for stewardship to curb global spread.

Parasitic Causes

Parasitic infections account for a significant portion of gastroenteritis cases, particularly in regions with poor sanitation or among travelers to endemic areas, where protozoan parasites are the primary culprits due to their fecal-oral transmission route via contaminated water or food.^[34] Among these, Giardia lamblia (also known as Giardia duodenalis or Giardia intestinalis) is one of the most common protozoans causing giardiasis, a condition that often presents with prolonged watery diarrhea, abdominal cramps, bloating, and foul-smelling fatty stools indicative of malabsorption.^[35] The incubation period for giardiasis typically ranges from 1 to 2 weeks after ingestion of cysts, and without treatment, infections can become chronic, leading to persistent symptoms and nutrient deficiencies, especially in developing regions where prevalence is heightened by inadequate water treatment.^[36]^[35] Cryptosporidium species, particularly Cryptosporidium parvum and Cryptosporidium hominis, cause cryptosporidiosis, which manifests as profuse watery diarrhea, abdominal pain, nausea, and low-grade fever, with symptoms usually appearing 2 to 10 days post-infection and lasting 1 to 2 weeks in immunocompetent individuals.^[37] This parasite is notably chlorine-resistant, allowing survival in inadequately treated recreational or drinking water, and it poses a greater risk of severe, prolonged, or chronic diarrhea in immunocompromised hosts, such as those with HIV, where it can lead to life-threatening dehydration and malabsorption.^[38]^[39] Entamoeba histolytica is the causative agent of amebiasis, which can result in invasive intestinal disease characterized by bloody diarrhea (dysentery), abdominal pain, and tenesmus, typically developing gradually over 1 to 3 weeks after cyst ingestion.^[40] While many infections remain asymptomatic, symptomatic cases are more prevalent in tropical and subtropical areas with poor sanitation, and untreated invasive amebiasis can cause chronic colonic ulceration and malabsorption.^[41] Cyclospora cayetanensis, another coccidian protozoan, is less commonly associated with sporadic acute gastroenteritis but has caused notable outbreaks linked to consumption of contaminated fresh produce, such as raspberries, basil, or cilantro imported from endemic regions.^[42] Infections lead to self-limited watery diarrhea, fatigue, and anorexia, with an incubation period of about 7 days, though chronic symptoms may occur without intervention, particularly in those with underlying health issues.^[43] Helminthic parasites, such as certain nematodes, infrequently cause acute gastroenteritis but can contribute to chronic gastrointestinal disturbances through mechanisms like partial intestinal obstruction or secondary malabsorption in endemic settings with poor hygiene.^[44] Diagnosis of these parasitic causes generally involves stool microscopy to detect oocysts, cysts, or trophozoites, confirming infection in suspected cases.^[45]

Noninfectious Causes

Noninfectious causes of gastroenteritis encompass a range of environmental, pharmacological, and physiological triggers that induce symptoms such as diarrhea, nausea, vomiting, and abdominal pain without involvement of pathogens.^[46] These etiologies are often linked to specific exposures or underlying conditions and typically lack systemic signs like fever, distinguishing them from infectious forms.^[47] Symptoms generally resolve upon removal of the offending agent or trigger, though severe cases may require targeted interventions.^[48] Chemical toxins represent a significant noninfectious category, including heavy metals like arsenic and organophosphates, which can irritate the gastrointestinal mucosa and cause acute diarrhea.^[47] For instance, ingestion of contaminated water or food with arsenic leads to abdominal cramping and watery stools, often within hours of exposure.^[48] Scombroid poisoning, resulting from histamine accumulation in improperly stored fish such as tuna or mackerel, mimics allergic reactions with flushing, headache, and diarrhea onset typically 10-60 minutes post-ingestion.^[49] Food additives and preservatives may also provoke symptoms in sensitive individuals, though these are less common.^[46] Medications frequently contribute to noninfectious gastroenteritis through direct mucosal irritation or disruption of gut flora. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen and naproxen, inhibit prostaglandin synthesis, leading to erosive damage in the stomach and intestines, with symptoms including nausea, dyspepsia, and diarrhea.^[50] Other culprits include antibiotics, which can induce osmotic diarrhea or Clostridioides difficile-associated issues; laxatives and sorbitol-containing products, causing osmotic effects; and chemotherapeutic agents, which damage rapidly dividing intestinal cells.^[48] Colchicine and metformin similarly provoke gastrointestinal upset via mechanisms like microtubule disruption or altered glucose absorption.^[47] Allergic reactions and intolerances often present with gastroenteritis-like episodes triggered by specific dietary components. Lactose intolerance arises from lactase deficiency, resulting in undigested lactose fermenting in the colon to produce bloating, flatulence, and diarrhea after dairy consumption.^[51] Celiac disease flare-ups, induced by gluten exposure in genetically susceptible individuals, cause villous atrophy and malabsorption, manifesting as acute abdominal pain and profuse diarrhea.^[47] Artificial sweeteners like sorbitol and fructose can also draw water into the bowel, exacerbating symptoms in those with irritable bowel syndrome or sensitivities.^[46] Additional noninfectious triggers include radiation therapy and ischemic events. Radiation enteritis, a complication of pelvic or abdominal radiotherapy for cancers like prostate or cervical, damages intestinal epithelium, leading to diarrhea, cramping, and mucus discharge during or shortly after treatment.^[52] Ischemic bowel, due to reduced mesenteric blood flow from atherosclerosis or embolism, presents with severe postprandial pain, bloody diarrhea, and urgency, particularly in older adults with vascular risk factors.^[53] These conditions highlight the importance of exposure history in identifying noninfectious etiologies.^[46]

Transmission Modes

Gastroenteritis is predominantly transmitted via the fecal-oral route, where pathogens from infected individuals' feces are ingested through contaminated hands, food, or water. This route facilitates the spread of viral, bacterial, and parasitic agents alike, often exacerbated by inadequate sanitation and hygiene practices.^[3]^[54] Person-to-person transmission occurs directly through close contact or indirectly via poor hand hygiene after using the toilet or changing diapers, particularly in high-density settings like childcare centers and schools where young children are frequent shedders of pathogens such as norovirus and rotavirus. In these environments, outbreaks can rapidly affect multiple individuals due to shared facilities and limited handwashing opportunities. Shigella, a bacterial cause, also spreads efficiently person-to-person, with 88% of U.S. outbreaks attributed to such contact or environmental contamination (2009–2013 data).^[5] Foodborne transmission involves consuming contaminated foods, including undercooked meats like poultry harboring Campylobacter, unpasteurized dairy products, and salads washed with tainted water; norovirus outbreaks are commonly linked to shellfish from polluted waters or foods handled by infected food workers. This mode underscores the role of food preparation hygiene in preventing widespread illness.^[55]^[56]^[57] Waterborne spread arises from ingesting untreated or contaminated water sources, a primary vector for parasites like Giardia and Cryptosporidium in recreational waters or drinking supplies, as well as Vibrio cholerae in areas with poor sewage infrastructure leading to cholera epidemics. These transmissions are especially prevalent in developing regions but can occur anywhere with compromised water treatment.^[58]^[37]^[59] Additional modes include contact with fomites such as contaminated surfaces in healthcare or food service settings, and aerosols generated from vomiting, particularly with norovirus, which can disperse virus particles in enclosed spaces. Zoonotic transmission from animals, notably Campylobacter from poultry or pets, adds another pathway, often through direct contact or unpasteurized milk. Incubation periods vary by agent, typically ranging from hours to days, influencing outbreak dynamics.^[60]^[61]^[56] High-risk settings amplify transmission risks, including international travel to areas with suboptimal sanitation, and closed environments like cruise ships and schools where norovirus outbreaks frequently occur due to communal dining and close quarters. Person-to-person contact drives over half of reported acute gastroenteritis outbreaks in such contexts, followed by foodborne routes.^[62]^[5]

Pathophysiology

Mechanisms of Disease

Gastroenteritis arises through diverse mechanisms depending on the causative agent, primarily involving disruption of intestinal homeostasis leading to fluid and electrolyte imbalances. In cases driven by enterotoxin-producing pathogens, such as Vibrio cholerae, the cholera toxin binds to GM1 ganglioside receptors on enterocytes, facilitating the entry of its A subunit into the cell, where it ADP-ribosylates the Gs alpha subunit of adenylate cyclase, resulting in persistent activation and a surge in cyclic AMP (cAMP) levels.^[63] This elevated cAMP inhibits sodium absorption while stimulating chloride (Cl-) secretion into the intestinal lumen via the cystic fibrosis transmembrane conductance regulator (CFTR), accompanied by passive water efflux, culminating in voluminous secretory diarrhea.^[64] Similar enterotoxin-mediated pathways occur with Escherichia coli heat-labile toxin, which also elevates cAMP, underscoring the central role of cyclic nucleotide dysregulation in noninflammatory, watery diarrhea syndromes.^[63] Invasive pathogens like Shigella species and Campylobacter jejuni employ direct mucosal penetration to induce tissue damage and inflammatory responses. Shigella invades colonic epithelial cells via type III secretion systems, injecting effector proteins that trigger actin polymerization for uptake, followed by intracellular replication and induction of apoptosis in infected cells, which provokes a robust neutrophil influx and cytokine release, manifesting as mucosal ulceration and bloody, mucoid stools.^[65] Campylobacter similarly adheres to and invades the intestinal mucosa, particularly in the ileum and colon, eliciting an inflammatory cascade with production of pro-inflammatory cytokines such as IL-8, leading to edema, erythema, and bloody diarrhea through disruption of the epithelial barrier and secondary bacterial translocation.^[66] These mechanisms contrast with toxin-mediated processes by directly compromising the structural integrity of the mucosa, often resulting in dysentery-like symptoms. Viral agents, exemplified by rotavirus, exert cytopathic effects primarily on mature villus enterocytes in the small intestine. Rotavirus infection disrupts the actin cytoskeleton and tight junctions, impairing sodium-glucose cotransporter function and causing villus atrophy through enterocyte lysis, which reduces absorptive surface area and leads to malabsorption of nutrients, osmotic gradients, and watery diarrhea.^[67] Additionally, rotavirus nonstructural protein 4 (NSP4) acts as an enterotoxin, elevating intracellular calcium and activating chloride secretion, further contributing to fluid loss independent of cell death.^[68] Parasitic agents, such as Giardia lamblia and Cryptosporidium parvum, cause gastroenteritis primarily through adherence to and invasion of the small intestinal epithelium. Giardia trophozoites colonize the duodenum and jejunum, adhering via a ventral disc and disrupting microvilli and tight junctions, which impairs nutrient absorption, induces epithelial apoptosis, and leads to osmotic diarrhea with steatorrhea. Cryptosporidium sporozoites excyst and invade enterocytes, forming intracellular but extracytoplasmic parasitophorous vacuoles that cause villus blunting, increased intestinal permeability, chloride secretion, and malabsorption, resulting in a mix of secretory and osmotic diarrhea.^[69] Noninfectious triggers, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and certain toxins, damage the gastrointestinal mucosa without microbial involvement. NSAIDs inhibit cyclooxygenase enzymes, reducing prostaglandin synthesis essential for maintaining mucosal bicarbonate secretion and blood flow, thereby allowing luminal acid and irritants to erode the epithelial barrier and initiate inflammatory cascades via activation of nuclear factor-kappa B (NF-κB) pathways, resulting in erosions, inflammation, and diarrhea.^[70] Other irritants like bile acids or food toxins similarly permeabilize the mucosal layer, triggering mast cell degranulation and chemokine release that amplify local inflammation.^[71] Host factors, particularly age-related immunological vulnerabilities, modulate disease severity and exacerbate tissue damage. In children under five, immature innate immunity and underdeveloped gut microbiota impair effective pathogen clearance, prolonging epithelial exposure and intensifying malabsorptive effects from enterocyte damage.^[72] Conversely, in the elderly, immunosenescence diminishes T-cell responses and mucosal IgA production, allowing unchecked pathogen replication and heightened susceptibility to invasive damage and dehydration.^[73] These age-specific gaps in host defense amplify the core pathological processes, linking to severe outcomes like prolonged diarrhea.

Immune Response

The innate immune response to gastroenteritis pathogens begins at the mucosal barrier of the gastrointestinal tract, where secretory immunoglobulin A (sIgA) antibodies play a pivotal role in preventing microbial adhesion and invasion. These antibodies, produced by plasma cells in the lamina propria, bind to pathogen surface proteins, neutralizing their ability to attach to epithelial cells and thereby inhibiting colonization and subsequent tissue penetration.^[74] In parallel, for bacterial causes, the response involves rapid recruitment of neutrophils to the site of invasion; epithelial cells release chemokines like interleukin-8 in response to bacterial signals, drawing neutrophils across the epithelium to phagocytose and eliminate invaders through oxidative bursts and antimicrobial granule release.^[75] This neutrophil influx helps contain the infection but can contribute to symptoms such as fever via pro-inflammatory cytokine signaling.^[76] The adaptive immune system further bolsters clearance, particularly against viral etiologies, through T-cell mediated mechanisms. CD4+ and CD8+ T lymphocytes, activated in the gut-associated lymphoid tissue, migrate to the infected mucosa to orchestrate cytotoxic responses and cytokine production that facilitate viral elimination from epithelial cells.^[77] In severe cases, however, dysregulated adaptive responses can escalate into a cytokine storm, characterized by excessive release of pro-inflammatory mediators like tumor necrosis factor-alpha and interleukins, which prolong mucosal inflammation and exacerbate tissue damage.^[78] These T-cell dynamics also contribute to long-term protection, reducing the likelihood of reinfection by establishing memory responses. In immunocompromised individuals, such as those with HIV and CD4+ T-cell depletion below 100 cells/µL, the immune response is severely impaired, leading to chronicity in infections like Cryptosporidium parvum gastroenteritis; without immune reconstitution via antiretroviral therapy, the parasite persists due to inadequate T-cell control over protozoal replication in enterocytes.^[79] Rotavirus vaccines exemplify how targeted enhancement of adaptive immunity, particularly through increased sIgA production, can mitigate severe disease; these oral vaccines induce robust intestinal IgA responses, achieving approximately 80% efficacy against hospitalization for severe rotavirus gastroenteritis in vaccinated children.^[80]^[81] Post-infection, immune-mediated alterations in the gut microbiome, known as dysbiosis, can hinder recovery by disrupting microbial homeostasis and barrier integrity, with shifts in bacterial composition persisting for months.^[82] Such dysbiosis is strongly linked to the development of post-infectious irritable bowel syndrome (IBS), where acute gastroenteritis triggers lasting changes in microbiota diversity that amplify visceral hypersensitivity and motility issues through immune-microbe crosstalk.^[83]

Diagnosis

Clinical Assessment

The clinical assessment of suspected gastroenteritis begins with a detailed history taking to identify potential causes and gauge severity. Clinicians inquire about the onset and duration of symptoms, such as diarrhea and vomiting, to distinguish acute from chronic presentations. Recent travel history is crucial, as it may indicate exposure to pathogens like enterotoxigenic Escherichia coli in high-risk areas. Food exposure, including consumption of undercooked meats, unpasteurized dairy, or contaminated water, is assessed to evaluate for foodborne etiologies. Contact with ill individuals, such as household members or those in daycare settings, helps identify possible person-to-person transmission. Severity is further evaluated by stool frequency and volume, with more than six loose stools per day or large-volume diarrhea suggesting higher risk of dehydration.^[84]^[85]^[86] Physical examination focuses on general appearance and specific findings to support the diagnosis and assess complications. Vital signs are evaluated for signs of dehydration, including tachycardia (heart rate >100 beats per minute in adults) and hypotension (systolic blood pressure <90 mmHg), which indicate fluid loss. Abdominal examination typically reveals mild, diffuse tenderness without peritoneal signs, though significant guarding or rebound may suggest alternative diagnoses. In children, additional checks for sunken fontanelles or dry mucous membranes may be noted, but these are interpreted cautiously. The exam is often otherwise unremarkable in uncomplicated cases.^[87]^[85] Risk stratification identifies patients vulnerable to severe outcomes. Young children under 5 years are at heightened risk due to immature immune systems and higher fluid loss relative to body weight. Elderly individuals over 65 years face increased complications from comorbidities and reduced physiologic reserve. Immunocompromised patients, such as those with HIV, chemotherapy, or organ transplants, experience prolonged symptoms and greater dehydration risk. These groups warrant closer monitoring and prompt intervention.^[85]^[88] Patients should seek medical care for persistent symptoms lasting more than 48 hours, as this may indicate bacterial infection or dehydration requiring evaluation. The presence of blood in the stool signals potential invasive pathogens like Shigella or Campylobacter and necessitates urgent assessment. High fever exceeding 101°F (38.3°C) in adults or 102°F (38.9°C) in children, especially with severe abdominal pain, prompts immediate evaluation to rule out serious complications.^[7]^[1]

Dehydration Evaluation

Evaluating dehydration in patients with gastroenteritis is essential, as fluid loss from diarrhea and vomiting can rapidly lead to significant morbidity, particularly in children and infants.^[3] Clinical assessment relies primarily on physical examination findings to classify dehydration severity, guiding timely intervention to prevent complications such as shock.^[89] The World Health Organization (WHO) provides a widely used clinical scale for assessing dehydration in children with acute diarrhea. No dehydration is indicated by the absence of specific signs. Some dehydration is present if two or more of the following are observed: restlessness or irritability, sunken eyes, and eager drinking with thirst. Severe dehydration requires at least two of: lethargy or unconsciousness, sunken eyes, inability to drink or drinking poorly, and very slow skin pinch return (≥2 seconds). In infants, a sunken fontanelle is an additional sign often associated with moderate to severe dehydration.^[3]^[89] Vital signs offer objective measures to support clinical evaluation. Tachycardia, typically an increase in heart rate beyond age-adjusted norms (e.g., >160 bpm in infants under 12 months), signals moderate dehydration, while severe cases may show marked tachycardia or hypotension. Prolonged capillary refill time greater than 2 seconds indicates reduced perfusion and is a reliable indicator of dehydration severity.^[89]^[90] Laboratory markers can confirm dehydration when clinical signs are equivocal, though they are not routinely needed for initial assessment. An elevated blood urea nitrogen (BUN) to creatinine ratio (>20:1) reflects prerenal azotemia due to hypovolemia. Urine specific gravity exceeding 1.020 suggests concentrated urine from fluid conservation by the kidneys.^[90]^[91] Management thresholds are based on estimated fluid deficit as a percentage of body weight, determined by clinical scales or pre- and post-illness weight comparisons. Mild dehydration (<5% loss) is managed with oral rehydration. Moderate dehydration (5-10% loss) also favors oral therapy if tolerated. Severe dehydration (>10% loss) necessitates intravenous fluids to rapidly restore volume.^[90]^[92]

Differential Diagnosis

Gastroenteritis, characterized by acute diarrhea, vomiting, and abdominal pain, can mimic a variety of other conditions, necessitating careful clinical evaluation to distinguish it from potentially serious alternatives. Appendicitis often presents with initial diffuse abdominal discomfort that localizes to the right lower quadrant, accompanied by rebound tenderness and fever, unlike the more generalized cramping in gastroenteritis. Similarly, Clostridium difficile colitis, particularly following antibiotic use, causes profuse watery or bloody diarrhea with severe abdominal pain, but it is distinguished by a history of recent antimicrobial exposure and pseudomembranous findings on colonoscopy. Noninfectious conditions can also imitate gastroenteritis symptoms. Inflammatory bowel disease (IBD) flares, such as in Crohn's disease or ulcerative colitis, may involve bloody diarrhea, weight loss, and extraintestinal manifestations like joint pain, contrasting with the self-limited nature of most infectious gastroenteritis episodes. Lactose intolerance triggers bloating, flatulence, and diarrhea after dairy consumption, without fever or vomiting, and is confirmed by symptom resolution on a lactose-free diet. Additionally, gastrointestinal manifestations of COVID-19 occur in approximately 50% of cases, including diarrhea and nausea, but are often accompanied by respiratory symptoms or anosmia, and persist longer in some patients. Systemic illnesses must be considered, especially in vulnerable populations. In children, urinary tract infections (UTIs) can present with abdominal pain, fever, and vomiting mimicking gastroenteritis, but urinalysis reveals pyuria and bacteriuria. Early pregnancy may cause nausea and vomiting resembling viral gastroenteritis, yet is differentiated by a positive pregnancy test and absence of diarrhea. Diabetic ketoacidosis (DKA) in diabetics can lead to nausea, vomiting, and abdominal pain due to metabolic derangements, with rapid onset of hyperglycemia and acidosis on labs. Red flags warrant urgent investigation to rule out severe mimics. Chronic or recurrent symptoms, such as persistent diarrhea with blood or mucus, suggest underlying IBD rather than acute gastroenteritis. Neurological signs like descending paralysis or cranial nerve palsies indicate botulism, which can initially present with gastrointestinal complaints from toxin ingestion. Long-term gastrointestinal sequelae post-COVID-19, including persistent dysbiosis, can mimic recurrent gastroenteritis episodes with ongoing diarrhea and abdominal discomfort, often linked to alterations in gut microbiota lasting months after acute infection. Laboratory tests play a key role in ruling out these differentials by identifying specific markers absent in uncomplicated gastroenteritis.

Laboratory Confirmation

Laboratory confirmation of the causative agent in gastroenteritis is typically reserved for severe, prolonged, or atypical cases, outbreaks, or patients who are immunocompromised, as routine testing is not recommended for mild, self-limited viral infections.^[93] Stool specimens are the primary sample for etiologic testing, with fresh diarrheal stool preferred to ensure viability of pathogens.^[93] Stool culture remains a standard method for identifying bacterial pathogens such as Salmonella, Shigella, Campylobacter, Yersinia, and Shiga toxin-producing Escherichia coli (STEC), particularly in cases with fever, bloody or mucoid stools, or signs of sepsis.^[93] A single stool specimen is usually sufficient, though additional samples may improve yield in persistent diarrhea.^[93] For broader detection, multiplex polymerase chain reaction (PCR) panels, such as the FilmArray Gastrointestinal Panel, simultaneously identify bacterial, viral (e.g., norovirus, rotavirus), and parasitic agents with higher sensitivity than culture and less dependence on specimen quality; results should be interpreted in clinical context, as they detect nucleic acids rather than viable organisms.^[93] Blood tests, including complete blood count (CBC) to assess for leukocytosis suggestive of bacterial infection and serum electrolytes to evaluate for imbalances from fluid loss, support overall management but do not directly confirm etiology.^[93] In STEC infections, CBC monitoring of hemoglobin, platelets, and renal function is crucial to detect hemolytic uremic syndrome.^[93] Blood cultures are indicated in infants under 3 months, suspected septicemia, enteric fever, or immunocompromised hosts.^[93] Imaging studies like ultrasound are rarely used for routine etiologic confirmation but may be employed in children to evaluate complications such as intussusception, which can follow viral gastroenteritis (e.g., adenovirus or rotavirus), with ultrasound serving as the preferred modality due to its non-invasive nature and high sensitivity for detecting the "target" or "doughnut" sign.^[94] Emerging techniques, such as microbiome sequencing of stool samples, are being explored to characterize dysbiosis and its role in post-infectious complications like irritable bowel syndrome following gastroenteritis, offering potential for molecular epidemiology and personalized insights beyond traditional pathogen detection.^[95]

Prevention

Hygiene and Sanitation

Hygiene and sanitation practices are essential for interrupting the fecal-oral transmission route of gastroenteritis pathogens, such as norovirus and rotavirus, thereby reducing infection risk in both community and institutional settings.^[96] These measures complement food and water safety efforts by targeting personal and environmental cleanliness to prevent contamination spread.^[97] Handwashing with soap and water for at least 20 seconds is a cornerstone of prevention, particularly after using the toilet, changing diapers, or before preparing or eating food, as it removes pathogens more effectively than alcohol-based sanitizers, which are ineffective against non-enveloped viruses like norovirus.^[98]^[97] In healthcare and community settings, this practice has been shown to reduce diarrheal diseases, a primary manifestation of gastroenteritis, by approximately 30%.^[98] A systematic review further estimates that handwashing with soap can lower diarrhea risk by up to 48% in populations with poor baseline hygiene.^[99] Access to clean water and proper sewage disposal forms the infrastructural backbone of sanitation, with the World Health Organization emphasizing that inadequate facilities contribute to nearly 90% of diarrhea-related deaths, predominantly in children under five.^[96] The Sustainable Development Goal 6 targets universal access to safely managed drinking water and sanitation by 2030 to mitigate such risks, including those from gastroenteritis transmission.^[100] Improvements in sanitation, such as latrines or sewer connections, can reduce diarrhea incidence by 36%, while enhanced water quality contributes an additional 17% reduction.^[99] In households and schools, protocols include isolating individuals with symptoms to limit close contact and disinfecting contaminated surfaces with a chlorine bleach solution (1,000–5,000 ppm) effective against norovirus, as alcohol sanitizers fail here too.^[97]^[101] These combined hygiene and sanitation interventions in low-resource settings have demonstrated reductions in gastroenteritis incidence ranging from 30% to 50%, highlighting their scalability for public health impact.^[102]^[99]

Vaccination Strategies

Vaccination strategies for gastroenteritis focus on preventing infections from key viral and bacterial pathogens, with rotavirus vaccines representing the most widely implemented approach. The two primary rotavirus vaccines, Rotarix (a monovalent live-attenuated vaccine) and RotaTeq (a pentavalent live-attenuated vaccine), are administered orally and have been recommended by the World Health Organization (WHO) for inclusion in routine infant immunization programs since 2009.^[103] These vaccines target the leading cause of severe viral gastroenteritis in young children, providing protection through induction of neutralizing antibodies and mucosal immunity. As of August 2025, rotavirus vaccines have been introduced nationally or subnationally in 135 countries, significantly expanding access in both high- and low-income settings.^[104] Clinical trials and real-world data demonstrate that Rotarix and RotaTeq achieve approximately 66% effectiveness against severe rotavirus gastroenteritis in high-mortality settings, with higher rates (up to 90%) observed in low-mortality countries.^[105] Effectiveness is measured primarily against hospitalization and severe dehydration outcomes, with protection lasting at least two years post-vaccination. The vaccines' live-attenuated nature mimics natural infection to stimulate robust intestinal immunity, though performance can vary due to strain diversity and nutritional factors in endemic areas.^[106] For norovirus, the second major viral cause of gastroenteritis, no licensed vaccines exist as of 2025, but several candidates are advancing through clinical trials. Phase 3 trials for norovirus vaccines, including mRNA-based candidates like Moderna's mRNA-1403, are ongoing as of November 2025, aiming to address the virus's high burden in children and adults, though enrollment has been challenging due to low case rates.^[107] A key challenge in norovirus vaccine development is the pathogen's genetic diversity, with emerging variants like GII.17 complicating broad protection and necessitating multivalent formulations.^[108] Bacterial pathogens contributing to gastroenteritis, such as enterotoxigenic Escherichia coli (ETEC) and Shigella, lack licensed vaccines but have experimental candidates in development. The oral inactivated whole-cell vaccine ETVAX, which includes key ETEC antigens like colonization factors and the heat-labile toxin B subunit, has completed phase 2b trials demonstrating safety, immunogenicity, and efficacy against moderate-to-severe diarrhea in travelers to endemic areas.^[109] Ongoing studies explore combining ETVAX with Shigella components to create a broader-spectrum vaccine for high-risk populations, including children in low- and middle-income countries.^[110] Rotavirus vaccination schedules typically involve 2 doses of Rotarix at ages 2 and 4 months or 3 doses of RotaTeq at ages 2, 4, and 6 months, integrated into infancy immunization programs to maximize early protection.^[111] Widespread adoption has generated herd immunity, reducing rotavirus-related hospitalizations among children by 70% or more in vaccinated populations, thereby lowering overall disease transmission and burden.^[112] These strategies enhance immune responses against enteric pathogens and contribute to declining epidemiological trends in severe gastroenteritis.

Food and Water Safety

Ensuring the safety of food and water is essential to prevent the transmission of gastroenteritis-causing pathogens such as Escherichia coli, Salmonella, and norovirus through contaminated supplies. Effective water treatment methods include boiling, which kills most bacteria, viruses, and parasites by reaching temperatures above 60°C for at least one minute, as recommended by health authorities for household use in areas with unreliable water sources.^[113] Chlorination is another common disinfection technique using household bleach or tablets to achieve 0.5–2 mg/L free chlorine, effectively eliminating many microbial threats, though it is less effective against chlorine-tolerant parasites like Cryptosporidium parvum, which can survive standard concentrations for extended periods.^[113]^[114] Filtration systems, such as ceramic or membrane filters with pores smaller than 1 micron, provide an additional barrier by physically removing pathogens, often combined with chemical treatments for comprehensive protection.^[113] Safe storage practices are critical post-treatment; treated water should be kept in clean, covered containers to avoid recontamination from dust, insects, or unclean hands, thereby maintaining its potability.^[115] In food handling, proper practices minimize the risk of introducing or spreading pathogens that lead to gastroenteritis. Cooking foods to an internal temperature of at least 74°C (165°F) for poultry, ground meats, and leftovers denatures proteins in bacteria like Salmonella and E. coli, rendering them non-viable, as verified by food thermometers.^[116] Avoiding cross-contamination involves using separate cutting boards, utensils, and storage areas for raw and cooked items, along with thorough cleaning of surfaces with hot soapy water to prevent transfer of fecal-oral pathogens.^[117] Washing fruits and vegetables under running water removes surface dirt and some microorganisms, though it does not eliminate internalized pathogens; for added safety, produce should be consumed fresh or cooked when possible.^[118] Pasteurization of dairy products and juices heats them to 72°C for 15 seconds or equivalent, destroying heat-sensitive bacteria such as Campylobacter and Listeria that can cause gastrointestinal illness, making these products safer for consumption.^[119]^[120] Regulatory frameworks in the food industry enforce these measures through systems like Hazard Analysis and Critical Control Points (HACCP), a preventive approach mandated by the FDA for seafood, juice, and certain low-acid canned foods, and by the USDA for meat and poultry, to identify and control contamination risks at key production stages.^[121]^[122] FDA and USDA guidelines outline specific standards, such as microbial testing and sanitation protocols, to reduce the incidence of foodborne gastroenteritis outbreaks.^[123] For travelers, advisories from the CDC and WHO recommend using factory-sealed bottled water or treating tap water to avoid exposure to contaminated sources in high-risk areas, as bottled water provides a reliable barrier against local waterborne pathogens.^[124]^[125] Outbreak control often involves rapid identification and removal of contaminated products from the supply chain. For instance, the 2024 E. coli O157:H7 outbreak linked to romaine lettuce, which sickened 89 people across 15 U.S. states and resulted in one death, led to investigations by the FDA and CDC, though no public recall was issued, highlighting the role of surveillance in preventing further spread.^[126] Such responses emphasize traceability and voluntary withdrawals to mitigate risks from produce contaminated during farming or processing.^[127]

Management

Rehydration Therapy

Rehydration therapy serves as the foundational treatment for gastroenteritis, aimed at correcting fluid and electrolyte deficits to mitigate dehydration-related morbidity and mortality. This approach prioritizes oral methods when feasible, given their efficacy, safety, and accessibility, while reserving intravenous options for critical cases. Effective rehydration not only restores volume but also supports recovery by maintaining organ perfusion and electrolyte balance. Oral rehydration solution (ORS) forms the core of therapy, with the World Health Organization (WHO) endorsing a reduced-osmolarity formulation containing 75 mmol/L sodium, 75 mmol/L glucose, and an osmolality of 245 mOsm/L. This solution facilitates sodium-glucose cotransport in the intestine, enhancing water absorption even during diarrheal states. Implementation of ORS has saved an estimated 50 million lives worldwide since the 1970s, significantly reducing child mortality from diarrhea, primarily through widespread use in both community and clinical settings. Administration begins with deficit replacement—typically 50–100 mL/kg body weight over 2–4 hours for mild (3%–5% body weight loss) to moderate (6%–9%) dehydration—followed by maintenance fluids (about 100 mL/kg/day) plus compensation for ongoing losses from vomiting or stool. In mild cases without significant deficit, ORS can be offered ad libitum in small, frequent sips to encourage tolerance and prevent escalation. Intravenous fluids are indicated for severe dehydration (>10% body weight loss), hypovolemic shock, or inability to tolerate oral intake due to protracted vomiting. Ringer's lactate solution is preferred for its balanced electrolytes, starting with a 20 mL/kg bolus over 20–30 minutes, repeatable up to 60 mL/kg until hemodynamic stability is achieved, then transitioning to maintenance rates. This method ensures rapid correction but carries risks like electrolyte imbalances if not monitored. Adjunctive zinc supplementation enhances rehydration outcomes in children under 5 years, particularly in developing countries where deficiencies are prevalent. The WHO recommends 20 mg elemental zinc daily for 10–14 days, which shortens diarrhea duration by approximately 25% and reduces stool volume by 30%, thereby aiding faster recovery and lowering recurrence risk.

Dietary Interventions

Dietary interventions for gastroenteritis emphasize maintaining nutritional intake to support recovery while minimizing gastrointestinal irritation, complementing rehydration therapy to prevent malnutrition. Early feeding is crucial, particularly continuing breastfeeding in infants, as it provides essential nutrients and antibodies without increasing diarrhea risk.^[128] The traditional BRAT diet (bananas, rice, applesauce, toast), once commonly recommended, is now considered outdated and unnecessarily restrictive, offering inadequate nutrition and no proven benefits over a normal age-appropriate diet once tolerated.^[129] Instead, guidelines advocate prompt reintroduction of usual foods to restore caloric balance and intestinal function.^[130] Certain foods should be avoided temporarily to reduce symptoms. Dairy products may exacerbate diarrhea in cases of secondary lactose intolerance, which can develop post-infection due to temporary damage to the intestinal lining and persists for several weeks in some patients; lactose-free alternatives are recommended during this period.^[131] High-fat foods, such as fried items or fast food, and high-fiber foods should also be limited initially, as they can prolong diarrhea by slowing digestion or irritating the gut, though complete fat avoidance is challenging and not always necessary.^[130]^[92] Probiotics have shown limited overall benefit in managing acute gastroenteritis, according to a 2020 Cochrane review analyzing 82 randomized trials. However, specific strains like Lactobacillus rhamnosus GG may shorten diarrhea duration by approximately 25 hours (95% CI 16 to 34) in children, based on 12 studies involving infants and young children, though effects vary by strain and setting.^[132] During recovery, a gradual reintroduction of diverse foods is advised to rebuild nutritional status, with monitoring for signs of post-infectious malabsorption, such as persistent diarrhea or weight loss, which may require temporary adjustments like lactose restriction. This approach helps mitigate complications like prolonged nutrient deficits without imposing long-term dietary changes.^[92]

Antiemetic Medications

Antiemetic medications are used in the management of gastroenteritis to control vomiting, particularly when it hinders oral rehydration therapy. These agents target symptoms in cases where vomiting is moderate to severe and prevents adequate fluid intake, but they are not recommended for routine use in mild cases.^[133]^[134] Ondansetron, a selective 5-HT3 receptor antagonist, is the most commonly recommended antiemetic for children with acute gastroenteritis. The typical dose for children is 0.15 mg/kg orally, administered as a single dose, with adjustments based on weight (e.g., 2 mg for 8-15 kg, 4 mg for 15-30 kg). Clinical trials have shown that ondansetron reduces the number of vomiting episodes by approximately 50% compared to placebo, thereby facilitating successful oral rehydration and reducing the need for intravenous fluids. This benefit is particularly relevant in viral gastroenteritis, the predominant cause, where symptom relief supports rehydration without addressing the underlying infection.^[135]^[136]^[137] Common side effects of ondansetron include constipation and headache, which are generally mild and transient. It is contraindicated in patients with congenital long QT syndrome or those taking other QT-prolonging drugs due to the risk of torsades de pointes. Although increased diarrhea has been reported in some studies, it does not typically outweigh the benefits in appropriate cases.^[138] Alternatives to ondansetron include metoclopramide, a prokinetic agent that enhances gastric motility. However, metoclopramide carries a higher risk of extrapyramidal side effects, such as dystonia, particularly in children, making it less preferred. Network meta-analyses confirm ondansetron's superior efficacy and safety profile over metoclopramide for vomiting control in pediatric gastroenteritis.^[134]^[139]

Antibiotic Use

Antibiotics are indicated for bacterial gastroenteritis in cases of severe illness, such as bloody diarrhea, high fever greater than 38.5°C, or symptoms persisting beyond 7 days, as well as in immunocompromised patients or those at high risk of complications like bacteremia.^[140]^[46] Empiric therapy may be initiated promptly in these scenarios, with choices guided by local resistance patterns; for example, azithromycin is recommended for Campylobacter infections, while ciprofloxacin is used for susceptible Salmonella strains.^[140]^[141] For Shigella, azithromycin or ciprofloxacin are preferred options to shorten the duration of fever and diarrhea by approximately 2 days.^[142] Routine antibiotic use is avoided in uncomplicated or viral gastroenteritis, as it does not improve outcomes and can prolong diarrhea in certain bacterial cases like Shiga toxin-producing E. coli.^[140] Such indiscriminate use promotes antimicrobial resistance and increases the risk of Clostridioides difficile infection, particularly with broad-spectrum agents like fluoroquinolones or cephalosporins.^[143]^[144] Antibiotic resistance is a major concern, with high rates of multidrug resistance among Shigella isolates in certain regions, such as over 90% in parts of Southeast Asia as of 2019, necessitating susceptibility testing.^[145] The Infectious Diseases Society of America (IDSA) guidelines emphasize antimicrobial stewardship, recommending culture-guided therapy to optimize efficacy and minimize resistance development, with trends showing increasing resistance as of 2023.^[140]^[146] In special populations, such as travelers with acute diarrhea, empiric non-absorbed antibiotics like rifaximin (200 mg three times daily for 3 days) are effective against noninvasive pathogens like enterotoxigenic E. coli, reducing symptom duration without systemic absorption.^[147]^[148]

Antimotility Agents

Antimotility agents are pharmacological interventions used to alleviate symptoms of diarrhea in gastroenteritis by slowing intestinal motility, thereby reducing stool frequency and urgency. These agents are particularly considered for symptom control in adults after initial rehydration, but their use requires careful patient selection to avoid complications in infectious cases.^[149] Loperamide, a synthetic opioid agonist acting on mu-opioid receptors in the intestinal wall, is the primary antimotility agent employed for this purpose. It inhibits peristalsis and prolongs intestinal transit time without affecting central opioid receptors due to its poor blood-brain barrier penetration. The standard adult dosing regimen is an initial 4 mg dose, followed by 2 mg after each unformed stool, not exceeding 16 mg per day for up to 2 days. In mild noninfectious or early viral gastroenteritis, loperamide effectively reduces stool frequency and can shorten the overall duration of diarrhea in adults.^[150]^[149]^[151] However, loperamide is contraindicated in cases of bloody diarrhea or suspected invasive bacterial infections, such as those caused by Shigella or other pathogens presenting with dysentery features like fever and mucoid stools, as it may prolong bacterial shedding and exacerbate illness. It is also avoided in Clostridium difficile-associated diarrhea due to the risk of toxic megacolon, a life-threatening complication involving colonic dilation and perforation. Use in children under 12 years is not recommended owing to reports of serious adverse events, including ileus, lethargy, and rare fatalities.^[149]^[152]^[150]^[140] Bismuth subsalicylate serves as an alternative antimotility option for mild cases of gastroenteritis, exerting antisecretory effects on the intestinal mucosa to decrease fluid secretion and stool output, alongside mild antimicrobial properties. It is dosed as 524 mg (two tablets or 30 mL) every 30 to 60 minutes for up to eight doses in 24 hours, but it is generally less effective than loperamide and may cause side effects such as temporary blackening of the tongue and stools. Caution is advised in patients with salicylate sensitivity or those at risk of toxicity, including pregnant individuals.^[149]^[153]

Epidemiology

Global Burden and Trends

Gastroenteritis, encompassing acute diarrhoeal diseases, imposes a substantial global health burden, with an estimated 1.7 billion cases occurring annually among children worldwide. In 2021, these conditions accounted for approximately 1.17 million deaths globally (95% uncertainty interval: 0.793–1.62 million), representing a 60.3% decline from 2.93 million deaths in 1990, though children under five years remain disproportionately affected, suffering around 340,000 deaths (95% UI: 244,000–480,000) yearly. Norovirus, a leading viral cause, contributes significantly to this toll, causing about 685 million cases of acute gastroenteritis each year, including 200 million among children under five, and resulting in roughly 200,000 deaths worldwide, with over 70,000 occurring in developing countries.^[4]^[3]^[154]^[155] Trends in gastroenteritis burden reflect both successes and emerging challenges, particularly with pathogen-specific interventions. Rotavirus vaccination programs, introduced globally since 2006 and expanding post-2011, have driven a substantial decline in rotavirus-associated mortality, reducing under-five deaths from approximately 346,000 in 2006 to 143,000 in 2019—a roughly 59% decrease—and preventing an estimated 139,000 deaths in that period. Conversely, norovirus outbreaks have surged in recent years; in the United States alone, 2,675 outbreaks were reported from August 2024 to July 2025, compared to 1,478 in the prior season, with the GII.17 variant accounting for 75% of cases during the 2024–2025 season, overtaking the previously dominant GII.4 strain.^[156]^[156]^[157]^[27] The burden is unevenly distributed, with the highest incidence and mortality concentrated in low-resource regions such as sub-Saharan Africa and South Asia, where deficits in water, sanitation, and hygiene (WASH) exacerbate transmission through contaminated sources. In Western sub-Saharan Africa, for instance, the age-standardized rate of disability-adjusted life years (DALYs) due to diarrhoeal diseases reached 3,660 per 100,000 in 2019 (95% UI: 2,618–4,785), far exceeding global averages, while South Asia reports similarly elevated child mortality rates linked to inadequate WASH infrastructure; globally, this affects 2.1 billion people without safely managed drinking water and 3.4 billion without safely managed sanitation as of 2023.^[158]^[3]^[159]^[160] In high-income settings like the United States, adult mortality from gastroenteritis has remained relatively stable from 2018 to 2023, with rates concentrated among older age groups—such as 4.54 to 5.31 per 100,000 among females aged 75–84—though emergency department visits for diarrhoeal complaints averaged 3.3–3.7 million annually through 2021. The COVID-19 pandemic influenced these patterns, with lockdowns and social distancing reducing gastrointestinal pathogen transmission by disrupting fecal-oral routes, leading to fewer outbreaks in 2020–2021; however, a rebound occurred post-restrictions, with case increases of up to 18% for certain pathogens like giardiasis in 2021–2022, alongside surges in stress-related gastrointestinal issues.^[161]^[162]^[163]^[164]

Risk Factors and Outbreaks

Certain populations are particularly vulnerable to gastroenteritis due to physiological, environmental, and socioeconomic factors. Children under five years of age bear a significant portion of severe outcomes, accounting for approximately 29% of global diarrhea-related deaths as of 2021, primarily because their immature immune systems and higher fluid requirements exacerbate dehydration risks.^[4] The elderly are also at elevated risk, as age-related declines in immune function and comorbidities increase susceptibility to complications like severe dehydration and hospitalization from pathogens such as norovirus.^[165] Malnourished individuals, especially in low-resource settings, face heightened vulnerability, as nutritional deficiencies impair gut barrier integrity and immune responses, leading to more frequent and prolonged episodes.^[3] Travelers to endemic regions, particularly in low- and middle-income countries, experience significantly higher incidence rates, with attack rates of 30-70% during short trips due to exposure to contaminated food and water.^[166] Outbreaks of gastroenteritis often occur in confined, high-density environments that facilitate rapid person-to-person transmission. Daycare centers and schools are common sites for pediatric outbreaks, exemplified by the 2024-2025 norovirus surge in US schools, where over 1,000 outbreaks were reported across participating states by early 2025, driven by close contact among children.^[167] Nursing homes frequently see norovirus clusters among residents, with attack rates up to 50% in affected facilities due to shared living spaces and vulnerable hosts.^[62] Cruise ships represent another hotspot, with at least 20 confirmed gastrointestinal outbreaks in 2025 (as of October), 15 attributed to norovirus, highlighting the role of communal dining and close quarters in amplifying spread.^[168] The dynamics of these outbreaks involve swift dissemination in crowded settings, often through fecal-oral routes via contaminated surfaces or food handlers. Public health investigations typically employ contact tracing to identify index cases and genotyping to track strains, such as norovirus GII.17 clusters, which have emerged in multiple global outbreaks since 2014, including school-based events in Italy and China, allowing for targeted containment.^[169] Emerging trends indicate that climate change is exacerbating waterborne risks by increasing extreme weather events that contaminate water sources, potentially raising incidence of bacterial and protozoal gastroenteritis in affected regions.^[170] Post-2023 surveillance data further reveal viral pathogens, particularly norovirus, dominating positivity trends in acute gastroenteritis cases across age groups, underscoring their role in ongoing outbreaks.^[171]

Societal Aspects

Economic and Public Health Impact

Gastroenteritis imposes a substantial economic burden worldwide, primarily through direct medical costs, lost productivity, and hospitalizations. In the United States, foodborne illnesses—a primary cause of gastroenteritis—impose an annual economic burden of approximately $75 billion (as of 2023), including medical costs and lost productivity. Norovirus, a leading cause, accounts for about $10.6 billion yearly. Rotavirus, a major cause of severe cases in children, contributed approximately $1 billion annually in the US prior to vaccine introduction, with medical costs alone accounting for $264 million. Globally, norovirus—a leading viral pathogen—generates an estimated $60.3 billion in societal costs each year (2016 estimate), including $4.2 billion in direct healthcare expenditures, highlighting the scale of viral gastroenteritis impacts.^[172]^[173]^[174] Public health responses to gastroenteritis emphasize surveillance and preventive infrastructure to mitigate outbreaks and transmission. The World Health Organization (WHO) and UNICEF promote Water, Sanitation, and Hygiene (WASH) programs, which have been shown to reduce diarrheal disease risk by 27% to 53% through improved access to safe water, sanitation, and handwashing practices. In the United States, the Centers for Disease Control and Prevention (CDC) utilizes the National Outbreak Reporting System (NORS) to track enteric disease outbreaks, including those caused by norovirus and other gastroenteritis agents, enabling rapid response and policy adjustments. These systems facilitate early detection and containment, reducing the overall public health strain. The COVID-19 pandemic illustrated both protective and adverse effects on gastroenteritis incidence. Lockdown measures led to approximately 50% to 67% reductions in acute gastroenteritis cases, attributed to decreased social interactions and improved hygiene behaviors. However, the pandemic also drove a surge in antibiotic prescriptions—up to 100% in some hospitalized COVID-19 patients—exacerbating antimicrobial resistance among bacterial pathogens associated with gastroenteritis. Key interventions have alleviated the economic and public health impacts through targeted policies. Global rotavirus vaccination campaigns, introduced in over 100 countries since 2006, have averted more than 500,000 hospitalizations annually (as of 2019), with vaccines reducing severe rotavirus disease by 37–50% in vaccinated populations. By 2024, rotavirus vaccine coverage reached approximately 50% globally, further reducing child mortality from diarrhea. Enhanced food safety regulations, such as those under the FDA's Food Code, have contributed to declines in foodborne outbreaks by promoting hygiene standards in food service, with studies indicating potential reductions in norovirus transmission through compliance. Post-COVID, gastroenteritis cases have rebounded in some regions, underscoring ongoing needs for surveillance.^[175]^[176]

Historical and Cultural Context

The recognition of gastroenteritis as a major public health concern evolved significantly through the 19th and 20th centuries, driven by devastating cholera outbreaks that highlighted the role of contaminated water in disease transmission. Between 1817 and 1923, six cholera pandemics originating from the Ganges Delta in India spread globally, claiming millions of lives and prompting widespread sanitation reforms in Europe and North America.^[177] These epidemics, caused by Vibrio cholerae, exposed the inadequacies of urban infrastructure, leading to initiatives like improved sewage systems and water treatment; for instance, the 1848 Public Health Act in the United Kingdom established local boards of health to address sanitation deficiencies revealed by the outbreaks.^[178] A pivotal milestone occurred in 1854 during the London cholera epidemic, when physician John Snow mapped cases around the Broad Street pump in Soho, demonstrating through epidemiological analysis that removing the pump handle halted the outbreak, thus establishing waterborne transmission as a key mechanism for infectious diarrhea.^[179] Advances in virology further transformed understanding of non-bacterial gastroenteritis in the late 20th century. In 1973, Australian researchers Ruth Bishop and colleagues identified rotavirus as a major cause of severe diarrheal illness in children using electron microscopy on duodenal biopsies, shifting focus from solely bacterial pathogens to viral agents responsible for up to 40% of cases worldwide.^[180] This discovery paved the way for vaccine development, though early efforts faced setbacks; the first rotavirus vaccine, RotaShield, was licensed in the United States in 1998 but withdrawn in 1999 due to a rare association with intussusception, a bowel obstruction condition. Subsequent vaccines, such as RotaTeq approved in 2006, incorporated safety modifications to minimize this risk, marking a critical step in preventing rotavirus-induced gastroenteritis and reducing global child mortality from diarrhea. Terminology surrounding gastroenteritis has reflected both scientific progress and cultural perceptions. The phrase "stomach flu" emerged as a common but inaccurate colloquialism for viral gastroenteritis, misleadingly linking it to influenza despite distinct etiologies, which has persisted in public discourse and complicated health education efforts.^[181] Similarly, "traveler's diarrhea" encapsulates a culturally associated form of the illness, often linked to international journeys to regions with suboptimal sanitation, evoking historical tropes of colonial-era exploration and modern tourism risks, such as Montezuma's revenge in Mexico.^[182] Culturally, gastroenteritis, particularly diarrhea, carries stigma in many societies, deterring care-seeking and exacerbating outcomes, especially among women and children in low-resource settings. In parts of sub-Saharan Africa and South Asia, embarrassment over symptoms leads to delayed medical consultation, with caregivers opting for home management to avoid social judgment.^[183] Traditional remedies remain prevalent, including herbal teas from plants like Ocimum lamiifolium in Ethiopia or chamomile infusions in various Asian contexts, brewed for their perceived antidiarrheal and soothing properties, often integrated with modern care in rural communities.^[184] These practices underscore a blend of indigenous knowledge and historical resilience against recurrent outbreaks.

Veterinary Aspects

Gastroenteritis in Animals

Gastroenteritis in animals refers to inflammation of the stomach and intestines, commonly presenting with symptoms such as vomiting, diarrhea, lethargy, and dehydration, which parallel those observed in humans but vary by species and etiology.^[185] In veterinary medicine, it affects a wide range of species, including companion animals and livestock, often requiring prompt supportive care to prevent severe complications like electrolyte imbalances or secondary infections. In dogs, canine parvovirus (CPV) is a major viral cause of acute gastroenteritis, particularly in unvaccinated puppies aged 6 weeks to 6 months, leading to parvoviral enteritis characterized by rapid onset of lethargy, anorexia, fever, vomiting, and profuse hemorrhagic or nonhemorrhagic diarrhea.^[186] Another common form is acute hemorrhagic diarrhea syndrome (AHDS), which manifests suddenly with profuse bloody diarrhea, vomiting, and rapid dehydration, often in young adult dogs without an identifiable infectious agent in many cases.^[187] Treatment for both conditions emphasizes supportive therapy, including intravenous fluid replacement with balanced electrolytes to correct dehydration, antiemetics like maropitant for vomiting control, and judicious use of broad-spectrum antibiotics (e.g., ampicillin) to prevent bacterial translocation; early enteral nutrition is also beneficial.^[186] Prevention of CPV relies on modified-live virus vaccination administered at 6–8, 10–12, and 14–16 weeks of age, followed by boosters every 3 years in low-risk environments.^[186] In cats, feline enteric coronavirus (FECV) is a prevalent viral pathogen causing mild, self-limiting gastroenteritis, especially in multi-cat households, through fecal-oral transmission via contaminated litter or direct contact.^[188] Symptoms typically include transient vomiting and diarrhea, occasionally with respiratory signs like sneezing, though most infections are subclinical or resolve without intervention.^[188] Management focuses on supportive measures such as fluid therapy and electrolyte supplementation for dehydrated animals, with no specific antiviral treatment available; isolation and hygiene prevent spread.^[188] Among livestock, enterotoxigenic Escherichia coli (ETEC) is a leading bacterial cause of gastroenteritis in neonatal calves, often termed "scours," striking within the first week of life via ingestion of contaminated colostrum or environment.^[189] Affected calves exhibit profuse, watery to pasty yellow diarrhea, dehydration, weakness, and hypothermia, potentially progressing to septicemia if untreated.^[189] Treatment involves aggressive oral or intravenous fluid and electrolyte replacement, along with antibiotics like ampicillin for systemic involvement, while maternal vaccination during pregnancy provides protective colostral antibodies.^[189] Bacterial gastroenteritis in poultry is frequently due to Salmonella species, such as S. Enteritidis or S. Typhimurium, which cause paratyphoid infections through vertical transmission in eggs or horizontal spread in flocks.^[190] Chicks and poults display diarrhea, decreased feed intake, ruffled feathers, and high mortality in outbreaks, with lesions including fibrinonecrotic enteritis.^[190] Supportive care includes fluid administration and biosecurity measures, with antibiotics (e.g., fluoroquinolones) reserved for septicemic cases to avoid promoting carrier states; vaccination programs in breeders reduce flock prevalence.^[191] Parasitic causes, such as Giardia species in pets like dogs and cats, lead to chronic or intermittent gastroenteritis via ingestion of cysts in contaminated water or feces.^[192] In dogs, infections often result in weight loss, foul-smelling diarrhea, and poor coat condition, though some animals remain asymptomatic.^[192] Treatment typically involves metronidazole (25 mg/kg PO q12h for 5–7 days) or fenbendazole, combined with thorough environmental disinfection to eliminate cysts.^[192] Overall, across species, antibiotics are used cautiously in bacterial cases to mitigate antimicrobial resistance, prioritizing fluid therapy and nutrition.^[193]

Zoonotic Transmission

Zoonotic transmission plays a significant role in human cases of gastroenteritis, particularly through bacterial pathogens like Campylobacter and Salmonella that originate in animal reservoirs. Campylobacter jejuni, the most common species causing campylobacteriosis, is primarily associated with poultry, where it colonizes the intestinal tract asymptomatically; consumption of undercooked poultry accounts for 50 to 80% of human cases.^[194] Raw or unpasteurized milk from cattle or other livestock also serves as a key source, with contamination occurring during milking due to fecal shedding. Similarly, Salmonella species, including non-typhoidal strains, are frequently transmitted from reptiles and amphibians, which carry the bacteria in their gastrointestinal tracts without showing illness; these pets are responsible for a notable portion of sporadic infections, especially among vulnerable populations.^[57]^[195] Transmission routes encompass direct contact, the food chain, and environmental exposure. Direct contact occurs through handling infected animals or their feces, such as petting dogs, cats, or reptiles, allowing bacteria to spread via contaminated hands to the mouth. In the food chain, pathogens enter human diets via undercooked meat from contaminated poultry or livestock, or through cross-contamination during food preparation. Environmental routes involve ingestion of water or produce tainted by wildlife feces, such as birds or rodents shedding Campylobacter into surface waters used for irrigation or drinking. These pathways highlight the interspecies dynamics, where animal colonization facilitates spillover to humans.^[57]^[196]^[195] Certain occupational and demographic groups face elevated risks due to frequent animal exposure. Farmers and veterinarians are particularly susceptible through handling livestock or poultry, with higher incidence rates of Campylobacter and Salmonella infections from occupational contact. Children, especially those under 5 years old interacting with household pets like puppies or reptiles, represent another high-risk group, as their hygiene practices may be inconsistent and immune systems less robust. For instance, in 2023, a multistate outbreak of Salmonella linked to contaminated dry dog food affected at least seven people, underscoring the dangers of pet-related exposures in homes with young children.^[197]^[198]^[199] Control measures focus on interrupting transmission at animal-human interfaces, emphasizing prevention in reservoirs and hygiene practices. Vaccination of poultry against Campylobacter and Salmonella has shown efficacy in reducing shedding, with live and inactivated vaccines implemented in some production systems to lower contamination levels by up to 90% in flocks. Thorough cooking of meat to internal temperatures of at least 74°C eliminates viable bacteria, while pet hygiene protocols—such as handwashing after contact and avoiding kitchen surfaces—mitigate direct risks. The One Health approach integrates veterinary, public health, and environmental efforts to monitor and control zoonoses, promoting coordinated surveillance and interventions across sectors to curb outbreaks.^[200]^[57]^[201]

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Understanding Viral Gastroenteritis | Johns Hopkins Medicine
Symptoms of viral gastroenteritis often begin about 1 to 2 days after the virus gets into the body. Common symptoms include: Nausea. Vomiting. Watery diarrhea.
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Signs and Symptoms of Shigella Infection - CDC
Mar 14, 2024 · Common symptoms of Shigella infection include diarrhea, fever, stomach pain, and feeling the need to pass stool (poop) even when the bowels are ...
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Rotavirus infections WPRO - World Health Organization (WHO)
Rotavirus is the most common cause of severe diarrhoeal disease in infants and young children globally. It is transmitted through the oral-faecal route.
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Shigellosis - StatPearls - NCBI Bookshelf - NIH
Feb 26, 2024 · The most common symptoms of shigellosis are mucoid bloody diarrhea, fever, abdominal pain, and tenesmus. Shigellosis occurs globally but is most ...Introduction · Pathophysiology · Evaluation · Treatment / Management
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Symptoms & Causes of Viral Gastroenteritis (“Stomach Flu”) - NIDDK
The symptoms listed below may suggest that an adult or child has a severe case of viral gastroenteritis, dehydration, or a more serious health problem instead ...
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Gastroenteritis: What It Is, Symptoms, Causes & Treatment
Diarrhea. Nausea and vomiting. Loss of appetite. Abdominal pain and cramping. Fever. Chills. Fatigue. Body aches.
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Oral Rehydration, Maintenance, and Nutritional Therapy - CDC
The clinical signs and symptoms of mild dehydration (3%-5% fluid deficit) include increased thirst and slightly dry mucous membranes, whereas moderate ...
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Gastroenteritis - PMC - PubMed Central - NIH
Table 6.23. Complications of acute gastroenteritis. Immediate. Dehydration. Electrolyte imbalance: Hypernatraemia. Hyponatremia. Hypokalaemia. Acid–base ...
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Electrolytes - StatPearls - NCBI Bookshelf - NIH
Jul 24, 2023 · Among the electrolyte disorders, hyponatremia is the most frequent. Hyponatremia is diagnosed when the serum sodium level is less than 135 mmol/ ...Missing: gastroenteritis | Show results with:gastroenteritis
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Electrolyte disorders related emergencies in children - PMC
Severe hypokalemia can lead to more serious consequences including paralysis, respiratory failure, and arrhythmias.
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Postinfection Irritable Bowel Syndrome - PMC - PubMed Central
A subset of patients develop new onset Rome criteria positive irritable bowel syndrome (IBS), called postinfection IBS (PI-IBS).
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Small Intestinal Bacterial Overgrowth | Current Infectious Disease ...
Aug 22, 2024 · SIBO is a chronic gastrointestinal disorder wherein excessive and abnormal growth of bacteria in the small bowel generally causes abdominal pain, bloating, and ...
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This so called post-infectious IBS (PI-IBS) represents the persistence of symptoms like diarrhea and abdominal discomfort well after resolution of the culprit ...
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May 14, 2024 · Infection with Shiga toxin-producing E. coli (STEC) can lead to a serious health condition called hemolytic uremic syndrome (HUS). HUS can lead ...Kinds of E. coli · View All E. coli infection · Prevention · Risk Factors
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Campylobacter Species and Guillain-Barré Syndrome - PMC
Campylobacter infection is now known as the single most identifiable antecedent infection associated with the development of GBS.
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Long-term gastrointestinal outcomes of COVID-19 - Nature
Mar 7, 2023 · We show that beyond the first 30 days of infection, people with COVID-19 exhibited increased risks and 1-year burdens of incident gastrointestinal disorders.
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This review provides a better understanding of the association between gut microbiota and the long-term consequences of COVID-19.
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Norovirus - StatPearls - NCBI Bookshelf - NIH
Feb 17, 2025 · Worldwide, norovirus is responsible for an estimated 685 million cases of gastroenteritis, 150,000 adult deaths, and 50,000 child deaths ...
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Increasing Predominance of Norovirus GII.17 over GII.4 ... - CDC
Jun 2, 2025 · In the United States, the norovirus season typically starts in early December (1,4), but in 2024–25, the onset of the season was in early ...
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About Rotavirus - CDC
Apr 22, 2024 · Rotavirus commonly causes severe watery diarrhea and vomiting in infants and young children. · Children may become dehydrated and need to be ...How It Spreads · Rotavirus Spreads Easily... · Treatment And Recovery
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A decade of experience with rotavirus vaccination in the United States
Vaccine introduction resulted in a median decline in rotavirus-associated hospitalizations and emergency department visits of 80% and 57%, respectively, along ...
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Non-Norovirus Viral Gastroenteritis Outbreaks Reported to the ...
During 2009-2018, four adenovirus, 10 astrovirus, 123 rotavirus, and 107 sapovirus gastroenteritis outbreaks were reported to the US National Outbreak ...
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Norovirus | Yellow Book - CDC
Apr 23, 2025 · Infected people usually experience acute onset of vomiting and non-bloody diarrhea. The incubation period ranges from 12 to 48 hours. Other ...Introduction · Epidemiology · Diagnosis<|control11|><|separator|>
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Jan 2, 2025 · Surveillance data from the Centers for Disease Control and Prevention (CDC) indicate a spike in norovirus outbreaks in the United States.
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Jul 12, 2024 · Protozoa such as Cryptosporidium spp., Giardia intestinalis, and Cyclospora cayetanensis most commonly cause diarrhea and other gastrointestinal ...Blood · Food And Water · Animals (zoonotic)
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Giardiasis - StatPearls - NCBI Bookshelf
Feb 12, 2024 · Giardiasis is the most prevalent enteric protozoal infection globally, affecting nearly 2% of adults and 8% of children in developed countries.Continuing Education Activity · Epidemiology · Evaluation · Treatment / Management
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Giardia lamblia infection increases risk of chronic gastrointestinal ...
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May 27, 2025 · Symptoms of cryptosporidiosis generally begin 2 to 10 days (average 7 days) after infection and last 1 to 2 weeks. The most common symptom of ...Missing: immunocompromised | Show results with:immunocompromised
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Cryptosporidiosis - StatPearls - NCBI Bookshelf - NIH
Chronic diarrhea can occur in patients with immunocompromising conditions, particularly human immunodeficiency virus (HIV) infections.
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Cryptosporidium Infection: Epidemiology, Pathogenesis, and ... - NIH
Cryptosporidium is a protozoan that infects a wide variety of vertebrates, including humans, causing acute gastroenteritis.
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Entamoeba histolytica Infection - StatPearls - NCBI Bookshelf - NIH
... amebiasis caused by Entamoeba histolytica ... Symptoms typically have a gradual onset, usually over one to three weeks. Common symptoms include diarrhea, bloody ...
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Amebiasis - CDC
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Outbreak of Cyclosporiasis Among Patrons of a Mexican-Style ...
Apr 17, 2025 · In June 2023, a total of 47 cases of cyclosporiasis were associated with consumption of food from a Mexican-style restaurant in Alabama.
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Cyclospora cayetanensis and Cyclosporiasis: An Update - PMC
Cyclospora cayetanensis is a coccidian parasite of humans, with a direct fecal–oral transmission cycle. It is globally distributed and an important cause of ...<|control11|><|separator|>
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Parasitic Infections of the Gastrointestinal Track and Liver - PMC
Four groups of protozoa, Giardia, Cryptosporidia, Isosopora, and Amoeba or Entamoeba, can cause gastroenteritis. Outbreaks of protozoal gastroenteritis usually ...
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Simultaneous Detection of Entamoeba histolytica, Giardia lamblia ...
Entamoeba histolytica, Giardia lamblia, and Cryptosporidium are three of the most important diarrhea-causing parasitic protozoa.
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Feb 1, 2014 · Noninfectious causes include medication adverse effects, acute abdominal processes, gastroenterologic disease, and endocrine disease.
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Aug 20, 2025 · Box 1. Non-infectious causes of acute gastroenteritis. Medication. • Antibiotics. • Laxative abuse. • Sorbitol. • Colchicine. • Cardiac ...Initial Evaluation Of Acute... · Figure 1 · Antibiotic Therapy
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Drug-Related Gastroenteritis and Chemical-Related Gastroenteritis
Although it is usually caused by infection with a microorganism, it can also be caused by ingesting drugs, medications, or chemicals.
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Scombroid and Histamine Toxicity - StatPearls - NCBI Bookshelf - NIH
The most common symptoms are rash, flushing, headache, and diarrhea. Less common symptoms include abdominal cramps, blurred vision, cold-like sensation, ...
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Lactose Intolerance - StatPearls - NCBI Bookshelf
Aug 6, 2025 · Lactose intolerance is a clinical syndrome characterized by gastrointestinal symptoms, such as bloating, abdominal pain, flatulence, nausea, ...
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Radiation Enteritis - StatPearls - NCBI Bookshelf
Radiation enteritis is damage to the small and/or large intestines secondary to radiation. Different terms like radiation colitis, radiation enteropathy, ...Continuing Education Activity · Treatment / Management · Radiation Oncology
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Bowel Ischemia - StatPearls - NCBI Bookshelf
Intestinal ischemia occurs when at least a 75% reduction in intestinal blood flow for more than 12 hours. Abdominal pain is the most common symptom in patients ...
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Apr 24, 2024 · You can get norovirus by accidentally getting tiny particles of feces (poop) or vomit in your mouth from a person infected with norovirus.
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Jan 10, 2024 · Symptoms. Symptoms usually start 1–2 days after infection and last 7 days. Most people with shigellosis experience: Diarrhea that can be bloody ...
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Jun 6, 2014 · Transmission of norovirus occurs primarily via the fecal-oral route, including direct person-to-person contact, consumption of contaminated food ...
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May 10, 2024 · Outbreaks of Campylobacter infections among people have been linked to many sources. Some of these sources include: Poultry · Raw ...Preventing · Campylobacter | CDC · Campylobacter · Symptoms
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DPDx - Giardiasis - CDC
Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with ...
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Nov 23, 2018 · Norovirus spread throughout the restaurant could have occurred by aerosol, person-to-person, fomite, or foodborne routes. Inadequate employee ...
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Norovirus Outbreaks - CDC
Most norovirus outbreaks happen when infected people spread the virus to others through direct contact. Norovirus outbreaks have been reported in many settings.
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The classical secretory diarrhea caused by cholera toxin (CT) is due to cAMP-dependent activation of the cystic fibrosis transmembrane conductance regulator ...
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A number of secretory stimuli can cause diarrhea. These include bacterial enterotoxins, hormones generated by endocrine neoplasms, dihydroxy bile acids, ...
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Invasive Diarrheas: Invasive bacteria, such as Shigella and Campylobacter, penetrate the intestinal mucosa. A bloody, mucoid diarrheal stool with inflammatory ...
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Campylobacter species produce disease primarily by direct invasion of the colonic epithelium and may induce inflammatory changes that are endoscopically ...<|control11|><|separator|>
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Nov 9, 2017 · Rotavirus primarily infects enterocytes and induces diarrhoea through the destruction of absorptive enterocytes (leading to malabsorption) ...Missing: cytopathic | Show results with:cytopathic
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Thus, inhibition of prostaglandin synthesis by NSAIDs reduces mucus and bicarbonate synthesis, impairs mucosal blood flow, and increases gastric acid secretion ...<|control11|><|separator|>
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The burden of norovirus disease is vast, and older adults are particularly at risk for severe outcomes, including prolonged symptoms and death.
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IgA binds surface proteins that mediate cell attachment of intestinal microbial pathogens thereby preventing colonization and cell invasion. The large complexes ...
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Following enteric bacterial infection, neutrophils are rapidly recruited into intestinal tissues where they eliminate microorganisms through phagocytosis and ...
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Jul 9, 2018 · Recent studies have demonstrated that an imbalance in gut bacterial communities, or “dysbiosis”, may be a contributor to the pathophysiology of IBS.
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Feb 1, 2019 · The history should include onset and duration of symptoms, caregiver reports of fluid intake and output, and red flag symptoms that require ...
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May 4, 2025 · Viral gastroenteritis is a widespread infectious illness caused by various viruses, including rotavirus, norovirus, adenovirus, and astrovirus, ...Continuing Education Activity · Introduction · Etiology · Treatment / Management
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Jan 17, 2023 · The history and physical examination serve 2 vital functions: (1) differentiating gastroenteritis from other causes of vomiting and diarrhea ...
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Jul 25, 2025 · Viruses are the suspected cause of acute gastroenteritis when vomiting is prominent, when the incubation period is longer than 14 hours, and ...
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Jul 25, 2025 · Bacterial (15-20%) causes of gastroenteritis. Salmonella. Salmonella is the second most common agent among outbreaks with known pathogens. It ...
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Oct 1, 2009 · The most useful individual signs for identifying dehydration in children are prolonged capillary refill time, abnormal skin turgor, and abnormal respiratory ...
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Jun 8, 2024 · Most cases of dehydration caused by gastroenteritis are isonatremic, and the serum sodium is between 130 and 150 mEq/L. Hyponatremia is a serum ...
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Dehydration and electrolyte losses associated with untreated diarrhea cause the primary morbidity of acute gastroenteritis. Diarrhea can be among the initial ...
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Ultrasound is the test of choice for the diagnosis of intussusception. The ... The differential diagnosis of intussusception includes acute gastroenteritis ...
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Therapies targeting the microbiome, such as probiotics, antibiotics, diet, and fecal microbiota transplants, improve IBS symptoms.
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Lack of access to safe, clean drinking-water and basic sanitation, as well as poor hygiene cause nearly 90% of all deaths from diarrhoea, mainly in children.
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Jan 13, 2025 · To disinfect, use a chlorine bleach solution with a concentration of 1,000 to 5,000 ppm (5 to 25 tablespoons of household bleach [5% to 8%] per ...Norovirus at Youth Camps · Norovirus Fact Sheet for Food...
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Apr 17, 2024 · Handwashing can prevent about 30% of diarrhea-related sicknesses and about 20% of respiratory infections (e.g., colds). Antibiotics often ...Washing Hands Prevents... · Wet Your Hands With Clean... · Scrubbing Your Hands For At...
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We propose diarrhoea risk reductions of 48, 17 and 36%, associated respectively, with handwashing with soap, improved water quality and excreta disposal.
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Mar 22, 2024 · A WHO study in 2012 calculated that for every US$ 1.00 invested in sanitation, there was a return of US$ 5.50 in lower health costs, more ...
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Mar 21, 2024 · Provide education to staff, patients, and visitors, including recognition of norovirus symptoms, preventing infection, and modes of transmission ...
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In December 2009, WHO recommended routine immunization of infants for prevention of rotavirus disease, the most common cause of serious gastroenteritis among ...
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All four vaccines are considered highly effective in preventing severe gastrointestinal disease. In low income countries, vaccine efficacy can be lower than ...
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HilleVax is developing HIL-214, a norovirus bivalent GI.1/GII.4 virus-like particle (VLP) vaccine intended for active immunization for the prevention of acute ...
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Dec 19, 2021 · This short article reviews the recent progress in norovirus vaccine development, focusing on those from recent clinical studies.
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Building a Broader Understanding of Enterotoxigenic Escherichia coli
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May 13, 2025 · These findings underscore the feasibility of combining ETEC and Shigella vaccine candidates into a single formulation without compromising immunogenicity.
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Apr 25, 2024 · Moderate or severe acute illnesses, including gastroenteritis (defer until symptoms improve) ... mild acute gastroenteritis or other mild acute ...
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Effects of the rotavirus vaccine program across age groups in the ...
Feb 22, 2019 · Overall, among all age groups combined, rotavirus hospitalization rates declined by nearly 70% after introduction of the vaccine. The youngest ...Vaccination Status · Rvge Time Series · Young Children, 0--9 Years...
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Apr 22, 2024 · There are many ways to make water safe from harmful germs. The most common methods are boiling, adding chlorine, using filters, and exposing water to sunlight.Key Points · Overview · Ways To Make Water Safe
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Cryptosporidium (or “Crypto”) is an extremely chlorine-tolerant parasite. This means Crypto can spread among swimmers even when the free chlorine.
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[PDF] Household water storage, handling and point-of-use treatment
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Sep 18, 2023 · Separate: Don't Cross Contaminate Use separate plates and utensils for cooked and raw foods. Use hot, soapy water to thoroughly wash plates, ...
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Mar 5, 2024 · To keep your family safer from food poisoning, follow these four simple steps: clean, separate, cook, and chill. CLEAN. Handwashing for Food ...
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Most human outbreaks of infection of Campylobacter jejuni that are associated with dairy products have been linked to raw milk or inadequately pasteurized milk.
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Bottled or canned drinks: Drinks from unopened, factory-sealed bottles or cans are safer than tap water; however, use caution as vendors in some countries may ...
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Contaminated water can look clean but still have harmful bacteria, viruses, and parasites. Factory-sealed bottled water is the safest option for most travelers.
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FDA Did Not Disclose Fatal E. coli Outbreak Linked to Lettuce in 2024
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Check recent Food Recalls and Safety Alerts. The following is a list of outbreak and adverse event investigations primarily being managed by FDA's CORE Response ...Escherichia coli (E. coli) · Salmonella (Salmonellosis) · See · Safe Food Handling
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Chapter 5 Fluid management · continue breastfeeding and other milk feeds · encourage fluid intake · discourage the drinking of fruit juices and carbonated drinks, ...<|control11|><|separator|>
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Research shows that following a restricted diet does not help treat viral gastroenteritis. Most experts do not recommend fasting or following a restricted diet.
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If caused by Campylobacter jejuni or Shigella, symptoms may progress to colitis, bloody diarrhea, and tenesmus.
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