Background
Acute gastroenteritis, a nonspecific term for various pathologic states of the gastrointestinal (GI) tract in which the primary manifestation is diarrhea associated with nausea and vomiting, is a common cause of morbidity and mortality worldwide. Conservative estimates put diarrhea in the top five causes of deaths worldwide, with most occurring in young children in developing nations. In industrialized countries, diarrheal diseases are a significant cause for morbidity across all age groups.
Prior to the coronavirus disease 2019 (COVID-19) pandemic, an estimated 179 million cases of acute gastroenteritis occurred every year in the United States. A sharp decline in the incidence of norovirus outbreaks was observed in early 2020 owing to COVID-19–related measures, including limiting travel, physical distancing, mask-wearing, handwashing, and surface disinfection. [1] As such measures have become increasingly relaxed, there has been an uptick in cases, and it is projected that norovirus cases will return to prepandemic levels by 2026. Current data from the CDC NoroSTAT system shows a significant increase in reported norovirus outbreaks when compared to the pre-COVID and during COVID time periods. [1, 2]
Etiologies of gastroenteritis include bacteria, viruses, parasites, toxins, and drugs. Viruses are responsible for a significant percentage of cases affecting patients of all ages; in the United States, viruses are the leading cause of acute gastroenteritis. [3, 4] Viral gastroenteritis ranges from a self-limited watery diarrheal illness (usually < 1 wk) associated with symptoms of nausea, vomiting, anorexia, malaise, or fever, to severe dehydration resulting in hospitalization or even death.
The clinician generally encounters acute viral gastroenteritis in three settings:
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Epidemic gastroenteritis, which occurs either in semiclosed communities (eg, families, institutions, ships, vacation spots) or as a result of classic food-borne or water-borne pathogens [6] ; most of these infections are caused by caliciviruses such as norovirus
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Sporadic acute gastroenteritis of adults, which most likely is caused by caliciviruses, rotaviruses, astroviruses, or adenoviruses
Etiology
Viral (50-70%) causes of gastroenteritis
Norovirus
Norovirus is the leading cause of viral gastroenteritis in the United States. Noroviruses (formerly known as Norwalk virus in the United States and as small, round structured virus [SRSV] in the United Kingdom), along with the sapoviruses (formerly known as Sapporo-like viruses), are members of the Caliciviridae family of viruses. The norovirus is a small, 26-40 nm, nonenveloped, single-stranded RNA virus. Sapoviruses, a cause of gastroenteritis, predominantly in children, are also in the Caliciviridae family.
Five norovirus genogroups have been identified: GI, GII, GIII, GIV, and GV; many clusters (genotypes) have also been identified. In 2010, the land-based experience was far busier than usual. The dominating strain was GII-4 (New Orleans). The most recent data from the CDC suggests that the 2024-2025 norovirus season has surpassed pre-COVID outbreak levels. The typical season is considered to be from November to April, and the most often identified strain is the GII.17, which has not been found at this time to cause more severe disease than other strains. [1, 2] Norovirus is often called the "winter vomiting disease" in Britain and the incidence seems to be higher in colder weather.
Norovirus is a highly infectious virus—with as few as 10-100 particles necessary for transmission—and is quite resistant to quaternary ammonia compounds, alcohol, detergent-based compounds, freezing, and heat (to 60o C). It is a very difficult virus to culture and measure; thus, studies on norovirus are limited, with researchers using a "surrogate," nonenveloped virus, Feline calicivirus (FCV), to assess the efficacy of disinfectants and other mitigation strategies. Some researchers have questioned the use of FCV as a surrogate as FCV is a respiratory virus and norovirus is a GI virus and likely is more resilient than FCV due to the need for norovirus to survive in the hostile environment of the gut. Therefore, the results of testing performed to validate the efficacy of disinfectants and hand sanitizers possibly overestimate the actual effectiveness of these products on human norovirus.
It has been suggested that murine norovirus (MNV) can serve as a useful tool in assessing the risk of infection with human norovirus. It has been used as a surrogate to evaluate the resistance of human norovirus to disinfectants due to its similar characteristics (ie, resistance to basic and acidic pHs, capsid structure, genomic organization, and replication cycle) to human norovirus. [7]
Various modes of transmission exist including fecal-oral transmission (predominant), person to person, fecal contamination of food and/or water, fomite transmission, and airborne spread when in close proximity to someone vomiting, as the virus is easily aerosolized.
Between January 1996 and November 2000, 348 outbreaks of norovirus were reported to the Centers for Disease Control and Prevention (CDC). Of these, 39% of patients were contaminated by food, 12% by person to person, 3% by water, and 18% by unidentified sources. [8] A reported 2,407 US outbreaks occurred between August 1, 2024 to April 9th, 2025, which is nearly double the reported outbreaks during the same time period in the previous season (1,230 outbreaks). [2] Most of the food sources responsible were identified as oysters, salads, salad dressing, sandwiches, deli meats, cake and frosting, raspberries, drinking water, and ice. Shellfish have been implicated in some outbreaks, but it is not a frequent source on cruise ships, where the predominant mode of infection is believed to be fecal-oral and person-to-person from individuals who come onto the ships ill and do not report the illness nor quarantine themselves in their cabins. [8]
Public vomiting episodes with aerosolization of the virus is likely a major source of spread in congested public locations such as cruise ships, schools, and casinos. The same study revealed that 39% of people contracted the disease in restaurants, 30% in nursing homes, 12% at school, 10% on vacation, and 9% remain unidentified [8]
The CDC National Outbreak Reporting System (NORS) and BEAM (Bacteria, Enterics, Ameba, and Mycotics) Dashboard, a web-based platform for reporting waterborne, foodborne, and enteric disease outbreak and viewing data related to these outbreaks has been updated to 2023. Between 2020 and 2023, 10,506 acute gastroenteritis outbreaks were reported, with primary transmission modes of person-to-person contact, foodborne, and unknown. Norovirus accounted for largest percentage of outbreaks (60%) and cases (68%). [9]
The incubation period for the norovirus is between 12 and 48 hours. Some of the early symptoms include nausea, a sudden onset of vomiting, moderate diarrhea, headache, fever (~50%), chills, and myalgia, and will last 12-60 hours. The clinical features suggestive of norovirus include the patient's presentation and the sudden onset of symptoms, with uncontrolled vomiting being a classic sign. Usually, more vomiting than diarrhea occurs. The virus is noninvasive of the colon; therefore, white blood cells (WBCs) are not seen in the stool, and hematochezia is rare. The severity and length of illness seen is often related to the then-current predominant strain.
The natural course of this illness usually provides resolution within 36 hours. Unless the patient is very young, very old, debilitated with severe underlying disease, or immunocompromised, they usually do very well with this self-limited illness, responding to oral rehydration and a rapid return to a normal diet once the vomiting has ceased. The only therapy is oral and/or intravenous hydration with the occasional need for antiemetics. The usual cautions concerning the use of antiemetics in very young patients apply.
Although viral shedding has been reported for up to 2 weeks or more, the polymerase chain reaction (PCR) testing used to determine this may just be detecting inactivated RNA. The length of viral shedding and the large number of viruses shed in stool (millions) relative to the number required for infection (10-100) explains the communicability and the need for education regarding meticulous hand hygiene.
There are many norovirus strains with no cross-immunity, so repeat infections are possible throughout one's lifetime.
Caliciviruses
Various caliciviruses, other than norovirus, are likely responsible for many outbreaks of previously unidentified viral gastroenteritis.
Rotavirus may cause severe dehydration.
Rotavirus is a nonenveloped, double-stranded RNA virus of the Reoviridae family with a wheel-like appearance under electron microscopy—hence the name. The virus is extremely contagious. Nearly all children are infected with rotavirus at some point before age 5 years, unless immunized. There are two commercially available vaccines in the United States, each with antibodies to multiple strains. The vaccines are shown to prevent infection in approximately 70% of vaccinated children and severe infection in approximately 90%. [10] Prior to this, there were 55,000–70,000 hospitalizations per year in United States. [11] The illness lasts 3-8 days and usually starts with some vomiting, followed by severe foul-smelling (distinctive) diarrhea, potentially leading to severe dehydration.
Adults can be infected with rotavirus, although symptoms are usually not as severe. Those adults most likely to be infected include people with children affected by the virus, elderly persons, and the immunocompromised. There are multiple strains (four are common in the United States), so people can be infected with rotavirus multiple times. Usually, the first infection is the most severe. Most initial infections occur by age 2 years. Rotavirus is considered the most significant etiologic agent for acute GI illness in children worldwide, with up to 500,000 global deaths annually. [11] The peak rotavirus season is November to April (cooler weather) in temperate weather and year-round in tropical climates.
Other viruses that can also cause gastroenteritis include the following:
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Astrovirus
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Coronavirus
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Pestivirus
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Torovirus
Bacterial (15-20%) causes of gastroenteritis
Salmonella is the second most common agent among outbreaks with known pathogens. It is manifested by acute enterocolitis, with abdominal pain, diarrhea, nausea, headache, sometimes vomiting, and almost always fever. Infected persons may develop a localized infection or septicemia. Salmonellosis is predominantly foodborne, and, on average, the onset of symptoms occurs 12-36 hours after ingestion of the contaminated source. It is estimated that Salmonella is responsible for approximately 1.35 million infections in the United States each year, with 26,500 hospitalizations and 420 deaths. [12] Over 2,500 serotypes of Salmonella have been described, but S typhimurium and S enteritidis are the most commonly detected in infected persons.
The incidence of S typhimurium has increased since 1997, and it was the cause of a multistate outbreak associated with peanut butter and other peanut-containing products that resulted in 714 cases across 46 states. The outbreak began in the summer of 2008; however, the epidemiologic investigation was initiated in November due to the inherent time lag in reporting (stool sample results may take 2 weeks). The problem became evident when there was a growing cluster of Salmonella serotype typhimurium isolates with the same pulsed-field gel electrophoresis (PFGE) pattern in several states.
Review of detailed epidemiologic questionnaires, assessment of foods, and results of case-control studies in industrialized settings where clusters appeared led to the assumption of peanut butter being the common source of the outbreak. The FDA inspected the facility where the peanut butter was produced and positive test results from finished peanut butter obtained on site confirmed the presence of the outbreak strain. Being an ingredient-driven outbreak, many products distributed through various channels had the potential of being contaminated. As a result of the findings, recalls of peanut butter and peanut-containing foods were issued for products dated as far back as January 2007. In addition, the producing facility was directed to stop production and distribution of all products.
Clostridium difficile, often referred to as “C diff,” is a gram-positive, spore-forming, toxin-producing bacillus that typically affects patients receiving antibiotic treatment, especially with broad-spectrum drugs (eg, cephalosporins, clindamycin, fluoroquinolones). Clinical symptoms of C difficile infection include watery diarrhea, fever, nausea, loss of appetite, and abdominal pain or tenderness. Complications that may result from infection include pseudomembranous colitis, toxic megacolon, perforations of the colon, sepsis, and even death, although it is rare. In some cases, infection resolves within 2-3 days of discontinuing the offending antibiotic. However, there are cases that require a full course of an appropriate antibiotic; several antibiotics are effective against C difficile. Severe cases may require surgery to remove the infected portion of the intestine.
C difficile incidence and severity have increased during relatively recent years due to the emergence of a more virulent epidemic strain. It is the leading cause of US hospital-acquired GI illness, with annual costs of $3.2 billion. [13] Host susceptibility is greater in hospitalized persons and those with underlying medical conditions. The bacterium is shed in feces and can be acquired from contact with contaminated surfaces, devices, or hands; it is considered to be a healthcare-associated infection.
Elderly individuals are more commonly affected; however, infection may occur at any age and over the last few years its appearance in populations considered low risk has increased (ie, healthy outpatients, children, and people with no recent history of taking antibiotics). In cases of community-acquired infection, obesity has been reported to be a possible risk factor. [14] The use and application of evidence-based management and prevention strategies are important factors in the collaboration to reduce incidence of C difficile. New treatment strategies are under investigation.
Other bacterial causes include the following:
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E coli: Enterohemorrhagic O157:H7, enterotoxigenic, enteroadherent, enteroinvasive
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Aeromonas
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B cereus
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Clostridium perfringens
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M avium-intracellulare (MAI), immunocompromised
Parasitic (10-15%) causes of gastroenteritis
Giardia lamblia (also called Giardia intestinalis), a flagellate protozoan parasite, lives primarily in the upper part of the small intestine of an organism. Some infected individuals present with symptoms including diarrhea, bloating, greasy stools that tend to float, abdominal cramps, nausea/vomiting, and dehydration, whereas others may be asymptomatic. The average incubation period is 7-10 days, and symptoms may persist for 1-2 weeks. Most infections occur in children aged 1-9 years, but its predominance is in those younger than 5 years. It is also seen in adults aged 25-44 years.
Infected persons may excrete cysts intermittently, making it difficult to diagnose. Several stool samples should be collected on various days and enzyme-linked immunosorbent assay (ELISA) or direct fluorescent antibody methods are usually performed to identify the parasite.
Transmission occurs from person to person or even from animals to humans via the fecal-oral route, through the ingestion of contaminated water. For example, it can be acquired from drinking downstream where a cow or other animal(s) may have contaminated the water. The risk of becoming infected is higher for travelers around the world, persons participating in outdoor activities/recreational water facilities, and those who consume unfiltered/untreated water (ie, hikers, campers). The majority of cases are observed during the months of June to October, coinciding with the months of increased travel and outdoor/recreational water activities. There is increased risk in daycare centers and for close contacts of infected persons as well.
Giardiasis occurs worldwide, with higher prevalence in areas where there is poor hygiene and sanitation. However, it is the most common intestinal parasitic disease in the United States, with an excess of 19,000 infections reported each year.
It has two stages, cyst and trophozoite. Both forms are passed in feces; however, the cyst is the infective stage and the one that can survive outside of a host and in the environment for weeks or months. It has moderate tolerance to chlorine and is capable of living in cold water for significant periods. Individuals infected with Giardia may shed 1 to 10 billion cysts daily, while the infectious dose is approximately 10 cysts, sometimes even as few as 1 or 2.
Other parasitic causes include the following:
Food-borne toxigenic diarrhea
Preformed toxins include S aureus and B cereus
Postcolonization toxins include V cholera, C perfringens, enterotoxigenic E coli, and Aeromonas.
Shellfish poisoning and poisoning from other marine animals
Shellfish and marine animal poisoning include the following:
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Paralytic shellfish poisoning (PSP) - Saxitoxin
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Neurologic shellfish poisoning (NSP) - Brevetoxin
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Diarrheal shellfish poisoning (DSP) - Okadaic acid
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Amnesic shellfish poisoning - Domoic acid
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Ciguatera (ciguatoxins)
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Scombroid (conversion of histidine to histamine)
Drug-associated diarrhea
Medications associated with diarrhea include the following:
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Antibiotics, due to alteration of normal flora
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Laxatives, including magnesium-containing antacids
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Colchicine
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Quinidine
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Cholinergics
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Sorbitol
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Proton pump inhibitors (PPIs): In a prospective population-based study of 38,109 middle-aged and older Australian adults, there was an association between use of PPIs and a significantly higher risk of hospitalization for infectious gastroenteritis, regardless of the PPI used. [15] There was a dose-response relationship noted.
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GLP1 inhibitors
Pseudomembranous colitis
Pseudomembranous colitis occurs as an overgrowth of C difficile.C difficile assay findings are positive.
Other causes
Other causes of diarrhea include the following:
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Unknown agents, especially in developing countries
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Ischemic colitis
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Ulcerative colitis
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Crohn disease
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Acquired immunodeficiency syndrome (AIDS)
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Dumping or short bowel syndrome
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Radiation or chemotherapy
Pathophysiology
Viral spread from person to person occurs by fecal-oral transmission of contaminated food and water. Some viruses, like noroviruses, may be transmitted by an airborne route. Clinical manifestations are related to intestinal infection, but the exact mechanism of the induction of diarrhea is not clear; several mechanisms, including adherence, mucosal invasion, enterotoxin production, and/or cytotoxin production have been implicated, resulting in increased fluid secretion and/or decreased absorption and producing an increased luminal fluid content that cannot be adequately reabsorbed, leading to dehydration and the loss of electrolytes and nutrients.
Diarrheal illnesses may be classified as follows:
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Osmotic, due to an increase in the osmotic load presented to the intestinal lumen, either through excessive intake or diminished absorption
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Inflammatory (or mucosal), when the mucosal lining of the intestine is inflamed leading to poor absorption of fluids and electrolytes
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Secretory, when ion channels are affected leading to excessive electrolyte and fluid loss
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Motile, caused by intestinal motility disorders which decrease transit time through the GI tract
The small intestine is the prime absorptive surface of the GI tract. The colon then absorbs additional fluid, transforming a relatively liquid fecal stream in the cecum to well-formed solid stool in the rectosigmoid. Disorders of the small intestine result in increased amounts of diarrheal fluid with a concomitantly greater loss of electrolytes and nutrients.
The exact mechanism of vomiting in acute diarrheal illness is not known, although serotonin release has been postulated as a cause, stimulating visceral afferent input to the chemoreceptor trigger zone in the lower brainstem.
The most extensive studies on viral gastroenteritis have been done with rotavirus. Rotaviruses attach and enter mature enterocytes at the tips of small intestinal villi. They cause structural changes to the small bowel mucosa, including villus shortening and mononuclear inflammatory infiltrate in the lamina propria.
The current knowledge on the mechanisms leading to diarrheal disease by rotavirus is as follows [11, 16] :
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Rotavirus infections induce maldigestion of carbohydrates, and their accumulation in the intestinal lumen, as well as a malabsorption of nutrients and a concomitant inhibition of water reabsorption, can lead to a malabsorption component of diarrhea.
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Rotavirus secretes an enterotoxin, NSP4, which leads to a Ca2+ -dependent Cl- secretory mechanism. Mobilization of intracellular calcium associated with NSP4 expressed endogenously or added exogenously is known to induce transient chloride secretion.
Morphologic abnormalities can be minimal, and studies demonstrate that rotavirus can be released from infected epithelial cells without destroying them. Viral attachment and entry into the epithelial cell without cell death may be enough to initiate diarrhea. The epithelial cell synthesizes and secretes numerous cytokines and chemokines, which can direct the host immune response and potentially regulate cell morphology and function. Studies also suggest that one of the nonstructural viral proteins may act as an enterotoxin, promoting active chloride secretion mediated through increases in intracellular calcium concentration. Toxin-mediated diarrhea would explain the observation that villus injury is not necessarily linked to diarrhea.
An animal study in zebrafish suggests that the viral capsid and possibly the minor capsid protein VP2 may have key roles in human norovirus symptomatology, perhaps behaving functionally as a viral enterotoxin. [17]
Epidemiology
United States data
Rotavirus
Rotavirus is the most common etiologic agent of health care–acquired diarrhea in pediatric patients. Community- and health care–acquired infections have similar temporal distributions; they are caused by the same viral subtypes; and they affect children of the same age groups. All of the health care–acquired infections with known viral subtypes occurred while the same subtype was still active in the community, suggesting that health care–acquired infections arise from repeated introduction of the community-acquired rotavirus into the hospital setting. [11, 16]
Before the 2006 advent of rotavirus vaccine, which prevents infection in approximately 70% of vaccinated children and severe infection in approximately 90%, acute viral gastroenteritis resulted in more than 400,000 office visits, 200,000 emergency department visits, 55,000-70,000 hospitalizations, and 20-60 deaths. [11] However, a US Centers for Disease Control and Prevention (CDC) study by Tate et al demonstrated a decline in the seasonality of rotavirus following the 2006 introduction of the rotavirus vaccine. [18]
The investigators evaluated data for July 2000 through June 2008 to assess national, regional, and local trends in rotavirus testing and detection and found not only was the onset of the 2007-2008 rotavirus season delayed 15 weeks and the peak delayed 8 weeks relative to the prevaccine rotavirus season from 2000 to 2006, but the 2007-2008 season also lasted a little over half (14 wk) of the median prevaccine seasons (26 weeks). [18] Moreover, there was a 67% decline in the number and a 69% decline in the proportion of 2007-2008 rotavirus-positive test results compared with the median in 2000-2006.
Statistics on sporadic cases of adult viral gastroenteritis are not known; however, food- and water-borne epidemics of viral gastroenteritis are monitored by the CDC surveillance programs.
Norovirus
The genus Norovirus, formerly called the Norwalk-like virus (or small, round structured virus [SRSV] in the United Kingdom), is a member of the family Caliciviridae. Norovirus is the leading cause of gastroenteritis outbreaks, causing an annual 19-21 million US cases of acute gastroenteritis occur, resulting in 2.27 million outpatient visits, 109,000 hospitalizations, 465,000 emergency department visits, primarily in young children. [19] It contributes to an estimated 900 deaths, mainly affecting children and the elderly. The CDC estimates that norovirus alone causes 58% of cases of food-related illness each year. [19]
Noroviruses are recognized as a common cause of gastroenteritis in new settings, including nursing homes and other healthcare settings, cruise ships, in other travelers, and in immunocompromised patients. Various modes of transmission exist including fecal-oral transmission (predominant), person to person, fecal contamination of food and/or water, fomite transmission, and airborne spread when in close proximity to someone vomiting, as the virus is easily aerosolized. Data from the CDC suggests that the 2024-2025 norovirus season surpassed pre-COVID outbreak levels. [1, 19]
The frequency is seasonal, typically November to April, although acute gastroenteritis outbreaks most frequently occur during the winter (December-February). [1, 19] Cruise ship outbreaks of noroviruses are more common during the summer months.
International data
Acute viral gastroenteritis is a leading cause of infant mortality throughout the world. By age 3 years, virtually all children become infected with the most common agents.
Globally, Norovirus causes an estimated 20% of cases of acute gastroenteritis [19] and is considered the most common of this condition (most common strain: genogroup II genotype 4 [20] ). It is responsible for over 700 million cases annually, [18] with 200 million cases involving children younger than 5 years and resulting in an estimated 50,000 child deaths every year, primarily in developing countries. [4, 19]
The occurrence of noroviruses on cruise ships has led to the use of the term "the cruise ship virus" as another name for these viruses. [21] Some illnesses previously attributed to sea sickness are now recognized to be caused by norovirus infections.
A 2-year retrospective study (2021-2022) comprising data from 8356 adults who presented with acute diarrhea in a tertiary care hospital (real time polymerase chain reaction testing on 8886 stool samples) found 10.3% of cases were caused by enteric viruses, predominantly norovirus (63.8%), and then rotavirus (26.7%) and adenovirus (9.4%). [22]
Race-, sex-, and age-related demographics
Significantly higher mortality is observed among women and non-Hispanic White individuals. [23]
Acute viral gastroenteritis occurs throughout life. Severe cases are seen in the very young and in the elderly. [24] It is a major cause of mortality among children younger than 5 years in developing countries, and persons aged 65 years or older account for the majority of hospitalizations and deaths in the United States. [24] The etiology also varies with age; in infants, most cases are due to rotavirus, whereas in adults, the most common cause is norovirus.
Prognosis
Acute gastroenteritis is generally self-limited and has a good prognosis.
Morbidity/mortality
Severe cases are seen in the elderly, infant, and immunosuppressed populations, including transplant patients.
Rotavirus infantile gastroenteritis is an important cause of infant mortality in the developing world.
In the United States, elderly persons have the highest risk of death from gastroenteritis.
Caliciviruses may kill more people in the United States than do rotaviruses.
Noroviruses are the most common cause of gastroenteritis in nursing homes, and several such outbreaks have resulted in deaths due to aspiration or exacerbation of another chronic disease. Norovirus infections in hospitalized patients are more severe than those seen in otherwise healthy persons. [25]
Complications
Complications of viral gastroenteritis include the following:
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Dehydration
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Malabsorption
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Transient lactose intolerance
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Chronic diarrhea
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Persistent diarrhea
Patient Education
Patients should be educated on the importance and proper methods of oral rehydration and early appropriate feeding.
All patients, especially the parents of infants and young children, must be extensively educated about the signs and symptoms of dehydration.
Patients with food-borne exposures should be educated on deterrence.
Immunocompromised patients and individuals with liver disease should be educated not to consume raw shellfish, especially oysters.
Travelers to underdeveloped areas should be made aware of proper avoidance measures, appropriate treatment, and current endemic illnesses.