The word "gastroenteritis" originates from the Greek word gastron, meaning "stomach," and enteron, meaning "small intestine." So the word "gastroenteritis" means "inflammation of the stomach and small intestine." Medically, gastroenteritis is defined as a diarrheal disease, in other words, an increase in bowel movement frequency with or without vomiting, fever, and abdominal pain. An increase in bowel movement frequency is defined by three or more watery or loose bowel movements in 24 hours or at least 200 grams of stool per day. It is classified in many ways, but according to the duration of symptoms, it is described as acute, persistent, chronic, or recurrent.
Causes of gastroenteritis include bacterial, viral, fungal, and parasitic, but this article will focus on bacterial causes. Causes of infectious diarrhea vary among different geographical regions, urban to rural areas, and depend on co-morbidities and host immune status. However, the most common cause of acute infectious diarrhea are viruses (norovirus, rotavirus, adenovirus, and others). This is indicated by the observation that stool cultures are positive in less than 5% of cases in most studies. Other than norovirus, important causes of watery diarrhea include Clostridium perfringens, and enterotoxigenic Escherichia coli (ETEC). Bacterial causes are more responsible for severe cases of infectious diarrhea than other infectious etiologies. For example, a single study found that in otherwise healthy adults with diagnosed severe diarrheal illness, defined as greater than or equal to four watery/loose stools per day for 3 or more days, a bacterial pathogen was identified in 87% of cases. Among these severe bacterial causes, nontyphoidal Salmonella and Campylobacter spp are the most common causes in the United States. The incidence rate per 100,000 persons in 2016 was estimated by the Centers for Disease Control and Prevention controlled active surveillance program, FoodNet, survey with results as follows:
Acute infectious diarrhea is a very common disease worldwide, even in a developed country like the United States. It is among the leading causes of illness globally and associated with 1.5 to 2.5 million deaths per year. In children younger than 5 years, diarrheal disease is the second most common cause of death by infectious diseases. Worldwide, it affects more than 3 to 5 billion children each year. In the United States, there are more than 350 million cases of acute gastroenteritis annually, and among these, food-borne bacteria are the cause of 48 million cases. It accounts for 1.5 million visits to primary care doctors each year and approximately 200,000 hospital admissions of children under 5 years of age. In the United States, it rarely causes death, but it is still responsible for 300 deaths per year. In general, developed countries like the United States, the United Kingdom, and Canada have lower hospital admissions rates in comparison to developing countries. Traveler's diarrhea affects more than 50% of people traveling from developed to developing countries. In the United States, children under 5 years of age are admitted to the hospital in 9 out of 1000 cases per year. In the United Kingdom and Australia, the admission rate is around 12 per 1000 annually. Additionally, the prevalence of Clostridium difficile is also increasing in adults and children.
The gut bacteria cause diarrhea by different mechanisms including adherence, mucosal invasion, and toxin production. Knowledge of pathophysiology and the mechanism of these pathogenic strategies also help in the evaluation and management of the disease. One of the main functions of the small intestine is to absorb fluids. With the disorder of the small intestine, the fluid does not get absorbed properly, and the action of different toxins causes the intestinal lining to start excreting fluid which results in relatively loose or watery stools.
Inoculum size is one of the important virulence factors that cause pathology. For Shigella and enterohemorrhagic Escherichia coli (EHEC), at a minimum of 10–100 bacteria can cause infection, while one hundred thousand or one million of Vibrio cholerae bacteria are required to cause infection. For this reason, infective doses of different pathogens differ in a great range and depend on the host as well as bacteria.
Adherence is another virulence factor for enteric pathogens. Some bacteria need to adhere themselves to the mucosal lining of the gastrointestinal tract initially. They produce various adhesins and other cell-surface proteins which help them to attach to intestinal cells. V. cholerae, for example, adheres to the brush border of small-intestinal enterocytes via specific surface adhesins, including the toxin-coregulated pilus and other accessory colonization factors. Enterotoxigenic E. coli, which causes watery diarrhea, produces an adherence protein called colonization factor antigen. This is necessary for colonization of the upper small intestine by the organism before the production of enterotoxin, causing disease.
Both cytotoxin production and bacterial invasion and destruction of intestinal mucosal cells can cause dysentery. Shigella and enteroinvasive E. coli infections are characterized by the organisms’ invasion of mucosal epithelial cells, intraepithelial multiplication, and subsequent spread to adjacent cells.
Toxin production is another important virulence factor. These toxins include enterotoxins, which cause watery diarrhea by acting directly on secretory mechanisms in the intestinal mucosa, and cytotoxins, which destroy mucosal cells and associated inflammatory diarrhea.
GI infectious diseases can cause mucosal inflammation which represents various patterns of tissue response. Histologic patterns of GI infections can be classified as follows:
Campylobacter jejuni, Shigella spp, Salmonella spp, Yersinia and E. coli and few other pathogens all have resembling histopathology. The histopathological picture shows a thick layer of mucosa and cluster of bacteria plus neutrophils in the intraepithelial surface; neutrophils accumulate in the lumen and the basal part of the intestinal crypts as well.
The most common history findings for a patient with gastroenteritis are as follows:
On physical examination, the abdomen would be soft, but there may be voluntary guarding. Palpation may elicit mild to moderate tenderness. Fever suggests the cause is invasive pathogens. Signs of dehydration are the most important thing to look for while performing the physical examination; some cases may be alarming and help to identify that which patient needs hospitalization. The following are red flags:
Initial evaluation requires good history taking and physical exam, particularly food and medical history, an assessment of duration, frequency, current volume status, and any other alarming signs and symptoms of the patient. Many cases of acute bacterial gastroenteritis may not require any testing to determine a specific etiology, but in a case of severe volume depletion, a serum electrolyte panel should be indicated to check for any electrolyte derangements. A complete blood count cannot distinguish between bacterial etiologies but helps in suggesting severe disease or potential complications, for example, a high white blood count indicates invasive bacteria or pseudomembranous colitis and low platelets counts indicate the development of the hemolytic-uremic syndrome. Blood culture should be obtained in a patient with high fever or other severe constitutional symptoms.
Stool testing for bacterial pathogens is indicated in the presence of severe illness (e.g., signs of dehydration/hypovolemia, severe abdominal pain, or need for hospitalization) high-risk host features (e.g., pregnant women, age greater than 70 years, immunocompromised state, or other co-morbidities), and other signs and symptoms of inflammatory diarrhea (e.g., mucus or blood in diarrhea, high-grade fever). A routine stool culture can identify three common bacteria: Salmonella, Campylobacter, and Shigella. Suspicion of other bacterial pathogens (e.g., Vibrio, Yersinia, Aeromonas, and Listeria) should warrant specific microbiology and culture analysis. In case of bloody diarrhea, additional testing for Shiga toxin and leukocytes in stool for EHEC should be ordered in addition to stool culture. In case of persistent diarrhea, the practitioner should send stool samples for ova and parasite testing.
The majority of cases of noninflammatory diarrhea are self-limited.
Differential diagnosis of acute bacterial gastroenteritis includes other causes of gastroenteritis such as viral and parasitic gastroenteritis. Common foodborne illnesses also should be considered in differentials. Other diseases that can cause watery diarrhea are Crohn disease, pseudomembranous colitis, microscopic colitis, acute HIV infection, irritable bowel disease, and lactose intolerance. Bloody diarrheal disease other than dysentery includes ulcerative colitis. Celiac disease and malabsorption syndromes also cause diarrhea.
Dehydration and depletion of electrolytes are the most common complications above all. Other complications that are common after acute gastroenteritis are the transformation of acute into chronic diarrhea which can lead to lactose intolerance or small-bowel bacterial overgrowth. Some other post-diarrhea complications include exacerbation of inflammatory bowel disease, septicemia, enteric fever, and Guillain-Barre syndrome, a complication likely after Campylobacter infection. Reactive arthritis may occur, particularly after Shigella, Salmonella, Campylobacter, or Yersinia.
The diagnosis and management of bacterial gastroenteritis is best done with an interprofessional team that includes the primary care provider, nurse practitioner, infectious disease consult and the emergency department physician. The key aim of treatment is to prevent dehydration and electrolyte alterations. The majority can be treated as outpatients but children and the elderly may require admission, depending on their hydration status. Some other post-diarrhea complications include exacerbation of inflammatory bowel disease, septicemia, enteric fever, and Guillain-Barre syndrome, a complication likely after Campylobacter infection. Reactive arthritis may occur, particularly after Shigella, Salmonella, Campylobacter, or Yersinia. With proper treatment the outcomes are excellent but any delay in treatment can lead to significant morbidity and mortality. 
|||Typhoidal Salmonella serovars: Ecological opportunity and the evolution of a new pathovar., Hiyoshi H,Tiffany CR,Bronner DN,Bäumler AJ,, FEMS microbiology reviews, 2018 May 21 [PubMed PMID: 29790924]|
|||Evaluating Previous Antibiotic Use as a Risk Factor for Acute Gastroenteritis Among Children in Davidson County, Tennessee, 2014-2015., Kolsin JM,Lopman BA,Payne DC,Wikswo ME,Dunn JR,Halasa NB,Hall AJ,, Journal of the Pediatric Infectious Diseases Society, 2018 May 19 [PubMed PMID: 29788403]|
|||Virulence Factors in Salmonella Typhimurium: The Sagacity of a Bacterium., Dos Santos AMP,Ferrari RG,Conte-Junior CA,, Current microbiology, 2018 May 21 [PubMed PMID: 29785632]|
|||Epidemiology of acute diarrhea caused by rotavirus in sentinel surveillance sites of Vietnam, 2012-2015., Huyen DTT,Hong DT,Trung NT,Hoa TTN,Oanh NK,Thang HV,Thao NTT,Hung DM,Iijima M,Fox K,Grabovac V,Heffelfinger J,Batmunkh N,Anh DD,, Vaccine, 2018 May 18 [PubMed PMID: 29784467]|
|||Correlative study between C-reactive protein, clinical severity, and nerve conduction studies in Guillain-Barrè syndrome., Altaweel YA,Abdelaziz S,Fathy HA,AbdelBadea S,, The Egyptian journal of neurology, psychiatry and neurosurgery, 2018 [PubMed PMID: 29780224]|
|||Gut microbiome analysis identifies potential aetiological factors in acute gastroenteritis., Castaño-Rodríguez N,Underwood AP,Merif J,Riordan SM,Rawlinson WD,Mitchell HM,Kaakoush NO,, Infection and immunity, 2018 Apr 23 [PubMed PMID: 29685983]|
|||Organoid and Enteroid Modeling of <i>Salmonella</i> Infection., Yin Y,Zhou D,, Frontiers in cellular and infection microbiology, 2018 [PubMed PMID: 29670862]|
|||Hospitalisations due to bacterial gastroenteritis: A comparison of surveillance and hospital discharge data., Scallan E,Griffin PM,McLean HQ,Mahon BE,, Epidemiology and infection, 2018 Apr 15 [PubMed PMID: 29655383]|
|||Epidemiologic characteristics of health care-associated outbreaks and lessons learned from multiple outbreak investigations with a focus on the usefulness of routine molecular analysis., Kanamori H,Weber DJ,Gergen MF,DiBiase LM,Sickbert-Bennett EE,Rutala WA,, American journal of infection control, 2018 Mar 16 [PubMed PMID: 29555145]|
|||Menta PLR,Andrade MER,Leocádio PCL,Fraga JR,Dias MTS,Cara DC,Cardoso VN,Borges LF,Capettini LSA,Aguilar EC,Alvarez-Leite JI, Wheat gluten intake increases the severity of experimental colitis and bacterial translocation by weakening of the proteins of the junctional complex. The British journal of nutrition. 2018 Dec 17; [PubMed PMID: 30554574]|
|||Mathew S,Smatti MK,Al Ansari K,Nasrallah GK,Al Thani AA,Yassine HM, Mixed Viral-Bacterial Infections and Their Effects on Gut Microbiota and Clinical Illnesses in Children. Scientific reports. 2019 Jan 29; [PubMed PMID: 30696865]|
|||Shelke YP,Deotale VS,Maraskolhe DL, Spectrum of infections in acute febrile illness in central India. Indian journal of medical microbiology. 2017 Oct-Dec; [PubMed PMID: 29405137]|