The World Health Organization recommends the following:

- Food should be properly cooked and hot when served.

- Consume only pasteurized or boiled milk and milk products, never raw milk products.

- Make sure that ice is from safe water.

- If you are not sure of the safety of drinking water, boil it, or disinfect it with chemical disinfectant.

- Wash hands thoroughly and frequently with soap, especially after using the toilet and after contact with pets and farm animals.

- Wash fruits and vegetables thoroughly, especially if they are to be eaten raw. Peel fruits and vegetables whenever possible.

- Food handlers, professionals and at home, should observe hygienic rules during food preparation.

- Professional food handlers should immediately report to their employer any fever, diarrhea, vomiting or visible infected skin lesions.

The infection is usually self-limiting, and in most cases, symptomatic treatment by liquid and electrolyte replacement is enough in human infections.

Enteroinvasive "Escherichia coli" (EIEC) is a type of pathogenic bacteria whose infection causes a syndrome that is identical to shigellosis, with profuse diarrhea and high fever. EIEC are highly invasive, and they use adhesin proteins to bind to and enter intestinal cells. They produce no toxins, but severely damage the intestinal wall through mechanical cell destruction.

It is closely related to "Shigella".

After the "E. coli" strain penetrates through the epithelial wall, the endocytosis vacuole gets lysed, the strain multiplies using the host cell machinery, and extends to the adjacent epithelial cell. In addition, the plasmid of the strain carries genes for a type III secretion system that is used as the virulent factor. Although it is an invasive disease, the invasion usually does not pass the submucosal layer. The similar pathology to shigellosis may be because both strains of bacteria share some virulent factors. The invasion of the cells can trigger a mild form of diarrhea or dysentery, often mistaken for dysentery caused by "Shigella" species. The illness is characterized by the appearance of blood and mucus in the stools of infected individuals or a condition called colitis.

Dysentery caused by EIEC usually occurs within 12 to 72 hours following the ingestion of contaminated food. The illness is characterized by abdominal cramps, diarrhea, vomiting, fever, chills, and a generalized malaise. Dysentery caused by this organism is generally self-limiting with no known complications.

Enterovirulent classes of "E. coli" are referred to as the EEC group (enterovirulent "E. coli"):

1. Enteroinvasive "E. coli" (EIEC) invades (passes into) the intestinal wall to produce severe diarrhea.

2. Enterohemorrhagic "E. coli" (EHEC): A type of EHEC, "E. coli" 0157:H7, can cause bloody diarrhea and hemolytic uremic syndrome (anemia and kidney failure).

3. Enterotoxigenic "E. coli" (ETEC) produces a toxin that acts on the intestinal lining, and is the most common cause of traveler's diarrhea.

4. Enteropathogenic "E. coli" (EPEC) can cause diarrhea outbreaks in newborn nurseries.

5. Enteroaggregative "E. coli" (EAggEC) can cause acute and chronic (long-lasting) diarrhea in children.

It is currently unknown what foods may harbor EIEC, but any food contaminated with human feces from an ill individual, either directly or via contaminated water, could cause disease in others. Outbreaks have been associated with hamburger meat and unpasteurized milk.

To date, no licensed vaccines specifically target ETEC, though several are in various stages of development. Studies indicate that protective immunity to ETEC develops after natural or experimental infection, suggesting that vaccine-induced ETEC immunity should be feasible and could be an effective preventive strategy. Prevention through vaccination is a critical part of the strategy to reduce the incidence and severity of diarrheal disease due to ETEC, particularly among children in low-resource settings. The development of a vaccine against this infection has been hampered by technical constraints, insufficient support for coordination, and a lack of market forces for research and development. Most vaccine development efforts are taking place in the public sector or as research programs within biotechnology companies. ETEC is a longstanding priority and target for vaccine development for the World Health Organization.

Treatment for ETEC infection includes rehydration therapy and antibiotics, although ETEC is frequently resistant to common antibiotics. Improved sanitation is also key. Since the transmission of this bacterium is fecal contamination of food and water supplies, one way to prevent infection is by improving public and private health facilities. Another simple prevention of infection is by drinking factory bottled water—this is especially important for travelers and traveling military—though it may not be feasible in developing countries, which carry the greatest disease burden.

Some studies reported up to 80% of patients with irritable bowel syndrome (IBS) have SIBO (using the hydrogen breath test). Subsequent studies demonstrated statistically significant reduction in IBS symptoms following therapy for SIBO.

There is a lack of consensus however, regarding the suggested link between IBS and SIBO. Other authors concluded that the abnormal breath results so common in IBS patients do not suggest SIBO, and state that "abnormal fermentation timing and dynamics of the breath test findings support a role for abnormal intestinal bacterial distribution in IBS." There is general consensus that breath tests are abnormal in IBS; however, the disagreement lies in whether this is representative of SIBO. More research is needed to clarifiy this possible link.

The best known of these strains is , but non-O157 strains cause an estimated 36,000 illnesses, 1,000 hospitalizations and 30 deaths in the United States yearly. Food safety specialists recognize "Big Six" strains; O26, O45, O103, O111, O121, and O145. A was caused by another STEC, . This strain has both enteroaggregative and enterohemorrhagic properties. Both the O145 and O104 strains can cause hemolytic-uremic syndrome; the former strain shown to account for 2% to 51% of known HUS cases; an estimated 56% of such cases are caused by O145 and 14% by other EHEC strains.

EHECs that induce bloody diarrhea lead to HUS in 10% of cases. The clinical manifestations of postdiarrheal HUS include acute renal failure, microangiopathic hemolytic anemia, and thrombocytopenia. The verocytotoxin (shiga-like toxin) can directly damage renal and endothelial cells. Thrombocytopenia occurs as platelets are consumed by clotting. Hemolytic anemia results from intravascular fibrin deposition, increased fragility of red blood cells, and fragmentation.

Antibiotics are of questionable value and have not shown to be of clear clinical benefit. Antibiotics that interfere with DNA synthesis, such as fluoroquinolones, have been shown to induce the Stx-bearing bacteriophage and cause increased production of toxins. Attempts to block toxin production with antibacterials which target the ribosomal protein synthesis are conceptually more attractive. Plasma exchange offers a controversial but possibly helpful treatment. The use of antimotility agents (medications that suppress diarrhea by slowing bowel transit) in children under 10 years of age or in elderly patients should be avoided, as they increase the risk of HUS with EHEC infections.

The clinical presentation ranges from a mild and uncomplicated diarrhea to a hemorrhagic colitis with severe abdominal pain. Serotype O157:H7 may trigger an infectious dose with 100 bacterial cells or fewer; other strain such as 104:H4 has also caused an outbreak in Germany 2011. Infections are most common in warmer months and in children under five years of age and are usually acquired from uncooked beef and unpasteurized milk and juice. Initially a non-bloody diarrhea develops in patients after the bacterium attaches to the epithelium or the terminal ileum, cecum, and colon. The subsequent production of toxins mediates the bloody diarrhea. In children, a complication can be hemolytic uremic syndrome which then uses cytotoxins to attack the cells in the gut, so that bacteria can leak out into the blood and cause endothelial injury in locations such as the kidney by binding to globotriaosylceramide (Gb3).

Intestinal bacteria may play a causal role in the dermatological condition rosacea. A recent study subjected patients to a hydrogen breath test to detect the occurrence of SIBO. It was found that significantly more patients were hydrogen-positive than controls indicating the presence of bacterial overgrowth (47% v. 5%, p<0.001).

Hydrogen-positive patients were then given a 10-day course of rifaximin, a non-absorbable antibiotic that does not leave the digestive tract and therefore does not enter the circulation or reach the skin. 96% of patients experienced a complete remission of rosacea symptoms that lasted beyond 9 months. These patients were also negative when retested for bacterial overgrowth. In the 4% of patients that experienced relapse, it was found that bacterial overgrowth had returned. These patients were given a second course of rifaximin which again cleared rosacea symptoms and normalized hydrogen excretion.

In another study, it was found that some rosacea patients that tested hydrogen-negative were still positive for bacterial overgrowth when using a methane breath test instead. These patients showed little improvement with rifaximin, as found in the previous study, but experienced clearance of rosacea symptoms and normalization of methane excretion following administration of the antibiotic metronidazole, which is effective at targeting methanogenic intestinal bacteria.

These results suggest that optimal antibiotic therapy may vary between patients and that diverse species of intestinal bacteria appear to be capable of mediating rosacea symptoms.

This may also explain the improvement in symptoms experienced by some patients when given a reduced carbohydrate diet. Such a diet would restrict the available material necessary for bacterial fermentation and thereby reduce intestinal bacterial populations.

Enterocolitis or coloenteritis is an inflammation of the digestive tract, involving enteritis of the small intestine and colitis of the colon. It may be caused by various infections, with bacteria, viruses, fungi, parasites, or other causes. Common clinical manifestations of enterocolitis are frequent diarrheal defecations, with or without nausea, vomiting, abdominal pain, fever, chills, alteration of general condition. General manifestations are given by the dissemination of the infectious agent or its toxins throughout the body, or – most frequently – by significant losses of water and minerals, the consequence of diarrhea and vomiting.

Among the causal agents of acute enterocolitis are:

- bacteria: "Salmonella", "Shigella", "Escherichia coli", "Campylobacter" etc.;

- viruses: enteroviruses, rotaviruses, Norwalk virus, adenoviruses;

- fungi: candidiasis, especially in immunosuppressed patients or who have previously received prolonged antibiotic treatment;

- parasites: "Giardia lamblia" (with high frequency of infestation in the population, but not always with clinical manifestations), "Balantidium coli", "Blastocystis homnis", "Cryptosporidium" (diarrhea in people with immunosuppression), "Entamoeba histolytica" (produces the amebian dysentery, common in tropical areas).

The Infectious Disease Society of America (IDSA) recommends treating uncomplicated methicillin resistant staph aureus (MRSA) bacteremia with a 14-day course of intravenous vancomycin. Uncomplicated bacteremia is defined as having positive blood cultures for MRSA, but having no evidence of endocarditis, no implanted prostheses, negative blood cultures after 2–4 days of treatment, and signs of clinical improvement after 72 hrs.

The antibiotic treatment of choice for streptococcal and enteroccal infections differs by species. However, it is important to look at the antibiotic resistance pattern for each species from the blood culture to better treat infections caused by resistant organisms.

Specific types of enterocolitis include:

- necrotizing enterocolitis (most common in premature infants)

- pseudomembranous enterocolitis (also called "Pseudomembranous colitis")

The presence of bacteria in the blood almost always requires treatment with antibiotics. This is because there are high mortality rates from progression to sepsis if antibiotics are delayed.

The treatment of bacteremia should begin with empiric antibiotic coverage. Any patient presenting with signs or symptoms of bacteremia or a positive blood culture should be started on intravenous antibiotics. The choice of antibiotic is determined by the most likely source of infection and by the characteristic organisms that typically cause that infection. Other important considerations include the patient's past history of antibiotic use, the severity of the presenting symptoms, and any allergies to antibiotics. Empiric antibiotics should be narrowed, preferably to a single antibiotic, once the blood culture returns with a particular bacteria that has been isolated.

Shigatoxigenic "Escherichia coli (STEC) and verotoxigenic "E. coli (VTEC) are strains of the bacterium "Escherichia coli" that produce either Shiga toxin or Shiga-like toxin (verotoxin). Only a minority of the strains cause illness in humans. The ones that do are collectively known as enterohemorrhagic "E. coli" (EHEC) and are major causes of foodborne illness. When infecting humans, they often cause gastroenteritis, enterocolitis, and bloody diarrhea (hence the name "enterohemorrhagic") and sometimes cause the severe complication of hemolytic-uremic syndrome (HUS). The group and its subgroups are known by various names. They are distinguished from other pathotypes of intestinal pathogenic "E. coli" including enterotoxigenic "E. coli" (ETEC), enteropathogenic "E. coli" (EPEC), enteroinvasive "E. coli" (EIEC), enteroaggregative "E. coli" (EAEC), and diffusely adherent "E. coli" (DAEC).

Mild cases usually do not require treatment and will go away after a few days in healthy people. In cases where symptoms persist or when it is more severe, specific treatments based on the initial cause may be required.

In cases where diarrhoea is present, replenishing fluids lost is recommended, and in cases with prolonged or severe diarrhoea which persists, intravenous rehydration therapy or antibiotics may be required. A simple oral rehydration therapy (ORS) can be made by dissolving one teaspoon of salt, eight teaspoons of sugar and the juice of an orange into one litre of clean water. Studies have shown the efficacy of antibiotics in reducing the duration of the symptoms of infectious enteritis of bacterial origin, however antibiotic treatments are usually not required due to the self-limiting duration of infectious enteritis.

the only form of prevention from viral infection of the neonate is a caesarean section form of delivery if the mother is showing symptoms of infection.

Prevention of neonatal meningitis is primarily intrapartum (during labor) antibiotic prophylaxis (prevention) of pregnant mothers to decrease chance of early-onset meningitis by GBS. For late-onset meningitis, prevention is passed onto the caretakers to stop the spread of infectious microorganisms. Proper hygiene habits are first and foremost, while stopping improper antibiotic use; such as over-prescriptions, use of broad spectrum antibiotics, and extended dosing times will aid prevention of late-onset neonatal meningitis. A possible prevention may be vaccination of mothers against GBS and "E. coli", however, this is still under development.

Travelers often get diarrhea from eating and drinking foods and beverages that have no adverse effects on local residents. This is due to immunity that develops with constant, repeated exposure to pathogenic organisms. The extent and duration of exposure necessary to acquire immunity has not been determined; it may vary with each individual organism. A study among expatriates in Nepal suggests that immunity may take up to seven years to develop—presumably in adults who avoid deliberate pathogen exposure.

Conversely, immunity acquired by American students while living in Mexico disappeared, in one study, as quickly as eight weeks after cessation of exposure.

Dysentery is managed by maintaining fluids by using oral rehydration therapy. If this treatment cannot be adequately maintained due to vomiting or the profuseness of diarrhea, hospital admission may be required for intravenous fluid replacement. In ideal situations, no antimicrobial therapy should be administered until microbiological microscopy and culture studies have established the specific infection involved. When laboratory services are not available, it may be necessary to administer a combination of drugs, including an amoebicidal drug to kill the parasite, and an antibiotic to treat any associated bacterial infection.

If shigellosis is suspected and it is not too severe, letting it run its course may be reasonable — usually less than a week. If the case is severe, antibiotics such as ciprofloxacin or TMP-SMX may be useful. However, many strains of "Shigella" are becoming resistant to common antibiotics, and effective medications are often in short supply in developing countries. If necessary, a doctor may have to reserve antibiotics for those at highest risk for death, including young children, people over 50, and anyone suffering from dehydration or malnutrition.

Amoebic dysentery is often treated with two antimicrobial drug such as metronidazole and paromomycin or iodoquinol.

Recovery from an anaerobic infection depends on adequate and rapid management. The main principles of managing anaerobic infections are neutralizing the toxins produced by anaerobic bacteria, preventing the local proliferation of these organisms by altering the environment and preventing their dissemination and spread to healthy tissues.

Toxin can be neutralized by specific antitoxins, mainly in infections caused by Clostridia (tetanus and botulism). Controlling the environment can be attained by draining the pus, surgical debriding of necrotic tissue, improving blood circulation, alleviating any obstruction and by improving tissue oxygenation. Therapy with hyperbaric oxygen (HBO) may also be useful. The main goal of antimicrobials is in restricting the local and systemic spread of the microorganisms.

The available parenteral antimicrobials for most infections are metronidazole, clindamycin, chloramphenicol, cefoxitin, a penicillin (i.e. ticarcillin, ampicillin, piperacillin) and a beta-lactamase inhibitor (i.e. clavulanic acid, sulbactam, tazobactam), and a carbapenem (imipenem, meropenem, doripenem, ertapenem). An antimicrobial effective against Gram-negative enteric bacilli (i.e. aminoglycoside) or an anti-pseudomonal cephalosporin (i.e. cefepime ) are generally added to metronidazole, and occasionally cefoxitin when treating intra-abdominal infections to provide coverage for these organisms. Clindamycin should not be used as a single agent as empiric therapy for abdominal infections. Penicillin can be added to metronidazole in treating of intracranial, pulmonary and dental infections to provide coverage against microaerophilic streptococci, and Actinomyces.

Oral agents adequate for polymicrobial oral infections include the combinations of amoxicillin plus clavulanate, clindamycin and metronidazole plus a macrolide. Penicillin can be added to metronidazole in the treating dental and intracranial infections to cover "Actinomyces" spp., microaerophilic streptococci, and "Arachnia" spp. A macrolide can be added to metronidazole in treating upper respiratory infections to cover "S. aureus" and aerobic streptococci. Penicillin can be added to clindamycin to supplement its coverage against "Peptostreptococcus" spp. and other Gram-positive anaerobic organisms.

Doxycycline is added to most regimens in the treatment of pelvic infections to cover chlamydia and mycoplasma. Penicillin is effective for bacteremia caused by non-beta lactamase producing bacteria. However, other agents should be used for the therapy of bacteremia caused by beta-lactamase producing bacteria.

Because the length of therapy for anaerobic infections is generally longer than for infections due to aerobic and facultative anaerobic bacteria, oral therapy is often substituted for parenteral treatment. The agents available for oral therapy are limited and include amoxacillin plus clavulanate, clindamycin, chloramphenicol and metronidazole.

In 2010 the American Surgical Society and American Society of Infectious Diseases have updated their guidelines for the treatment of abdominal infections.

The recommendations suggest the following:

For mild-to-moderate community-acquired infections in adults, the agents recommended for empiric regimens are: ticarcillin- clavulanate, cefoxitin, ertapenem, moxifloxacin, or tigecycline as single-agent therapy or combinations of metronidazole with cefazolin, cefuroxime, ceftriaxone, cefotaxime, levofloxacin, or ciprofloxacin. Agents no longer recommended are: cefotetan and clindamycin ( Bacteroides fragilis group resistance) and ampicillin-sulbactam (E. coli resistance) and ainoglycosides (toxicity).

For high risk community-acquired infections in adults, the agents recommended for empiric regimens are: meropenem, imipenem-cilastatin, doripenem, piperacillin-tazobactam, ciprofloxacin or levofloxacin in combination with metronidazole, or ceftazidime or cefepime in combination with metronidazole. Quinolones should not be used unless hospital surveys indicate >90% susceptibility of "E. coli" to quinolones.

Aztreonam plus metronidazole is an alternative, but addition of an agent effective against gram-positive cocci is recommended. The routine use of an aminoglycoside or another second agent effective against gram-negative facultative and aerobic bacilli is not recommended in the absence of evidence that the infection is caused by resistant organisms that require such therapy.

Empiric use of agents effective against enterococci is recommended and agents effective against methicillin-resistant "S. aureus" (MRSA) or yeast is not recommended in the absence of evidence of infection due to such organisms.

Empiric antibiotic therapy for health care-associated intra-abdominal should be driven by local microbiologic results. Empiric coverage of likely pathogens may require multidrug regimens that include agents with expanded spectra of activity against gram-negative aerobic and facultative bacilli. These include meropenem, imipenem-cilastatin, doripenem, piperacillin-tazobactam, or ceftazidime or cefepime in combination with metronidazole. Aminoglycosides or colistin may be required.

Antimicrobial regimens for children include an aminoglycoside-based regimen, a carbapenem (imipenem, meropenem, or ertapenem), a beta-lactam/beta-lactamase-inhibitor combination (piperacillin-tazobactam or ticarcillin-clavulanate), or an advanced-generation cephalosporin (cefotaxime, ceftriaxone, ceftazidime, or cefepime) with metronidazole.

Clinical judgment, personal experience, safety and patient compliance should direct the physician in the choice of the appropriate antimicrobial agents. The length of therapy generally ranges between 2 and 4 weeks, but should be individualized depending on the response. In some instances treatment may be required for as long as 6–8 weeks, but can often be shortened with proper surgical drainage.

"E. histolytica" infections occur in both the intestine and (in people with symptoms) in tissue of the intestine and/or liver. As a result, two different classes of drugs are needed to treat the infection, one for each location. Such anti-amoebic drugs are known as amoebicides.

Recommendations include avoidance of questionable foods and drinks, on the assumption that TD is fundamentally a sanitation failure, leading to bacterial contamination of drinking water and food. While the effectiveness of this strategy has been questioned, given that travelers have little or no control over sanitation in hotels and restaurants, and little evidence supports the contention that food vigilance reduces the risk of contracting TD, guidelines continue to recommend basic, common-sense precautions when making food and beverage choices:

- Maintain good hygiene and use only safe water for drinking and brushing teeth.

- Safe beverages include bottled water, bottled carbonated beverages, and water boiled or appropriately treated by the traveler (as described below). Caution should be exercised with tea, coffee, and other hot beverages that may be only heated, not boiled.

- In restaurants, insist that bottled water be unsealed in your presence; reports of locals filling empty bottles with untreated tap water and reselling them as purified water have surfaced. When in doubt, a bottled carbonated beverage is the safest choice, since it is difficult to simulate carbonation when refilling a used bottle.

- Avoid ice, which may not have been made with safe water.

- Avoid green salads, because the lettuce and other uncooked ingredients are unlikely to have been washed with safe water.

- Avoid eating raw fruits and vegetables unless cleaned and peeled personally.

If handled properly, thoroughly cooked fresh and packaged foods are usually safe. Raw or undercooked meat and seafood should be avoided. Unpasteurized milk, dairy products, mayonnaise, and pastry icing are associated with increased risk for TD, as are foods and beverages purchased from street vendors and other establishments where unhygienic conditions may be present.

Note that, in neonates, sepsis is difficult to diagnose clinically. They may be relatively asymptomatic until hemodynamic and respiratory collapse is imminent, so, if there is even a remote suspicion of sepsis, they are frequently treated with antibiotics empirically until cultures are sufficiently proven to be negative. In addition to fluid resuscitation and supportive care, a common antibiotic regimen in infants with suspected sepsis is a beta-lactam antibiotic (usually ampicillin) in combination with an aminoglycoside (usually gentamicin) or a third-generation cephalosporin (usually cefotaxime—ceftriaxone is generally avoided in neonates due to the theoretical risk of kernicterus.) The organisms which are targeted are species that predominate in the female genitourinary tract and to which neonates are especially vulnerable to, specifically Group B Streptococcus, "Escherichia coli", and "Listeria monocytogenes" (This is the main rationale for using ampicillin versus other beta-lactams.) Of course, neonates are also vulnerable to other common pathogens that can cause meningitis and bacteremia such as "Streptococcus pneumoniae" and "Neisseria meningitidis". Although uncommon, if anaerobic species are suspected (such as in cases where necrotizing enterocolitis or intestinal perforation is a concern, clindamycin is often added.

Granulocyte-macrophage colony stimulating factor (GM-CSF) is sometimes used in neonatal sepsis. However, a 2009 study found that GM-CSF corrects neutropenia if present but it has no effect on reducing sepsis or improving survival.

Trials of probiotics for prevention of neonatal sepsis have generally been too small and statistically underpowered to detect any benefit, but a randomized controlled trial that enrolled 4,556 neonates in India reported that probiotics significantly reduced the risk of developing sepsis. The probiotic used in the trial was "Lactobacillus plantarum".

A very large meta-analysis investigated the effect of probiotics on preventing late-onset sepsis (LOS) in neonates. Probiotics were found to reduce the risk of LOS, but only in babies who were fed human milk exclusively. It is difficult to distinguish if the prevention was a result of the probiotic supplementation or if it was a result of the properties of human milk. It is also still unclear if probiotic administration reduces LOS risk in extremely low birth weight infants due to the limited number of studies that investigated it. Out of the 37 studies included in this systematic review, none indicated any safety problems related to the probiotics. It would be beneficial to clarify the relationship between probiotic supplementation and human milk for future studies in order to prevent late onset sepsis in neonates.

One study suggests that on very long trips in the wilderness, taking multivitamins may reduce the incidence of diarrhea.

It is recommended that breast-fed infants continue to be nursed in the usual fashion, and that formula-fed infants continue their formula immediately after rehydration with ORT. Lactose-free or lactose-reduced formulas usually are not necessary. Children should continue their usual diet during episodes of diarrhea with the exception that foods high in simple sugars should be avoided. The BRAT diet (bananas, rice, applesauce, toast and tea) is no longer recommended, as it contains insufficient nutrients and has no benefit over normal feeding.

Some probiotics have been shown to be beneficial in reducing both the duration of illness and the frequency of stools. They may also be useful in preventing and treating antibiotic associated diarrhea. Fermented milk products (such as yogurt) are similarly beneficial. Zinc supplementation appears to be effective in both treating and preventing diarrhea among children in the developing world.

With correct treatment, most cases of amoebic and bacterial dysentery subside within 10 days, and most individuals achieve a full recovery within two to four weeks after beginning proper treatment. If the disease is left untreated, the prognosis varies with the immune status of the individual patient and the severity of disease. Extreme dehydration can delay recovery and significantly raises the risk for serious complications.

In Germany, 90% of cases of infectious enteritis are caused by four pathogens, Norovirus, Rotavirus, "Campylobacter" and "Salmonella". Other common causes of infectious enteritis include bacteria such as "Shigella" and "E. coli," as well as viruses such as adenovirus, astrovirus and calicivirus. Other less common pathogens include "Bacillus cereus, Clostridium perfringens, Clostridium difficile" and "Staphylococcus aureus".

"Campylobacter jejuni" is one of the most common sources of infectious enteritis, and the most common bacterial pathogen found in 2 year old and smaller children with diarrhoea. It has been linked to consumption of contaminated water and food, most commonly poultry and milk. The disease tends to be less severe in developing countries, due to the constant exposure which people have with the antigen in the environment, leading to early development of antibodies.

Rotavirus is responsible for infecting 140 million people and causing 1 million deaths each year, mostly in children younger than 5 years. This makes it the most common cause of severe childhood diarrhoea and diarrhea-related deaths in the world. It selectively targets mature enterocytes in the small intestine, causing malabsorption, as well as inducing secretion of water. It has also been observed to cause villus ischemia, and increase intestinal motility. The net result of these changes is induced diarrhoea.

Enteritis necroticans is an often fatal illness, caused by β-toxin of "Clostridium perfringens". This causes inflammation and segments of necrosis throughout the gastrointestinal tract. It is most common in developing countries, however has also been documented in post-World War II Germany. Risk factors for enteritis necroticans include decreased trypsin activity, which prevent intestinal degradation of the toxin, and reduced intestinal motility, which increases likelihood of toxin accumulation.