One of the most common causes of infectious diarrhea, is a lack of clean water. Often, improper fecal disposal leads to contamination of groundwater. This can lead to widespread infection among a population, especially in the absence of water filtration or purification. Human feces contains a variety of potentially harmful human pathogens.

Open defecation is a leading cause of infectious diarrhea leading to death.

Poverty is a good indicator of the rate of infectious diarrhea in a population. This association does not stem from poverty itself, but rather from the conditions under which impoverished people live. The absence of certain resources compromises the ability of the poor to defend themselves against infectious diarrhea. "Poverty is associated with poor housing, crowding, dirt floors, lack of access to clean water or to sanitary disposal of fecal waste (sanitation), cohabitation with domestic animals that may carry human pathogens, and a lack of refrigerated storage for food, all of which increase the frequency of diarrhea... Poverty also restricts the ability to provide age-appropriate, nutritionally balanced diets or to modify diets when diarrhea develops so as to mitigate and repair nutrient losses. The impact is exacerbated by the lack of adequate, available, and affordable medical care."

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.

With most infections, the key is to block the spread of the organism.

- Wash hands frequently

- Eat properly prepared and stored food.

- Bleach soiled laundry

- Vaccinations for "Vibrio cholerae" and rotavirus have been developed. Rotavirus vaccination is recommended for infants in the U.S. Vaccines for "V. cholerae" may be administered to individuals traveling to at-risk areas

Depending on the cause of the inflammation, symptoms may last from one day to more than a week.

Gastroenteritis caused by viruses may last one to two days. Most people recover easily from a short episode of vomiting and diarrhea by drinking clear fluids to replace the fluid that was lost and then gradually progressing to a normal diet. But for others, especially infants and the elderly, the loss of bodily fluid with gastroenteritis can cause dehydration, which can be a life-threatening illness unless it is treated and fluids in the body are replaced.

The primary source of infection is ingestion of fecally contaminated food or water. Attack rates are similar for men and women.

The most important determinant of risk is the traveler's destination. High-risk destinations include developing countries in Latin America, Africa, the Middle East, and Asia. Among backpackers, additional risk factors include drinking untreated surface water and failure to maintain personal hygiene practices and clean cookware. Campsites often have very primitive (if any) sanitation facilities, making them potentially as dangerous as any developing country.

Although traveler's diarrhea usually resolves within three to five days (mean duration: 3.6 days), in about 20% of cases, the illness is severe enough to require bedrest, and in 10%, the illness duration exceeds one week. For those prone to serious infections, such as bacillary dysentery, amoebic dysentery, and cholera, TD can occasionally be life-threatening. Others at higher-than-average risk include young adults, immunosuppressed persons, persons with inflammatory bowel disease or diabetes, and those taking H2 blockers or antacids.

Transmission may occur via consumption of contaminated water, or when people share personal objects. In places with wet and dry seasons, water quality typically worsens during the wet season, and this correlates with the time of outbreaks. In areas of the world with four seasons, infections are more common in the winter. Bottle-feeding of babies with improperly sanitized bottles is a significant cause on a global scale. Transmission rates are also related to poor hygiene, especially among children, in crowded households, and in those with pre-existing poor nutritional status. After developing tolerance, adults may carry certain organisms without exhibiting signs or symptoms, and thus act as natural reservoirs of contagion. While some agents (such as "Shigella") only occur in primates, others may occur in a wide variety of animals (such as "Giardia").

There are a number of non-infectious causes of inflammation of the gastrointestinal tract. Some of the more common include medications (like NSAIDs), certain foods such as lactose (in those who are intolerant), and gluten (in those with celiac disease). Crohn's disease is also a non-infectious source of (often severe) gastroenteritis. Disease secondary to toxins may also occur. Some food-related conditions associated with nausea, vomiting, and diarrhea include: ciguatera poisoning due to consumption of contaminated predatory fish, scombroid associated with the consumption of certain types of spoiled fish, tetrodotoxin poisoning from the consumption of puffer fish among others, and botulism typically due to improperly preserved food.

In the United States, rates of emergency department use for noninfectious gastroenteritis dropped 30% from 2006 until 2011. Of the twenty most common conditions seen in the emergency department, rates of noninfectious gastroenteritis had the largest decrease in visits in that time period.

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.

Smoking has been linked to a variety of disorders of the stomach. Tobacco is known to stimulate acid production and impairs production of the protective mucus. This leads to development of ulcers in the majority of smokers.

Chronic stomach problems have also been linked to excess intake of alcohol. It has been shown that alcohol intake can cause stomach ulcer, gastritis and even stomach cancer. Thus, avoidance of smoking and excess alcohol consumption can help prevent the majority of chronic stomach disorders.

One of the most causes of chronic stomach problems is use of medications. Use of aspirin and other non-steroidal anti-inflammatory drugs to treat various pain disorders can damage lining of the stomach and cause ulcers. Other medications like narcotics can interfere with stomach emptying and cause bloating, nausea, or vomiting.

The majority of chronic stomach problems are treated medically. However, there is evidence that a change in life style may help. Even though there is no specific food responsible for causing chronic stomach problems, experts recommend eating a healthy diet which consists of fruits and vegetables. Lean meat should be limited. Moreover, people should keep a diary of foods that cause problems and avoid them.

Fibromyalgia is a poorly understood pain condition. Lactulose breath testing has shown that patients with fibromyalgia have a more pronounced degree of abnormal results compared to both IBS patients and the general population. This study also demonstrated positive correlation between the amount of pain and the degree of abnormality on the breath test. A subsequent study also demonstrated increased prevalence of intestinal hyperpermeability, which some believe occurs commonly with SIBO.

Insufficient data exists, but "Shigella" is estimated to have caused the death of 34,000 children under the age of five in 2013, and 40,000 deaths in people over five years of age. "Amebiasis" infects over 50 million people each year, of whom 50,000 die.

The prevalence of IBS varies by country and by age range examined. The bar graph at right shows the percentage of the population reporting symptoms of IBS in studies from various geographic regions (see table below for references). The following table contains a list of studies performed in different countries that measured the prevalence of IBS and IBS-like symptoms:

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

Cancers of the stomach are rare and the incidence has been declining worldwide. Stomach cancers usually occur due to fluctuations in acidity level and may present with vague symptoms of abdominal fullness, weight loss and pain. The actual cause of stomach cancer is not known but has been linked to infection with "Helicobacter pylori", pernicious anemia, Menetriere's disease, and nitrogenous preservatives in food.

There is considerable research into the causes, diagnosis and treatments for FGIDs. Diet, microbiome, genetics, neuromuscular function and immunological response all interact. Heightened mast cell activation has been proposed to be a common factor among FGIDs, contributing to visceral hypersensitivity as well as epithelial, neuromuscular, and motility dysfunction.

Dysentery results from viral, bacterial, or parasitic infestations. These pathogens typically reach the large intestine after entering orally, through ingestion of contaminated food or water, oral contact with contaminated objects or hands, and so on.

Each specific pathogen has its own mechanism or pathogenesis, but in general, the result is damage to the intestinal lining, leading to the inflammatory immune response. This can cause elevated temperature, painful spasms of the intestinal muscles (cramping), swelling due to water leaking from capillaries of the intestine (edema), and further tissue damage by the body's immune cells and the chemicals, called cytokines, which are released to fight the infection. The result can be impaired nutrient absorption, excessive water and mineral loss through the stools due to breakdown of the control mechanisms in the intestinal tissue that normally remove water from the stools, and in severe cases, the entry of pathogenic organisms into the bloodstream.

Extensive cellular damage or death is required to cause bleeding. Bacteria can do this either by invading into intestinal mucosa or by secreting toxins that cause cell death. Bacterial infections that cause bloody diarrhea are typically classified as being either invasive or toxogenic. Invasive species cause damage directly by invading into the mucosa. The toxogenic species do not invade, but cause cellular damage by secreting toxins, resulting in bloody diarrhea. This is also in contrast to toxins that cause watery diarrhea, which usually do not cause cellular damage, but rather they take over cellular machinery for a portion of life of the cell.

Some microorganisms – for example, bacteria of the genus "Shigella" – secrete substances known as cytotoxins, which kill and damage intestinal tissue on contact. Shigella is thought to cause bleeding due to invasion rather than toxin, because even non-toxogenic strains can cause dysentery, but E. coli with shiga-like toxins do not invade the intestinal mucosa, and are therefore toxin dependent. Viruses directly attack the intestinal cells, taking over their metabolic machinery to make copies of themselves, which leads to cell death.

Definitions of dysentery can vary by region and by medical specialty. The U. S. Centers for Disease Control and Prevention (CDC) limits its definition to "diarrhea with visible blood". Others define the term more broadly. These differences in definition must be taken into account when defining mechanisms. For example, using the CDC definition requires that intestinal tissue be so severely damaged that blood vessels have ruptured, allowing visible quantities of blood to be lost with defecation. Other definitions require less specific damage.

The risk of acquiring infectious diarrhea in the wilderness arises from inadvertent ingestion of pathogens. Various studies have sought to estimate diarrhea attack rates among wilderness travelers, and results have ranged widely. The variation of diarrhea rate between studies may depend on the time of year, the location of the study, the length of time the hikers were in the wilderness,

the prevention methods used, and the study methodology.

The National Outdoor Leadership School (NOLS), which emphasizes strict hand-washing techniques, water disinfection and washing of common cooking utensils in their programs, reports that gastrointestinal illnesses occurred at a rate of only 0.26 per 1000 program days. In contrast, a survey of long-distance Appalachian Trail hikers found more than half the respondents reported at least one episode of diarrhea that lasted an average of two days. (Infectious diarrhea may last longer than an average of two days; certain forms of non-infectious diarrhea, caused by diet change etc., can be of very brief duration). Analysis of this survey found occurrence of diarrhea was positively associated with the duration of exposure in the wilderness. During any given four-week period, as many as 7.2% of Americans may experience some form of infectious or non-infectious diarrhea. A number of behaviors each individually reduced the incidence of diarrhea: treating water; routinely washing hands with soap and water after defecation and urination; cleaning cooking utensils with soap and warm water; and taking multi-vitamins.

A variety of pathogens can cause infectious diarrhea, and most cases among backpackers appear to be caused by bacteria from feces. A study at Grand Teton National Park found 69% of diarrhea affected visitors had no identifiable cause, that 23% had diarrhea due to "Campylobacter" and 8% of patients with diarrhea had giardiasis. Campylobacter enteritis occurred most frequently in young adults who had hiked in wilderness areas and drunk untreated surface water in the week prior. Another study tested 35 individuals before and after a trip to the Desolation Wilderness of California. Giardia cysts were found in fecal samples from two people after the trip, but they were asymptomatic. A third person was empirically treated for symptoms of giardiasis.

Fecal-oral transmission may be the most common vector for wilderness acquired diarrhea. There are differing opinions regarding the importance of routine disinfection of water during relatively brief backcountry visits.

While the causes of IBS are still unknown, it is believed that the entire gut–brain axis is affected.

The risk of developing IBS increases six-fold after acute gastrointestinal infection. Postinfection, further risk factors are young age, prolonged fever, anxiety, and depression. Psychological factors, such as depression or anxiety, have not been shown to cause or influence the onset of IBS, but may play a role in the persistence and perceived severity of symptoms. Nevertheless, they may worsen IBS symptoms and the patient quality of life. Antibiotic use also appears to increase the risk of developing IBS. Research has found that genetic defects in innate immunity and epithelial homeostasis increase the risk of developing both post-infectious as well as other forms of IBS.

To date, the precise causative factor has not been verified, and the disease has been attributed by various sources to viruses, parasites, bacteria, use of antibiotics and sulfonamides, and heavy metal poisoning. Other possible causes include peracute salmonellosis, clostridial enterocolitis, and endotoxemia. "Clostridium difficile" toxins isolated in the horse have a genotype like the current human "epidemic strain", which is associated with human "C. difficile"-associated disease of greater than historical severity. "C. difficile" can cause pseudomembranous colitis in humans, and in hospitalized patients who develop it, fulminant "C. difficile" colitis is a significant and increasing cause of death.

Horses under stress appear to be more susceptible to developing colitis X. Disease onset is often closely associated with surgery or transport. Excess protein and lack of cellulose content in the diet (a diet heavy on grain and lacking adequate hay or similar roughage) is thought to be the trigger for the multiplication of clostridial organisms. A similar condition may be seen after administration of tetracycline or lincomycin to horses. These factors may be one reason the condition often develops in race horses, having been responsible for the deaths of the Thoroughbred filly Landaluce,

the Quarter Horse stallion Lightning Bar,

and is one theory for the sudden death of Kentucky Derby winner Swale.

The link to stress suggests the condition may be brought on by changes in the microflora of the cecum and colon that lower the number of anaerobic bacteria, increase the number of Gram-negative enteric bacteria, and decrease anaerobic fermentation of soluble carbohydrates, resulting in damage to the cecal and colonic mucosa and allowing increased absorption of endotoxins from the lumen of the gut.

The causative agent may be "Clostridium perfringens", type A, but the bacteria are recoverable only in the preliminary stages of the disease.

The suspect toxin could also be a form of "Clostridium difficile". In a 2009 study at the University of Arizona, "C. difficile" toxins A and B were detected, large numbers of "C. difficile" were isolated, and genetic characterization revealed them to be North American pulsed-field gel electrophoresis type 1, polymerase chain reaction ribotype 027, and toxinotype III. Genes for the binary toxin were present, and toxin negative-regulator tcdC contained an 18-bp deletion. The individual animal studied in this case was diagnosed as having peracute typhlocolitis, with lesions and history typical of those attributed to colitis X.

Use of antibiotics may also be associated with some forms of colitis-X. In humans, "C. difficile" is the most serious cause of antibiotic-associated diarrhea, often a result of eradication of the normal gut flora by antibiotics. In one equine study, colitis was induced after pretreatment with clindamycin and lincomycin, followed by intestinal content from horses which had died from naturally occurring idiopathic colitis. (A classic adverse effect of clindamycin in humans is "C. difficile"-associated diarrhea.) In the experiment, the treated horses died. After necropsy, "Clostridium cadaveris" was present, and is proposed as another possible causative agent in some cases of fatal colitis.

Treatment for colitis-X usually does not save the horse. The prognosis is average to poor, and mortality is 90% to 100%. However, treatments are available, and one famous horse that survived colitis-X was U.S. Triple Crown winner Seattle Slew, that survived colitis-X in 1978 and went on to race as a four-year-old.

Large amounts of intravenous fluids are needed to counter the severe dehydration, and electrolyte replacement is often necessary. Flunixin meglumine (Banamine) may help block the effects of toxemia. Mortality rate has been theorized to fall to 75% if treatment is prompt and aggressive, including administration of not only fluids and electrolytes, but also blood plasma, anti-inflammatory and analgesic drugs, and antibiotics. Preventing dehydration is extremely important. Nutrition is also important. Either parenteral or normal feeding can be used to support the stressed metabolism of the sick horse. Finally, the use of probiotics is considered beneficial in the restoration of the normal intestinal flora. The probiotics most often used for this purpose contain "Lactobacillus" and "Bifidobacterium".

Functional gastrointestinal disorders (FGID) include a number of separate idiopathic disorders which affect different parts of the gastrointestinal tract and involve visceral hypersensitivity and impaired gastrointestinal motility.

Specific types of enterocolitis include:

- necrotizing enterocolitis (most common in premature infants)

- pseudomembranous enterocolitis (also called "Pseudomembranous colitis")

The causes are divided into benign or malignant.

- Benign

- Peptic ulcer disease

- Infections, such as tuberculosis; and infiltrative diseases, such as amyloidosis.

- A rare cause of gastric outlet obstruction is blockage with a gallstone, also termed "Bouveret's syndrome".

- In children congenital pyloric stenosis / congenital hypertrophic pyloric stenosis may be a cause.

- A pancreatic pseudocyst can cause gastric compression.

- Pyloric mucosal diaphragm could be a rare cause.

- Malignant

- Tumours of the stomach, including adenocarcinoma (and its linitis plastica variant), lymphoma, and gastrointestinal stromal tumours

An increasing number of people are now surviving cancer, with improved treatments producing cure of the malignancy (cancer survivors). There are now over 14 million such people in the US, and this figure is expected to increase to 18 million by 2022. More than half are survivors of abdominal or pelvic cancers, with about 300,000 people receiving abdominal and pelvic radiation each year. It has been estimated there are 1.6 million people in the US with post-radiation intestinal dysfunction, a greater number than those with inflammatory bowel disease such as Crohn's disease or ulcerative colitis.