The systemic use of corticosteroids in the context of inflammatory bowel disease.

Many hypotheses have been raised for environmental factors contributing to the pathogenesis of ulcerative colitis. They include the following:

- Diet: as the colon is exposed to many dietary substances which may encourage inflammation, dietary factors have been hypothesized to play a role in the pathogenesis of both ulcerative colitis and Crohn's disease. Few studies have investigated such an association; one study showed no association of refined sugar on the prevalence of ulcerative colitis. High intake of unsaturated fat and vitamin B6 may enhance the risk of developing ulcerative colitis. Other identified dietary factors that may influence the development and/or relapse of the disease include meat protein and alcoholic beverages. Specifically, sulfur has been investigated as being involved in the etiology of ulcerative colitis, but this is controversial. Sulfur restricted diets have been investigated in patients with UC and animal models of the disease. The theory of sulfur as an etiological factor is related to the gut microbiota and mucosal sulfide detoxification in addition to the diet.

- Breastfeeding: Some reports of the protection of breastfeeding in the development of inflammatory bowel disease contradict each other. One Italian study showed a potential protective effect.

- One study of isotretinoin found a small increase in the rate of ulcerative colitis.

The usual treatment is antivirals, specifically ganciclovir or valganciclovir. Severe CMV colitis may lead a colectomy.

Research has not revealed any difference in overall risk of dying in patients with ulcerative colitis from that of the background population. The cause-of-death distribution may be different from that of the background population. It is thought that the disease primarily affects quality of life, and not lifespan.

Specific types of enterocolitis include:

- necrotizing enterocolitis (most common in premature infants)

- pseudomembranous enterocolitis (also called "Pseudomembranous colitis")

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.

Crohn's disease – also known as regional enteritis, it can occur along any surface of the gastrointestinal tract. In 40% of cases it is limited to the small intestine.

Coeliac disease – caused by an autoimmune reaction to gluten by genetically predisposed individuals.

Eosinophilic enteropathy – a condition where eosinophils build up in the gastrointestinal tract and blood vessels, leading to polyp formation, necrosis, inflammation and ulcers. It is most commonly seen in patients with a history of atopy, however is overall relatively uncommon.

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).

As a result of microbial symbiosis and immunity, alterations in enteral bacteria may contribute to inflammatory gut diseases. IBD-affected individuals have been found to have 30–50 percent reduced biodiversity of commensal bacteria, such as decreases in Firmicutes (namely Lachnospiraceae) and Bacteroidetes. Further evidence of the role of gut flora in the cause of inflammatory bowel disease is that IBD-affected individuals are more likely to have been prescribed antibiotics in the 2–5 year period before their diagnosis than unaffected individuals. The enteral bacteria can be altered by environmental factors, such as concentrated milk fats (a common ingredient of processed foods and confectionery) or oral medications such as antibiotics and oral iron preparations.

Incidence and prevalence of microscopic colitis nears those of ulcerative colitis and Crohn’s disease. Recent studies in North America found incidence rates of 7.1 per 100,000 person-years and 12.6 per 100,000 person-years for collagenous colitis for lymphocytic colitis, respectively.

A higher incidence of autoimmune diseases, for example arthritis, Sjögren's syndrome, thyroid disorders, and coeliac disease, has been reported in patients with microscopic colitis. Associations with various drugs have been found, especially proton pump inhibitors, H blockers, selective serotonin reuptake inhibitors (SSRIs), and non-steroidal anti-inflammatory drugs (NSAIDs). Bile acid diarrhea is found in 41% of patients with collagenous colitis and 29% with lymphocytic colitis. Additionally, smoking has been identified as a significant risk factor of microscopic colitis.

The increased incidence of Crohn's in the industrialized world indicates an environmental component. Crohn's is associated with an increased intake of animal protein, milk protein and an increased ratio of omega-6 to omega-3 polyunsaturated fatty acids.

Those who consume vegetable proteins appear to have a lower incidence of Crohn's disease. Consumption of fish protein has no association.

Smoking increases the risk of the return of active disease (flares). The introduction of hormonal contraception in the United States in the 1960s is associated with a dramatic increase in incidence, and one hypothesis is that these drugs work on the digestive system in ways similar to smoking. Isotretinoin is associated with Crohn's. Although stress is sometimes claimed to exacerbate Crohn's disease, there is no concrete evidence to support such claim. Dietary microparticles, such as those found in toothpaste, have been studied as they produce effects on immunity, but they were not consumed in greater amounts in patients with Crohn's.

Chemical colitis is a type of colitis, an inflammation of the large intestine or colon, caused by the introduction of harsh chemicals to the colon by an enema or other procedure. Chemical colitis can resemble ulcerative colitis, infectious colitis and pseudomembranous colitis endoscopically.

Prior to 1950, hydrogen peroxide enemas were commonly used for certain conditions. This practice will often result in chemical colitis.

Soap enemas may also cause chemical colitis.

Harsh chemicals, such as compounds used to clean colonoscopes, are sometimes accidentally introduced into the colon during colonoscopy or other procedures. This can also lead to chemical colitis.

Chemical colitis may trigger a flare of ulcerative colitis or Crohn's colitis. Symptoms of colitis are assessed using the Simple Clinical Colitis Activity Index.

High protein intake, specifically animal protein via meat and fish consumption has been significantly associated with inflammatory bowel disease as well as ulcerative colitis. There was no such association related to plant proteins in the prospective study consisting of over 65,000 patients over a 10-year period. Animal proteins have greater amounts of sulphur containing amino acids such as methionine, which the colonic microflora accrues into hydrogen sulfide, resulting in the pathogenesis of IBD and ulcerative colitis. Such bacteria-derived cell poisons in the form of hydrogen sulfide are specifically elaborated by animal or meat and fish intake, and not by plant foods.

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.

In histology, cryptitis refers to inflammation of an intestinal crypt.

Cryptitis is a non-specific histopathologic finding that is seen in several conditions, e.g. inflammatory bowel disease, diverticular disease, radiation colitis, infectious colitis.

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").

A subtype of infectious colitis is "Clostridium difficile" colitis, which is informally abbreviated as "c diff colitis". It classically forms and is often referred to as pseudomembranous colitis, which is its (nonspecific) histomorphologic description.

Enterohemorrhagic colitis may be caused by Shiga toxin in "Shigella dysenteriae" or "Shigatoxigenic group" of "Escherichia coli" (STEC), which includes serotype and other enterohemorrhagic "E. coli".

Parasitic infections, like those caused by "Entamoeba histolytica", can also cause colitis.

In the developed world "Campylobacter jejuni" is the primary cause of bacterial gastroenteritis, with half of these cases associated with exposure to poultry. In children, bacteria are the cause in about 15% of cases, with the most common types being "Escherichia coli", "Salmonella", "Shigella", and "Campylobacter" species. If food becomes contaminated with bacteria and remains at room temperature for a period of several hours, the bacteria multiply and increase the risk of infection in those who consume the food. Some foods commonly associated with illness include raw or undercooked meat, poultry, seafood, and eggs; raw sprouts; unpasteurized milk and soft cheeses; and fruit and vegetable juices. In the developing world, especially sub-Saharan Africa and Asia, cholera is a common cause of gastroenteritis. This infection is usually transmitted by contaminated water or food.

Toxigenic "Clostridium difficile" is an important cause of diarrhea that occurs more often in the elderly. Infants can carry these bacteria without developing symptoms. It is a common cause of diarrhea in those who are hospitalized and is frequently associated with antibiotic use. "Staphylococcus aureus" infectious diarrhea may also occur in those who have used antibiotics. Acute "traveler's diarrhea" is usually a type of bacterial gastroenteritis, while the persistent form is usually parasitic. Acid-suppressing medication appears to increase the risk of significant infection after exposure to a number of organisms, including "Clostridium difficile", "Salmonella", and "Campylobacter" species. The risk is greater in those taking proton pump inhibitors than with H2 antagonists.

Colitis is an inflammation of the colon. Colitis may be acute and self-limited or long-term. It broadly fits into the category of digestive diseases.

In a medical context, the label "colitis" (without qualification) is used if:

- The cause of the inflammation in the colon is undetermined; for example, "colitis" may be applied to "Crohn's disease" at a time when the diagnosis is unknown, or

- The context is clear; for example, an individual with ulcerative colitis is talking about their disease with a physician who knows the diagnosis.

Crohn's disease can lead to several mechanical complications within the intestines, including obstruction, fistulae, and abscesses. Obstruction typically occurs from strictures or adhesions that narrow the lumen, blocking the passage of the intestinal contents. A fistula can develop between two loops of bowel, between the bowel and bladder, between the bowel and vagina, and between the bowel and skin. Abscesses are walled off concentrations of infection, which can occur in the abdomen or in the perianal area. Crohn's is responsible for 10% of vesicoenteric fistulae, and is the most common cause of ileovesical fistulae.

Crohn's disease also increases the risk of cancer in the area of inflammation. For example, individuals with Crohn's disease involving the small bowel are at higher risk for small intestinal cancer. Similarly, people with Crohn's colitis have a relative risk of 5.6 for developing colon cancer. Screening for colon cancer with colonoscopy is recommended for anyone who has had Crohn's colitis for at least eight years. Some studies suggest there is a role for chemoprotection in the prevention of colorectal cancer in Crohn's involving the colon; two agents have been suggested, folate and mesalamine preparations. Also, immunomodulators and biologic agents used to treat this disease may promote developing extra-intestinal cancers.

Individuals with Crohn's disease are at risk of malnutrition for many reasons, including decreased food intake and malabsorption. The risk increases following resection of the small bowel. Such individuals may require oral supplements to increase their caloric intake, or in severe cases, total parenteral nutrition (TPN). Most people with moderate or severe Crohn's disease are referred to a dietitian for assistance in nutrition.

The major significant complications of Crohn's disease include bowel obstruction, abscesses, free perforation and hemorrhage, which in rare cases may be fatal.

Crohn's disease can be problematic during pregnancy, and some medications can cause adverse outcomes for the fetus or mother. Consultation with an obstetrician and gastroenterologist about Crohn's disease and all medications facilitates preventative measures. In some cases, remission occurs during pregnancy. Certain medications can also lower sperm count or otherwise adversely affect a man's fertility.

Inflammation can spread to other parts of the gut in patients with typhlitis. The condition can also cause the cecum to become distended and can cut off its blood supply. This and other factors can result in necrosis and perforation of the bowel, which can cause peritonitis and sepsis.

Historically, the mortality rate for typhlitis was as high as 50%, mostly because it is frequently associated with bowel perforation. More recent studies have demonstrated better outcomes with prompt medical management, generally with resolution of symptoms with neutrophil recovery without death

Anoscopy can be used to diagnose the majority of cases of proctocolitis.

Proctocolitis has many possible causes. Common infectious causes of proctocolitis include Chlamydia trachomatis, LGV (Lymphogranuloma venereum), Neisseria gonorrhoeae, HSV, and Helicobacter species. It can also be idiopathic (see colitis), vascular (as in ischemic colitis), or autoimmune (as in inflammatory bowel disease).

No definite cause has been determined. Some reports have implicated long-term usage of NSAIDs, proton pump inhibitors, and selective serotonin reuptake inhibitors, and other drugs. Associations with other autoimmune disorders suggests that overactive immune responses occur.