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.

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.

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.

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.

In the majority of cases, amoebas remain in the gastrointestinal tract of the hosts. Severe ulceration of the gastrointestinal mucosal surfaces occurs in less than 16% of cases. In fewer cases, the parasite invades the soft tissues, most commonly the liver. Only rarely are masses formed (amoebomas) that lead to intestinal obstruction.(Mistaken for Ca caecum and appendicular mass) Other local complications include bloody diarrhea, pericolic and pericaecal abscess.

Complications of hepatic amoebiasis includes subdiaphragmatic abscess, perforation of diaphragm to pericardium and pleural cavity, perforation to abdominal cavital "(amoebic peritonitis)" and perforation of skin "(amoebiasis cutis)".

Pulmonary amoebiasis can occur from hepatic lesion by haemotagenous spread and also by perforation of pleural cavity and lung. It can cause lung abscess, pulmono pleural fistula, empyema lung and broncho pleural fistula. It can also reach the brain through blood vessels and cause amoebic brain abscess and amoebic meningoencephalitis. Cutaneous amoebiasis can also occur in skin around sites of colostomy wound, perianal region, region overlying visceral lesion and at the site of drainage of liver abscess.

Urogenital tract amoebiasis derived from intestinal lesion can cause amoebic vulvovaginitis "(May's disease)", rectovesicle fistula and rectovaginal fistula.

"Entamoeba histolytica" infection is associated with malnutrition and stunting of growth.

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.

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.

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

In 2010 it caused about 55,000 deaths worldwide down from 68,000 in 1990.

In older textbooks it is often stated that 10% of the world's population is infected with "Entamoeba histolytica". It is now known that at least 90% of these infections are due to "E. dispar". Nevertheless, this means that there are up to 50 million true "E. histolytica" infections and approximately seventy thousand die each year, mostly from liver abscesses or other complications. Although usually considered a tropical parasite, the first case reported (in 1875) was actually in St Petersburg in Russia, near the Arctic Circle. Infection is more common in warmer areas, but this is both because of poorer hygiene and the parasitic cysts surviving longer in warm moist conditions.

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.

Some intestinal parasitic infections may play a role in irritable bowel syndrome and other long-term sequelae.

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.

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.

human intestinal spirochetosis, also intestinal spirochetes, colonic spirochetosis and colonic spirochetes, is an infection of the colonic-type mucosa with spirochete microorganisms.

The CDC recommends hand-washing and avoiding potentially contaminated food and untreated water.

Boiling suspect water for one minute is the surest method to make water safe to drink and kill disease-causing microorganisms such as "Giardia lamblia" if in doubt about whether water is infected. Chemical disinfectants or filters may be used.

According to a review of the literature from 2000, there is little evidence linking the drinking of water in the North American wilderness and Giardia. CDC surveillance data (for 2005 and 2006) reports one outbreak (6 cases) of waterborne giardiasis contracted from drinking wilderness river water in Colorado. However, less than 1% of reported giardiasis cases are associated with outbreaks.

Person-to-person transmission accounts for the majority of "Giardia" infections and is usually associated with poor hygiene and sanitation. "Giardia" is found on the surface of the ground, in the soil, in undercooked foods, and in water, and on hands without proper cleaning after handling infected feces. Water-borne transmission is associated with the ingestion of contaminated water. In the U.S., outbreaks typically occur in small water systems using inadequately treated surface water. Venereal transmission happens through fecal-oral contamination. Additionally, diaper changing and inadequate hand washing are risk factors for transmission from infected children. Lastly, food-borne epidemics of "Giardia" have developed through the contamination of food by infected food-handlers.

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.

Dysentery may also be caused by shigellosis, an infection by bacteria of the genus "Shigella", and is then known as bacillary dysentery (or Marlow syndrome). The term "bacillary dysentery" etymologically might seem to refer to any dysentery caused by any bacilliform bacteria, but its meaning is restricted by convention to "Shigella" dysentery.

Horses may develop pharyngitis, laryngitis, or esophagitis secondary to indwelling nasogastric tube. Other complications include thrombophlebitis, laminitis (which subsequently reduces survival rate), and weight loss. Horses are also at increased risk of hepatic injury.

Survival rates for DPJ are 25–94%. Horses that survive the incident rarely have reoccurrence.

Colitis X, equine colitis X or peracute toxemic colitis is a catchall term for various fatal forms of acute or peracute colitis found in horses, but particularly a fulminant colitis where clinical signs include sudden onset of severe diarrhea, abdominal pain, shock, and dehydration. Death is common, with 90% to 100% mortality, usually in less than 24 hours. The causative factor may be "Clostridium difficile", but it also may be caused by other intestinal pathogens. Horses under stress appear to be more susceptible to developing colitis X, and like the condition pseudomembranous colitis in humans, there also is an association with prior antibiotic use. Immediate and aggressive treatment can sometimes save the horse, but even in such cases, 75% mortality is considered a best-case scenario.

Human intestinal spirochetosis is caused by "Brachyspira pilosicoli" and "Brachyspira aalborgi". Porcine and avian intestinal spirochetosis are caused by "Brachyspira pilosicoli".

Avoiding food or water that may be contaminated with stool can help prevent the infection of "Cystoisospora" (Isosporiasis). Good hand-washing, and personal-hygiene practices should be used as well. One should wash their hands with soap and warm water after using the toilet, changing diapers, and before handling food (CDC.gov). It is also important to teach children the importance of washing their hands, and how to properly wash their hands.

Patients with ascites underwent routine paracentesis, the incidence of active SBP ranged from 10% to 27% at the time of hospital admission.

The coccidian parasite "Isospora belli" infects the epithelial cells of the small intestine, and is the least common of the three intestinal coccidia that infect humans ("Toxoplasma", "Cryptosporidium", and "Isospora").

Due to the difficulty of exploring host and amebic factors involved in the pathogenesis of amebic liver abscess in humans, most studies have been conducted with animal models (e.g., mice, gerbils, and hamsters). Histopathological findings revealed that the chronic phase of amebic liver abscess in humans corresponds to lytic or liquefactive necrosis, whereas in rodent models there is granulomatous inflammation. However, the use of animal models has provided important information on molecules and mechanisms of the host/parasite interaction in amebic liver abscess.

The incidence of colic can be reduced by restricted access to simple carbohydrates including sugars from feeds with excessive molasses, providing clean feed and drinking water, preventing the ingestion of dirt or sand by using an elevated feeding surface, a regular feeding schedule, regular deworming, regular dental care, a regular diet that does not change substantially in content or proportion and prevention of heatstroke. Horses that bolt their feed are at risk of colic, and several management techniques may be used to slow down the rate of feed consumption.

Supplementing with previously mentioned form of pysllium fiber may reduce risk of sand colic if in a high-risk area. Most supplement forms are given one week per month and available wherever equine feed is purchased.

Turnout is thought to reduce the likelihood of colic, although this has not been proven. It is recommended that a horse receive ideally 18 hours of grazing time each day, as in the wild. However, many times this is difficult to manage with competition horses and those that are boarded, as well as for animals that are easy keepers with access to lush pasture and hence at risk of laminitis. Turnout on a dry lot with lower-quality fodder may have similar beneficial effects.