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.

Small intestine bacterial overgrowth (SIBO), also termed bacterial overgrowths, or small bowel bacterial overgrowth syndrome (SBBOS), is a disorder of excessive bacterial growth in the small intestine. Unlike the colon (or large bowel), which is rich with bacteria, the small bowel usually has fewer than 10,000 organisms per millilitre. Patients with bacterial overgrowth typically develop symptoms including nausea, bloating, vomiting, diarrhea, malnutrition, weight loss and malabsorption, which is caused by a number of mechanisms.

The diagnosis of bacterial overgrowth is made by a number of techniques, with the gold standard being an aspirate from the jejunum that grows in excess of 10 bacteria per millilitre. Risk factors for the development of bacterial overgrowth include dysmotility; anatomical disturbances in the bowel, including fistulae, diverticula and blind loops created after surgery, and resection of the ileo-cecal valve; gastroenteritis-induced alterations to the small intestine; and the use of certain medications, including proton pump inhibitors.

Small bowel bacterial overgrowth syndrome is treated with an elemental diet or antibiotics, which may be given in a cyclic fashion to prevent tolerance to the antibiotics, sometimes followed by prokinetic drugs to prevent recurrence if dysmotility is a suspected cause.

Bacterial overgrowth can cause a variety of symptoms, many of which are also found in other conditions, making the diagnosis challenging at times. Many of the symptoms are due to malabsorption of nutrients due to the effects of bacteria which either metabolize nutrients or cause inflammation of the small bowel, impairing absorption. The symptoms of bacterial overgrowth include nausea, flatus, constipation, bloating, abdominal distension, abdominal pain or discomfort, diarrhea, fatigue, and weakness. SIBO also causes an increased permeability of the small intestine. Some patients may lose weight. Children with bacterial overgrowth may develop malnutrition and have difficulty attaining proper growth. Steatorrhea, a sticky type of diarrhea where fats are not properly absorbed and spill into the stool, may also occur.

Patients with bacterial overgrowth that is longstanding can develop complications of their illness as a result of malabsorption of nutrients. Anemia may occur from a variety of mechanisms, as many of the nutrients involved in production of red blood cells are absorbed in the affected small bowel. Iron is absorbed in the more proximal parts of the small bowel, the duodenum and jejunum, and patients with malabsorption of iron can develop a microcytic anemia, with small red blood cells. Vitamin B is absorbed in the last part of the small bowel, the ileum, and patients who malabsorb vitamin B can develop a megaloblastic anemia with large red blood cells.

In older adults, small bowel bacterial overgrowth is associated with a higher frequency of diarrhea, a lower body mass index, and a significantly lower serum albumin concentration.

Colitis-X is a term used for colitis cases in which no definitive diagnosis can be made and the horse dies. Clinical signs include sudden, watery diarrhea that is usually accompanied by symptoms of hypovolemic shock and usually leads to death in 3 to 48 hours, usually in less than 24 hours. Other clinical signs include tachycardia, tachypnea, and a weak pulse. Marked depression is present. An explosive diarrhea develops, resulting in extreme dehydration. Hypovolemic and endotoxic shock are manifest by increased capillary refill time, congested or cyanotic (purplish) mucous membranes, and cold extremities. While there may initially be a fever, temperature usually returns to normal.

Clinical signs are similar to those of other diarrheal diseases, including toxemia caused by "Clostridium", Potomac horse fever, experimental endotoxic shock, and anaphylaxis.

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

The most common form of dysentery is bacillary dysentery, which is typically a mild illness, causing symptoms normally consisting of mild stomach pains and frequent passage of stool or diarrhea. Symptoms normally present themselves after one to three days, and are usually no longer present after a week. The frequency of urges to defecate, the large volume of liquid feces passed, and the presence of mucus, pus, and blood depends on the pathogen causing the disease. Temporary lactose intolerance can occur, as well. In some caustic occasions severe abdominal pain, fever, shock, and delirium can all be symptoms.

In extreme cases, dysentery patients may pass more than one litre of fluid per hour. More often, individuals will complain of nausea, abdominal pain, and frequent watery and usually foul-smelling diarrhea, accompanied by mucus, blood, rectal pain, and fever. Vomiting, rapid weight-loss, and generalized muscle aches sometimes also accompany dysentery. On rare occasions, the amoebic parasite will invade the body through the bloodstream and spread beyond the intestines. In such cases, it may more seriously infect other organs such as the brain, lungs, and most commonly the liver.

Signs and symptoms of enteritis are highly variable and vary based on the specific cause and other factors such as individual variance and stage of disease.

Symptoms may include abdominal pain, cramping, diarrhoea, dehydration, fever, nausea, vomiting and weight loss.

Dysentery is a type of gastroenteritis that results in diarrhea with blood. Other symptoms may include fever, abdominal pain, and a feeling of incomplete defecation.

It is caused by several types of infections such as bacteria, viruses, parasitic worms, or protozoa. The mechanism is an inflammatory disorder of the intestine, especially of the colon.

The onset of TD usually occurs within the first week of travel, but may occur at any time while traveling, and even after returning home, depending on the incubation period of the infectious agent. Bacterial TD typically begins abruptly, but "Cryptosporidium" may incubate for seven days, and "Giardia" for 14 days or more, before symptoms develop. Typically, a traveler experiences four to five loose or watery bowel movements each day. Other commonly associated symptoms are abdominal cramping, bloating, fever, and malaise. Appetite may decrease significantly. Though unpleasant, most cases of TD are mild, and resolve in a few days without medical intervention.

Blood or mucus in the diarrhea, significant abdominal pain, or high fever suggests a more serious cause, such as cholera, characterized by a rapid onset of weakness and torrents of watery diarrhea with flecks of mucus (described as "rice water" stools). Medical care should be sought in such cases; dehydration is a serious consequence of cholera, and may trigger serious sequelae—including, in rare instances, death—as rapidly as 24 hours after onset if not addressed promptly.

Infection causes acute, non-bloody diarrhea with crampy abdominal pain, which can last for weeks and result in malabsorption and weight loss. In immunodepressed patients, and in infants and children, the diarrhea can be severe. Eosinophilia may be present (differently from other protozoan infections).

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.

Enteritis is inflammation of the small intestine. It is most commonly caused by food or drink contaminated with pathogenic microbes. but may have other causes such as NSAIDs, cocaine, radiation therapy as well as autoimmune conditions like Crohn's disease and coeliac disease. Symptoms include abdominal pain, cramping, diarrhoea, dehydration, and fever. Related diseases include inflammation of the stomach (gastritis) and large intestine (colitis).

Duodenitis, jejunitis and ileitis are subtypes of enteritis which are only localised to a specific part of the small intestine. Inflammation of both the stomach and small intestine is referred to as gastroenteritis. Inflammation of related organs of the gastrointestinal system are:

- gastritis

- gastroenteritis

- colitis

- enterocolitis

Symptoms vary from none to severe diarrhea with poor absorption of nutrients. It can result in weakness, loss of appetite, stomach cramps, vomiting, bloating, excessive gas, and burping. Symptoms typically develop 9–15 days after exposure, but may occur as early as one day.

Symptoms are caused by "Giardia" organisms infecting the cells of the duodenum and jejunum of the small intestine and blocking nutrient absorption. Most people are asymptomatic; only about a third of those infected exhibit symptoms. If the infection is not treated, these symptoms may last for six weeks or more.

Symptomatic infections are well recognized as causing lactose intolerance, which, while usually temporary, may become permanent. Although hydrogen breath tests indicate poorer rates of carbohydrate absorption in those asymptomatically infected, such tests are not diagnostic of infection. It has been suggested that these observations are explained by symptomatic giardia infection allowing for the overgrowth of other bacteria.

Some studies have shown giardiasis should be considered as a cause of vitamin B deficiency as a result of the problems caused within the intestinal absorption system.

The average incubation periods for giardiasis and cryptosporidiosis are each 7 days. Certain other bacterial and viral agents have shorter incubation periods, although hepatitis may take weeks to manifest itself. The onset usually occurs within the first week of return from the field, but may also occur at any time while hiking.

Most cases begin abruptly and usually result in increased frequency, volume, and weight of stool. Typically, a hiker experiences at least four to five loose or watery bowel movements each day. Other commonly associated symptoms are nausea, vomiting, abdominal cramping, bloating, low fever, urgency, and malaise, and usually the appetite is affected. The condition is much more serious if there is blood or mucus in stools, abdominal pain, or high fever. Dehydration is a possibility. Life-threatening illness resulting from WAD is extremely rare but can occur in people with weakened immune systems.

Some people may be carriers and not exhibit symptoms.

No clear association exists with complaints. However, potential associations exist with include watery diarrhea and abdominal pain, which may be seen with blood; these findings are not specific, i.e. may be seen due to number of other causes.

Isosporiasis, also known as cystoisosporiasis, is a human intestinal disease caused by the parasite "Isospora belli" (now known as "Cystoisospora belli"). It is found worldwide, especially in tropical and subtropical areas. Infection often occurs in immuno-compromised individuals, notably AIDS patients, and outbreaks have been reported in institutionalized groups in the United States. The first documented case was in 1915. It is usually spread indirectly, normally through contaminated food or water (CDC.gov).

Signs and symptoms depend on the type of infection. Intestinal parasites produce a variety of symptoms in those affected, most of which manifest themselves in gastrointestinal complications and general weakness. Gastrointestinal complications include diarrhea, nausea, dysentery, and abdominal pain. These symptoms negatively impact nutritional status, including decreased absorption of micronutrients, loss of appetite, weight loss, and intestinal blood loss that can often result in anemia. It may also cause physical and mental disabilities, delayed growth in children, and skin irritation around the anus and vulva.

Traveler's diarrhea (TD) is a stomach and intestinal infection. TD is defined as the passage of unformed stool (one or more by some definitions, three or more by others) while traveling. It may be accompanied by abdominal cramps, nausea, fever, and bloating. Occasionally bloody diarrhea may occur. Most travelers recover within four days with little or no treatment. About 10% of people may have symptoms for a week.

Bacteria are responsible for more than half of cases. The bacteria enterotoxigenic "Escherichia coli" (ETEC) are typically the most common except in Southeast Asia, where "Campylobacter" is more prominent. About 10% to 20% of cases are due to norovirus. Protozoa such as "Giardia" may cause longer term disease. The risk is greatest in the first two weeks of travel and among young adults. People affected are more often from the developed world.

Recommendations for prevention include eating only properly cleaned and cooked food, drinking bottled water, and frequent hand washing. The oral cholera vaccine, while effective for cholera, is of questionable use for traveler's diarrhea. Preventative antibiotics are generally discouraged. Primary treatment includes drinking lots of fluids and replacing lost salts (oral rehydration therapy). Antibiotics are recommended for significant or persistent symptoms, and can be taken with loperamide to decrease diarrhea. Hospitalization is required in less than 3% of cases.

Estimates of the percentage of people affected range from 20 to 50% among travelers to the developing world. TD is particularly common among people travelling to Asia (except Japan), the Middle East, Africa, Mexico, and Central and South America. The risk is moderate in Southern Europe, Russia, and China. TD has been linked to later irritable bowel syndrome and Guillain–Barré syndrome. It has colloquially been known by a number of names, including "Montezuma's revenge" and "Delhi belly".

Most infected people, about 90%, are asymptomatic, but this disease has the potential to make the sufferer dangerously ill. It is estimated that about 40,000 to 100,000 people worldwide die annually due to amoebiasis.

Infections can sometimes last for years. Symptoms take from a few days to a few weeks to develop and manifest themselves, but usually it is about two to four weeks. Symptoms can range from mild diarrhea to severe dysentery with blood and mucus. The blood comes from lesions formed by the amoebae invading the lining of the large intestine. In about 10% of invasive cases the amoebae enter the bloodstream and may travel to other organs in the body. Most commonly this means the liver, as this is where blood from the intestine reaches first, but they can end up almost anywhere in the body.

Onset time is highly variable and the average asymptomatic infection persists for over a year. It is theorized that the absence of symptoms or their intensity may vary with such factors as strain of amoeba, immune response of the host, and perhaps associated bacteria and viruses.

In asymptomatic infections the amoeba lives by eating and digesting bacteria and food particles in the gut, a part of the gastrointestinal tract. It does not usually come in contact with the intestine itself due to the protective layer of mucus that lines the gut. Disease occurs when amoeba comes in contact with the cells lining the intestine. It then secretes the same substances it uses to digest bacteria, which include enzymes that destroy cell membranes and proteins. This process can lead to penetration and digestion of human tissues, resulting first in flask-shaped ulcers in the intestine. "Entamoeba histolytica" ingests the destroyed cells by phagocytosis and is often seen with red blood cells (a process known as erythrophagocytosis) inside when viewed in stool samples. Especially in Latin America, a granulomatous mass (known as an amoeboma) may form in the wall of the ascending colon or rectum due to long-lasting immunological cellular response, and is sometimes confused with cancer.

"Theoretically, the ingestion of one viable cyst can cause an infection."

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.

Diarrhea acquired in the wilderness or other remote areas is typically a form of infectious diarrhea, itself classified as a type of secretory diarrhea. These are all considered forms of gastroenteritis. The term may be applied in various remote areas of non-tropical developed countries (U.S., Canada, western Europe, etc.), but is less applicable in developing countries, and in the tropics, because of the different pathogens that are most likely to cause infection.

Giardiasis, popularly known as beaver fever, is a parasitic disease caused by "Giardia lamblia". About 10% of those infected have no symptoms. When symptoms occur they may include diarrhea, abdominal pain, and weight loss. Vomiting, blood in the stool, and fever are less common. Symptoms usually begin 1 to 3 weeks after exposure and without treatment may last up to six weeks.

Giardia usually spreads when "Giardia lamblia" cysts within feces contaminate food or water which is then eaten or drunk. It may also spread between people and from other animals. Risk factors include travel in the developing world, changing diapers, eating food without cooking it, and owning a dog. Cysts may survive for nearly three months in cold water. Diagnosis is via stool tests.

Prevention is typically by improved hygiene. Those without symptoms do not usually need treatment. When symptoms are present treatment is typically with either tinidazole or metronidazole. People may become temporarily lactose intolerant after an infection and therefore it is often recommended milk be avoided for a few weeks. Resistance to treatment may occur.

Giardia is one of the most common parasitic human diseases globally. In 2013, there were about 280 million people worldwide with symptomatic giardiasis. Rates are as high as 7% in the developed world and 30% in the developing world. The World Health Organization classified it as a neglected disease.

An intestinal parasite infection is a condition in which a parasite infects the gastro-intestinal tract of humans and other animals. Such parasites can live anywhere in the body, but most prefer the intestinal wall.

Routes of exposure and infection include ingestion of undercooked meat, drinking infected water, fecal-oral transmission and skin absorption.

Some types of helminths and protozoa are classified as intestinal parasites that cause infection—those that reside in the intestines. These infections can damage or sicken host (humans or other animals). If the intestinal parasite infection is caused by helminths, the infection is called helminthiasis.

Proximal enteritis, also known as anterior enteritis or duodenitis-proximal jejunitis (DPJ), is inflammation of the duodenum and upper jejunum. It produces a functional stasis of the affected intestine (ileus) and hypersecretion of fluid into the lumen of that intestine. This leads to large volumes of gastric reflux, dehydration, low blood pressure, and potentially shock. Although the exact cause is not yet definitively known, proximal enteritis requires considerable supportive care.

Signs and symptoms of spontaneous bacterial peritonitis include fevers, chills, nausea, vomiting, abdominal tenderness, and general malaise. Affected individuals may complain of abdominal pain and worsening ascites. Thirteen percent of patients have no signs or symptoms. Hepatic encephalopathy may be the only manifestation of SBP; in the absence of a clear precipitant for the encephalopathy, all patients should undergo paracentesis, or sampling of the ascites fluid, in order to assess for SBP.