Infection with ETEC can cause profuse, watery diarrhea with no blood or leukocytes and abdominal cramping. Fever, nausea with or without vomiting, chills, loss of appetite, headache, muscle aches and bloating can also occur, but are less common.

Enterotoxins produced by ETEC include heat-labile enterotoxin (LT) and heat-stable enterotoxin (ST).

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.

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

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.

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.

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

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

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

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

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.

Gram-negative bacterial infection refers to a disease caused by gram-negative bacteria. One example is E. coli.

It is important to recognize that this class is defined morphologically (by the presence of a bacterial outer membrane), and not histologically (by a pink appearance when stained), though the two usually coincide.

One reason for this division is that the outer membrane is of major clinical significance: it can play a role in the reduced effectiveness of certain antibiotics, and it is the source of endotoxin.

The gram status of some organisms is complex or disputed:

- Mycoplasma are sometimes considered gram-negative, but because of its lack of a cell wall and unusual membrane composition, it is sometimes considered separately from other gram-negative bacteria.

- Gardnerella is often considered gram-negative, but it is classified in MeSH as both gram-positive and gram-negative. It has some traits of gram-positive bacteria, but has a gram-negative appearance. It has been described as a "gram-variable rod".

Carbapenem-resistant Enterobacteriaceae (CRE) have been defined as carbapenem-nonsusceptible and extended-spectrum cephalosporin-resistant "Escherichia coli, Enterobacter aerogenes, Enterobacter cloacae" complex, "Klebsiella pneumoniae", or "Klebsiella oxytoca". Some exclude ertapenem resistance from the definition.

Secondary peritonitis and intra-abdominal abscesses including splenic and hepatic abscesses generally occur because of the entry of enteric micro-organisms into the peritoneal cavity through a defect in the wall of the intestine or other viscus as a result of obstruction, infarction or direct trauma. Perforated appendicitis, diverticulitis, inflammatory bowel disease with perforation and gastrointestinal surgery are often associated with polymicrobial infections caused by aerobic and anaerobic bacteria, where the number of isolates can average 12 (two-thirds are generally anaerobes). The most common aerobic and facultative bacteria are "Escherichia coli", "Streptococcus" spp. (including Enterococcus spp.), and the most frequently isolated anaerobic bacteria are the "B. fragilis" group, "Peptostreptococcus" spp., and "Clostridium" spp.

Abdominal infections are characteristically biphasic: an initial stages of generalized peritonitis associated with "Escherichia coli" sepsis, and a later stages, in which intra abdominal abscesses harboring anaerobic bacteria ( including "B. fragilis" group ) emerge.

The clinical manifestations of secondary peritonitis are a reflection of the underlying disease process. Fever, diffuse abdominal pain, nausea and vomiting are common. Physical examination generally show signs of peritoneal inflammation, isuch as rebound tenderness, abdominal wall rigidity and decrease in bowel sounds. These early findings may be followed by signs and symptoms of shock.

Biliary tract infection is usually caused by "E. coli, Klebsiella" and "Enterococcus" spp. Anaerobes (mostly "B. fragilis" group, and rarely "C. perfringens") can be recovered in complicated infections associated with carcinoma, recurrent infection, obstruction, bile tract surgery or manipulation.

Laboratory studies show elevated blood leukocyte count and predominance of polymorphonuclear forms. Radiographs studies may show free air in the peritoneal cavity, evidence of ileus or obstruction and obliteration of the psoas shadow. Diagnostic ultrasound, gallium and CT scanning may detect appendiceal or other intra-abdominal abscesses. Polymicrobial postoperative wound infections can occur.

Treatment of mixed aerobic and anaerobic abdominal infections requires the utilization of antimicrobials effective against both components of the infection as well as surgical correction and drainage of pus. Single and easily accessible abscesses can be drained percutaneously.

Carbapenem-resistant Enterobacteriaceae (CRE) or carbapenemase-producing Enterobacteriaceae (CPE) are Gram-negative bacteria that are resistant to the carbapenem class of antibiotics, considered the drugs of last resort for such infections. They are resistant because they produce an enzyme called a carbapenemase that disables the drug molecule. The resistance can vary from moderate to severe. Enterobacteriaceae are common commensals and infectious agents. Experts fear CRE as the new "superbug". The bacteria can kill up to half of patients who get bloodstream infections. Tom Frieden, former head of the Centers for Disease Control and Prevention has referred to CRE as "nightmare bacteria". Types of CRE are sometimes known as KPC (Klebsiella pneumoniae carbapenemase) and NDM (New Delhi Metallo-beta-lactamase). KPC and NDM are enzymes that break down carbapenems and make them ineffective. Both of these enzymes, as well as the enzyme VIM (Verona Integron-Mediated Metallo-β-lactamase) have also been reported in Pseudomonas.

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".

Anaerobes can be isolated from most types of upper respiratory tract and head and neck and infection and are especially common in chronic ones. These include tonsillar, peritonsillar and retropharyngeal abscesses, chronic otitis media, sinusitis and mastoiditis, eye ocular) infections, all deep neck space infections, parotitis, sialadenitis, thyroiditis, odontogenic infections, and postsurgical and nonsurgical head and neck wounds and abscesses., The predominant organisms are of oropharyngeal flora origin and include AGNB, "Fusobacterium" and Peptostreptococcus spp.

Anaerobes involve almost all dental infections. These include dental abscesses, endodontal pulpitis and periodontal (gingivitis and periodontitis) infections, and perimandibular space infection. Pulpitis can lead to abscess formation and eventually spread to the mandible and other neck spaces. In addition to strict anaerobic bacteria, microaerophilic streptococci and "Streptococcus salivarius" can also be present.

"Fusobacterium" spp. and anaerobic spirochetes are often the cause of acute necrotizing ulcerative gingivitis (or Vincent's angina) which is a distinct form of ulcerative gingivitis.

Deep neck infections that develop as a consequence of oral, dental and pharyngeal infections are generally polymicrobial in nature. These include extension of retropharyngeal cellulitis or abscess, mediastinitis following esophagus perforation, and dental or periodontal abscess.

Amoebiasis, also known amoebic dysentery, is an infection caused by any of the amoebas of the "Entamoeba" group. Symptoms are most common during infection by "Entamoeba histolytica". Amoebiasis can be present with no, mild, or severe symptoms. Symptoms may include abdominal pain, diarrhea, or bloody diarrhea. Complications can include inflammation of the colon with tissue death or perforation, which may result in peritonitis. People affected may develop anemia due to loss of blood.

Cysts of "Entamoeba" can survive for up to a month in soil or for up to 45 minutes under fingernails. Invasion of the intestinal lining can cause bloody diarrhea. If the parasite reaches the bloodstream it can spread through the body, most frequently ending up in the liver where it can cause amoebic liver abscesses. Liver abscesses can occur without previous diarrhea. Diagnosis is typical by stool examination using a microscope, but may not reliably exclude infection or separate between specific types. An increased white blood cell count may be present in severe cases. The most accurate test is finding specific antibodies in the blood, but it may remain positive following treatment. Bacterial colitis can result in similar symptoms.

Prevention of amoebiasis is by improved sanitation, including separating food and water from faeces. There is no vaccine. There are two treatment options depending on the location of the infection. Amoebiasis in tissues is treated with either metronidazole, tinidazole, nitazoxanide, dehydroemetine or chloroquine, while luminal infection is treated with diloxanide furoate or iodoquinoline. Effective treatment against all stages of the disease may require a combination of medications. Infections without symptoms do not require treatment but infected individuals can spread the parasite to others and treatment can be considered. Treatment of other "Entamoeba" infections apart from "E. histolytica" is not needed.

Amoebiasis is present all over the world. About 480 million people are infected with amoebiasis and this results in the death of between 40,000–110,000 people a year. Most infections are now believed due to "E. dispar". "E. dispar" is more common in certain areas and symptomatic cases may be less common than previously reported. The first case of amoebiasis was documented in 1875 and in 1891 the disease was described in detail, resulting in the terms "amoebic dysentery" and "amoebic liver abscess". Further evidence from the Philippines in 1913 found that upon swallowing cysts of "E. histolytica" volunteers developed the disease.

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."

Symptoms can be local due to involvement of the intestinal mucosa, or systemic in nature and include either diarrhea or constipation.

Bacteremia (also bacteraemia) is the presence of bacteria in the blood. Blood is normally a sterile environment, so the detection of bacteria in the blood (most commonly accomplished by blood cultures) is always abnormal. It is distinct from sepsis, which is the host response to the bacteria.

Bacteria can enter the bloodstream as a severe complication of infections (like pneumonia or meningitis), during surgery (especially when involving mucous membranes such as the gastrointestinal tract), or due to catheters and other foreign bodies entering the arteries or veins (including during intravenous drug abuse). Transient bacteremia can result after dental procedures or brushing of teeth.

Bacteremia can have several important health consequences. The immune response to the bacteria can cause sepsis and septic shock, which has a high mortality rate. Bacteria can also spread via the blood to other parts of the body (which is called hematogenous spread), causing infections away from the original site of infection, such as endocarditis or osteomyelitis. Treatment for bacteremia is with antibiotics, and prevention with antibiotic prophylaxis can be given in high risk situations.

Bacteremia is the presence of bacteria in the bloodstream that are alive and capable of reproducing. It is a type of bloodstream infection. Bacteremia is defined as either a primary or secondary process. In primary bacteremia, bacteria have been directly introduced into the bloodstream. Injection drug use may lead to primary bacteremia. In the hospital setting, use of blood vessel catheters contaminated with bacteria may also lead to primary bacteremia. Secondary bacteremia occurs when bacteria have entered the body at another site, such as the cuts in the skin, or the mucous membranes of the lungs (respiratory tract), mouth or intestines (gastrointestinal tract), bladder (urinary tract), or genitals. Bacteria that have infected the body at these sites may then spread into the lymphatic system and gain access to the bloodstream, where further spread can occur.

Bacteremia may also be defined by the timing of bacteria presence in the bloodstream: transient, intermittent, or persistent. In transient bacteremia, bacteria are present in the bloodstream for minutes to a few hours before being cleared from the body, and the result is typically harmless in healthy people. This can occur after manipulation of parts of the body normally colonized by bacteria, such as the mucosal surfaces of the mouth during teeth brushing, flossing, or dental procedures, or instrumentation of the bladder or colon. Intermittent bacteremia is characterized by periodic seeding of the same bacteria into the bloodstream by an existing infection elsewhere in the body, such as an abscess, pneumonia, or bone infection, followed by clearing of that bacteria from the bloodstream. This cycle will often repeat until the existing infection is successfully treated. Persistent bacteremia is characterized by the continuous presence of bacteria in the bloodstream. It is usually the result of an infected heart valve, a central line-associated bloodstream infection (CLABSI), an infected blood clot (suppurative thrombophlebitis), or an infected blood vessel graft. Persistent bacteremia can also occur as part of the infection process of typhoid fever, brucellosis, and bacterial meningitis. Left untreated, conditions causing persistent bacteremia can be potentially fatal.

Bacteremia is clinically distinct from sepsis, which is a condition where the blood stream infection is associated with an inflammatory response from the body, often causing abnormalities in body temperature, heart rate, breathing rate, blood pressure, and white blood cell count.

Gastroenteritis typically involves both diarrhea and vomiting, or less commonly, presents with only one or the other. Abdominal cramping may also be present. Signs and symptoms usually begin 12–72 hours after contracting the infectious agent. If due to a viral agent, the condition usually resolves within one week. Some viral causes may also be associated with fever, fatigue, headache, and muscle pain. If the stool is bloody, the cause is less likely to be viral and more likely to be bacterial. Some bacterial infections may be associated with severe abdominal pain and may persist for several weeks.

Children infected with rotavirus usually make a full recovery within three to eight days. However, in poor countries treatment for severe infections is often out of reach and persistent diarrhea is common. Dehydration is a common complication of diarrhea, and a child with a significant degree of dehydration may have a prolonged capillary refill, poor skin turgor, and abnormal breathing. Repeat infections are typically seen in areas with poor sanitation, and malnutrition, stunted growth, and long-term cognitive delays can result.

Reactive arthritis occurs in 1% of people following infections with "Campylobacter" species, and Guillain–Barré syndrome occurs in 0.1%. Hemolytic uremic syndrome (HUS) may occur due to infection with Shiga toxin-producing "Escherichia coli" or "Shigella" species, causing low platelet counts, poor kidney function, and low red blood cell count (due to their breakdown). Children are more predisposed to getting HUS than adults. Some viral infections may produce benign infantile seizures.

New or progressive infiltrate on the chest X-ray with one of the following:

- Fever > 37.8 °C (100 °F)

- Purulent sputum

- Leukocytosis > 10,000 cells/μl

In an elderly person, the first sign of hospital-acquired pneumonia may be mental changes or confusion.

Other symptoms may include:

- A cough with greenish or pus-like phlegm (sputum)

- Fever and chills

- General discomfort, uneasiness, or ill feeling (malaise)

- Loss of appetite

- Nausea and vomiting

- Sharp chest pain that gets worse with deep breathing or coughing

- Shortness of breath

- Decreased blood pressure and fast heart rate

Onset of symptoms begins one to nine days following exposure (with an average of five). Initial symptoms include changes in taste and smell, headache, fever, nausea, vomiting, back pain, and a stiff neck. Secondary symptoms are also meningitis-like including confusion, hallucinations, lack of attention, ataxia, cramp and seizures. After the start of symptoms, the disease progresses rapidly over three to seven days, with death usually occurring anywhere from seven to fourteen days later, although it can take longer. In 2013, a man in Taiwan died twenty-five days after being infected by "Naegleria fowleri".

It affects healthy children or young adults who have recently been exposed to bodies of fresh water. Some people have presented with a clinical triad of edematous brain lesions, immune suppression, and fever.

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).

Balantidiasis is a protozoan infection caused by infection with "Balantidium coli".

Naegleriasis (also known as primary amoebic meningoencephalitis) is an infection of the brain by the free-living unicellular "Naegleria fowleri".

"N. fowleri" is typically found in warm bodies of fresh water, such as ponds, lakes, rivers, and hot springs. It is also found in soil, poorly maintained municipal water supplies, water heaters, near warm-water discharges of industrial plants, and in poorly chlorinated or unchlorinated swimming pools, in an amoeboid or temporary flagellate stage. There is no evidence of it living in salt water. As the disease is rare, it is often not considered. Symptoms are similar to those of meningitis.

Although infection occurs rarely, it nearly always results in death, with a case fatality rate greater than 95%.