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.

Amoebiasis is usually transmitted by the fecal-oral route, but it can also be transmitted indirectly through contact with dirty hands or objects as well as by anal-oral contact. Infection is spread through ingestion of the cyst form of the parasite, a semi-dormant and hardy structure found in feces. Any non-encysted amoebae, or "trophozoites", die quickly after leaving the body but may also be present in stool: these are rarely the source of new infections. Since amoebiasis is transmitted through contaminated food and water, it is often endemic in regions of the world with limited modern sanitation systems, including México, Central America, western South America, South Asia, and western and southern Africa.

Amoebic dysentery is often confused with "traveler's diarrhea" because of its prevalence in developing nations. In fact, most traveler's diarrhea is bacterial or viral in origin.

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.

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

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.

Currently, no licensed vaccine targeting "Shigella" exists. Several vaccine candidates for "Shigella" are in various stages of development including live attenuated, conjugate, ribosomal, and proteosome vaccines. "Shigella" has been a longstanding World Health Organization target for vaccine development, and sharp declines in age-specific diarrhea/dysentery attack rates for this pathogen indicate that natural immunity does develop following exposure; thus, vaccination to prevent the disease should be feasible. Shigellosis is resistant to many antibiotics used to treat the disease, so vaccination is an important part of the strategy to reduce morbidity and mortality.

Insufficient data exist, but it is estimated to have caused the death of 34,000 children under the age of five in 2013, and 40,000 deaths in people over five years of age. "Shigella" also causes about 580,000 cases annually among travelers and military personnel from industrialized countries.

An estimated 500,000 cases of shigellosis occur annually in the United States. Infants, the elderly, and the critically ill are susceptible to the most severe symptoms of disease, but all humans are susceptible to some degree. Individuals with acquired immune deficiency syndrome (AIDS) are more frequently infected with "Shigella". Shigellosis is a more common and serious condition in the developing world; fatality rates of shigellosis epidemics in developing countries can be 5–15%.

Orthodox Jewish communities (OJCs) are a known risk group for shigellosis; "Shigella sonnei" is cyclically epidemic in these communities in Israel, with sporadic outbreaks occurring elsewhere in among these communities. "Through phylogenetic and genomic analysis, we showed that strains from outbreaks in OJCs outside of Israel are distinct from strains in the general population and relate to a single multidrug-resistant sublineage of "S. sonnei" that prevails in Israel. Further Bayesian phylogenetic analysis showed that this strain emerged approximately 30 years ago, demonstrating the speed at which antimicrobial drug–resistant pathogens can spread widely through geographically dispersed, but internationally connected, communities."

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

Transmission is fecal-oral and is remarkable for the small number of organisms that may cause disease (10 ingested organisms cause illness in 10% of volunteers, and 500 organisms cause disease in 50% of volunteers). "Shigella" bacteria invade the intestinal mucosal cells but do not usually go beyond the lamina propria. Dysentery is caused when the bacteria escape the epithelial cell phagolysosome, multiply within the cytoplasm, and destroy host cells. Shiga toxin causes hemorrhagic colitis and hemolytic-uremic syndrome by damaging endothelial cells in the microvasculature of the colon and the glomeruli, respectively. In addition, chronic arthritis secondary to "S. flexneri" infection, called reactive arthritis, may be caused by a bacterial antigen; the occurrence of this syndrome is strongly linked to HLA-B27 genotype, but the immunologic basis of this reaction is not understood.

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

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

When properly treated, people with malaria can usually expect a complete recovery. However, severe malaria can progress extremely rapidly and cause death within hours or days. In the most severe cases of the disease, fatality rates can reach 20%, even with intensive care and treatment. Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria. Chronic infection without severe disease can occur in an immune-deficiency syndrome associated with a decreased responsiveness to "Salmonella" bacteria and the Epstein–Barr virus.

During childhood, malaria causes anemia during a period of rapid brain development, and also direct brain damage resulting from cerebral malaria. Some survivors of cerebral malaria have an increased risk of neurological and cognitive deficits, behavioural disorders, and epilepsy. Malaria prophylaxis was shown to improve cognitive function and school performance in clinical trials when compared to placebo groups.

Bacillary dysentery is a type of dysentery, and is a severe form of shigellosis.

Bacillary dysentery is associated with species of bacteria from the Enterobacteriaceae family. The term is usually restricted to "Shigella" infections.

Shigellosis is caused by one of several types of "Shigella" bacteria. Three species are associated with bacillary dysentery: "Shigella sonnei, Shigella flexneri" and "Shigella dysenteriae". A study in China indicated that "Shigella flexneri" 2a was the most common serotype.

Salmonellosis caused by "Salmonella enterica" (serovar "Typhimurium") has also been described as a cause of bacillary dysentery, though this definition is less common. It is sometimes listed as an explicit differential diagnosis of bacillary dysentery, as opposed to a cause.

Bacillary dysentery should not be confused with diarrhea caused by other bacterial infections. One characteristic of bacillary dysentery is blood in stool, which is the result of invasion of the mucosa by the pathogen.

Rates of infection increase in conditions of crowding and poor sanitation, and are higher in military personnel and mental institutions.

The true extent of disease has yet to emerge, as most laboratories do not use techniques to adequately identify this organism. An Australian study identified a large number of patients, considered to have irritable bowel syndrome, who were actually infected with "Dientamoeba fragilis".

Although "D. fragilis" has been described as an infection "emerging from obscurity", it has become one of the most prevalent gastrointestinal infections in industrialized countries, especially among children and young adults. A Canadian study reported a prevalence of around 10% in boys and girls aged 11–15 years, a prevalence of 11.5% in individuals aged 16–20, and a lower incidence of 0.3–1.9% in individuals over age 20.

Malaria parasites belong to the genus "Plasmodium" (phylum Apicomplexa). In humans, malaria is caused by "P. falciparum", "P. malariae", "P. ovale", "P. vivax" and "P. knowlesi". Among those infected, "P. falciparum" is the most common species identified (~75%) followed by "P. vivax" (~20%). Although "P. falciparum" traditionally accounts for the majority of deaths, recent evidence suggests that "P. vivax" malaria is associated with potentially life-threatening conditions about as often as with a diagnosis of "P. falciparum" infection. "P. vivax " proportionally is more common outside Africa. There have been documented human infections with several species of "Plasmodium" from higher apes; however, except for "P. knowlesi"—a zoonotic species that causes malaria in macaques—these are mostly of limited public health importance.

Global warming is likely to affect malaria transmission, but the severity and geographic distribution of such effects is uncertain.

As many individuals are asymptomatic carriers of "D. fragilis", pathogenic and nonpathogenic variants are proposed to exist. A study of "D. fragilis" isolates from 60 individuals with symptomatic infection in Sydney, Australia, found all were infected with the same genotype, which is the most common worldwide, but differed from the genotype first described from a North American isolate and later also detected in Europe.

Experimental infection in immunocompetent and immunocompromised mice has produced intestinal inflammation, altered bowel habits, lethargy and death. Chronic diarrhea has been reported in non-human higher primates.

As resistance to ampicillin, chloramphenicol, trimethoprim-sulfamethoxazole, and streptomycin is now common, these agents have not been used as first–line treatment of typhoid fever for almost 20 years. Typhoid resistant to these agents is known as multidrug-resistant typhoid (MDR typhoid).

Ciprofloxacin resistance is an increasing problem, especially in the Indian subcontinent and Southeast Asia. Many centres are shifting from using ciprofloxacin as the first line for treating suspected typhoid originating in South America, India, Pakistan, Bangladesh, Thailand, or Vietnam. For these people, the recommended first-line treatment is ceftriaxone. Also, azithromycin has been suggested to be better at treating typhoid in resistant populations than both fluoroquinolone drugs and ceftriaxone. Azithromycin significantly reduces relapse rates compared with ceftriaxone.

A separate problem exists with laboratory testing for reduced susceptibility to ciprofloxacin: current recommendations are that isolates should be tested simultaneously against ciprofloxacin (CIP) and against nalidixic acid (NAL), and that isolates that are sensitive to both CIP and NAL should be reported as "sensitive to ciprofloxacin", but that isolates testing sensitive to CIP but not to NAL should be reported as "reduced sensitivity to ciprofloxacin". However, an analysis of 271 isolates showed that around 18% of isolates with a reduced susceptibility to ciprofloxacin (MIC 0.125–1.0 mg/l) would not be picked up by this method. How this problem can be solved is not certain, because most laboratories around the world (including the West) are dependent on disk testing and cannot test for MICs.

According to Centers for Disease Control and Prevention, a multistate outbreak of human "Campylobacter" infections have been reported since September 11, 2017. Total 55 cases have been reported from 12 states (Florida, Kansas, Maryland, Missouri, New Hampshire, New York, Ohio, Pennsylvania, Tennessee, Utah, Wisconsin and Wyoming). Epidemiological and laboratory evidence indicated that puppies sold through Petland stores are a likely source of this outbreak. 50 people out of 55 cases reported were either employees of Petland of have recently purchased a puppy at Petland or visited before illness began. 5 people out of 55 cases reported were exposed to puppies from various sources.

"Campylobacter" can spread through contact with dog feces. It usually does not spread from one person to another. However, activities such as changing an infected person's diapers or sexual contact with an infected person can lead to infection. Regardless of where they are from, any puppies and dogs may carry "Campylobacter" germs.

Most of these public health concerns have focused on children who are infected with hookworm. This focus on children is largely due to the large body of evidence that has demonstrated strong associations between hookworm infection and impaired learning, increased absences from school, and decreased future economic productivity.

In 2001, the 54th World Health Assembly passed a resolution demanding member states to attain a minimum target of regular deworming of at least 75% of all at-risk school children by the year 2010. A 2008 World Health Organization publication reported on these efforts to treat at-risk school children. Some of the interesting statistics were as follows: 1) only 9 out of 130 endemic countries were able to reach the 75% target goal; and 2) less than 77 million school-aged children (of the total 878 million at risk) were reached, which means that only 8.78% of at-risk children are being treated for hookworm infection.

Campylobacteriosis is usually self-limited without any mortality (assuming proper hydration is maintained). However, there are several possible complications.

In 2000, typhoid fever caused an estimated 21.7 million illnesses and 217,000 deaths. It occurs most often in children and young adults between 5 and 19 years old. In 2013 it resulted in about 161,000 deaths – down from 181,000 in 1990. Infants, children, and adolescents in south-central and Southeast Asia experience the greatest burden of illness. Outbreaks of typhoid fever are also frequently reported from sub-Saharan Africa and countries in Southeast Asia. Historically, in the pre-antibiotic era, the case fatality rate of typhoid fever was 10–20%. Today, with prompt treatment, it is less than 1%. However, about 3–5% of individuals who are infected will develop a chronic infection in the gall bladder. Since "S." Typhi is human-restricted, these chronic carriers become the crucial reservoir, which can persist for decades for further spread of the disease, further complicating the identification and treatment of the disease. Lately, the study of Typhi associated with a large outbreak and a carrier at the genome level provides new insights into the pathogenesis of the pathogen.

In industrialized nations, water sanitation and food handling improvements have reduced the number of cases. Developing nations, such as those found in parts of Asia and Africa, have the highest rates of typhoid fever. These areas have a lack of access to clean water, proper sanitation systems, and proper health care facilities. For these areas, such access to basic public health needs is not in the near future.

Humans contract "Blastocystis" infection by drinking water or eating food contaminated with feces from an infected human or animal. "Blastocystis" infection can be spread from animals to humans, from humans to other humans, from humans to animals, and from animals to animals. Risk factors for infection have been reported as following:

- International travel: Travel to less developed countries has been cited in development of symptomatic Blastocystis infection. A 1986 study in the United States found that all individuals symptomatically infected with "Blastocystis" reported recent travel history to less developed countries. In the same study, all hospital employees working in New York who were screened for "Blastocystis" were found to have asymptomatic infections.

- Military service: Several studies have identified high rates of infection in military personnel. An early account described infection of British troops in Egypt in 1916 who recovered following treatment with emetine. A 1990 study published in "Military Medicine" from Lackland AFB in Texas concluded symptomatic infection was more common in foreign nationals, children, and immunocompromised individuals. A 2002 study published in "Military Medicine" of army personnel in Thailand identified a 44% infection rate. Infection rates were highest in privates who had served the longest at the army base. A follow-up study found a significant correlation between infection and symptoms, and identified the most likely cause as contaminated water. A 2007 newspaper article suggested the infection rate of US military personnel returning from the Gulf War was 50%, quoting the head of Oregon State University's Biomedicine department.

- Consumption of Untreated Water (well water): Many studies have linked "Blastocystis" infection with contaminated drinking water. A 1993 study of children infected symptomatically with "Blastocystis" in Pittsburgh indicated that 75% of them had a history of drinking well water or travel in less developed countries. Two studies in Thailand linked "Blastocystis" infection in military personnel and families to drinking of unboiled and untreated water. A book published in 2006 noted that in an Oregon community, infections are more common in winter months during heavy rains. A research study published in 1980 reported bacterial contamination of well water in the same community during heavy rainfall. A 2007 study from China specifically linked infection with "Blastocystis sp. subtype 3" with drinking untreated water. Recreational contact with untreated water, for example though boating, has also been identified as a risk factor. Studies have shown that "Blastocystis" survives sewage treatment plants in both the United Kingdom and Malaysia. "Blastocystis" cysts have been shown to be resistant to chlorination as a treatment method and are among the most resistant cysts to ozone treatment.

- Contaminated Food: Contamination of leafy vegetables has been implicated as a potential source for transmission of "Blastocystis" infection, as well as other gastrointestinal protozoa. A Chinese study identified infection with "Blastocystis sp. subtype 1" as specifically associated with eating foods grown in untreated water.

- Daycare facilities: A Canadian study identified an outbreak of "Blastocystis" associated with daycare attendance. Prior studies have identified outbreaks of similar protozoal infections in daycares.

- Geography: Infection rates vary geographically, and variants which produce symptoms may be less common in industrialized countries. For example, a low incidence of "Blastocystis" infection has been reported in Japan. A study of individuals infected with "Blastocystis" in Japan found that many (43%, 23/54) carried "Blastocystis sp. subtype 2", which was found to produce no symptoms in 93% (21/23) of patients studied, in contrast to other variants which were less common but produced symptoms in 50% of Japanese individuals. Studies in urban areas of industrialized countries have found "Blastocystis" infection associated with a low incidence of symptoms. In contrast, studies in developing countries generally show "Blastocystis" to be associated with symptoms. In the United States, a higher incidence of "Blastocystis" infection has been reported in California and West Coast states.

- Prevalence over Time: A 1989 study of the prevalence of "Blastocystis" in the United States found an infection rate of 2.6% in samples submitted from all 48 states. The study was part of the CDC's MMWR Report. A more recent study, in 2006, found an infection rate of 23% in samples submitted from all 48 states. However, the more recent study was performed by a private laboratory located in the Western US, and emphasized samples from Western states, which have previously been reported to have a higher infection rate.

Research studies have suggested the following items are not risk factors for contracting "Blastocystis" infection:

- Consumption of municipal water near water plant (not a risk factor): One study showed that municipal water was free of "Blastocystis", even when drawn from a polluted source. However, samples taken far away from the treatment plant showed cysts. The researchers suggested that aging pipes may permit intrusion of contaminated water into the distribution system.

- Human-to-Human transmission among adults (not a risk factor): Some research suggests that direct human-to-human transmission is less common even in households and between married partners. One study showed different members of the same household carried different subtypes of Blastocystis.

The prevalence of intestinal parasites is the highest among children that are living in the poorest communities in developing nations. The most common causes of intestinal parasites are through consumption of contaminated water, infected soil, inadequate sanitation and hygiene, and improper hygiene. Specifically, lack of access to facilities for safe disposal of human waste can result in intestinal parasites and disease. Poor hygiene habits or lacking available hygiene resources, such as hand washing facilities, also negatively impact rates of disease. Parasitic contamination can also occur from eating raw vegetables and fruits, soil-eating behavior, and lack of available safe water.

Parasites can get into the intestine by going through the mouth from uncooked or unwashed food, contaminated water or hands, or by skin contact with larva infected soil; they can also be transferred by the sexual act of anilingus in some cases.

When the organisms are swallowed, they move into the intestine, where they can reproduce and cause symptoms. Children are particularly susceptible if they are not thoroughly cleaned after coming into contact with infected soil that is present in environments that they may frequently visit such as sandboxes and school playgrounds. People in developing countries are also at particular risk due to drinking water from sources that may be contaminated with parasites that colonize the gastrointestinal tract.

There is no vaccine to control "Cyclospora" infection in humans at present, but one is available for reduction of fetal losses in sheep.