Several studies found that healthcare-associated pneumonia is the second most common type of pneumonia, occurring less commonly than community-acquired pneumonia but more frequently than hospital-acquired pneumonia and ventilator-associated pneumonia. In a recent observational study, the rates for CAP, HCAP and HAP were 60%, 25% and 15% respectively. Patients with HCAP are older and more commonly have simultaneous health problems (such as previous stroke, heart failure and diabetes).

The number of residents in long term care facilities is expected to rise dramatically over the next 30 years. These older adults are known to develop pneumonia 10 times more than their community-dwelling peers, and hospital admittance rates are 30 times higher.

Healthcare-associated pneumonia seems to have fatality rates similar to hospital-acquired pneumonia, worse than community-acquired pneumonia but less severe than pneumonia in ventilated patients. Besides clinical markers like tachypnea (fast breathing) or a high white cell count (leukocytosis), the prognosis seems to be influenced by the underlying associated diseases (comorbidities) and functional capacities (for example, the ADL score). Many patients have a decreased health condition after the episode.

CAP is common worldwide, and a major cause of death in all age groups. In children, most deaths (over two million a year) occur in newborn period. According to a World Health Organization estimate, one in three newborn deaths are from pneumonia. Mortality decreases with age until late adulthood, with the elderly at risk for CAP and its associated mortality.

More CAP cases occur during the winter than at other times of the year. CAP is more common in males than females, and more common in black people than Caucasians. Patients with underlying illnesses (such as Alzheimer's disease, cystic fibrosis, COPD, tobacco smoking, alcoholism or immune-system problems) have an increased risk of developing pneumonia.

There are several risk factors that increase the likelihood of developing bacteremia from any type of bacteria. These include:

- HIV infection

- Diabetes Mellitus

- Chronic hemodialysis

- Solid organ transplant

- Stem cell transplant

- Treatment with glucocorticoids

- Liver failure

Gram negative bacterial species are responsible for approximately 24% of all cases of healthcare-associated bacteremia and 45% of all cases of community-acquired bacteremia. In general, gram negative bacteria enter the bloodstream from infections in the respiratory tract, genitourinary tract, gastrointestinal tract, or hepatobiliary system. Gram-negative bacteremia occurs more frequently in elderly populations (65 years or older) and is associated with higher morbidity and mortality in this population.

"E.coli" is the most common cause of community-acquired bacteremia accounting for approximately 75% of cases. E.coli bacteremia is usually the result of a urinary tract infection. Other organisms that can cause community-acquired bacteremia include "pseudomonas aeruginosa", "klebsiella pneumoniae", and "proteus mirabilis". "Salmonella" infection, despite mainly only resulting in gastroenteritis in the developed world, is a common cause of bacteremia in Africa. It principally affects children who lack antibodies to Salmonella and HIV+ patients of all ages.

Among healthcare-associated cases of bacteremia, gram negative organisms are an important cause of bacteremia in the ICU. Catheters in the veins, arteries, or urinary tract can all create a way for gram negative bacteria to enter the bloodstream. Surgical procedures of the genitourinary tract, intestinal tract, or hepatobiliary tract can also lead to gram negative bacteremia. "Pseudomonas" and "enterobacter" species are the most important causes of gram negative bacteremia in the ICU.

A full spectrum of microorganisms is responsible for CAP in adults, and patients with certain risk factors are more susceptible to infections of certain groups of microorganisms. Identifying people at risk for infection by these organisms aids in appropriate treatment.

Many less-common organisms can cause CAP in adults, and are identified from specific risk factors or treatment failure for common causes.

With treatment, most types of bacterial pneumonia will stabilize in 3–6 days. It often takes a few weeks before most symptoms resolve. X-ray finding typically clear within four weeks and mortality is low (less than 1%). In the elderly or people with other lung problems, recovery may take more than 12 weeks. In persons requiring hospitalization, mortality may be as high as 10%, and in those requiring intensive care it may reach 30–50%. Pneumonia is the most common hospital-acquired infection that causes death. Before the advent of antibiotics, mortality was typically 30% in those that were hospitalized.

Complications may occur in particular in the elderly and those with underlying health problems. This may include, among others: empyema, lung abscess, bronchiolitis obliterans, acute respiratory distress syndrome, sepsis, and worsening of underlying health problems.

Clinical prediction rules have been developed to more objectively predict outcomes of pneumonia. These rules are often used in deciding whether or not to hospitalize the person.

- Pneumonia severity index (or "PSI Score")

- CURB-65 score, which takes into account the severity of symptoms, any underlying diseases, and age

Prevention of bacterial pneumonia is by vaccination against "Streptococcus pneumoniae" (pneumococcal polysaccharide vaccine for adults and pneumococcal conjugate vaccine for children), "Haemophilus influenzae" type B, meningococcus, "Bordetella pertussis", "Bacillus anthracis", and "Yersinia pestis".

People who have difficulty breathing due to pneumonia may require extra oxygen. An extremely sick individual may require artificial ventilation and intensive care as life-saving measures while his or her immune system fights off the infectious cause with the help of antibiotics and other drugs.

The most common causative organisms are (often intracellular living) bacteria:

- "Chlamydophila pneumoniae": Mild form of pneumonia with relatively mild symptoms.

- "Chlamydophila psittaci": Causes psittacosis.

- "Coxiella burnetii": Causes Q fever.

- "Francisella tularensis": Causes tularemia.

- "Legionella pneumophila": Causes a severe form of pneumonia with a relatively high mortality rate, known as legionellosis or Legionnaires' disease.

- "Mycoplasma pneumoniae": Usually occurs in younger age groups and may be associated with neurological and systemic (e.g. rashes) symptoms.

Atypical pneumonia can also have a fungal, protozoan or viral cause.In the past, most organisms were difficult to culture. However, newer techniques aid in the definitive identification of the pathogen, which may lead to more individualized treatment plans.

When comparing the bacterial-caused atypical pneumonias with these caused by real viruses (excluding bacteria that were wrongly considered as viruses), the term "atypical pneumonia" almost always implies a bacterial cause and is contrasted with viral pneumonia.

Known viral causes of atypical pneumonia include respiratory syncytial virus (RSV), influenza A and B, parainfluenza, adenovirus, severe acute respiratory syndrome (SARS)

and measles.

CRE resistance depends upon a number of factors such as the health of the patient, whether the patient has recently undergone a transplant, risk of co-infection, and use of multiple antibiotics.

Carbapenem minimal inhibitory concentrations (MICs) results may be more predictive of clinical patient outcomes than the current categorical classification of the MICs being listed as susceptible, intermediate, or resistant. The study aimed to define an all-cause hospital mortality breakpoint for carbapenem MICs that were adjusted for risk factors. Another objective was to determine if a similar breakpoint existed for indirect outcomes, such as the time to death and length of stay after infection for survivors. Seventy-one patients were included, of which 52 patients survived and 19 patients died. Classification and regression tree analysis determined a split of organism MIC between 2 and 4 mg/liter and predicted differences in mortality (16.1% for 2 mg/liter versus 76.9% for 4 mg/liter). In logistic regression controlling for confounders, each imipenem MIC doubling dilution doubled the probability of death. This classification scheme correctly predicted 82.6% of cases. Patients were accordingly stratified to MICs of ≤2 mg/liter (58 patients) and ≥4 mg/liter (13 patients). Patients in the group with a MIC of ≥4 mg/liter tended to be more ill. Secondary outcomes were also similar between groups. Patients with organisms that had an MIC of ≥4 mg/liter had worse outcomes than those with isolates of an MIC of ≤2 mg/liter.

At New York Presbyterian Hospital, part of Columbia University Medical Center in New York, NY, a study was conducted on the significant rise in carbapenem resistance in "K. pneumoniae" from 1999 to 2007. Following a positive blood culture from a patient, overall mortality was 23% in 7 days, 42% in 30 days, and 60% by the end of hospitalization. The overall in-hospital mortality rate was 48%.

At Soroka Medical Center, an Israeli university teaching hospital, a study was done between October 2005 and October 2008 to determine the direct mortality rate associated with carbapenem-resistant "K. pneumoniae" bloodstream infections. The crude mortality rate for those with the resistant bacteremia was 71.9%, and the attributable mortality rate was determined to be 50% with a 95% confidence interval. The crude mortality rate for control subjects was 21.9%. As a result of the study, Soroka Medical Center started an intensive program designed to prevent the spread of carbapenem-resistant "K. pneumoniae."

A 2013 retrospective study at the Shaare Zedek Medical Center of patients with urinary tract infections (bacteriuria) caused by carbapenem-resistant "Klebsiella pneumoniae" (CRKp) showed no statistically significant difference in mortality rates from patients with bacteriuria caused by carbapenem-susceptible "K. pneumoniae" (CSKp). A 29% mortality rate was seen in patients with CRKp infection compared to a 25% mortality rate in patients with CSKp infections that produced extended-spectrum beta-lactamase (ESBL). Both mortality rates were considerably higher than that of patients with drug-susceptible urosepsis. Most patients in the study suffered from other illnesses, including dementia, immune compromise, renal failure, or diabetes mellitus. The main risk factor for death found by the study was being bedridden, which significantly increased the chance of death. This suggests that the deaths were due to reasons other than bacteriuria. Total length of hospitalization was somewhat longer in patients with CRKp infections (28 ± 33 days compared to 22 ± 28 days for patients with CSKp infection).

In a case-control study of 99 patients compared with 99 controls at Mount Sinai Hospital (Manhattan), a 1,171 bed tertiary care teaching hospital, 38% of patients in long-term care that were afflicted with CRE died from "K. pneumoniae" infection. Patients had risk factors including diabetes, HIV infection, heart disease, liver disease, renal insufficiency, one was a transplant recipient. 72% of patients who were released from the hospital with CRE were readmitted within 90 days.

A 2008 study at Mount Sinai identified outcomes associated with Carbapenem-resistant "Klebsiella pneumoniae" infections, in which patients in need of organ or stem cell transplants, mechanical ventilation, prolonged hospitalization, or prior treatment with carbapenems, had an increased probability of infection with Carbapenem-resistant "K. pneumoniae". A combination of antibiotics worked to treat infection and survival rates of infected patients increased when the focus of infection was removed.

CRE infections can set in about 12 days after liver transplantation, and 18% of those patients died a year after transplantation in a 2012 study.

The newborn`s exposure to the maternal vaginal bacterial flora which contains aerobic and anaerobic bacterial flora can lead to the development of anaerobic bacterial infection. These infections include cellulitis of the site of fetal monitoring (caused by "Bacterodes" spp.), bacteremia, aspiration pneumonia (caused by "Bacterodes" spp.), conjunctivitis (caused by clostridia,) omphalitis (caused by mixed flora), and infant botulism. Clostridial species may play a role in necrotizing enterocolitis. Management of these infection necessitates treating of the underlying condition(s) when present, and administration of proper antimicrobial therapy

Condition predisposing to anaerobic infections include: exposure of a sterile body location to a high inoculum of indigenous bacteria of mucous membrane flora origin, inadequate blood supply and tissue necrosis which lower the oxidation and reduction potential which support the growth of anaerobes. Conditions which can lower the blood supply and can predispose to anaerobic infection are: trauma, foreign body, malignancy, surgery, edema, shock, colitis and vascular disease. Other predisposing conditions include splenectomy, neutropenia, immunosuppression, hypogammaglobinemia, leukemia, collagen vascular disease and cytotoxic drugs and diabetes mellitus. A preexisting infection caused by aerobic or facultative organisms can alter the local tissue conditions and make them more favorable for the growth of anaerobes. Impairment in defense mechanisms due to anaerobic conditions can also favor anaerobic infection. These include production of leukotoxins (by "Fusobacterium" spp.), phagocytosis intracellular killing impairments (often caused by encapsulated anaerobes and by succinic acid ( produced by "Bacteroides" spp.), chemotaxis inhibition (by "Fusobacterium, Prevotella" and "Porphyromonas" spp.), and proteases degradation of serum proteins (by Bacteroides spp.) and production of leukotoxins (by "Fusobacterium" spp.).

The hallmarks of anaerobic infection include suppuration, establishment of an abscess, thrombophlebitis and gangrenous destruction of tissue with gas generation. Anaerobic bacteria are very commonly recovered in chronic infections, and are often found following the failure of therapy with antimicrobials that are ineffective against them, such as trimethoprim–sulfamethoxazole (co-trimoxazole), aminoglycosides, and the earlier quinolones.

Some infections are more likely to be caused by anaerobic bacteria, and they should be suspected in most instances. These infections include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia and lung abscesses, amnionitis, endometritis, septic abortions, tubo-ovarian abscess, peritonitis and abdominal abscesses following viscus perforation, abscesses in and around the oral and rectal areas, pus-forming necrotizing infections of soft tissue or muscle and postsurgical infections that emerge following procedures on the oral or gastrointestinal tract or female pelvic area. Some solid malignant tumors, ( colonic, uterine and bronchogenic, and head and neck necrotic tumors, are more likely to become secondarily infected with anaerobes. The lack of oxygen within the tumor that are proximal to the endogenous adjacent mucosal flora can predispose such infections.

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.

The current incidence in the United States is somewhere around 0.5% per year; overall, the incidence rate for developed world falls between 0.2–0.7%. In developing countries, the incidence of omphalitis varies from 2 to 7 for 100 live births. There does not appear to be any racial or ethnic predilection.

Like many bacterial infections, omphalitis is more common in those patients who have a weakened or deficient immune system or who are hospitalized and subject to invasive procedures. Therefore, infants who are premature, sick with other infections such as blood infection (sepsis) or pneumonia, or who have immune deficiencies are at greater risk. Infants with normal immune systems are at risk if they have had a prolonged birth, birth complicated by infection of the placenta (chorioamnionitis), or have had umbilical catheters.

Hospitals are primary transmission sites for CRE-based infections. Up to 75% of hospital admissions attributed to CRE were from long-term care facilities or transferred from another hospital. Suboptimal maintenance practices are the largest cause of CRE transmission. This includes the failure to adequately clean and disinfect medication cabinets, other surfaces in patient rooms, and portable medical equipment, such as X-ray and ultrasound machines that are used for both CRE and non-CRE patients.

Thus far, CRE have primarily been nosocomial infectious agents. Almost all CRE infections occur in people receiving significant medical care in hospitals, long-term acute care facilities, or nursing homes. Independent risk factors for CRE infection include use of beta-lactam antibiotics and the use of mechanical ventilation. Patients with diabetes have also been shown to be at an elevated risk for acquiring CRE infections. When compared to other hospitalized patients, those admitted from long-term acute care (LTAC) facilities have significantly higher incidence of colonization and infection rates. Another 2012 multicenter study found that over 30% of patients with recent exposure to LTAC were colonized or infected with CRE. A person susceptible to CRE transmission is more likely to be female, have a greater number of parenteral nutrition-days (meaning days by which the person received nutrition via the bloodstream), and to have had a significant number of days breathing through a ventilator.

Infections with carbapenem-resistant "Klebsiella pneumoniae" were associated with organ/stem cell transplantation, mechanical ventilation, exposure to antimicrobials, and overall longer length of stay in hospitals.

People most likely to acquire carbapenem-resistant bacteria are those already receiving medical attention. In a study carried out at Sheba medical center, there was a trend toward worse Charleson Comorbidity scores in patients who acquired CRKP during ICU stay. Those at highest risk are patients receiving an organ or stem cell implantation, use of mechanical ventilation, or have to have an extended stay in the hospital along with exposure to antimicrobials. In a study performed in Singapore, the acquisition of ertapenem-resistant Enterobacteriaceae to the acquisition of CRE. Exposure to antibiotics, especially fluoroquinolones, and previous hospitalization dramatically increased the risk of acquisition carbapenem-resistant bacteria. This study found that carbapenem-resistant acquisition has a significantly higher mortality rate and poorer clinical response compared to that of the ertapenem-resistance acquisition.

Bacteruria (also known as urinary tract infection) caused by CRKp and CSKp have similar risk factors. These include prior antibiotic use, admittance to an ICU, use of a permanent urinary catheter, and previous invasive procedures or operations. A retrospective study of patients with CRKp and CSKp infection asserted that the use of cephalosporins (a class of β-lactam antibiotics) used before invasive procedures was higher in patients with CRKp infection, suggesting that it is a risk factor.

In a three-year study, the prevalence of CRE was shown to be proportional to the lengths of stays of the patients in those hospitals. Policies regarding contact precaution for patients infected or colonized by Gram-negative pathogens were also observed in hospitals reporting decreases in CRE prevalence.

One case study showed that patients with a compromised immune response are especially susceptible to both CRE exposure and infection. In one study, an elderly patient with acute lymphoblastic leukemia being treated in a long-term care facility contracted a CRE infection. Her age and condition, combined with her environment and regulation by a catheter and mechanical ventilation, all contributed to a higher susceptibility. This highlights the importance of finding the source of the bacteria, as members of this class of patients are at continued risk for infection. Infection control and prevention of CRE should be the main focus in managing patients at high risk.

Another major risk factor is being in a country with unregulated antibiotic distribution. In countries where antibiotics are over-the counter and obtainable without a prescription, the incidence and prevalence of CRE infections were higher. One study from Japan found that 6.4% of healthy adults carried ESBL (mostly cefotaximase)-producing strains compared to 58.4% in Thailand, where antibiotics are available over the counter and without prescription. An Egyptian research group found that 63.3% of healthy adults were colonized.

In February 2015, the FDA reported about a transmission risk when people undergo a gastroenterology procedure called endoscopic retrograde cholangiopancreatography, where an endoscope enters the mouth, passes the stomach, and ends in the duodenum; if incompletely disinfected, the device can transmit CRE from one patient to another. The FDA's safety communication came a day after the UCLA Health System, Los Angeles, notified more than 100 patients that they may have been infected with CRE during endoscopies between October 2014 and January 2015. The FDA had issued its first notice about the devices in 2009.

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.

A study performed at Strong Memorial Hospital in Rochester, New York, showed that infants ≤ 60 days old meeting the following criteria were at low-risk for having a serious bacterial illness:

- generally well-appearing

- previously healthy

- full term (at ≥37 weeks gestation)

- no antibiotics perinatally

- no unexplained hyperbilirubinemia that required treatment

- no antibiotics since discharge

- no hospitalizations

- no chronic illness

- discharged at the same time or before the mother

- no evidence of skin, soft tissue, bone, joint, or ear infection

- White blood cells (WBCs) count 5,000-15,000/mm

- absolute band count ≤ 1,500/mm

- urine WBC count ≤ 10 per high power field (hpf)

- stool WBC count ≤ 5 per high power field (hpf) "only in infants with diarrhea"

Those meeting these criteria likely do not require a lumbar puncture, and are felt to be safe for discharge home without antibiotic treatment, or with a single dose of intramuscular antibiotics, but will still require close outpatient follow-up.

One risk for Group B streptococcal infection (GBS) is Preterm rupture of membranes. Screening women for GBS (via vaginal and rectal swabbing) and treating culture positive women with intrapartum chemoprophylaxis is reducing the number of neonatal sepsis caused by GBS.

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.

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.

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

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

Transmission may occur via consumption of contaminated water, or when people share personal objects. In places with wet and dry seasons, water quality typically worsens during the wet season, and this correlates with the time of outbreaks. In areas of the world with four seasons, infections are more common in the winter. Bottle-feeding of babies with improperly sanitized bottles is a significant cause on a global scale. Transmission rates are also related to poor hygiene, especially among children, in crowded households, and in those with pre-existing poor nutritional status. After developing tolerance, adults may carry certain organisms without exhibiting signs or symptoms, and thus act as natural reservoirs of contagion. While some agents (such as "Shigella") only occur in primates, others may occur in a wide variety of animals (such as "Giardia").