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".

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.

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.

Vancomycin-resistant "Enterococcus", or vancomycin-resistant enterococci (VRE), are bacterial strains of the genus "Enterococcus" that are resistant to the antibiotic vancomycin.

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).

Once the individual has VRE, it is important to ascertain which "strain".

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.

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.

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.

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

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

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.

Spontaneous bacterial peritonitis (SBP) is the development of a bacterial infection in the peritoneum causing peritonitis, despite the absence of an obvious source for the infection. It occurs almost exclusively in people with portal hypertension (increased pressure over the portal vein), usually as a result of cirrhosis of the liver. It can also occur in patients with nephrotic syndrome.

The diagnosis of SBP requires paracentesis (aspiration of fluid with a needle) from the abdominal cavity. If the fluid contains bacteria or large numbers of neutrophil granulocytes (>250 cells/µL) (a type of white blood cells), infection is confirmed and antibiotics are required to avoid complications. In addition to antibiotics, infusions of albumin are usually administered.

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

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).

An overwhelming post-splenectomy infection (OPSI) or Overwhelming post-splenectomy sepsis (OPSS) is a rare but rapidly fatal infection occurring in individuals following removal of the spleen. The infections are typically characterized by either meningitis or sepsis, and are caused by encapsulated organisms including "Streptococcus pneumoniae".

The risk of OPSI is 0.23–0.42 percent per year, with a lifetime risk of 5 percent. Most infections occur in the first few years following splenectomy, but the risk of OPSI is lifelong. OPSI is almost always fatal without treatment, and modern treatment has decreased the mortality to approximately 40–70 percent. Individuals with OPSI are most commonly treated with antibiotics and supportive care. Measures to prevent OPSI include vaccination and prophylactic antibiotics.

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.

Hospital-acquired pneumonia (HAP) or nosocomial pneumonia refers to any pneumonia contracted by a patient in a hospital at least 48–72 hours after being admitted. It is thus distinguished from community-acquired pneumonia. It is usually caused by a bacterial infection, rather than a virus.

HAP is the second most common nosocomial infection (after urinary tract infections) and accounts for 15–20% of the total. It is the most common cause of death among nosocomial infections and is the primary cause of death in intensive care units.

HAP typically lengthens a hospital stay by 1–2 weeks.

Common symptoms of "Staphylococcus aureus" food poisoning include: a rapid onset which is usually 1–6 hours, nausea, explosive vomiting for up to 24 hours, abdominal cramps/pain, headache, weakness, diarrhea and usually a subnormal body temperature. Symptoms usually start one to six hours after eating and last less than 12 hours. The duration of some cases may take two or more days to fully resolve.

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.

The following is a list of common signs and symptoms found with neonatal meningitis.

- Fever

- poor appetite

- anterior fontanelle bulging

- seizure

- jitteriness

- dyspnea

- irritability

- anorexia

- vomiting

- diarrhea

- abdominal distention (increase in abdominal size)

- neck rigidity

- cyanosis

- jaundice

- and sunset eyes (downward gaze of the eyes)

- abnormal body temperature (hypo-or hyperthermia)

- change of activity (lethargy or irritability)

Unfortunately these symptoms are unspecific and may point to many different conditions.

Laboratory features that are characteristic of neonatal bacterial meningitis include:

- Isolation of a bacterial pathogen from the cerebrospinal fluid (CSF) by culture and/or visualization by Gram stain

- Increased CSF white blood cell (WBC) count (typically >1000 WBC/mL, but may be lower, especially with gram-positive organisms) with a predominance of neutrophils

- Elevated CSF protein concentration (>150 mg/dL in preterm (premature birth) and >100 mg/dL in term (on time) infants)

- Decreased CSF glucose concentration (<20 mg/dL [1.1 mmol/L] in preterm (premature birth) and <30 mg/dL [1.7 mmol/L] in term (on time) infants)

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

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

The 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.

Staphylococcal enteritis is an inflammation that is usually caused by eating or drinking substances contaminated with staph enterotoxin. The toxin, not the bacterium, settles in the small intestine and causes inflammation and swelling. This in turn can cause abdominal pain, cramping, dehydration, diarrhea and fever.

"Staphylococcus aureus" is a Gram-positive, facultative anaerobe, coccal (round shaped) bacteria that appears in grape-like clusters that can thrive in high salt and low water activity habitats. "S. aureus" bacteria can live on the skin which is one of the primary modes of transmission. "S. aureus" can cause a range of illnesses from minor skin infections to Staphylococcus aureus food poisoning enteritis. Since humans are the primary source, cross-contamination is the most common way the microorganism is introduced into foods. Foods at high risks are those prepared in large quantities.

Staphylococcus aureus is a true food poisoning organism. It produces a heat stable enterotoxin when allowed to grow for several hours in foods such as cream-filled baked goods, poultry meat, gravies, eggs, meat salads, puddings and vegetables. It is important to note that the toxins may be present in dangerous amounts in foods that have no signs of spoilage, such as a bad smell, any off color, odor, or textural or flavor change.

Enteritis is the inflammation of the small intestine. It is generally caused by eating or drinking substances that are contaminated with bacteria or viruses. The bacterium and/or toxin settles in the small intestine and cause inflammation and swelling. This in turn can cause abdominal pain, cramping, diarrhea, fever, and dehydration. There are other types of enteritis, the types include: bacterial gastroenteritis, "Campylobacter" enteritis, "E. coli" enteritis, radiation enteritis, "Salmonella" enteritis and "Shigella" enteritis.