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.

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.

The main manifestations of peritonitis are acute abdominal pain, abdominal tenderness and abdominal guarding, which are exacerbated by moving the peritoneum, e.g., coughing (forced cough may be used as a test), flexing one's hips, or eliciting the Blumberg sign (a.k.a. rebound tenderness, meaning that pressing a hand on the abdomen elicits less pain than releasing the hand abruptly, which will aggravate the pain, as the peritoneum snaps back into place). Rigidity (involuntary contraction of the abdominal muscles) is the most specific exam finding for diagnosing peritonitis (+ likelihood ratio: 3.9). The presence of these signs in a patient is sometimes referred to as peritonism. The localization of these manifestations depends on whether peritonitis is localized (e.g., appendicitis or diverticulitis before perforation), or generalized to the whole abdomen. In either case, pain typically starts as a generalized abdominal pain (with involvement of poorly localizing innervation of the visceral peritoneal layer), and may become localized later (with the involvement of the somatically innervated parietal peritoneal layer). Peritonitis is an example of an acute abdomen.

In normal conditions, the peritoneum appears greyish and glistening; it becomes dull 2–4 hours after the onset of peritonitis, initially with scarce serous or slightly turbid fluid. Later on, the exudate becomes creamy and evidently suppurative; in dehydrated patients, it also becomes very inspissated. The quantity of accumulated exudate varies widely. It may be spread to the whole peritoneum, or be walled off by the omentum and viscera. Inflammation features infiltration by neutrophils with fibrino-purulent exudation.

"Streptococcus pneumoniae" () is the most common bacterial cause of pneumonia in all age groups except newborn infants. "Streptococcus pneumoniae" is a Gram-positive bacterium that often lives in the throat of people who do not have pneumonia.

Other important Gram-positive causes of pneumonia are "Staphylococcus aureus" () and "Bacillus anthracis".

Intraabdominal infection (IAI) is a group of infections that occur within the abdominal cavity. They vary from appendicitis to fecal peritonitis. Risk of death despite treatment is often high.

The presentation of acute appendicitis includes abdominal pain, nausea, vomiting, and fever. As the appendix becomes more swollen and inflamed, it begins to irritate the adjoining abdominal wall. This leads to the localization of the pain to the right lower quadrant. This classic migration of pain may not be seen in children under three years. This pain can be elicited through signs and can be severe. Signs include localized findings in the right iliac fossa. The abdominal wall becomes very sensitive to gentle pressure (palpation). There is severe pain on sudden release of deep pressure in the lower abdomen (rebound tenderness). If the appendix is retrocecal (localized behind the cecum), even deep pressure in the right lower quadrant may fail to elicit tenderness (silent appendix). This is because the cecum, distended with gas, protects the inflamed appendix from pressure. Similarly, if the appendix lies entirely within the pelvis, there is usually complete absence of abdominal rigidity. In such cases, a digital rectal examination elicits tenderness in the rectovesical pouch. Coughing causes point tenderness in this area (McBurney's point), historically called Dunphy's sign.

Inflammation can spread to other parts of the gut in patients with typhlitis. The condition can also cause the cecum to become distended and can cut off its blood supply. This and other factors can result in necrosis and perforation of the bowel, which can cause peritonitis and sepsis.

Historically, the mortality rate for typhlitis was as high as 50%, mostly because it is frequently associated with bowel perforation. More recent studies have demonstrated better outcomes with prompt medical management, generally with resolution of symptoms with neutrophil recovery without death

The clinical presentation of both the adult and pediatric patient with pleural empyema depends upon several factors, including the causative micro-organism. Most cases present themselves in the setting of a pneumonia, although up to one third of patients do not have clinical signs of pneumonia and as many as 25% of cases are associated with trauma (including surgery). Typical symptoms include cough, chest pain, shortness of breath and fever.

Signs and symptoms of typhlitis may include diarrhea, a distended abdomen, fever, chills, nausea, vomiting, and abdominal pain or tenderness.

Bacterial pneumonia is a type of pneumonia caused by bacterial infection.

Pleural empyema is a collection of pus in the pleural cavity caused by microorganisms, usually bacteria. Often it happens in the context of a pneumonia, injury, or chest surgery. It is one of various kinds of pleural effusion. There are three stages: exudative, when there is an increase in pleural fluid with or without the presence of pus; fibrinopurulent, when fibrous septa form localized pus pockets; and the final organizing stage, when there is scarring of the pleura membranes with possible inability of the lung to expand. Simple pleural effusions occur in up to 40% of bacterial pneumonias. They are usually small and resolve with appropriate antibiotic therapy. If however an empyema develops additional intervention is required.

Pylephlebitis (also called pyelophlebitis and infective suppurative thrombosis of the portal vein) is an uncommon thrombophlebitis of the portal vein or any of its branches (i.e. a portal vein thrombosis) that is caused by infection. It is usually a complication of intraabdominal sepsis, most often following diverticulitis, perforated appendicitis, or peritonitis. Considered uniformly lethal in the pre-antibiotic era, it still carries a mortality of 10-30%.

It typically presents with fever, rigors, and right upper quadrant abdominal pain, but sometimes abdominal pain may be absent. Liver function test abnormalities are usually present but frank jaundice is uncommon. In the modern era, it is usually diagnosed by CT scans of the abdomen and pelvis. Bacteriology is often polymicrobial and blood cultures are positive in some cases. A significant fraction of people presenting with this condition have an underlying hypercoagulable state.

Treatment is with a prolonged course of broad-spectrum antibiotics, with the addition of anticoagulants if other clots are present outside the portal vein or if fever persists on antibiotic therapy.

It is a cause of portal hypertension and can cause bowel ischemia sometimes leading to bowel infarction.

Usually the atypical causes also involve atypical symptoms:

- No response to common antibiotics such as sulfonamide and beta-lactams like penicillin.

- No signs and symptoms of lobar consolidation, meaning that the infection is restricted to small areas, rather than involving a whole lobe. As the disease progresses, however, the look can tend to lobar pneumonia.

- Absence of leukocytosis.

- Extrapulmonary symptoms, related to the causing organism.

- Moderate amount of sputum, or no sputum at all (i.e. non-productive).

- Lack of alveolar exudate.

- Despite general symptoms and problems with the upper respiratory tract (such as high fever, headache, a dry irritating cough followed later by a productive cough with radiographs showing consolidation), there are in general few physical signs. The patient looks better than the symptoms suggest.

Acute abdomen is occasionally used synonymously with peritonitis. While this is not entirely incorrect, peritonitis is the more specific term, referring to inflammation of the peritoneum. It manifests on physical examination as rebound tenderness, or pain upon "removal" of pressure more than on "application" of pressure to the abdomen. Peritonitis may result from several of the above diseases, notably appendicitis and pancreatitis. While rebound tenderness is commonly associated with peritonitis, the most specific finding is rigidity.

Twenty percent of infants born with meconium peritonitis will have vomiting and dilated bowels on x-rays which necessitates surgery.

Meconium peritonitis is sometimes diagnosed on prenatal ultrasound where it appears as calcifications within the peritoneum.

Pneumococcal infection is an infection caused by the bacterium "Streptococcus pneumoniae". "S. pneumoniae" is a common member of the bacterial flora colonizing the nose and throat of 5–10% of healthy adults and 20–40% of healthy children. However, it is also the cause of significant disease being a leading cause of pneumonia, bacterial meningitis, and sepsis. The World Health Organization estimate that in 2005 pneumococcal infections were responsible for the death of 1.6 million children worldwide.

The differential diagnoses of acute abdomen include but are not limited to:

1. Acute appendicitis

2. Acute peptic ulcer and its complications

3. Acute cholecystitis

4. Acute pancreatitis

5. Acute intestinal ischemia (see section below)

6. Acute diverticulitis

7. Ectopic pregnancy with tubal rupture

8. Ovarian torsion

9. Acute peritonitis (including hollow viscus perforation)

10. Acute ureteric colic

11. Bowel volvulus

12. Bowel obstruction

13. Acute pyelonephritis

14. Adrenal crisis

15. Biliary colic

16. Abdominal aortic aneurysm

17. Familial Mediterranean fever

18. Hemoperitoneum

19. Ruptured spleen

20. Kidney stone

21. Sickle cell anaemia

Additional problems may occur in the early stage of the illness. These may require specific treatment, and sometimes indicate severe illness or worse prognosis. The infection may trigger sepsis, a systemic inflammatory response syndrome of falling blood pressure, fast heart rate, high or abnormally low temperature, and rapid breathing. Very low blood pressure may occur at an early stage, especially but not exclusively in meningococcal meningitis; this may lead to insufficient blood supply to other organs. Disseminated intravascular coagulation, the excessive activation of blood clotting, may obstruct blood flow to organs and paradoxically increase the bleeding risk. Gangrene of limbs can occur in meningococcal disease. Severe meningococcal and pneumococcal infections may result in hemorrhaging of the adrenal glands, leading to Waterhouse-Friderichsen syndrome, which is often fatal.

The brain tissue may swell, pressure inside the skull may increase and the swollen brain may herniate through the skull base. This may be noticed by a decreasing level of consciousness, loss of the pupillary light reflex, and abnormal posturing. The inflammation of the brain tissue may also obstruct the normal flow of CSF around the brain (hydrocephalus). Seizures may occur for various reasons; in children, seizures are common in the early stages of meningitis (in 30% of cases) and do not necessarily indicate an underlying cause. Seizures may result from increased pressure and from areas of inflammation in the brain tissue. Focal seizures (seizures that involve one limb or part of the body), persistent seizures, late-onset seizures and those that are difficult to control with medication indicate a poorer long-term outcome.

Inflammation of the meninges may lead to abnormalities of the cranial nerves, a group of nerves arising from the brain stem that supply the head and neck area and which control, among other functions, eye movement, facial muscles, and hearing. Visual symptoms and hearing loss may persist after an episode of meningitis. Inflammation of the brain (encephalitis) or its blood vessels (cerebral vasculitis), as well as the formation of blood clots in the veins (cerebral venous thrombosis), may all lead to weakness, loss of sensation, or abnormal movement or function of the part of the body supplied by the affected area of the brain.

Signs and symptoms usually include a fever greater than , chills, low abdominal pain, and possibly bad smelling vaginal discharge.

In adults, the most common symptom of meningitis is a severe headache, occurring in almost 90% of cases of bacterial meningitis, followed by nuchal rigidity (the inability to flex the neck forward passively due to increased neck muscle tone and stiffness). The classic triad of diagnostic signs consists of nuchal rigidity, sudden high fever, and altered mental status; however, all three features are present in only 44–46% of bacterial meningitis cases. If none of the three signs are present, acute meningitis is extremely unlikely. Other signs commonly associated with meningitis include photophobia (intolerance to bright light) and phonophobia (intolerance to loud noises). Small children often do not exhibit the aforementioned symptoms, and may only be irritable and look unwell. The fontanelle (the soft spot on the top of a baby's head) can bulge in infants aged up to 6 months. Other features that distinguish meningitis from less severe illnesses in young children are leg pain, cold extremities, and an abnormal skin color.

Nuchal rigidity occurs in 70% of bacterial meningitis in adults. Other signs include the presence of positive Kernig's sign or Brudziński sign. Kernig's sign is assessed with the person lying supine, with the hip and knee flexed to 90 degrees. In a person with a positive Kernig's sign, pain limits passive extension of the knee. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary flexion of the knee and hip. Although Kernig's sign and Brudzinski's sign are both commonly used to screen for meningitis, the sensitivity of these tests is limited. They do, however, have very good specificity for meningitis: the signs rarely occur in other diseases. Another test, known as the "jolt accentuation maneuver" helps determine whether meningitis is present in those reporting fever and headache. A person is asked to rapidly rotate the head horizontally; if this does not make the headache worse, meningitis is unlikely.

Other problems can produce symptoms similar to those above, but from non-meningitic causes. This is called meningism or pseudomeningitis.

Meningitis caused by the bacterium "Neisseria meningitidis" (known as "meningococcal meningitis") can be differentiated from meningitis with other causes by a rapidly spreading petechial rash, which may precede other symptoms. The rash consists of numerous small, irregular purple or red spots ("petechiae") on the trunk, lower extremities, mucous membranes, conjuctiva, and (occasionally) the palms of the hands or soles of the feet. The rash is typically non-blanching; the redness does not disappear when pressed with a finger or a glass tumbler. Although this rash is not necessarily present in meningococcal meningitis, it is relatively specific for the disease; it does, however, occasionally occur in meningitis due to other bacteria. Other clues on the cause of meningitis may be the skin signs of hand, foot and mouth disease and genital herpes, both of which are associated with various forms of viral meningitis.

"S. pneumoniae" is responsible for 15–50% of all episodes of community acquired pneumonia, 30–50% of all cases of acute otitis media, and a significant proportion of bloodstream infections and bacterial meningitis.

As estimated by WHO in 2005 it killed about 1.6 million children every year worldwide with 0.7–1 million of them being under the age of five. The majority of these deaths were in developing countries.

Diagnosis is based on a medical history (symptoms) and physical examination which can be supported by an elevation of neutrophilic white blood cells and imaging studies if needed. (Neutrophils are the primary white blood cells that respond to a bacterial infection.) Histories fall into two categories, typical and atypical.

Typical appendicitis includes several hours of generalized abdominal pain that begins in the region of the umbilicus with associated anorexia, nausea, or vomiting. The pain then "localizes" into the right lower quadrant where the tenderness increases in intensity. It is possible the pain could localize to the left lower quadrant in people with situs inversus totalis. The combination of pain, anorexia, leukocytosis, and fever is classic.

Atypical histories lack this typical progression and may include pain in the right lower quadrant as an initial symptom. Irritation of the peritoneum (inside lining of the abdominal wall) can lead to increased pain on movement, or jolting, for example going over speedbumps. Atypical histories often require imaging with ultrasound or CT scanning.

Subphrenic abscess is a disease characterized by an accumulation of infected fluid between the diaphragm, liver, and spleen. This abscess develops after surgical operations like splenectomy.

Presents with cough, increased respiratory rate with shallow respiration, diminished or absent breath sounds, hiccups, dullness in percussion, tenderness over the 8th–11th ribs, fever, chills, anorexia and shoulder tip pain on the affected side. Lack of treatment or misdiagnosis could quickly lead to sepsis, septic shock, and death. It is also associated with peritonitis.

Signs and symptoms may include a sudden pain in the epigastrium to the right of the midline indicating the perforation of a duodenal ulcer. In a gastric ulcer perforation creates a history of burning pain in epigastrium, with flatulence and dyspepsia.

In intestinal perforation, pain starts from the site of perforation and spreads across the abdomen.

Gastrointestinal perforation results in severe abdominal pain intensified by movement, nausea, vomiting and hematemesis. Later symptoms include fever and or chills. In any case, the abdomen becomes rigid with tenderness and rebound tenderness. After some time the abdomen becomes silent and heart sounds can be heard all over. Patient stops passing flatus and motion, abdomen is distended.

The symptoms of esophageal rupture may include sudden onset of chest pain.