Approximately 20–35% of people with severe sepsis and 30–70% of people with septic shock die. Lactate is a useful method of determining prognosis with those who have a level greater than 4 mmol/L having a mortality of 40% and those with a level of less than 2 mmol/L have a mortality of less than 15%.

There are a number of prognostic stratification systems such as APACHE II and Mortality in Emergency Department Sepsis. APACHE II factors in the person's age, underlying condition, and various physiologic variables to yield estimates of the risk of dying of severe sepsis. Of the individual covariates, the severity of underlying disease most strongly influences the risk of death. Septic shock is also a strong predictor of short- and long-term mortality. Case-fatality rates are similar for culture-positive and culture-negative severe sepsis. The Mortality in Emergency Department Sepsis (MEDS) score is simpler and useful in the emergency department environment.

Some people may experience severe long-term cognitive decline following an episode of severe sepsis, but the absence of baseline neuropsychological data in most people with sepsis makes the incidence of this difficult to quantify or to study.

"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.

"S. pneumoniae" is normally found in the nose and throat of 5–10% of healthy adults and 20–40% of healthy children. It can be found in higher amounts in certain environments, especially those where people are spending a great deal of time in close proximity to each other (day-care centers, military barracks). It attaches to nasopharyngeal cells through interaction of bacterial surface adhesins. This normal colonization can become infectious if the organisms are carried into areas such as the Eustachian tube or nasal sinuses where it can cause otitis media and sinusitis, respectively. Pneumonia occurs if the organisms are inhaled into the lungs and not cleared (again, viral infection, or smoking-induced ciliary paralysis might be contributing factors). The organism's polysaccharide capsule makes it resistant to phagocytosis and if there is no pre-existing anticapsular antibody alveolar macrophages cannot adequately kill the pneumococci. The organism spreads to the blood stream (where it can cause bacteremia) and is carried to the meninges, joint spaces, bones, and peritoneal cavity, and may result in meningitis, brain abscess, septic arthritis, or osteomyelitis.

"S. pneumoniae" has several virulence factors, including the polysaccharide capsule mentioned earlier, that help it evade a host's immune system. It has pneumococcal surface proteins that inhibit complement-mediated opsonization, and it secretes IgA1 protease that will destroy secretory IgA produced by the body and mediates its attachment to respiratory mucosa.

The risk of pneumococcal infection is much increased in persons with impaired IgG synthesis, impaired phagocytosis, or defective clearance of pneumococci. In particular, the absence of a functional spleen, through congenital asplenia, surgical removal of the spleen, or sickle-cell disease predisposes one to a more severe course of infection (overwhelming post-splenectomy infection) and prevention measures are indicated (see asplenia).

People with a compromised immune system, such as those living with HIV, are also at higher risk of pneumococcal disease. In HIV patients with access to treatment, the risk of invasive pneumoccal disease is 0.2–1% per year and has a fatality rate of 8%.

There is an association between pneumococcal pneumonia and influenza. Damage to the lining of the airways (respiratory epithelium) and upper respiratory system caused by influenza may facilitate pneumococcal entry and infection.

Other risk factors include smoking, injection drug use, Hepatitis C, and COPD.

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".

Gram-negative bacteria are seen less frequently: "Haemophilus influenzae" (), "Klebsiella pneumoniae" (), "Escherichia coli" (), "Pseudomonas aeruginosa" (), "Bordetella pertussis", and "Moraxella catarrhalis" are the most common.

These bacteria often live in the gut and enter the lungs when contents of the gut (such as vomit or faeces) are inhaled.

Sepsis causes millions of deaths globally each year and is the most common cause of death in people who have been hospitalized. The worldwide incidence of sepsis is estimated to be 18 million cases per year. In the United States sepsis affects approximately 3 in 1,000 people, and severe sepsis contributes to more than 200,000 deaths per year.

Sepsis occurs in 1–2% of all hospitalizations and accounts for as much as 25% of ICU bed utilization. Due to it rarely being reported as a primary diagnosis (often being a complication of cancer or other illness), the incidence, mortality, and morbidity rates of sepsis are likely underestimated. A study by the Agency for Healthcare Research and Quality (AHRQ) of selected States found that there were approximately 651 hospital stays per 100,000 population with a sepsis diagnosis in 2010. It is the second-leading cause of death in non-coronary intensive care unit (ICU) and the tenth-most-common cause of death overall (the first being heart disease). Children under 12 months of age and elderly people have the highest incidence of severe sepsis. Among U.S. patients who had multiple sepsis hospital admissions in 2010, those who were discharged to a skilled nursing facility or long term care following the initial hospitalization were more likely to be readmitted than those discharged to another form of care. A study of 18 U.S. States found that, amongst Medicare patients in 2011, sepsis was the second most common principal reason for readmission within 30 days.

Several medical conditions increase a person's susceptibility to infection and developing sepsis. Common sepsis risk factors include age (especially the very young and old); conditions that weaken the immune system such as cancer, diabetes, or the absence of a spleen; and major trauma and burns.

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

The Centers for Disease Control and Prevention (CDC) estimated roughly 1.7 million hospital-associated infections, from all types of bacteria combined, cause or contribute to 99,000 deaths each year. Other estimates indicate 10%, or 2 million, patients a year become infected, with the annual cost ranging from $4.5 billion to $11 billion. In the USA, the most frequent type of infection hospitalwide is urinary tract infection (36%), followed by surgical site infection (20%), and bloodstream infection and pneumonia (both 11%).

In 2012 the Health Protection Agency reported the prevalence rate of HAIs in England was 6.4% in 2011, against a rate of 8.2% in 2006. With respiratory tract, urinary tract and surgical site infections the most common types of HAI reported.

The incidence of pleural empyema and the prevalence of specific causative microorganisms varies depending on the source of infection (community acquired vs. hospital acquired pneumonia), the age of the patient and host immune status. Risk factors include alcoholism, drug use, HIV infection, neoplasm and pre-existent pulmonary disease. Pleural empyema was found in 0.7% of 3675 patients needing hospitalization for a community acquired pneumonia in a recent Canadian single-center prospective study. A multi-center study from the UK including 430 adult patients with community acquired pleural empyema found negative pleural-fluid cultures in 54% of patients, Streptococcus milleri group in 16%, Staphylococcus aureus in 12%, Streptococcus pneumoniae in 8%, other Streptococci in 7% and anaerobic bacteria in 8%. Given the difficulties in culturing anaerobic bacteria the frequency of the latter (including mixed infections) might be underestimated.

The risk of empyema in children seems to be comparable to adults. Using the United States Kids’ Inpatient Database the incidence is calculated to be around 1.5% in children hospitalized for community acquired pneumonia, although percentages up to 30% have been reported in individual hospitals, a difference which may be explained by an transient endemic of highly invasive serotype or overdiagnosis of small parapneumonic effusions. The distribution of causative organisms does differ greatly from that in adults: in an analysis of 78 children with community acquired pleural empyema, no micro-organism was found in 27% of patients, Streptococcus pneumoniae in 51%, Streptococcus pyogenes in 9% and Staphylococcus aureus in 8%.

Although pneumococcal vaccination dramatically decreased the incidence of pneumonia in children, it did not have this effect on the incidence of complicated pneumonia. It has been shown that the incidence of empyema in children was already on the rise at the end of the 20th century, and that the widespread use of pneumococcal vaccination did not slow down this trend. This might in part be explained by a change in prevalence of (more invasive) pneumococcal serotypes, some of which are not covered by the vaccine, as well a rise in incidence of pneumonia caused by other streptococci and staphylococci. The incidence of empyema seems to be rising in the adult population as well, albeit at a slower rate.

In the western world, GBS (in the absence of effective prevention measures) is the main cause of bacterial infections in newborns, such as septicemia, pneumonia, and meningitis, which can lead to death or long-term after effects.

GBS infections in newborns are separated into two clinical types, early-onset disease (GBS-EOD) and late-onset disease (GBS-LOD). GBS-EOD manifests from 0 to 7 living days in the newborn, most of the cases of EOD being apparent within 24 h from birth. GBS-LOD starts between 7 and 90 days after birth.

The most common clinical syndromes of GBS-EOD are septicemia without apparent location, pneumonia, and less frequently meningitis. Bacteremia without a focus occurs in 80-85%, pneumonia in 10-15%, and meningitis in 5-10% of cases. The initial clinical findings are respiratory signs in more than 80% of cases. Neonates with meningitis often have an initial clinical presentation identical to presentation in those without meningeal affectation. An exam of the cerebrospinal fluid is often necessary to rule out meningitis.

Colonization with GBS during labour is the primary risk factor for the development of GBS-EOD. GBS-EOD is acquired vertically (vertical transmission), through exposure of the fetus or the baby to GBS from the vagina of a colonized woman, either "in utero" (because of ascending infection) or during birth, after rupture of membranes. Infants can also be infected during passage through the birth canal, nevertheless, newborns who acquire GBS through this route can only become colonized, and these colonized infants usually do not develop GBS-EOD.

Roughly 50% of newborns of GBS colonized mothers are also GBS colonized and (without prevention measures) 1-2% of these newborns will develop GBS-EOD.

In the past, the incidence of GBS-EOD ranged from 0.7 to 3.7 per thousand live births in the US, and from 0.2 to 3.25 per thousand in Europe.

In 2008, after widespread use of antenatal screening and intrapartum antibiotic prophylaxis, the Centers for Disease Control and Prevention of United States reported an incidence of 0.28 cases of GBS-EOD per thousand live births in the US.

Though maternal GBS colonization is the key determinant for GBS-EOD, other factors also increase the risk. These factors are:

- Onset of labour before 37 weeks of gestation (premature birth)

- Prolonged rupture of membranes (longer duration of membrane rupture) (≥18 h before delivery)

- Intrapartum (during childbirth) fever (>38 °C, >100.4 °F)

- Amniotic infections (chorioamnionitis)

- Young maternal age

Nevertheless, most babies who develop GBS-EOD are born to colonized mothers without any of these risk factors. Heavy GBS vaginal colonization is also associated with a higher risk for GBS-EOD. Women who had one of these risk factors but who are not GBS colonized at labour are at low risk for GBS-EOD compared to women who were colonized prenatally, but had none of the aforementioned risk factors.

Presence of low levels of anticapsular antibodies against GBS in the mother are also of great importance for the development of GBS-EOD.

Because of that, a previous sibling with GBS-EOD is also an important risk factor for the development of the infection in subsequent deliveries, probably reflecting the lack of protective antibodies in the mother.

Overall, the case fatality rates from GBS-EOD have declined, from 50% observed in studies from the 1970s to between 2 and 10% in recent years, mainly as a consequence of improvements in therapy and management. Fatal neonatal infections by GBS are more frequent among premature infants.

GBS-LOD affects infants from 7 days to 3 months of age and has a lower case fatality rate (1%-6%) than GBS-EOD. Clinical syndromes of GBS-EOD are bacteremia without a focus (65%), meningitis (25%), cellulitis, osteoarthritis, and pneumonia.

Prematurity has been reported to be the main risk factor. Each week of decreasing gestation increases the risk by a factor of 1.34 for developing GBS-LOD.

GBS-LOD is not acquired through vertical transmission during delivery; it can be acquired later from the mother from breast milk or from environmental and community sources.

GBS-LOD commonly shows nonspecific signs, and diagnosis should be made obtaining blood cultures in febrile newborns. Hearing loss and mental impairment can be a long-term consequence of GBS meningitis.

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.

Pneumococcal pneumonia is a type of bacterial pneumonia that is specifically caused by Streptococcus pneumoniae. "S. pneumoniae" is also called pneumococcus. It is the most common bacterial pneumonia found in adults. The estimated number of Americans with pneumococcal pneumonia is 900,000 annually, with almost 400,000 cases hospitalized and fatalities accounting for 5-7% of these cases.

The symptoms of pneumococcal pneumonia can occur suddenly, typically presenting as a severe chill, later including a severe fever, cough, shortness of breath, rapid breathing, and chest pains. Other symptoms like nausea, vomiting, headache, fatigue, and muscle aches could also accompany the original symptoms. Sometimes the coughing can produce rusty or blood-streaked sputum. In 25% of cases, a parapneumonic effusion may occur. Chest X-rays will typically show lobar consolidation or patchy infiltrates.

In most cases, once pneumococcal pneumonia has been identified, doctors will prescribe antibiotics. These antibiotic usually help alleviate and eliminate symptoms between 12 and 36 hours after being taken. Despite most antibiotics' effectiveness in treating the disease, sometimes the bacteria can resist the antibiotics, causing symptoms to worsen. Additionally, age and health of the infected patient can contribute to the effectiveness of the antibiotics. A vaccine has also been developed for the prevention of pneumococcal pneumonia, recommended to children under age five as well as adults over the age of 65.

While it has been commonly known that the influenza virus increases one's chances of contracting pneumonia or meningitis caused by the streptococcus pneumonaie bacteria, new medical research in mice indicates that the flu is actually a necessary component for the transmission of the disease. Researcher Dimitri Diavatopoulo from the Radboud University Nijmegen Medical Centre in the Netherlands describes his observations in mice, stating that in these animals, the spread of the bacteria only occurs between animals already infected with the influenza virus, not between those without it. He says that these findings have only been inclusive in mice, however, he believes that the same could be true for humans.

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.

Though GBS colonization is asymptomatic and, in general, does not cause problems, it can sometimes cause serious illness for the mother and the baby during gestation and after delivery. GBS infections in the mother can cause chorioamnionitis (intra-amniotic infection or severe infection of the placental tissues) infrequently, and postpartum infections (after birth). GBS urinary tract infections may induce labour and cause premature delivery (preterm birth) and miscarriage.

Vaccination helps prevent bronchopneumonia, mostly against influenza viruses, adenoviruses, measles, rubella, streptococcus pneumoniae, haemophilus influenzae, diphtheria, bacillus anthracis, chickenpox, and bordetella pertussis.

Lower respiratory infectious disease is the fifth-leading cause of death and the combined leading infectious cause of death, being responsible for 2·74 million deaths worldwide. This is generally similar to estimates in the 2010 Global Burden of Disease study.

This total only accounts for "Streptococcus pneumoniae" and "Haemophilus Influenzae" infections and does not account for atypical or nosocomial causes of lower respiratory disease, therefore underestimating total disease burden.

All patients with empyema require outpatient follow-up with a repeat chest X-ray and inflammatory biochemistry analysis within 4 weeks following discharge. Chest radiograph returns to normal in the majority of patients by 6 months. Patients should of course be advised to return sooner if symptoms redevelop. Long-term sequelae of pleural empyema are rare but include bronchopleural fistula formation, recurrent empyema and pleural thickening, which may lead to functional lung impairment needing surgical decortication.

Approximately 15% of adult patients with pleural infection die within 1 year of the event, although deaths are usually due to comorbid conditions and not directly due to sepsis from the empyema. Mortality in children is generally reported to be less than 3%. No reliable clinical, radiological or pleural fluid characteristics accurately determine patients’ prognosis at initial presentation.

In birds, "Chlamydia psittaci" infection is referred to as avian chlamydiosis (AC). Infected birds shed the bacteria through feces and nasal discharges, which can remain infectious for several months. Many strains remain quiescent in birds until activated under stress. Birds are excellent, highly mobile vectors for the distribution of chlamydial infection because they feed on, and have access to, the detritus of infected animals of all sorts.

"C. psittaci" in birds is often systemic and infections can be inapparent, severe, acute or chronic with intermittent shedding. Signs in birds include "inflamed eyes, difficulty in breathing, watery droppings and green urates."

Untreated, bacterial meningitis is almost always fatal. Viral meningitis, in contrast, tends to resolve spontaneously and is rarely fatal. With treatment, mortality (risk of death) from bacterial meningitis depends on the age of the person and the underlying cause. Of newborns, 20–30% may die from an episode of bacterial meningitis. This risk is much lower in older children, whose mortality is about 2%, but rises again to about 19–37% in adults. Risk of death is predicted by various factors apart from age, such as the pathogen and the time it takes for the pathogen to be cleared from the cerebrospinal fluid, the severity of the generalized illness, a decreased level of consciousness or an abnormally low count of white blood cells in the CSF. Meningitis caused by "H. influenzae" and meningococci has a better prognosis than cases caused by group B streptococci, coliforms and "S. pneumonia". In adults, too, meningococcal meningitis has a lower mortality (3–7%) than pneumococcal disease.

In children there are several potential disabilities which may result from damage to the nervous system, including sensorineural hearing loss, epilepsy, learning and behavioral difficulties, as well as decreased intelligence. These occur in about 15% of survivors. Some of the hearing loss may be reversible. In adults, 66% of all cases emerge without disability. The main problems are deafness (in 14%) and cognitive impairment (in 10%).

Tuberculous meningitis in children continues to be associated with a significant risk of death even with treatment (19%), and a significant proportion of the surviving children have ongoing neurological problems. Just over a third of all cases survives with no problems.

Treatment for gastroenteritis due to "Y. enterocolitica" is not needed in the majority of cases. Severe infections with systemic involvement (sepsis or bacteremia) often requires aggressive antibiotic therapy; the drugs of choice are doxycycline and an aminoglycoside. Alternatives include cefotaxime, fluoroquinolones, and co-trimoxazole.

Bacterial and viral meningitis are contagious, but neither is as contagious as the common cold or flu. Both can be transmitted through droplets of respiratory secretions during close contact such as kissing, sneezing or coughing on someone, but cannot be spread by only breathing the air where a person with meningitis has been. Viral meningitis is typically caused by enteroviruses, and is most commonly spread through fecal contamination. The risk of infection can be decreased by changing the behavior that led to transmission.

Long-term antibiotics, while they decrease rates of infection during treatment, have an unknown effect on long-term outcomes such as hearing loss. This method of prevention has been associated with emergence of antibiotic-resistant otitic bacteria. They are thus not recommended.

Pneumococcal conjugate vaccines (PCV) in early infancy, decreases the risk of acute otitis media in healthy infants. PCV is recommended for all children, and, if implemented broadly, PCV would have a significant public health benefit. Influenza vaccine is recommended annually for all children. PCV does not appear to decrease the risk of otitis media when given to high-risk infants or for older children who have previously experienced otitis media.

Risk factors such as season, allergy predisposition and presence of older siblings are known to be determinants of recurrent otitis media and persistent middle-ear effusions (MEE). History of recurrence, environmental exposure to tobacco smoke, use of daycare, and lack of breastfeeding have all been associated with increased risk of development, recurrence, and persistent MEE. Thus, cessation of smoking in the home should be encouraged, daycare attendance should be avoided or daycare facilities with the fewest attendees should be recommended, and breastfeeding should be promoted.

There is some evidence that breastfeeding for the first year of life is associated with a reduction in the number and duration of OM infections. Pacifier use, on the other hand, has been associated with more frequent episodes of AOM.

Evidence does not support zinc supplementation as an effort to reduce otitis rates except maybe in those with severe malnutrition such as marasmus.