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.

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.

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.

HCAP is a condition in patients who can come from the community, but have frequent contact with the healthcare environment. Historically, the etiology and prognosis of nursing home pneumonia appeared to differ from other types of community acquired pneumonia, with studies reporting a worse prognosis and higher incidence of multi drug resistant organisms as etiology agents. The definition criteria which has been used is the same as the one which has been previously used to identify bloodstream healthcare associated infections.

HCAP is no longer recognized as a clinically independent entity. This is due to increasing evidence from a growing number of studies that many patients defined as having HCAP are not at high risk for MDR pathogens. As a result, 2016 IDSA guidelines removed consideration of HCAP as a separate clinical entity.

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.

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.

A recent retrospective study of all cases of Ecthyma gangrenosum from 2004-2010 in a university hospital in Mexico shows that neutropenia in immunocompromised patients is the most common risk factor for ecthyma gangrenosum.

Serratia infection refers to a disease caused by a species in the genus "Serratia".

The species involved is usually "Serratia marcescens".

It can cause nosocomial infections.

Infection with "Y. enterocolitica" can cause a variety of symptoms depending on the age of the person infected, therefore it's often referred to as "monkey of diseases". Common symptoms in children are fever, abdominal pain, and diarrhea, which is often bloody. Symptoms typically develop 4 to 7 days after exposure and may last 1 to 3 weeks or longer. In older children and adults, right-sided abdominal pain and fever may be the predominant symptoms, and may be confused with appendicitis. In a small proportion of cases, complications such as skin rash, joint pains, ileitis, erythema nodosum, and sometimes septicemia, acute arthritis or the spread of bacteria to the bloodstream (bacteremia) can occur.

Acute renal failure occurs in 55–70% of patients with STEC-HUS, although up to 70–85% recover renal function. Patients with aHUS generally have poor outcomes, with up to 50% progressing to ESRD or irreversible brain damage; as many as 25% die during the acute phase. However, with aggressive treatment, more than 90% of patients survive the acute phase of HUS, and only about 9% may develop ESRD. Roughly one-third of persons with HUS have abnormal kidney function many years later, and a few require long-term dialysis. Another 8% of persons with HUS have other lifelong complications, such as high blood pressure, seizures, blindness, paralysis, and the effects of having part of their colon removed. The overall mortality rate from HUS is 5–15%. Children and the elderly have a worse prognosis.

Haemorrhagic septicaemia is one of the most economically important pasteurelloses. Haemorrhagic septicaemia in cattle and buffaloes was previously known to be associated with one of two serotypes of "P. multocida": Asian B:2 and African E:2 according to the Carter-Heddleston system, or 6:B and 6:E using the Namioka-Carter system.

The disease occurs mainly in cattle and buffaloes, but has also been reported in goats ("Capra aegagrus hircus"), African buffalo ("Syncerus nanus"), camels, horses and donkeys ("Equus africanus asinus"), in pigs infected by serogroup B, and in wild elephants ("Elephas maximus"). Serotypes B:1 and B:3,4 have caused a septicaemic disease in antelope ("Antilocapra americana") and elk ("Cervus canadensis"), respectively. Serotype B:4 was associated with the disease in bison ("Bison bison").

Serotypes E:2 and B:2 were associated with HS outbreaks in Africa and Asia respectively. Serotype E:2 was reported in Senegal, Mali, Guinea, Ivory Coast, Nigeria, Cameroon, the Central African Republic and Zambia. However, it is now inaccurate to associate outbreaks in Africa with serotype E:2 as many outbreaks of HS in Africa have now been associated with serogroup B. In the same manner, serogroup E has been associated with outbreaks in Asia. For instance, one record of "Asian serotype" (B:2) was reported in Cameroon. Some reports showed that serotype B:2 may be present in some East African countries. Both serogroups B and E have been reported in Egypt and Sudan.

Natural routes of infection are inhalation and/or ingestion. Experimental transmission has succeeded using intranasal aerosol spray or oral drenching. When subcutaneous inoculation is used experimentally, it results in rapid onset of the disease, a shorter clinical course and less marked pathological lesions compared to the longer course of disease and more profound lesions of oral drenching and the intranasal infection by aerosols.

When HS was introduced for the first time into a geographic area, morbidity and mortality rates were high, approaching 100% unless animals were treated in the very early stages of disease.

Haemorrhagic shock occurs in about 1–2% of trauma cases. Up to one-third of people admitted to the intensive care unit (ICU) are in circulatory shock.

Acute prostatitis is a serious bacterial infection of the prostate gland. This infection is a medical emergency. It should be distinguished from other forms of prostatitis such as chronic bacterial prostatitis and chronic pelvic pain syndrome (CPPS).

The organism enters directly through the breakdown of mechanical defense barriers such as mucosa or skin. Immunocompromised conditions make the patient more susceptible to this infection and septicemia. In case of septicemia, the bacteria reaches the skin via the bloodstream. Defective humoral or cellular immune system increases the risk because the organism is not able to be cleared from the bloodstream. The main mechanism of the organism that is causing the typical skin lesions is the invasion of the organism into the arteries and veins in the dermis and subcutaneous tissues of the skin. This perivascular invasion leads to nodular formation, ulceration, vasculitis and necrosis due to impaired blood supply. Perivascular involvement is achieved by direct entry of bacteria through the skin or hematogenous spreading in case of sepsis.

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 prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. Septic shock however, is a grave condition with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse with a mortality rate between 70% and 90%.

A wide variety of clinical signs have been described for HS in cattle and buffaloes. The incubation periods (the time between exposure and observable disease) for buffalo calves 4–10 months of age varies according to the route of infection. The incubation period is 12–14 hours, approximately 30 hours and 46–80 hours for subcutaneous infection, oral infection and natural exposure, respectively.

There is variability in the duration of the clinical course of the disease. In the case of experimental subcutaneous infection, the clinical course lasted only a few hours, while it persisted for 2–5 days following oral infection and in buffaloes and cattle that had been exposed to naturally-infected animals. It has also been recorded from field observations that the clinical courses of per-acute and acute cases were 4–12 hours and 2–3 days, respectively.

Generally, progression of the disease in buffaloes and cattle is divided into three phases. Phase one is characterised by fever, with a rectal temperature of , loss of appetite and depression. Phase two is typified by increased respiration rate (40–50/minute), laboured breathing, clear nasal discharge (turns opaque and mucopurulent as the disease progresses), salivation and submandibular oedema spreading to the pectoral (brisket) region and even to the forelegs. Finally, in phase three, there is typically recumbency, continued acute respiratory distress and terminal septicaemia. The three phases overlap when the disease course is short. In general, buffaloes have a more acute onset of disease than cattle, with a shorter duration.

Noma neonatorum is a cutaneous condition, a manifestation of infection, usually "Pseudomonas aeruginosa" septicemia, and has been reported almost exclusively in developing countries.

Causes (listed in order of decreasing frequency) include endometritis, urinary tract infection, pneumonia/atelectasis, wound infection, and septic pelvic thrombophlebitis. Septic risk factors for each condition are listed in order of the postpartum day (PPD) on which the condition generally occurs.

- PPD 0: atelectasis risk factors include general anesthesia, cigarette smoking, and obstructive lung disease.

- PPD 1–2: urinary tract infections risk factors include multiple catheterization during labor, multiple vaginal examinations during labor, and untreated bacteriuria.

- PPD 2–3: endometritis ( the most common cause ) risk factors include emergency cesarean section, prolonged membrane rupture, prolonged labor, and multiple vaginal examinations during labor.

- PPD 4–5: wound infection risk factors include emergency cesarean section, prolonged membrane rupture, prolonged labor, and multiple vaginal examination during labor.

- PPD 5–6: septic pelvic thrombophlebitis risk factors include emergency cesarean section, prolonged membrane rupture, prolonged labor, and diffuse difficult vaginal childbirth.

- PPD 7–21: mastitis risk factors include nipple trauma from breastfeeding.

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.

A superinfection is a second infection superimposed on an earlier one, especially by a different microbial agent of exogenous or endogenous origin, that is resistant to the treatment being used against the first infection. Examples of this in bacteriology are the overgrowth of endogenous "Clostridium difficile" which occurs following treatment with a broad-spectrum antibiotic, and pneumonia or septicemia from "Pseudomonas aeruginosa" in some immuno-compromised patients.

In virology, the definition is slightly different. Superinfection is the process by which a cell that has previously been infected by one virus gets co-infected with a different strain of the virus, or another virus, at a later point in time. Viral superinfections may be resistant to the antiviral drug or drugs that were being used to treat the original infection. Viral superinfections may also be less susceptible to the host's immune response.

Pneumococcal septicemia, or whole-body infection caused by the "Streptococcus pneumoniae" bacteria, has been reported to cause autosplenectomy but is a very rare and poorly understood complication of the infection.

The most efficient treatment in breeding flocks or laying hens is individual intramuscular injections of a long-acting tetracycline, with the same antibiotic in drinking water, simultaneously. The mortality and clinical signs will stop within one week, but the bacteria might remain present in the flock.

Recurrent pyogenic cholangitis is characterised by recurrent bouts of bacterial cholangitis with primary hepatolithiasis. It is prevalent in Hong Kong and East Asian including China, Taiwan, Korea, Japan, Indonesia and the Philippines. Apart from affecting humans it is also a common disease in cats.