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.

Some strains of group A streptococci (GAS) cause severe infection. Severe infections are usually invasive, meaning that the bacteria has entered parts of the body where bacteria are not usually found, such as the blood, lungs, deep muscle or fat tissue. Those at greatest risk include children with chickenpox; persons with suppressed immune systems; burn victims; elderly persons with cellulitis, diabetes, vascular disease, or cancer; and persons taking steroid treatments or chemotherapy. Intravenous drug users also are at high risk. GAS is an important cause of puerperal fever worldwide, causing serious infection and, if not promptly diagnosed and treated, death in newly delivered mothers. Severe GAS disease may also occur in healthy persons with no known risk factors.

All severe GAS infections may lead to shock, multisystem organ failure, and death. Early recognition and treatment are critical. Diagnostic tests include blood counts and urinalysis as well as cultures of blood or fluid from a wound site.

Severe Group A streptococcal infections often occur sporadically but can be spread by person-to-person contact.

Public Health policies internationally reflect differing views of how the close contacts of people affected by severe Group A streptococcal infections should be treated. Health Canada and the US CDC recommend close contacts see their doctor for full evaluation and may require antibiotics; current UK Health Protection Agency guidance is that, for a number of reasons, close contacts should not receive antibiotics unless they are symptomatic but that they should receive information and advice to seek immediate medical attention if they develop symptoms. However, guidance is clearer in the case of mother-baby pairs: both mother and baby should be treated if either develops an invasive GAS infection within the first 28 days following birth (though some evidence suggests that this guidance is not routinely followed in the UK).

Group A β-hemolytic streptococcus can cause infections of the throat and skin. These may vary from very mild conditions to severe, life-threatening diseases. Although it is not completely clear what causes different people to develop different diseases as a result of infection with the same pathogenic bacteria, it is suspected that host phenotypic and epigenetic factors are the source of such variation. Indeed, the many virulence factors of GAS can influence the epigenetics of the host. Furthermore, persons with suppressed or compromised immune systems may be more susceptible to certain diseases caused by GAS than other persons with intact immune systems.

Humans may also carry the GAS either on the skin or in the throat and show no symptoms. These carriers are less contagious than symptomatic carriers of the bacteria.

The non-invasive infections caused by GAS tend to be less severe and more common. They occur when the bacteria colonizes the throat area, where it recognizes epithelial cells. The two most prominent infections of GAS are both non-invasive: strep throat (pharyngitis) where it causes 15- 30% of the childhood cases and 10% of adult cases, and impetigo. These may be effectively treated with antibiotics. Scarlet fever is also a non-invasive infection caused by GAS, although much less common.

The invasive infections caused by Group A β-hemolytic streptococcus tend to be more severe and less common. These occurs when the bacterium is able to infect areas where bacteria are not usually found, such as blood and organs. The diseases that may be caused as a result of this include streptococcal toxic shock syndrome (STSS), necrotizing fasciitis (NF), pneumonia, and bacteremia.

In addition, infection of GAS may lead to further complications and health conditions, namely acute rheumatic fever and poststreptococcal glomerulonephritis.

Most Common:

- impetigo, cellulitis, and erysipelas – infections of the skin which can be complicated by necrotizing fasciitis – skin, fascia and muscle

- strep throat AKA strep pharyngitis – pharynx

Less Common:

- Bacteremia can be associated with these infections, but is not typical.

- septic arthritis – joints

- osteomyelitis – bones

- vaginitis – vagina (more common in pre-pubescent girls)

- meningitis* – meninges

- sinusitis* – sinuses

- pneumonia* – pulmonary alveolus

The symptoms of strep throat usually improve within three to five days, irrespective of treatment. Treatment with antibiotics reduces the risk of complications and transmission; children may return to school 24 hours after antibiotics are administered. The risk of complications in adults is low. In children, acute rheumatic fever is rare in most of the developed world. It is, however, the leading cause of acquired heart disease in India, sub-Saharan Africa and some parts of Australia.

Complications arising from streptococcal throat infections include:

- Acute rheumatic fever

- Scarlet fever

- Streptococcal toxic shock syndrome

- Glomerulonephritis

- PANDAS syndrome

- Peritonsillar abscess

- Cervical lymphadenitis

- Mastoiditis

The economic cost of the disease in the United States in children is approximately $350 million annually.

This disease is most common among the elderly, infants, and children. People with immune deficiency, diabetes, alcoholism, skin ulceration, fungal infections, and impaired lymphatic drainage (e.g., after mastectomy, pelvic surgery, bypass grafting) are also at increased risk.

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.

Most cases of erysipelas are due to "Streptococcus pyogenes" (also known as beta-hemolytic group A streptococci), although non-group A streptococci can also be the causative agent. Beta-hemolytic, non-group A streptococci include "Streptococcus agalactiae", also known as group B strep or GBS. Historically, the face was most affected; today, the legs are affected most often. The rash is due to an exotoxin, not the "Streptococcus" bacteria, and is found in areas where no symptoms are present; e.g., the infection may be in the nasopharynx, but the rash is found usually on the upper dermis and superficial lymphatics.

Erysipelas infections can enter the skin through minor trauma, insect bites, dog bites, eczema, athlete's foot, surgical incisions and ulcers and often originate from streptococci bacteria in the subject's own nasal passages. Infection sets in after a small scratch or abrasion spreads, resulting in toxaemia.

Erysipelas does not affect subcutaneous tissue. It does not release pus, only serum or serous fluid. Subcutaneous edema may lead the physician to misdiagnose it as cellulitis, but the style of the rash is much more well circumscribed and sharply marginated than the rash of cellulitis.

Strep throat is caused by group A beta-hemolytic streptococcus (GAS or S. pyogenes). Other bacteria such as non–group A beta-hemolytic streptococci and fusobacterium may also cause pharyngitis. It is spread by direct, close contact with an infected person; thus crowding, as may be found in the military and schools, increases the rate of transmission. Dried bacteria in dust are not infectious, although moist bacteria on toothbrushes or similar items can persist for up to fifteen days. Contaminated food can result in outbreaks, but this is rare. Of children with no signs or symptoms, 12% carry GAS in their pharynx, and, after treatment, approximately 15% of those remain positive, and are true "carriers".

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.

Streptococcus species are the cause of opportunistic infections in poultry leading to acute and chronic conditions in affected birds. Disease varies according to the Streptococcal species but common presentations include septicaemia, peritonitis, salpingitis and endocarditis.

Common species affecting poultry include:

- "S. gallinaceus" in broiler chickens

- "S. gallolyticus" which is a pathogen of racing pigeons and turkey poults

- "S. dysgalactiae" in broiler chickens

- "S. mutans" in geese

- "S. pluranimalium" in broiler chickens

- "S. equi subsp. zooepidemicus" in chickens and turkeys

- "S. suis" in psittacine birds

The elderly and those with a weakened immune system are especially vulnerable to contracting cellulitis. Diabetics are more susceptible to cellulitis than the general population because of impairment of the immune system; they are especially prone to cellulitis in the feet, because the disease causes impairment of blood circulation in the legs, leading to diabetic foot or foot ulcers. Poor control of blood glucose levels allows bacteria to grow more rapidly in the affected tissue, and facilitates rapid progression if the infection enters the bloodstream. Neural degeneration in diabetes means these ulcers may not be painful, thus often become infected. Those who have suffered poliomyelitis are also prone because of circulatory problems, especially in the legs.

Immunosuppressive drugs, and other illnesses or infections that weaken the immune system, are also factors that make infection more likely. Chickenpox and shingles often result in blisters that break open, providing a gap in the skin through which bacteria can enter. Lymphedema, which causes swelling on the arms and/or legs, can also put an individual at risk.

Diseases that affect blood circulation in the legs and feet, such as chronic venous insufficiency and varicose veins, are also risk factors for cellulitis.

Cellulitis is also common among dense populations sharing hygiene facilities and common living quarters, such as military installations, college dormitories, nursing homes, oil platforms, and homeless shelters.

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.

The disease is spread by an infected horse when nasal discharge or pus from the draining lymph nodes contaminate pastures, feed troughs, brushes, bedding, tack etc.

Equines of any age may contract the disease, although younger and elderly equines are more susceptible. Young equines may lack immunity to the disease because they have not had prior exposure. Geriatric equines may have a weaker immune system.

Bacterial infections of the orbit have long been associated with a risk of catastrophic local

sequelae and intracranial spread.

The natural course of the disease, as documented by Gamble (1933), in the pre-antibiotic era,

resulted in death in 17% of patients and permanent blindness in 20%.

A horse with strangles will typically develop abscesses in the lymph nodes of the head and neck causing coughing fits and difficulty swallowing. Clinical signs include fever up to 106 °F and yellow coloured nasal discharge from both the nose and eyes.

Abscesses may form in other areas of the body, such as the abdomen, lungs and brain. This is considered a chronic form of strangles called "bastard strangles" and can have serious implications if the abscesses rupture. Horses develop this form of strangles when their immune systems are compromised or if the bacteria rapidly invades the body.

Strangles has a 8.1% mortality rate. Mortality is lower in cases without complications than it is in cases of bastard strangles. The disease is very contagious and morbidity is high. Precautions to limit the spread of the illness are necessary and those affected are normally isolated. An isolation period of 4–6 weeks is usually necessary to ensure that the disease is not still incubating before ending the quarantine.

The most common cause is viral infection and includes adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus. It can also be caused by Epstein-Barr virus, herpes simplex virus, cytomegalovirus, or HIV. The second most common cause is bacterial infection of which the predominant is Group A β-hemolytic streptococcus (GABHS), which causes strep throat. Less common bacterial causes include: "Staphylococcus aureus" (including methicillin resistant Staphylococcus aureus or MRSA ),"Streptococcus pneumoniae", "Mycoplasma pneumoniae", "Chlamydia pneumoniae", "Bordetella pertussis", "Fusobacterium" sp., "Corynebacterium diphtheriae", "Treponema pallidum", and "Neisseria gonorrhoeae".

Anaerobic bacteria have been implicated in tonsillitis and a possible role in the acute inflammatory process is supported by several clinical and scientific observations.

Under normal circumstances, as viruses and bacteria enter the body through the nose and mouth, they are filtered in the tonsils. Within the tonsils, white blood cells of the immune system destroy the viruses or bacteria by producing inflammatory cytokines like phospholipase A2, which also lead to fever. The infection may also be present in the throat and surrounding areas, causing inflammation of the pharynx.

Sometimes, tonsillitis is caused by an infection of spirochaeta and treponema, in this case called Vincent's angina or Plaut-Vincent angina.

The organism should be cultured and antibiotic sensitivity should be determined before treatment is started. Amoxycillin is usually effective in treating streptococcal infections.

Biosecurity protocols and good hygiene are important in preventing the disease.

Vaccination is available against "S. gallolyticus" and can also protect pigeons.

Horses may acquire cellulitis, usually secondarily to a wound (which can be extremely small and superficial) or to a deep-tissue infection, such as an abscess or infected bone, tendon sheath, or joint. Cellulitis from a superficial wound usually creates less lameness (grade 1–2 of 5) than that caused by septic arthritis (grade 4–5). The horse exhibits inflammatory edema, which is hot, painful swelling. This swelling differs from stocking up in that the horse does not display symmetrical swelling in two or four legs, but in only one leg. This swelling begins near the source of infection, but eventually continues down the leg. In some cases, the swelling also travels distally. Treatment includes cleaning the wound and caring for it properly, the administration of NSAIDs, such as phenylbutazone, cold hosing, applying a sweat wrap or a poultice, and mild exercise. Veterinarians may also prescribe antibiotics.

Cellulitis is also seen in staphylococcal and corynebacterial mixed infections in bulls.

Since the advent of penicillin in the 1940s, a major preoccupation in the treatment of streptococcal tonsillitis has been the prevention of rheumatic fever, and its major effects on the nervous system (Sydenham's chorea) and heart. Recent evidence would suggest that the rheumatogenic strains of group A beta hemolytic strep have become markedly less prevalent and are now only present in small pockets such as in Salt Lake City, USA. This brings into question the rationale for treating tonsillitis as a means of preventing rheumatic fever.

Complications may rarely include dehydration and kidney failure due to difficulty swallowing, blocked airways due to inflammation, and pharyngitis due to the spread of infection.

An abscess may develop lateral to the tonsil during an infection, typically several days after the onset of tonsillitis. This is termed a peritonsillar abscess (or quinsy).

Rarely, the infection may spread beyond the tonsil resulting in inflammation and infection of the internal jugular vein giving rise to a spreading septicaemia infection (Lemierre's syndrome).

In chronic/recurrent cases (generally defined as seven episodes of tonsillitis in the preceding year, five episodes in each of the preceding two years or three episodes in each of the preceding three years), or in acute cases where the palatine tonsils become so swollen that swallowing is impaired, a tonsillectomy can be performed to remove the tonsils. Patients whose tonsils have been removed are still protected from infection by the rest of their immune system.

In strep throat, very rarely diseases like rheumatic fever or glomerulonephritis can occur. These complications are extremely rare in developed nations but remain a significant problem in poorer nations. Tonsillitis associated with strep throat, if untreated, is hypothesized to lead to pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS).

Note that, in neonates, sepsis is difficult to diagnose clinically. They may be relatively asymptomatic until hemodynamic and respiratory collapse is imminent, so, if there is even a remote suspicion of sepsis, they are frequently treated with antibiotics empirically until cultures are sufficiently proven to be negative. In addition to fluid resuscitation and supportive care, a common antibiotic regimen in infants with suspected sepsis is a beta-lactam antibiotic (usually ampicillin) in combination with an aminoglycoside (usually gentamicin) or a third-generation cephalosporin (usually cefotaxime—ceftriaxone is generally avoided in neonates due to the theoretical risk of kernicterus.) The organisms which are targeted are species that predominate in the female genitourinary tract and to which neonates are especially vulnerable to, specifically Group B Streptococcus, "Escherichia coli", and "Listeria monocytogenes" (This is the main rationale for using ampicillin versus other beta-lactams.) Of course, neonates are also vulnerable to other common pathogens that can cause meningitis and bacteremia such as "Streptococcus pneumoniae" and "Neisseria meningitidis". Although uncommon, if anaerobic species are suspected (such as in cases where necrotizing enterocolitis or intestinal perforation is a concern, clindamycin is often added.

Granulocyte-macrophage colony stimulating factor (GM-CSF) is sometimes used in neonatal sepsis. However, a 2009 study found that GM-CSF corrects neutropenia if present but it has no effect on reducing sepsis or improving survival.

Trials of probiotics for prevention of neonatal sepsis have generally been too small and statistically underpowered to detect any benefit, but a randomized controlled trial that enrolled 4,556 neonates in India reported that probiotics significantly reduced the risk of developing sepsis. The probiotic used in the trial was "Lactobacillus plantarum".

A very large meta-analysis investigated the effect of probiotics on preventing late-onset sepsis (LOS) in neonates. Probiotics were found to reduce the risk of LOS, but only in babies who were fed human milk exclusively. It is difficult to distinguish if the prevention was a result of the probiotic supplementation or if it was a result of the properties of human milk. It is also still unclear if probiotic administration reduces LOS risk in extremely low birth weight infants due to the limited number of studies that investigated it. Out of the 37 studies included in this systematic review, none indicated any safety problems related to the probiotics. It would be beneficial to clarify the relationship between probiotic supplementation and human milk for future studies in order to prevent late onset sepsis in neonates.

Orbital cellulitis occurs commonly from bacterial infection spread via the paranasal sinuses. Other ways in which orbital cellulitis may occur is from infection in the blood stream or from an eyelid skin infection. Upper respiratory infection, sinusitis, trauma to the eye, ocular or periocular infection and systemic infection all increase one's risk of orbital cellulitis.

"Staphylococcus aureus", "Streptococcus pneumoniae" and beta-hemolytic streptococci are three bacteria that can be responsible for orbital cellulitis.

- "Staphylococcus aureus" is a gram-positive bacterium which is the most common cause of staphylococcal infections. "Staphylococcus aureus" infection can spread to the orbit from the skin. These organisms are able to produce toxins which promote their virulence which leads to the inflammatory response seen in orbital cellulitis. "Staphylococcus" infections are identified by a cluster arrangement on gram stain. "Staphylococcus aureus" forms large yellow colonies (which is distinct from other Staph infections such as "Staphylococcus epidermidis" which forms white colonies).

- "Streptococcus pneumoniae" is also a gram-positive bacterium responsible for orbital cellulitis due to its ability to infect the sinuses (sinusitis). Streptococcal bacteria are able to determine their own virulence and can invade surrounding tissues causing an inflammatory response seen in orbital cellulitis (similar to "Staphyloccoccus aureus"). Streptococcal infections are identified on culture by their formation of pairs or chains. "Streptococcus pneumoniae" produce green (alpha) hemolysis, or partial reduction of red blood cell hemoglobin.

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.

Some cases of pharyngitis are caused by fungal infection such as Candida albicans causing oral thrush.

A number of different bacteria can infect the human throat. The most common is Group A streptococcus, but others include "Streptococcus pneumoniae", "Haemophilus influenzae", "Bordetella pertussis", "Bacillus anthracis", "Corynebacterium diphtheriae", "Neisseria gonorrhoeae", "Chlamydophila pneumoniae", and "Mycoplasma pneumoniae".

- Streptococcal pharyngitis

Streptococcal pharyngitis or strep throat is caused by group A beta-hemolytic streptococcus (GAS). It is the most common bacterial cause of cases of pharyngitis (15–30%). Common symptoms include fever, sore throat, and large lymph nodes. It is a contagious infection, spread by close contact with an infected individual. A definitive diagnosis is made based on the results of a throat culture. Antibiotics are useful to both prevent complications and speed recovery.

- Fusobacterium necrophorum

"Fusobacterium necrophorum" is a normal inhabitant of the oropharyngeal flora and can occasionally create a peritonsillar abscess. In 1 out of 400 untreated cases, Lemierre's syndrome occurs.

- Diphtheria

Diphtheria is a potentially life-threatening upper respiratory infection caused by "Corynebacterium diphtheriae" which has been largely eradicated in developed nations since the introduction of childhood vaccination programs, but is still reported in the Third World and increasingly in some areas in Eastern Europe. Antibiotics are effective in the early stages, but recovery is generally slow.

- Others

A few other causes are rare, but possibly fatal, and include parapharyngeal space infections: peritonsillar abscess ("quinsy"), submandibular space infection (Ludwig's angina), and epiglottitis.