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%.

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.

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.

Antibiotics are aimed at gram positive bacteria. Medical attention should be sought if symptoms persist beyond 2–3 days.

"Staphylococcus aureus", "Streptococcus pneumoniae", other streptococci, and anaerobes are the most common causes, depending on the origin of the infection.

The advent of the "Haemophilus influenzae" vaccine has dramatically decreased the incidence.

Cellulitis in 2015 resulted in about 16,900 deaths worldwide, up from 12,600 in 2005.

Risk factors for abscess formation include intravenous drug use. Another possible risk factor is a prior history of disc herniation or other spinal abnormality, though this has not been proven.

Abscesses are caused by bacterial infection, parasites, or foreign substances.

Bacterial infection is the most common cause. Often many different types of bacteria are involved in a single infection. In the United States and many other areas of the world the most common bacteria present is "methicillin-resistant Staphylococcus aureus". Among spinal subdural abscesses, methicillin-sensitive Staphylococcus aureus is the most common organism involved.

Rarely parasites can cause abscesses and this is more common in the developing world. Specific parasites known to do this include dracunculiasis and myiasis.

A variety of causes may lead to dacrocystitis. Most notably, obstruction of the nasolacrimal duct leads to stasis of the nasolacrimal fluid, which predisposes to infection. Staphylococcus aureus is a common bacterial pathogen causing infectious dacrocystitis. Sometimes, especially in women, stones may develop in the lacrimal gland, causing recurrent bouts of dacrocystitis; this condition is called "acute dacryocystic retention syndrome."

Also due to pneumococcus, infection due to surrounding structure such as paranasal sinuses.

Skin abscesses are common and have become more common in recent years. Risk factors include intravenous drug use with rates reported as high as 65% in this population. In 2005 in the United States 3.2 million people went to the emergency department for an abscess. In Australia around 13,000 people were hospitalized in 2008 for the disease.

About 60 percent of initial attacks of dacryocystitis will recur. Individuals with a poorly functioning immune system (immunocompromised) may develop orbital cellulitis, which may lead to optic neuritis, proptosis, motility abnormalities, or blindness.

Cavernous sinus thrombosis has a mortality rate of less than 20% in areas with access to antibiotics. Before antibiotics were available, the mortality was 80–100%. Morbidity rates also dropped from 70% to 22% due to earlier diagnosis and treatment.

Dental infections account for approximately 80% of cases of Ludwig's angina. Mixed infections, due to both aerobes and anaerobes, are of the cellulitis associated with Ludwig's angina. Typically, these include alpha-hemolytic streptococci, staphylococci and bacteroides groups.

The route of infection in most cases is from infected lower molars or from pericoronitis, which is an infection of the gums surrounding the partially erupted lower (usually third) molars. Although the widespread involvement seen in Ludwig's usually develops in immunocompromised persons, it can also develop in otherwise healthy individuals. Thus, it is very important to obtain dental consultation for lower-third molars at the first sign of any pain, bleeding from the gums, sensitivity to heat/cold or swelling at the angle of the jaw.

There has been a single case reported where Ludwig's angina was thought to be caused by a recent Tongue piercing. In addition, Filipino boxer Pancho Villa (1901–1925) died after contracting Ludwig's Angina following a bout with Jimmy McLarnin.

The newborn`s exposure to the maternal vaginal bacterial flora which contains aerobic and anaerobic bacterial flora can lead to the development of anaerobic bacterial infection. These infections include cellulitis of the site of fetal monitoring (caused by "Bacterodes" spp.), bacteremia, aspiration pneumonia (caused by "Bacterodes" spp.), conjunctivitis (caused by clostridia,) omphalitis (caused by mixed flora), and infant botulism. Clostridial species may play a role in necrotizing enterocolitis. Management of these infection necessitates treating of the underlying condition(s) when present, and administration of proper antimicrobial therapy

Condition predisposing to anaerobic infections include: exposure of a sterile body location to a high inoculum of indigenous bacteria of mucous membrane flora origin, inadequate blood supply and tissue necrosis which lower the oxidation and reduction potential which support the growth of anaerobes. Conditions which can lower the blood supply and can predispose to anaerobic infection are: trauma, foreign body, malignancy, surgery, edema, shock, colitis and vascular disease. Other predisposing conditions include splenectomy, neutropenia, immunosuppression, hypogammaglobinemia, leukemia, collagen vascular disease and cytotoxic drugs and diabetes mellitus. A preexisting infection caused by aerobic or facultative organisms can alter the local tissue conditions and make them more favorable for the growth of anaerobes. Impairment in defense mechanisms due to anaerobic conditions can also favor anaerobic infection. These include production of leukotoxins (by "Fusobacterium" spp.), phagocytosis intracellular killing impairments (often caused by encapsulated anaerobes and by succinic acid ( produced by "Bacteroides" spp.), chemotaxis inhibition (by "Fusobacterium, Prevotella" and "Porphyromonas" spp.), and proteases degradation of serum proteins (by Bacteroides spp.) and production of leukotoxins (by "Fusobacterium" spp.).

The hallmarks of anaerobic infection include suppuration, establishment of an abscess, thrombophlebitis and gangrenous destruction of tissue with gas generation. Anaerobic bacteria are very commonly recovered in chronic infections, and are often found following the failure of therapy with antimicrobials that are ineffective against them, such as trimethoprim–sulfamethoxazole (co-trimoxazole), aminoglycosides, and the earlier quinolones.

Some infections are more likely to be caused by anaerobic bacteria, and they should be suspected in most instances. These infections include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia and lung abscesses, amnionitis, endometritis, septic abortions, tubo-ovarian abscess, peritonitis and abdominal abscesses following viscus perforation, abscesses in and around the oral and rectal areas, pus-forming necrotizing infections of soft tissue or muscle and postsurgical infections that emerge following procedures on the oral or gastrointestinal tract or female pelvic area. Some solid malignant tumors, ( colonic, uterine and bronchogenic, and head and neck necrotic tumors, are more likely to become secondarily infected with anaerobes. The lack of oxygen within the tumor that are proximal to the endogenous adjacent mucosal flora can predispose such infections.

The cause of juvenile cellulitis is unknown. Cytologic examination of aspirates of affected lymph nodes, pustules, abscesses, and joint fluid rarely reveal bacteria, and culture results of intact lesion are always negative for bacterial growth, suggesting a nonbacterial etiology. As signs resolve following treatment with glucocorticoids, the cause is likely to be an immune disorder.

Most patients will fully recover from dacryoadenitis. For conditions with more serious causes, such as sarcoidosis, the prognosis is that of the underlying condition.

Mumps can be prevented by immunization. Gonococcus, bacteria can be avoided by the use of condoms. Most other causes cannot be prevented.

It has been hypothesized that biofilm bacterial infections may account for many cases of antibiotic-refractory chronic sinusitis. Biofilms are complex aggregates of extracellular matrix and inter-dependent microorganisms from multiple species, many of which may be difficult or impossible to isolate using standard clinical laboratory techniques. Bacteria found in biofilms have their antibiotic resistance increased up to 1000 times when compared to free-living bacteria of the same species. A recent study found that biofilms were present on the mucosa of 75% of people undergoing surgery for chronic sinusitis.

Acute sinusitis is usually precipitated by an earlier upper respiratory tract infection, generally of viral origin, mostly caused by rhinoviruses, coronaviruses, and influenza viruses, others caused by adenoviruses, human parainfluenza viruses, human respiratory syncytial virus, enteroviruses other than rhinoviruses, and metapneumovirus. If the infection is of bacterial origin, the most common three causative agents are "Streptococcus pneumoniae", "Haemophilus influenzae", and "Moraxella catarrhalis". Until recently, "Haemophilus influenzae" was the most common bacterial agent to cause sinus infections. However, introduction of the "H. influenza" type B (Hib) vaccine has dramatically decreased "H. influenza" type B infections and now non-typable "H. influenza" (NTHI) are predominantly seen in clinics. Other sinusitis-causing bacterial pathogens include "Staphylococcus aureus" and other streptococci species, anaerobic bacteria and, less commonly, gram negative bacteria. Viral sinusitis typically lasts for 7 to 10 days, whereas bacterial sinusitis is more persistent. Approximately 0.5% to 2% of viral sinusitis results in subsequent bacterial sinusitis. It is thought that nasal irritation from nose blowing leads to the secondary bacterial infection.

Acute episodes of sinusitis can also result from fungal invasion. These infections are typically seen in patients with diabetes or other immune deficiencies (such as AIDS or transplant patients on immunosuppressive anti-rejection medications) and can be life-threatening. In type I diabetics, ketoacidosis can be associated with sinusitis due to mucormycosis.

Chemical irritation can also trigger sinusitis, commonly from cigarette smoke and chlorine fumes. Rarely, it may be caused by a tooth infection.

Surgical drainage with sphenoidotomy is indicated if the primary site of infection is thought to be the sphenoidal sinuses.

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.

Large doses of glucocorticoids are the treatment of choice, and are administered until the signs have resolved. In uncomplicated cases, this can take up to a month. If dogs are not treated promptly and with high doses of steroids, severe scarring may occur. If there is evidence of secondary bacterial infection, treatment with antibiotics is required.

Cutaneous group B streptococcal infection may result in orbital cellulitis or facial erysipelas in neonates.

Treatment involves appropriate antibiotic medications, monitoring and protection of the airway in severe cases, and, where appropriate, urgent Otolaryngology-Head and Neck Surgery, maxillo-facial surgery and/or dental consultation to incise and drain the collections. The antibiotic of choice is from the penicillin group.

Incision and drainage of the abscess may be either intraoral or external. An intraoral incision and drainage procedure is indicated if the infection is localized to the sublingual space. External incision and drainage is performed if infection involves the perimandibular spaces.

A nasotracheal tube is sometimes warranted for ventilation if the tissues of the mouth make insertion of an oral airway difficult or impossible.

In cases where the patency of the airway is compromised, skilled airway management is mandatory. Fiberoptic intubation is common.

Ludwig's angina is a life-threatening condition, and carries a fatality rate of about 5%.

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.