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

Immediate treatment is very important for someone with orbital cellulitis. Treatment typically involves intravenous (IV) antibiotics in the hospital and frequent observation (every 4–6 hours). Along with this several laboratory tests are run including a complete blood count, differential, and blood culture.

- Antibiotic therapy – Since orbital cellulitis is commonly caused by "Staphylococcus" and "Streptococcus" species both penicillins and cephalosporins are typically the best choices for IV antibiotics. However, due to the increasing rise of MRSA (methicillin-resistant "Staphylococcus aureus") orbital cellulitis can also be treated with Vancomycin, Clindamycin, or Doxycycline. If improvement is noted after 48 hours of IV antibiotics, healthcare professions can then consider switching a patient to oral antibiotics (which must be used for 2–3 weeks).

- Surgical intervention – An abscess can threaten the vision or neurological status of a patient with orbital cellulitis, therefore sometimes surgical intervention is necessary. Surgery typically requires drainage of the sinuses and if a subperiosteal abscess is present in the medial orbit, drainage can be performed endoscopically. Post-operatively, patients must follow up regularly with their surgeon and remain under close observation.

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%.

Other conditions that may mimic cellulitis include deep vein thrombosis, which can be diagnosed with a compression leg ultrasound, and stasis dermatitis, which is inflammation of the skin from poor blood flow. Signs of a more severe infection such as necrotizing fasciitis or gas gangrene that would require prompt surgical intervention include purple bullae, skin sloughing, subcutaneous edema, and systemic toxicity. Misdiagnosis can occur in up to 30% of people with suspected lower-extremity cellulitis, leading to 50,000 to 130,000 unnecessary hospitalization and $195 to $515 million in avoidable healthcare spending annually in the United States.

Associated musculoskeletal findings are sometimes reported. When it occurs with acne conglobata, hidradenitis suppurativa, and pilonidal cysts, the syndrome is referred to as the follicular occlusion triad or tetrad.

Lyme disease can be misdiagnosed as staphylococcal- or streptococcal-induced cellulitis. Because the characteristic bullseye rash does not always appear in people infected with Lyme disease, the similar set of symptoms may be misdiagnosed as cellulitis. Standard treatments for cellulitis are not sufficient for curing Lyme disease. The only way to rule out Lyme disease is with a blood test, which is recommended during warm months in areas where the disease is endemic.

In those who have previously had cellulitis, the use of antibiotics may help prevent future episodes. This is recommended by CREST for those who have had more than two episodes.

For those with a history of intravenous drug use, an X-ray is recommended before treatment to verify that no needle fragments are present. In this population if there is also a fever present infectious endocarditis should be considered.

Abscesses should be differentiated from empyemas, which are accumulations of pus in a preexisting rather than a newly formed anatomical cavity.

Other conditions that can cause similar symptoms include: cellulitis, a sebaceous cyst and necrotising fasciitis. Cellulitis typically also has an erythematous reaction, but does not confer any purulent drainage.

"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.

CBC, ESR, blood cultures, and sinus cultures help establish and identify an infectious primary source. Lumbar puncture is necessary to rule out meningitis.

The diagnosis of Ludwig's angina is clinical. History and physical examination are usually enough to establish the diagnosis.

Sinus films are helpful in the diagnosis of sphenoid sinusitis. Opacification, sclerosis, and air-fluid levels are typical findings. Contrast-enhanced CT scan may reveal underlying sinusitis, thickening of the superior ophthalmic vein, and irregular filling defects within the cavernous sinus; however, findings may be normal early in the disease course.

A MRI using flow parameters and an MR venogram are more sensitive than a CT scan, and are the imaging studies of choice to diagnose cavernous sinus thrombosis. Findings may include deformity of the internal carotid artery within the cavernous sinus, and an obvious signal hyperintensity within thrombosed vascular sinuses on all pulse sequences.

Cerebral angiography can be performed, but it is invasive and not very sensitive. Orbital venography is difficult to perform, but it is excellent in diagnosing occlusion of the cavernous sinus.

Dacryoadenitis can be diagnosed by examination of the eyes and lids. Special tests such as a CT scan may be required to search for the cause. Sometimes biopsy will be needed to be sure that a tumor of the lacrimal gland is not present.

Puppies are first presented with what appears to be staphylococcal pyoderma. Definitive diagnosis requires cytologic and histopathologic evaluations. Cytologic examination of papulopustular lesions of juvenile cellulitis reveals pyogranulomatous inflammation with no microorganisms and carefully performed cultures are negative. Biopsies of early lesions reveal multiple discrete or confluent granulomas and pyogranulomas consisting of clusters of large epithelioid macrophages with variably sized cores of neutrophils. Cytological analysis of joint fluid often reveals sterile suppurative arthritis.

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

For sinusitis lasting more than 12 weeks a CT scan is recommended. On a CT scan, acute sinus secretions have a radiodensity of 10 to 25 Hounsfield units (HU), but in a more chronic state they become thickened, with a radiodensity of 30 to 60 HU.

Nasal endoscopy and clinical symptoms are also used to make a positive diagnosis. A tissue sample for histology and cultures can also be collected and tested. Allergic fungal sinusitis (AFS) is often seen in people with asthma and nasal polyps. In rare cases, sinusoscopy may be made.

Nasal endoscopy involves inserting a flexible fiber-optic tube with a light and camera at its tip into the nose to examine the nasal passages and sinuses. This is generally a completely painless (although uncomfortable) procedure which takes between five and ten minutes to complete.

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.

Health care providers distinguish bacterial and viral sinusitis by watchful waiting. If a person has had sinusitis for fewer than 10 days without the symptoms becoming worse, then the infection is presumed to be viral. When symptoms last more than 10 days or get worse in that time, then the infection is considered bacterial sinusitis. Imaging by either X-ray, CT or MRI is generally not recommended unless complications develop. Pain caused by sinusitis is sometimes confused for pain caused by pulpitis (toothache) of the maxillary teeth, and vice versa. Classically, the increased pain when tilting the head forwards separates sinusitis from pulpitis.

This disease is diagnosed mainly by the appearance of well-demarcated rash and inflammation. Blood cultures are unreliable for diagnosis of the disease, but may be used to test for sepsis. Erysipelas must be differentiated from herpes zoster, angioedema, contact dermatitis, and diffuse inflammatory carcinoma of the breast.

Erysipelas can be distinguished from cellulitis by its raised advancing edges and sharp borders. Elevation of the antistreptolysin O titer occurs after around 10 days of illness.

Recovery from an anaerobic infection depends on adequate and rapid management. The main principles of managing anaerobic infections are neutralizing the toxins produced by anaerobic bacteria, preventing the local proliferation of these organisms by altering the environment and preventing their dissemination and spread to healthy tissues.

Toxin can be neutralized by specific antitoxins, mainly in infections caused by Clostridia (tetanus and botulism). Controlling the environment can be attained by draining the pus, surgical debriding of necrotic tissue, improving blood circulation, alleviating any obstruction and by improving tissue oxygenation. Therapy with hyperbaric oxygen (HBO) may also be useful. The main goal of antimicrobials is in restricting the local and systemic spread of the microorganisms.

The available parenteral antimicrobials for most infections are metronidazole, clindamycin, chloramphenicol, cefoxitin, a penicillin (i.e. ticarcillin, ampicillin, piperacillin) and a beta-lactamase inhibitor (i.e. clavulanic acid, sulbactam, tazobactam), and a carbapenem (imipenem, meropenem, doripenem, ertapenem). An antimicrobial effective against Gram-negative enteric bacilli (i.e. aminoglycoside) or an anti-pseudomonal cephalosporin (i.e. cefepime ) are generally added to metronidazole, and occasionally cefoxitin when treating intra-abdominal infections to provide coverage for these organisms. Clindamycin should not be used as a single agent as empiric therapy for abdominal infections. Penicillin can be added to metronidazole in treating of intracranial, pulmonary and dental infections to provide coverage against microaerophilic streptococci, and Actinomyces.

Oral agents adequate for polymicrobial oral infections include the combinations of amoxicillin plus clavulanate, clindamycin and metronidazole plus a macrolide. Penicillin can be added to metronidazole in the treating dental and intracranial infections to cover "Actinomyces" spp., microaerophilic streptococci, and "Arachnia" spp. A macrolide can be added to metronidazole in treating upper respiratory infections to cover "S. aureus" and aerobic streptococci. Penicillin can be added to clindamycin to supplement its coverage against "Peptostreptococcus" spp. and other Gram-positive anaerobic organisms.

Doxycycline is added to most regimens in the treatment of pelvic infections to cover chlamydia and mycoplasma. Penicillin is effective for bacteremia caused by non-beta lactamase producing bacteria. However, other agents should be used for the therapy of bacteremia caused by beta-lactamase producing bacteria.

Because the length of therapy for anaerobic infections is generally longer than for infections due to aerobic and facultative anaerobic bacteria, oral therapy is often substituted for parenteral treatment. The agents available for oral therapy are limited and include amoxacillin plus clavulanate, clindamycin, chloramphenicol and metronidazole.

In 2010 the American Surgical Society and American Society of Infectious Diseases have updated their guidelines for the treatment of abdominal infections.

The recommendations suggest the following:

For mild-to-moderate community-acquired infections in adults, the agents recommended for empiric regimens are: ticarcillin- clavulanate, cefoxitin, ertapenem, moxifloxacin, or tigecycline as single-agent therapy or combinations of metronidazole with cefazolin, cefuroxime, ceftriaxone, cefotaxime, levofloxacin, or ciprofloxacin. Agents no longer recommended are: cefotetan and clindamycin ( Bacteroides fragilis group resistance) and ampicillin-sulbactam (E. coli resistance) and ainoglycosides (toxicity).

For high risk community-acquired infections in adults, the agents recommended for empiric regimens are: meropenem, imipenem-cilastatin, doripenem, piperacillin-tazobactam, ciprofloxacin or levofloxacin in combination with metronidazole, or ceftazidime or cefepime in combination with metronidazole. Quinolones should not be used unless hospital surveys indicate >90% susceptibility of "E. coli" to quinolones.

Aztreonam plus metronidazole is an alternative, but addition of an agent effective against gram-positive cocci is recommended. The routine use of an aminoglycoside or another second agent effective against gram-negative facultative and aerobic bacilli is not recommended in the absence of evidence that the infection is caused by resistant organisms that require such therapy.

Empiric use of agents effective against enterococci is recommended and agents effective against methicillin-resistant "S. aureus" (MRSA) or yeast is not recommended in the absence of evidence of infection due to such organisms.

Empiric antibiotic therapy for health care-associated intra-abdominal should be driven by local microbiologic results. Empiric coverage of likely pathogens may require multidrug regimens that include agents with expanded spectra of activity against gram-negative aerobic and facultative bacilli. These include meropenem, imipenem-cilastatin, doripenem, piperacillin-tazobactam, or ceftazidime or cefepime in combination with metronidazole. Aminoglycosides or colistin may be required.

Antimicrobial regimens for children include an aminoglycoside-based regimen, a carbapenem (imipenem, meropenem, or ertapenem), a beta-lactam/beta-lactamase-inhibitor combination (piperacillin-tazobactam or ticarcillin-clavulanate), or an advanced-generation cephalosporin (cefotaxime, ceftriaxone, ceftazidime, or cefepime) with metronidazole.

Clinical judgment, personal experience, safety and patient compliance should direct the physician in the choice of the appropriate antimicrobial agents. The length of therapy generally ranges between 2 and 4 weeks, but should be individualized depending on the response. In some instances treatment may be required for as long as 6–8 weeks, but can often be shortened with proper surgical drainage.

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.

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%.

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.

Depending on the severity, treatment involves either oral or intravenous antibiotics, using penicillins, clindamycin, or erythromycin. While illness symptoms resolve in a day or two, the skin may take weeks to return to normal.

Because of the risk of reinfection, prophylactic antibiotics are sometimes used after resolution of the initial condition. However, this approach does not always stop reinfection.

The best imaging modality for idiopathic orbital inflammatory disease is contrast-enhanced thin section magnetic resonance with fat suppression. The best diagnostic clue is a poorly marginated, mass-like enhancing soft tissue involving any area of the orbit.

Overall, radiographic features for idiopathic orbital inflammatory syndrome vary widely. They include inflammation of the extraocular muscles (myositis) with tendinous involvement, orbital fat stranding, lacrimal gland inflammation and enlargement (dacryoadenitis), involvement of the optic sheath complex, uvea, and sclera, a focal intraorbital mass or even diffuse orbital involvement. Bone destruction and intracranial extension is rare, but has been reported. Depending on the area of involvement, IOI may be categorized as:

- Myositic

- Lacrimal

- Anterior – Involvement of the globe, retrobulbar orbit

- Diffuse – Multifocal intraconal involvement with or without an extraconal component

- Apical – Involving the orbital apex and with intracranial involvement

Tolosa–Hunt syndrome is a variant of orbital pseudotumor in which there is extension into the cavernous sinus through the superior orbital fissure. Another disease variant is Sclerosing pseudotumor, which more often presents bilaterally and may extend into the sinuses.

CT findings

In non-enhanced CT one may observe a lacrimal, extra-ocular muscle, or other orbital mass. It may be focal or infiltrative and will have poorly circumscribed soft tissue. In contrast-enhanced CT there is moderate diffuse irregularity and enhancement of the involved structures. A dynamic CT will show an attenuation increase in the late phase, contrary to lymphoma where there is an attenuation decrease. Bone CT will rarely show bone remodeling or erosion, as mentioned above.

MR findings

On MR examination there is hypointensity in T1 weighted imaging (WI), particularly in sclerosing disease. T1WI with contrast will show moderate to marked diffuse irregularity and enhancement of involved structures. T2 weighted imaging with fat suppression will show iso- or slight hyperintensity compared to muscle. There is also decreased signal intensity compared to most orbital lesions due to cellular infiltrate and fibrosis. In chronic disease or sclerosing variant, T2WI with FS will show hypointensity (due to fibrosis). Findings on STIR (Short T1 Inversion Recovery) are similar to those on T2WI FS. In Tolosa–Hunt syndrome, findings include enhancement and fullness of the anterior cavernous sinus and superior orbital fissure in T1WI with contrast, while MRA may show narrowing of cavernous sinus internal carotid artery (ICA).

Ultrasonographic findings

On grayscale ultrasound there is reduced reflectivity, regular internal echoes, and weak attenuation, in a way, similar to lymphoproliferative lesions.

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.