Staphylococcus aureus, Haemophilus influenzae B, Moraxella catarrhalis, Streptococcus pneumoniae, and beta-hemolytic streptococci are 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 from the skin to the orbit. This organism is able to produce toxins which promotes its virulence, leading 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 when cultured (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. Streptococcal bacteria can invade surrounding tissues, causing the 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. Risk Factors
Risk factors for the development of orbital cellulitis include, but are not limited to:
Recent upper respiratory illness
Sinus infection
Younger age
Retained foreign bodies within the orbit
Trauma
Immunosuppression
Systemic infection
Dental infection

Diagnosis
Early diagnosis of orbital cellulitis is urgent, and it involves a complete and thorough physical examination. Common presenting signs include: a protruding eye (proptosis), eyelid edema (swelling), eye pain, vision loss, inability to move the eye completely (ophthalmoplegia), and fever.
Myeloperoxidase deficiency is a disorder featuring lack in either the quantity or the function of myeloperoxidase–an iron-containing protein expressed primarily in neutrophil granules. There are two types of myeloperoxidase deficiency: primary/inherited and secondary/acquired. Lack of functional myeloperoxidase leads to less efficient killing of intracellular pathogens, particularly Candida albicans, as well as less efficient production and release of neutrophil extracellular traps (NETs) from the neutrophils to trap and kill extracellular pathogens. Despite these characteristics, more than 95% of individuals with myeloperoxidase deficiency experience no symptoms in their lifetime. For those who do experience symptoms, the most common symptom is frequent infections by Candida albicans. Individuals with myeloperoxidase deficiency also experience higher rates of chronic inflammatory conditions. Myeloperoxidase deficiency is diagnosed using flow cytometry or cytochemical stains. There is no treatment for myeloperoxidase deficiency itself. Rather, in the rare cases that individuals experience symptoms, these infections should be treated. Pathophysiology
The innate immune system responds quickly to infection, with neutrophils (a type of white blood cells) being the first responders. Neutrophils enter the site of infection and begin to phagocytose (take up) pathogens. Once engulfed, the neutrophils must then degrade the captured pathogens–a process known as intracellular killing.One method of intracellular killing which takes place in the phagolysosomes of neutrophils involves the reaction of myeloperoxidase with hydrogen peroxide (H2O2) acquired in the cells from NADPH oxidase through the respiratory bursts. This reaction generates several acidic products including hypochlorous acid (HClO), which can break down pathogens.