Any of the various parts of the eye can be infected. For ease of discussion we can divide the eye into the: (1) eyelids and tissue surrounding the eye, (2) the conjunctiva, (3) the cornea, and (4) the intraocular area. Each of these areas can be infected. The etiological agents will vary with the type of tissue infected.

    (1)     Infections of the Eyelids and Tissue Surrounding the Eye
 
 

ETIOLOGICAL AGENT:       Demodex folliculorum (a mite), followed by bacterial infection
                                                with S. aureus or S. epidermidis.
 

DIAGNOSIS:

    The disease is due to an allergic reaction to the mite which resides in the eyelash or the eyebrow. Most often, there is concomitant seborrhea of the eyebrows, scalp, lateral nares, posterior auricular area, and hirsute portions of the chest. There is scaling of the epidermis, usually with bacterial invasion of the hair follicles. Abscesses may form in and around the follicles, destroying the follicles, with the loss of lashes and the formation of ulcers. Hordeola and chalazia may follow. Microscopically, there is lymphocytic infiltration, hyperemia, acanthosis, parakeratosis and desquamation. The clinical appearance of the eyelids is virtually diagnostic. There may be a history of itching and scaling of the lid since early childhood. The patient describes an incessant urge to pull on the lashes in an attempt to remove the scales.
 

TREATMENT:

    An appropriate antibiotic (depending on the secondarily infecting bacteria), a glucosteroid to reduce inflammation and washing of all hairy parts of the body with a shampoo containing selenium sulfide. CAUTION: IT IS ABSOLUTELY NECESSARY TO DETERMINE THAT THE PATIENT DOES NOT HAVE A PROPENSITY FOR HERPETIC INFECTIONS OF THE CORNEA. STEROID THERAPY IS ALWAYS CONTRAINDICATED IN CORNEAL INFECTIONS BY HERPESVIRUS.
 
 

ETIOLOGICAL AGENTS:     Generally Staphylococcus aureus, but may also be caused
                                                 by Pseudomonas aeruginosa and Proteus sp.
 

DIAGNOSIS:

    Obstruction of the orifice of a gland (Meibomian, Zeis, or Moll) seems to be the primary pathological event in the formation of hordeola. A red nodule that is quite painful develops and is surmounted with a yellowish top as the lesion matures. The histopathology is typical of acute suppurative inflammation.

    Chalazia evolve from hordeola that do not drain spontaneously or are not incised. There is usually persistent chronic inflammation, and granuloma formation may occur as sebaceous secretions are impounded.
 

TREATMENT:

    Injection of glucosteroid such as betamethasone. Neomycin. Surgical intervention may also be necessary to facilitate drainage.
 
 

ETIOLOGICAL AGENT:     Staphylococcus aureus, usually

    Periorbital cellulitis is secondary to the infection of contiguous structures-paranasal sinusitis, osteomyelitis of the facial bones, conjunctivitis, panophthalmitis, dental infections, or infections in the drainage of the facial veins. Edema and hyperemia of the orbital tissues may be intense and may be associated with the accumulation of exudate and foci of necrosis. Thrombi are sometimes evident in associated lymphatics and veins. Both systemic (chills, fever, malaise, leukocytosis) and local (tenderness, voluntary limitations of extraocular movements) symptoms may arise in periorbital cellulitis.
 

TREATMENT:

    Large doses of nafcillin or oxacillin for two weeks.
 
 

ETIOLOGICAL AGENT:     S. aureus, S. epidermidis, Streptococcus pneumoniae
 

DIAGNOSIS:

    This is an infection of the lacrimal sac, almost always secondary to obstruction of the lacrimal duct. The lacrimal apparatus has two functions. The main lacrimal gland and the accessory lacrimal glands produce the aqueous component of the tear film. The lacrimal sac, along with other structures, is concerned with the drainage of tears from the conjunctival cul-de-sac and tear lake to the nasal cavity. Pathologic processes affecting the main and the accessory lacrimal glands result in diminished tear production, whereas those affecting the lacrimal drainage apparatus cause obstruction resulting in epiphora.

    Acute dacryocystitis occurs when both the upper and lower ends of the drainage system become partially or totally obstructed. The major symptom is pain in the tear sac area. There are also erythema, edema, a purulent discharge and epiphora. Dacryocystitis, whether acute or chronic, should be considered a dangerous reservoir of infection, and its absence should be established before intraocular surgery.
 

TREATMENT:

    A penicillinase-resistant penicillin such as nafcillin or oxacillin.
 
 

ETIOLOGICAL AGENTS:     Streptococcus pneumoniae
                                                Hemophilus influenzae
                                                Candida albicans
                                                Aspergillus sp.
                                                Actinomyces sp.

DIAGNOSIS:

    Chronic dacryocystitis is usually caused by a single site of partial or complete obstruction within the lacrimal sac or within the nasolacrimal duct. The infection is usually the result, and not the cause, of obstruction. Tear fluid collects in the lacrimal sac because of the obstruction, and bacteria from the conjunctival surface that have washed into the sac find a stagnant pool of fluid in which they may multiply. Obstruction may be due to:

    1.     Trauma

    2.     Tumors

    3.     Foreign bodies

    4.     Delayed canalization in neonates

    5.     Closure of canal in post menopausal women

Symptoms are the same as for acute dacryocystitis.
 

TREATMENT:

    Penicillin for a bacterial infection, Amphotericin B for a fungal infection
 

    (2)     Infections of the Conjunctiva
 
 

ETIOLOGICAL AGENT:     Haemophilus aegypticus and/or Moraxella lacunata
 

DIAGNOSIS:

    The only symptoms are conjunctivitis, either chronic or acute, and severe inflammation of the cornea. Diagnosis is via isolation of the organism ( a Gam-negative slender rod).
 

TREATMENT:     0.25% solution of zinc sulfate or 1% ointment of chlortetracycline.
 
 

ETIOLOGICAL AGENT:     Chlamydia trachomatis
 

DIAGNOSIS:

    The newborn contracts the disease form the mother's genital tract. In the newborn, clinical signs appear five to 12 days after birth. The conjunctiva becomes inflamed and thickened, and there is often copious discharge of pus. Follicles can develop on the conjunctiva, but the disease is usually self-limiting, resolving spontaneously within a few months even without treatment.

    In the adult, too, the conjunctivitis resembles the early stages of trachoma, but usually does not progress to a chronic disease; blindness is not a threat. This is considered a disease of developed countries, in contrast to trachoma, which is a disease of developing countries. There are no unique clinical signs.
 

TREATMENT:     Tetracycline
 
 

ETIOLOGICAL AGENT:     Chlamydia trachomatis
 

DIAGNOSIS:

    This is a chlamydial disease transmitted to the fetus during passage down the birth canal. Inflammation begins about five days after birth and never results in follicle formation (thus, it differs from trachoma and inclusion conjunctivitis). Corneal scars, conjunctival scars, and micropannus formation occur. It is rarely a cause of blindness. There will be inclusions in the epithelial cells of the conjunctiva.
 

TREATMENT:     Tetracycline
 
 

ETIOLOGICAL AGENT:     Chlamydia trachomatis
 

PATHOLOGY:

    This disease is limited to man, infecting only epithelial cells of the eye and possibly the nasopharynx; no systemic involvement has been described. It is found worldwide, and is the greatest single cause of blindness.

    In endemic areas, children are generally infected soon after birth or during the first few years of life; although, the disease may begin at any age. Onset of the disease is generally abrupt, with inflamed conjunctivae; within a few weeks, accumulation of lymphocytes, polymorphonuclear leukocytes, neutrophils, and macrophages coalesce to form characteristic follicles beneath the conjunctival surface. Later, vacuolization of the cornea begins, usually at the upper limbus, followed by an infiltration of the cornea (termed pannus), which may produce partial or complete blindness. Scarring of the conjunctiva may cause the eyelids to turn inward so that the lashes scratch the cornea. Distortion of the structures of the external eye also interferes with normal lacrimal flow, growth of lashes, and function of glands; as a result, bacterial infections of trachomatous eyes are common.
 

DIAGNOSIS:
 

    Clinical diagnosis of trachoma rests on the finding of characteristic follicles and scars in the conjunctiva, and vascularization and infiltration of the cornea. In the typical case, diagnosis is easy; in mild cases or after distortion of the anatomy of the external eye, the diagnosis of activity may be difficult. The World Health Organization lists these stages of the disease:
 

        1.     TR-D is the symbol applied to trachoma dubium, or suspect trachoma. The clinical signs
                suggest an early conjunctival reaction, but either there are no follicles or they are atypical.
                Corneal changes are either not visible or are atypical. Inclusions are not demonstrated
                and the agent cannot be isolated via inoculation of seven-day chick embryos with
                conjunctival scrapings.

        2.     PR-TR represents prototrachoma or prefollicular trachoma. There is an early conjunctival
                lesion, but no follicles are visible; and, the corneal changes are not diagnostic. Either
                 Chlamydia trachomatis is isolated or inclusions are present.

        3.     TR-I represents trachoma stage I in which immature follicles are present on the upper
                tarsal conjunctiva, including the central area. Early corneal changes are visible.

        4.     TR-II is characterized by the presence of well-developed follicles, papillary hyperplasia,
                pannus, and infiltration extending from the upper limbus.

        5.     TR-III is the stage of scarring resulting from follicular necrosis. The signs of TR-II may
                also be noted.

        6.     TR-IV is the healing stage where the follicles and infiltrates of TR-III are replaced by
                scar tissue. This is the only stage that is NOT infectious.

    Blindness is progressive and irreversible. A recently developed diagnostic aid is a serological test of eye secretions for trachoma specific antibodies.
 

TREATMENT:

    The drug of choice is one of the sulfonamides administered orally over a minimum of three weeks. Tetracycline administered as an ophthalmic ointment is sometimes beneficial, but does not always cure the disease.
 
 

ETIOLOGICAL AGENTS:     Adenovirus, types 3,7 and 8
                                                Human Herpesvirus 1 (Herpes simplex 1 virus)
                                                Human Herpesvirus 2 (Herpes simplex 2 virus)
                                                Human Herpesvirus 3 (Varicella-Zoster virus)
                                                Human Herpesvirus 5 (cytomegalovirus)

DIAGNOSIS:

    Bilateral conjunctivitis which is usually self limited. It may be recurrent with herpesvirus. No constitutional symptoms are present.
 

TREATMENT:     None. GLUCOSTEROIDS ARE CONTRAINDICATED
 
 

ETIOLOGICAL AGENTS:     Candida albicans
                                                Sporothrix schenkii
                                                Allescheria sp.
                                                Aspergillus sp.
                                                Mucor sp.
 

DIAGNOSIS:

    An uncommon disease which can be acute or chronic. Often secondary to fungal infections of other parts of the body. Often aggravated by glucosteroids and initiated after antibiotic therapy. Diagnosed by isolation of the etiological agent.
 

TREATMENT:     Nystatin, Amphotericin B
 
 

ETIOLOGICAL AGENTS:     Onchocerca volvulus
                                                Loa loa
                                                Wuchereria bancrofti
                                                Trichinella spiralis
                                                Schistosoma haematobium
                                                Taenia solium
                                                Echinococcus sp.
                                                Thelazia sp.
 

DIAGNOSIS:

    Constitutional symptoms related to infection of other body parts by the parasite. Isolation of the parasite. These diseases are common in Africa and Central America.
 

TREATMENT:     Various antiparasitic drugs
 

    (3)     Infections of the Cornea
 
 

ETIOLOGICAL AGENTS:     Pseudomonas aeruginosa
                                                Streptococcus pneumoniae
                                                Staphylococcus aureus
                                                Streptococcus pyogenes
                                                Proteus sp.
                                                Neisseria sp.
                                                Corynebacterium sp.
                                                Haemophilus sp.
                                                Mycobacterium fortuitum
                                                Human Herpesvirus 1 (Herpes simplex 1 virus)
                                                Adenovirus types 3 and 8
                                                Fusarium sp.
                                                Aspergillus sp.
                                                Candida albicans

DIAGNOSIS:

    Corneal disease commonly provokes toxic reactions intraocularly in the form of hypopyon (leukocytes in the anterior chamber) and iritis (resulting in photophobia). The cornea itself has an epithelium that rapidly undergoes mitosis and that consequently heals quickly after trauma. It is held together by a collagen matrix; yet peculiarly, the corneal epithelium contains a collagen-destroying enzyme, collagenase. This enzyme is released whenever there is trauma to the corneal epithelium whether caused by physical, chemical or bacterial disruption.

    A number of predisposing factors may lead to corneal ulcers. These include the dry eye syndrome as caused by deficiency of ocular secretions, and exposure from the inability to close the lids. Trauma to the cornea markedly increases the risk of corneal infection, especially when there is decreased sensation - as follows long-continued wearing of contact lenses, old herpetic corneal disease, or fifth cranial nerve damage. Steroids have a marked collagenolytic effect that destroys the corneal matrix in addition to decreasing the local immune response.

    When glucosteroids and antimicrobics are used in the presence of a bacterial ulcer, the ulcer may well become sterile while increasing in size and depth, leading to perforation. Also, steroids markedly enhance corneal disease and lead to intraocular and perhaps systemic infection caused by herpes viruses. This effect, which cannot be prevented by the simultaneous use of idoxuridine (IDU) or other antiviral drugs, becomes apparent only late in the course of the disease.

    Because the cornea is avascular, the nearest vessels that can express an inflammatory response are in the adjacent conjunctiva. As exudate is formed, the cornea becomes cloudy and may opacify. If healing is delayed, there may be vascular ingrowth, with the proliferation of fibroblasts, yielding an opaque or opalescent vascularized membrane that covers the cornea partially or completely.

    Pain, a lack of corneal sensitivity, circumcorneal vascular congestion, hypopyon, iritis, photophobia, lid closure, and lacrimation constitute the manifestations of corneal infections. The severity varies with the etiologic agent and the speed with which ulceration proceeds.
 

THERAPY:

    The prompt application of specific antimicrobial agents is the therapeutic ideal. With many bacteria, 10 to 15 percent sulfacetamide solution applied topically at least hourly, around the clock, may be effective. Pseudomonas aeruginosa usually requires treatment with a polymyxin or gentamicin.

    Mycobacterium fortuitum poses a difficult problem in treatment because the usual antimicrobics are often without results. Rifampin has been used with good results in some patients.

    The treatment of ocular fungal infections is at best poor. Amphotericin B may be used topically and systemically. Nystatin may also be of value when used topically.
 
 

ETIOLOGICAL AGENT:     Neisseria gonorrhoeae
 

DIAGNOSIS:

    The disease is contracted from a mother with gonorrhea as the fetus passes down the birth canal. Infection does not occur in utero. At one time about 10% of all cases of blindness in the United States was due to this disease. Corneal inflammation is the major clinical sign.
 

TREATMENT:

    It is now common practice to prevent this disease by treating the eyes of the newborn with an antibacterial compound. Home childbirth bypasses this prophylactic procedure so that some cases are still occurring in the United States. The treatment for active cases is Penicillin G if the organism is sensitive to penicillin, or a broad spectrum antibiotic if the organism is resistant to penicillin (e.g., Spectinomycin).

    Most commonly this is an erythromycin or tetracycline ointment (1%). Silver nitrate solution has been used in the past but has been found to induce inflammation.
 

    (4)     Infections of the intraocular area
 
 

ETIOLOGICAL AGENTS:     Staphylococcus aureus             )     following intraocular
                                                Staphylococcus epidermidis     )     lens implantation

                                                Bacillus cereus - following trauma

                                                Staphylococcus aureus             )
                                                Streptococcus pneumoniae      )     endogenous
                                                Streptococcus pyogenes           )     (metastatic)

DIAGNOSIS:

    The most common presenting symptoms of endophthalmitis are:

        ocular pain
        decreased vision
        headache
        photophobia

    Clinical signs include conjunctival injection, eyelid swelling, cells in aqueous or vitreous, hypopyon and poor or sheltered red reflex
 

TREATMENT:

    A vitrectomy or vitreous aspiration is an incision and drainage procedure that is imperative for initial therapy of endophthalmitis. Antibiotic therapy may involve four modalities:

        1.     Intravitreal. Vancomycin, cefazolin and gentamicin are possible antibiotics to inject into
                the vitreous.

        2.     Systemic. Third generation cephalosporins (e.g., cefotaxime, ceftriaxone, moxalactam),
                third or fourth generation penicillins (e.g., piperacillin, ticarcillin) and quinolones (e.g.,
                ciprofloxacin, ofloxacin).

        3.     Subconjunctival. Cefazolin or tobramycin are sometimes used.

        4.     Topical. Antibiotic drops are given for the first several days of treatment every two-four
                hours.
 
 

    Nonpurulent uveitis seldom involves the entire uveal tract but may occur predominantly in the anterior segment (iritis, iridocyclitis) or the posterior segment (posterior uveitis, retinitis).

Anterior uveitis etiology:

    MOST COMMON:

        Mumps virus
        Human Herpesvirus 3 (Varicella-Zoster virus)
        Rubella virus
        Rubeola virus
        Human Herpesvirus 1 (Herpes simplex 1 virus)
 

    LESS COMMON

        Treponema pallidum
        Neisseria gonorrhoea
        Brucella sp.
        Borrelia burgdorferi
        Rickettsia rickettsii
        Human immunodeficiency virus
        Leptospira interrogans

Anterior uveitis diagnosis:

    Most patients present with the acute symptoms of unilateral red eye, deep ocular pain with a tender eyeball, papillary constriction, photophobia and tearing. This condition must be distinguished from conjunctivitis, which has minimal eye discomfort and no papillary changes

Anterior uveitis treatment: variable or non-existent.

Posterior uveitis (inflammation of the choroid) etiology:

    Toxoplasma gondii (25% of all cases)
    Toxocara sp.
    Cryptococcus neoformans
    Histoplasma capsulatum
    Mycobacterium tuberculosis
    Human Herpesvirus 5 (cytomegalovirus)
    Human Herpesvirus 1 (Herpes simplex 1 virus)
    Human immunodeficiency virus

Posterior uveitis diagnosis:

    Patients present with chronic symptoms of visual impairment, retinal lesions and cloudiness of the vitreous. Pain and signs of inflammation are absent.

Posterior uveitis treatment:     variable or non-existent