MM 373, 365; ID 1440-1460
 
 

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
 
 

OVERVIEW:

Blepharitis is an infestation of the eyelash follicle by a mite. This results in an allergic reaction which leads to an inflammatory reaction and secondary infection of normal skin flora.
 

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.
 
 

OVERVIEW:

Obstruction of the oriface of a gland (Meibomian, Zeis or Moll) that traps microorganisms within the gland results in an infection and inflammation of that gland. Chalazia (small benign tumors produced by chronic inflammation) evolve from hordeola that do not drain spontaneously or are not excised.
 

ETIOLOGICAL AGENTS:

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

DIAGNOSIS:

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.

With chalazia there is usually persistent chronic inflammation, and granuloma formation may occur as sebaceous secretions are impounded.

TREATMENT:

Injection of glucosteroid such as betamethasone. Topical bacitracin or erythromycin. Surgical intervention may also be necessary to facilitate drainage.
 
 

OVERVIEW:

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.

ETIOLOGICAL AGENT:    Staphylococcus aureus, usually
 

SYMPTOMOLOGY:

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:

Cefuroxime or cefoxitin or cefotetan
 
 

OVERVIEW:

Acute dacryocytitis as infection of the lacrimal sac; this is almost always secondary to infection of the lacrimal duct. This occurs when both the upper and lower ends of the drainage system become partially or completely blocked.

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

SYMPTOMS:

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:

First generation cephalosporin or penicillinase-resistant synthetic penicillin or erythromycin.
 
 

OVERVIEW:

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
 

ETIOLOGICAL AGENTS:    Streptococcus pneumoniae
                                                        Hemophilus influenzae
 

SYMPTOMS:

Symptoms are the same as for acute dacryocystitis.
 

TREATMENT:

First generation cephalosporin or penicillinase-resistant synthetic penicillin or erythromycin.

    (2) Infections of the Conjunctiva
 
 

OVERVIEW:

Pinkeye is a disease characterized by an inflamed, bright red conjunctiva with inflammation extending into the cornea. It is spread by direct person-to-person contact. It is no threat to eyesight.
 

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.

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

OVERIEW:

During the birth process, when the fetus passes down the birth canal, it can contract an eye infection from the mother's genital flora. If Chlamydia trachomatis of a particular serotype is obtained in this way it can cause an inclusion conjunctivitis after a 5-12 day incubation period.

ETIOLOGICAL AGENT:    Chlamydia trachomatis
 

SYMPTOMOLOGY:

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:     Erythromycin syrup
 
 

OVERVIEW:

As in inclusion conjunctivitis, a fetus can contract an eye infection by Chlamydia trachomatis during passage down the birth canal. However, if it is of a more virulent serotype than the strain causing inclusion conunctivitis, the presentation can be that of ocular lymphogranuloma venereum. This will occur 5-12 days after birth.

ETIOLOGICAL AGENT:    Chlamydia trachomatis
 

SYMPTOMOLOGY:

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:     Erythromycin syrup
 
 

OVERVIEW:

Trachoma is the most serious of the eye diseases caused by Chlamydia trachomatis. There is no genital involvement in this disease; the disease is spread person-to-person via the common use of towels and washcloths. Both children and adults can be infected. This is the leading cause of blindness in the world.

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.

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:     Azithromycin or doxycycline
 
 

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:

There is no treatment for adenoviruses. For human herpes viruses 1 and 2 adenine arabinoside, cytosine arabinoside, iododeoxyuridine or trifluorethymicline may be used. For human herpesvirus 5 foscarnet sodium may be used. GLUCOSTEROIDS ARE CONTRAINDICATED
 
 

ETIOLOGICAL AGENTS:    Candida albicans
                                                        Sporothrix schenckii
                                                        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 spp.
                                                        Thelazia spp.

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
 
 

OVERVIEW:

Keratitis, the formation of a corneal ulcer, occurs in people who are predisposed to infection due to dry eye syndrome, trauma to the cornea or use of steroids. The infection gives rise to hypopyon, iritis and possible blindness.
 

ETIOLOGICAL AGENTS:
 

Pseudomonas aeruginosa	Haemophilus sp.
Streptococcus pneumoniae	Mycobacterium fortuitum
Staphylococcus aureus	Human Herpesvirus 1 (Herpes simplex 1 virus)
Streptococcus pyogenes	Adenovirus types 3 and 8
Proteus sp.	Fusarium sp.
Neisseria sp.	Aspergillus sp.
Corynebacterium 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 tobramycin + piperacillin.

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.

Viral infections may be amenable to adenine arabinoside or cytosine arabinoside for human herpesvirus 1.
 
 

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
 
 

OVERVIEW:

Endophthalmitis, inflammation of the aqueous or vitreous humor, occurs most commonly following intraocular lens implantation or trauma or as an extension of an adjacent (endogenous) infection.

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 humor 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.
 
 

OVERVIEW:

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).

ETIOLOGY (Anterior uveitis):

    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
 

SYMPTOMOLOGY (Anterior uveitis):

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

TREATMENT (Anterior uveitis):     variable or non-existent.
 
 

ETIOLOGY (Posterior uveitis (inflammation of the choroid)):

    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
 

SYMPTOMOLOGY (Posterior uveitis):

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

TREATMENT (Posterior uveitis):     variable or non-existent