Acute conjunctivitis can be caused by numerous bacteria. Symptoms are hyperemia, lacrimation, irritation, and discharge. Diagnosis is clinical. Treatment is with topical antibiotics, augmented by systemic antibiotics in more serious cases.
Most bacterial conjunctivitis is acute; chronic bacterial conjunctivitis may be caused by Chlamydia and rarely Moraxella. Chlamydial conjunctivitis includes trachoma and adult or neonatal inclusion conjunctivitis.
Bacterial conjunctivitis is usually caused by Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus sp, or, less commonly, Chlamydia trachomatis (see Trachoma). Neisseria gonorrhoeae causes gonococcal conjunctivitis, which usually results from sexual contact with a person who has a genital infection.
Ophthalmia neonatorum (see Neonatal Conjunctivitis) is conjunctivitis that occurs in 20 to 40% of neonates delivered through an infected birth canal. It can be caused by maternal gonococcal or chlamydial infection.
Symptoms and Signs
Symptoms are typically unilateral but frequently spread to the opposite eye within a few days. Discharge is typically purulent.
The bulbar and tarsal conjunctivae are intensely hyperemic and edematous. Petechial subconjunctival hemorrhages, chemosis, photophobia, and an enlarged preauricular lymph node are typically absent. Eyelid edema is often moderate.
With adult gonococcal conjunctivitis, symptoms develop 12 to 48 h after exposure. Severe eyelid edema, chemosis, and a profuse purulent exudate are typical. Rare complications include corneal ulceration, abscess, perforation, panophthalmitis, and blindness.
Ophthalmia neonatorum caused by gonococcal infection appears 2 to 5 days after delivery. With ophthalmia neonatorum caused by a chlamydial infection, symptoms appear within 5 to 14 days. Symptoms of both are bilateral, intense papillary conjunctivitis with eyelid edema, chemosis, and mucopurulent discharge.
Diagnosis of conjunctivitis and differentiation between bacterial, viral, and noninfectious conjunctivitis are usually clinical. Smears and bacterial cultures should be done in patients with severe symptoms, immunocompromise, ineffective initial therapy, or a vulnerable eye (eg, after a corneal transplant, in exophthalmos due to Graves disease). Smears and conjunctival scrapings should be examined microscopically and stained with Gram stain to identify bacteria and stained with Giemsa stain to identify the characteristic epithelial cell basophilic cytoplasmic inclusion bodies of chlamydial conjunctivitis.
Bacterial conjunctivitis is very contagious, and standard infection control measures (see Overview of Conjunctivitis) should be followed.
If neither gonococcal nor chlamydial infection is suspected, most clinicians treat presumptively with moxifloxacin 0.5% drops tid for 7 to 10 days or another fluoroquinolone or trimethoprim/polymyxin B qid. A poor clinical response after 2 or 3 days indicates that the cause is resistant bacteria, a virus, or an allergy. Culture and sensitivity studies should then be done (if not done previously); results direct subsequent treatment.
Adult gonococcal conjunctivitis requires a single dose of ceftriaxone 1 g IM. Fluoroquinolones are no longer recommended because resistance is now widespread. Bacitracin 500 U/g or gentamicin 0.3% ophthalmic ointment instilled into the affected eye q 2 h may be used in addition to systemic treatment. Sex partners should also be treated. Because chlamydial genital infection is often present in patients with gonorrhea, patients should also receive a single dose of azithromycin 1 g po or doxycycline 100 mg po bid for 7 days.
Ophthalmia neonatorum is prevented by the routine use of silver nitrate eye drops or erythromycin ointment at birth. Infections that develop despite this treatment require systemic treatment. For gonococcal infection, ceftriaxone 25 to 50 mg/kg IV or IM (not exceeding 125 mg) is given as a single dose. Chlamydial infection is treated with erythromycin 12.5 mg/kg po or IV qid for 14 days. The parents should also be treated.
Last full review/revision October 2012 by Melvin I. Roat, MD, FACS
Content last modified September 2013