CITATION: Baum JL. 1997. Bacterial conjunctivitis: diagnosis and treatment. APUA Newsletter 15(4):1,4-5,8.


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Bacterial conjunctivitis: diagnosis and treatment
Jules L Baum, MD
Boston Eye Associates, Chestnut Hill, Massachusetts, USA

Infections of the conjunctiva, with few exceptions, constitute a benign, self-limited group of diseases caused by a variety of infectious agents(1). This article, addressed to the general practitioner, limits itself to a presentation of bacterial conjunctivitis. Except for infections due to Staphylococcus and, rarely, a few gram-negative species (e.g., Proteus and Moraxella/Branhamella), bacterial conjunctivitis characteristically resolves in 10-14 days with antibiotic treatment. Since, with the noted exceptions, it is unusual for a case of acute bacterial conjunctivitis not to respond rapidly to topical therapy, the choice of drug should be determined in large part by cost and the potential for an adverse reaction. This characteristic rapid response to treatment is probably due to our ability to deliver a concentration of drug to the ocular surface much greater than that used in the disk-diffusion assay.

In general, bactericidal rather than bacteriostatic agents are preferable, especially when the patient is immunosuppressed. Drug delivery by eyedrop is appropriate for daytime use by adults since ointments tend to blur vision. The use of an ointment, which increases drug contact time, is preferable prior to sleep and in infants and young children who often cry and squeeze their eyelids thus diluting the drug and reducing drug volume, respectively.

Host Defenses and Risk Factors for Corneal Infection
The conjunctiva, a mucous membrane exposed to the external world, is remarkably resistant to infection. Tears, in combination with eyelid action, mechanically flush the ocular surface to reduce an ever-present bacterial load. Further, the tears contain immunoglobulins and components of the complement pathways, lactoferrin, lysozyme and ß-lysin that help kill microorganisms and decrease their adherence to the ocular surface. Trauma or disease trigger polymorphonuclear and macrophage release from the conjunctival vessels into the tears. These cellular elements, combined with the relatively low temperature of the ocular surface and the trapping effect of bacteria by mucus, serve to limit acute infection. The conjunctiva also contains abundant lymphoid tissue, another component of its anti-microbial defense.

The eyelid margins, and to a lesser degree the conjunctival surface, are populated with a variety of aerobic and anaerobic organisms.(2) The normal flora consists mainly of staphylococci (>60%;mostly
Staphylococcus epidermidis), diphtheroids, and Propionobacterium acnes. Local risk factors for conjunctival infection include trauma, a foreign body, deranged tissue following disease (e.g., erythema multiforme major, ocular cicatricial pemphigoid) and an infected lacrimal outflow tract.

Much more serious is the risk of corneal infection following conjunctival infection, which carries the potential for severe permanent loss of vision. Risk factors for corneal infection include prolonged eyelid closure, the use of soft contact lenses (especially when worn overnight), dry eyes, and corneal epithelial
disruption following disease or trauma (3). It is especially important to instill an appropriate topical antibiotic as prophylaxis when the cornea is at risk or if there is a "bleb." A bleb, a surgical portal created to treat glaucoma, is usually located at the superior limbus and is covered only by conjunctiva. This opening provides the potential for bacterial endophthalmitis to develop. The cornea is at particular risk with eyelid closure, during sleep, or with corneal exposure, such as may occur in a comatose patient whose eyes may remain open with reduced blinking. In both of these situations, an antibiotic ointment should be administered. The cornea is also at risk after
Neisseria gonorrhoeae conjunctivitis in the newborn, because the organism can invade intact epithelium and because of pressure necrosis of the epithelium due to extensive purulent exudate under the closed eyelid.

Signs and Symptoms
Viral conjunctivitis, most often of adenoviral origin, is the most common form of infectious conjunctivitis. Recognition of the clinical signs and symptoms which differentiate between viral, allergic and bacterial disease is helpful in determining whether antibiotic administration is of value (Table 1). General practitioners, well acquainted with signs such as conjunctival injection and purulence, may have difficulty differentiating follicles from papillae without magnification. A loupe or a magnifying glass is often adequate.

Follicles, focal lymphoid tissue associated with viral disease, appear as 1-2 mm translucent elevations most easily seen on the lower palpebral conjunctiva or in the lower fornix, each displaying fine surface vessels. They may normally be seen along the superior border of the tarsus (e.g., cartilage plate within the upper lid) and on the tarsal conjunctiva of children. They are also associated with chlamydial (larger than in viral disease), some toxic, and
Moraxella/Branhamella conjunctivitis. Papillae are seen as a myriad of minute, opaque elevations on the tarsal conjunctiva, each with a central vascular core. Although non-specific, they are common in bacterial disease.

Disease Entities
Bacterial conjunctivitis is commonly divided into subtypes based on the degree of purulence (purulent, mucopurulent) and duration of infection (hyperacute, acute, chronic). Much less often, membrane formation and the presence of granuloma are used to subtype disease. Although a hyperacute, purulent infection in the newborn is characteristic of infection due to
N. gonorrhoeae, clinical signs rarely permit the diagnosis of a specific bacterial species in acute disease.

Since the vast majority of cases of bacterial conjunctivitis are of the relatively benign acute type and respond rapidly to topical therapy, laboratory diagnosis is rarely indicated, except, when necessary, to differentiate bacterial from other infectious conjunctivitis. When a diagnosis of hyperacute disease is clinically suspect however, a Gram stain and culture are mandatory. Gonococci are more readily seen on gram stain following scraping of the inferior palpebral conjunctiva with a platinum spatula than from a swab of the inferior fornix. Material for culture may be obtained by a brisk calcium alginate swab of the inferior palpebral conjunctiva or fornix. The swab should be taken before a topical anesthetic is instilled, as these agents and their preservatives may decrease the recovery of some bacteria.

Hyperacute Conjunctivitis
Hyperacute conjunctivitis has a more rapid and severe onset than that seen in acute conjunctivitis. The overwhelming preponderance of cases of hyperacute conjunctivitis is due to
N. gonorrhoeae. Conjunctivitis due to Neisseria meningitidis is seen more commonly in children than in adults and is a sentinel for potential or concomitant meningococcemia and meningitis. The eye disease from either bacterium is characterized by lid edema (at times severe enough to close the eye), marked conjunctival injection, chemosis (conjunctival edema), and a copious purulent discharge. When verbal, the patient often describes moderately severe ocular discomfort. The incubation period is typically 1-3 days. Most often, the adult has a concomitant genital infection whereas newborn disease stems from the mother's birth canal.

As stated above, the neonatal cornea is at risk for infection. Systemic therapy is indicated for the treatment of
N. gonorrhoeae and N. meningitidis conjunctivitis in all age groups to minimize the risk of systemic and corneal infection. Mothers of neonates and sexual partners of patients with gonococcal conjunctivitis and contacts of patients with meningicoccal conjunctivitis should also be evaluated and treated. Treatment for N. gonorrhoeae conjunctivitis in the adult consists of a single dose IM injection of ceftriaxone, 1 g.(4,5) In the neonate, a single dose of 25-50 mg/kg IV or IM and a concurrent one-time saline irrigation of the eye is suggested.(5) Since there may be a chlamydial co-infection, co-treatment should be considered.

Instillation of 1% silver nitrate eyedrops is the standard method of prophylaxis against
N. gonorrhoeae. Saline irrigation immediately following prophylaxis is not recommended. Recently, povidone-iodine, administered as a 2.5% eyedrop, was found to be more effective as a prophylactic agent against Chlamydia trachomatous than either silver nitrate or erythromycin.(6) All three agents were equally effective against N. gonorrhoeae.

Acute Conjunctivitis
Acute conjunctivitis is rapid in onset with infection soon affecting the contralateral eye. Characteristically, the discharge is mucopurulent and the bulbar conjunctiva is more inflamed than the palpebral conjunctiva. The latter exhibits a velvety papillary reaction. Symptoms generally subside in 10-14 days, sometimes without specific therapy. When due to
Staphylococcus or Moraxella/Branhamella, the disease may become chronic. Staphylococcus has an affinity to populate the eyelid margin and induce a chronic blepharitis. Most cases of bacterial conjunctivitis are caused by gram-positive cocci, (2,7) but with residual defects of the conjunctiva from prior abnormalities, the incidence of gram negative infection increases. Table 2 lists the organisms commonly seen.

In children,
Hemophilus influenzae, Streptococcus pneumoniae and S. aureus are common pathogens. S. aureus is the most frequent cause of bacterial conjunctivitis worldwide. S. pneumoniae infection is self-limited, may occur in epidemics, is more frequent in temperate climates and winter months and is associated with subconjunctival hemorrhages. Streptococcus pyogenes infection is associated with pseudomembrane formation, usually on the bulbar conjunctiva. Conjunctivitis due to H. influenzae, biogroup aegyptius, (previously classified as Hemophilus aegyptius, the Koch-Weeks bacillus), is often epidemic but may be endemic in warmer climates. It too is associated with subconjunctival hemorrhages. Moraxella/Branhamella, formally seen in urban derelict and alcoholic populations in the United States, is now rarely encountered. Pseudomonas aeruginosa is an uncommon cause of conjunctivitis except in neonates, who are infrequently at risk for bacteremia following this infection.(8) When the corneal surface is traumatized concurrent with P. aeruginosa conjunctivitis in any age group, or when soft contact lenses are worn, the risk of keratitis dramatically increases, with its potential for corneal scarring and perforation.

Treatment of acute conjunctivitis consists of the administration of a topical antibiotic(s). Table 3 lists the more common drugs commercially available in the United States. Eyedrops are usually instilled 1-4 hours initially and ointments 4 times daily. Treatment may be tapered towards the end of the usual 10-14 day course of the infection. The aminoglycosides, mainstays of treatment for years (except for streptococcal infection), have given way to the use of the fluoroquinolones. However, bacterial resistance to fluoroquinolones appears to be on the increase (9) and their use should be restricted, with few exceptions, to tissue-destroying ocular infections. Polymixin B- trimethoprim eyedrops and bacitracin-polymixin B ointment are effective broad-spectrum drug combinations. Systemic antibiotics are rarely used for uncomplicated acute conjunctivitis. Exceptions include their use in the treatment of
H. influenzae conjunctivitis in infants and children and the Brazilian clone of H. influenzae, biogroup aegyptius, which is associated with severe systemic consequences.(10)

Chronic Conjunctivitis
S.aureus is, by far, the most common organism associated with chronic bacterial conjunctivitis.(11) S. epidermidis, part of the normal ocular surface flora, is a less frequent pathogen. Chronic staphylococcal conjunctivitis, often protracted and associated with chronic staphylococcal blepharitis, usually responds slowly to topical antibiotic therapy. Bacitracin ointment, after a short initial period of more frequent application, may have to be applied before sleep for several months to effect a cure. Vancomycin 1% eyedrops, compounded from the parenteral product, may be required following identification of methicillin-resistant staphylococcus. Gram negative infection (see Table 1), associated with disease or treatment that compromises the conjunctiva, may, at times, be difficult to eradicate even after signs of inflammation have abated. Moraxella/Branhamella is encountered much less frequently than in the past (see above). Chronic unilateral conjunctivitis may stem from a silent infection of a portion of the lacrimal outflow tract (e.g., canaliculitis, dacryocystitis).

Antibiotic resistance
The widespread use of antibiotics for the treatment of infections of the eye raises concern about the potential development of bacterial resistance to these drugs. Available data are limited, but nonetheless concerning, with identification of increasing levels of fluoroquinolone-resistant corneal isolates (7,13,14) as fluoroquinolone ophthalmic solutions replace aminoglycoside
preparations for treatment of conjunctivitis. Clearly, more research is needed to better assess the scope of this problem. Mechanisms need to be developed to improve surveillance and to try to reduce the development of resistance through efficient and judicious antibiotic use.

In summary, bacterial conjunctivitis, ubiquitous and generally easily managed by the general practitioner may on occasion present special peculiarities and diagnostic or therapeutic difficulties. At times, referral to an ophthalmologist may be required.

References

  1. Soukiasian SH, Baum JL. In: Krachmer JH, Mannis MJ, Holland EJ, eds. Cornea, vol. 2. St. Louis, MO; 1997; 759-772.
  2. Perkins RE, Kundsin RB, Abrahamsen I, Leibowitz HM. J Clin Microbiol 1975; 1:147
  3. Baum JL. In Tassman W, Jaeger E, eds. Duane's Foundations of Clinical Ophthalmology, Philadelphia, PA; 1998; in press
  4. Haimovici T, Roussel TJ. Am J Ophthalmol 1989; 107:511-514
  5. Centers for Disease Control and Prevention. 1993 MMWR 42 (suppl RR-14):47
  6. Issenberg SJ, Apt L, Wood M. N Eng J Med 1995; 332:562
  7. Brook I, Pettit TH, Martin WJ, Feingold SM. Ann Ophthalmol 1979; 11:389
  8. Burns RP, Rhodes DH Jr. Arch Ophthalmol 1961; 65:517
  9. Hwang DG, Biswell R, Holsclaw DS et al. Ophthalmology 1995; 102 (9A):101
  10. Brazilian Purpuric Study Group. Lancet 1987; 2:758
  11. Mannis, MJ. In Tasman W, Jaeger EA, eds. Foundations of Clinical Ophthalmology. Philadelphia, PA; 1990 JB Lippincott pp 1-7
  12. Fraunfelder F, Bagby G, Kelly D. Am J Ophthalmol 1982; 93:356
  13. Ooishi M, Miyao M. Ophthalmologica 1997; 211(suppl 1): 15-24.
  14. Knauf HP, Silvany R, Southern PM Jr, Risser RC, Wilson SE. Cornea 1996;15(1):66-71.
 

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