The Microbiology of Contact Lens Wear

BY MICHAEL A. WARD, C.O.M.T., F.C.L.S.A.
SEPT. 1997

OCULAR FLORA

The incidence and densities of microorganisms vary with environmental conditions. Normal ocular flora are transient and sparse. Other organisms that drop in from the environment are usually washed away, seldom causing infection. Among the normal flora of the human conjunctiva, Staphylococcus epidermidis and Corynebacterium xerosis are the most common aerobic isolates. McNatt et al. (1978) reported that Propionibacterium acnes is the predominant anaerobic bacterium in conjunctival cultures. Although fungi have been isolated from the conjunctiva, they generally represent transient contamination and are not usually found in serial cultures.

OCULAR DEFENSE MECHANISMS

Donzis et al. (1987) reported that of 100 patients, 52 had contaminated contact lens care systems but were asymptomatic and free of infection, demonstrating the efficacy of the defense mechanisms of the eye. They include:

1. Decreased ocular temperature -- bacteria have specific temperature requirements.

2. Mechanical action of blinking -- a windshield wiper effect that physically pushes debris down into the lacrimal lake.

3. Irrigation by lacrimal secretions -- washes debris and unadhered microbes out of the ocular area, through the lacrimal drainage system and into the nasopharynx.

4. Intact epithelial surface -- very few pathogenic bacteria can penetrate an intact epithelial barrier. Maintaining a healthy epithelium is the most important defense against infection.

5. Lysozyme, lactoferrin, specific immunoglobulins and complement in tears -- these proteins, which are part of the normal defense system, act to eliminate microbial invaders.

Ocular defenses prevent initial colonization of opportunistic pathogens on the outer eye. If a large enough inoculum is present, these defenses may become overwhelmed and infection occurs. The body's immune system then triggers specific and nonspecific inflammatory responses to fight microbial invasion. Occasionally, the immunologic response is so severe that it not only attacks the offending organisms, but triggers excess inflammation that destroys host tissue.

HOW INFECTION OCCURS

Hand-to-eye contact is the most common route of transmission of potentially pathogenic microorganisms to the eye. However, contaminated contact lenses, lens care products, lens cases and office instruments may also transport microbes to the eye. In fact, the contact lens carrying case is the single most important reservoir for potential infection.

Bacteria, fungi, viruses and parasites are all potential pathogens. However, bacteria, particularly Pseudomonas aeruginosa, are the most feared due to their toxigenicity, their invasiveness and the speed with which they can destroy ocular tissues. Fortunately, bacteria are also most responsive to drug therapy.

BACTERIA

The four principal bacterial genera that may cause ocular infections are: Staphylococcus, Streptococcus, Pseudomonas and Serratia.

Staphylococcus epidermidis is an indigenous floral organism of the outer eye, seldom associated with outer eye infections. Staphylococcus aureus is an aerobic gram positive coccus, and is probably the most common cause of bacterial conjunctivitis in the western world. S. aureus has been isolated from hands, face, nose and skin of healthy patients. Direct and recurrent staphylococcal ocular infection is most likely due to hand-to-eye transfer.

Streptococcus pneumoniae and Streptococcus pyogenes are the two streptococci most implicated in ocular pathogenesis. S. pneumoniae (pneumococcus) is an aerobic gram positive diplococcus, often lancet-shaped or arranged in short chains, possessing a polysaccharide capsule. The virulence of this bacterium is a function of its capsule, which prevents phagocytosis (engulfing) by white blood cells. A normal inhabitant of the upper respiratory tract, it is likely transmitted via the nasolacrimal drainage system and hand-to-eye contact among individuals with upper respiratory infections or who are carriers of the organism.

S. pyogenes is an invasive, toxigenic, aerobic gram positive coccus, typically arranged in chains. Although not commonly associated with ocular infection, when it occurs, it is frequently severe with inflammatory membrane formation. It may cause a diffuse and rapidly spreading cellulitis that involves the tissues and extends along the lymphatic pathway into the bloodstream with subsequent septicemia. It is usually spread via droplets from the respiratory tract or skin of a person harboring the organism with clinical or subclinical disease. Ocular infection is usually from direct hand-to-eye contact.

The pseudomonads include gram negative, non-sporulating, motile rods that are frequently present in the normal intestinal flora and in soil, water, sewage and air. Pseudomonas aeruginosa is remarkably versatile with simple nutritional requirements. It can use 60 to 80 different organic compounds as sole carbon sources and energy. It may replicate in moist environments including eye drops, weak antiseptics, irrigating solutions and eye cosmetics. It can multiply over a relatively wide temperature range (10�C to >42�C) and even grow slowly in an anaerobic environment if nitrate is present. It is ubiquitous in our environment and may potentially contaminate distilled water, inhalation aerosols and medications. Pseudomonas is an opportunistic pathogen that can cause very rapidly spreading, severely destructive corneal ulcers (Fig. 1). It liberates exotoxins which inhibit protein synthesis similar to diphtheria toxin fragment A. Exotoxin A can result in rapid death of epithelial, stromal and endothelial cells and associated further necrosis. Proteolytic enzymes, leukocidin, hemolysis and endotoxins add to the virulent character of P. aeruginosa.

This organism produces glycocalyx (extracellular polysaccharide slime), which is associated with bacterial adhesion, persistence and survival of the bacteria in infected tissues and on the surface of hydrophilic contact lenses. In addition, the glycocalyx protects the organism from antibodies and complement as well as extraocular doses of antibiotics. In P. aeruginosa keratitis, PMNs aid in host defenses as well as in corneal destruction. PMN lysosomal enzymes (collagenase and proteoglycanase) and toxic oxygen metabolites are responsible for microbial killing and progressive corneal tissue destruction.

P. aeruginosa keratitis has been associated with hydrophilic contact lenses, both daily and extended wear. It appears that contact lenses can serve as vectors in transferring P. aeruginosa from contaminated solutions to the eye, since viable organisms readily adhere to hydrophilic lenses of varying water content and polymer composition and to silicone acrylate lenses.

Serratia marcescens is a small, motile, non-spore forming, gram negative rod of the Enterobacteriaceae family. Like pseudomonas, it is an opportunistic pathogen that becomes resistant to disinfectants and antibiotics and is capable of liquefactive keratitis and necrosis. It has been isolated from various preserved ophthalmic preparations, contaminated lens care products and corneal ulcers. S. marcescens has been reported to persist and grow in rigid contact lens wetting/soaking solutions preserved with chlorhexidine.

FUNGI, VIRUSES AND AMOEBAS

Filamentous fungi penetrate soft contact lenses in vitro and in vivo. Although uncommon, fungal corneal ulcers associated with contact lens wear have been reported (Fig. 2). Fungal invasion and infection is generally more prevalent in the southeastern United States due to environmental and nutritional factors. Aspergillus, Cladosporium, Curvularia and Fusarium genera have been associated with contact lens contamination. These fungi can attach to and penetrate a soft contact lens matrix and result in physical and metabolic degradation of the lens.

Fungal spores (Fig. 3) may seed the contact lens surface in vivo and use the lens and tears for carbon and energy sources. Certain species have been isolated from shower curtains, bathroom tiles and contact lens cases. The most likely route of transmission of fungi to the eye is lens-to-eye from a contaminated lens case or environmental seeding.

Viruses are rare and are not commonly associated with contact lens wear. Certain viruses, herpes simplex virus (HSV) and human immunodeficiency virus (HIV), have become more prevalent and have raised concerns regarding transmittance among patients and from practitioner to patient. Although HIV has been isolated in tears of some AIDS patients, there is no conclusive evidence that this virus can be transmitted via the tears or contact lenses. HSV may cause corneal ulceration and is widely reported in the literature. It's conceivable that a contact lens wearer could transfer the virus via hand-to-eye contact by touching an open cold sore just prior to lens insertion.

Acanthamoeba is also associated with keratitis among contact lens wearers (Fig. 4). Acanthamoeba are true, living, freshwater amoeba. They have been isolated from well water, hot tubs, tap water and other freshwater sources. Acanthamoebic keratitis is rare, but it is a devastatingly sight-threatening infection that is certainly preventable. The most probable route of transmission is lens-to-eye from a contaminated saline or lens case. The incidence has decreased in recent years, largely due to discontinued use of homemade saline.

PLAYING INTO THEIR HANDS

Many corneal ulcers associated with contact lens wear can be attributed to improper hygiene or patient noncompliance. In one study, patients did not wash their hands prior to lens manipulation, disinfected their lenses less than once a month or used no disinfection system at all. Some lens wearers do not regularly disinfect their carrying cases, so it's not surprising that microbial populations thrive in lens cases where nutrients from deposits or unwashed fingers have accumulated.

Plastic containers may become contaminated within the container and even within the neck of the dispensing tip. Even though lenses may be properly cleaned and thoroughly disinfected, individuals using contaminated solutions for moistening the lens before insertion, or using the solution as an eye drop, could conceivably self-inoculate the corneal surface with microorganisms.

Inadequately preserved cosmetics have also been identified as reservoirs for ulcer-causing bacteria. Wilson and Ahearn (1977) stated that corneal infection may occur after an accidental scratch of the epithelium with a contaminated mascara applicator.

PREVENTION IS KEY

Proper patient instruction -- oral and written -- is imperative in preventing ocular infections. We should emphasize the importance of good hygiene by washing our hands in front of the patient whenever we enter the examination room. When we deliver a contact lens care system, we should always demonstrate its use.

A typical contact lens care regimen should include:

1. daily cleaning with surfactant cleaner;

2. rinsing with a commercially prepared sterile saline;

3. disinfecting with appropriate heat, cold chemical or hydrogen peroxide system and storing overnight.

Patients should enzyme their lenses weekly when indicated. In the morning, they should rinse the case with hot tap water and allow it to air dry. Once a week, patients should disinfect the lens case by placing the opened case in freshly boiled water for 20 minutes. This prevents carryover of microbes.

Emphasize that patients should use only fresh, sterile, commercially prepared products, and they must not change any component of the care system without checking with your office first. At each follow-up visit, ask patients the brand names of the products they use and how they use them.

Infection prevention is a shared responsibility. It's our responsibility to provide proper patient instruction, demonstrating lens care and providing written reference material. The patient's responsibility is to follow the practitioner's instructions to the letter. The incidence of contact lens related ocular infections is quite low, but with proper instruction, it could be even lower. CLS

References are available upon request from the editors at Contact Lens Spectrum. To receive references via fax, call (800) 239-4684 and request document #28.

SPECTRUM SEPT. 1997