Pseudomonas: What We Really Know
What We Really Know
BY WILLIAM D. TOWNSEND, OD
When a contact lens patient calls complaining of a painful red eye, we all hope it's not infectious keratitis caused by Pseudomonas aeruginosa. Pseudomonas ulcers are bad, and often do not respond
in a typical way to treatment. We are only now beginning to understand the characteristics that make this organism so dangerous.
What is Pseudomonas?
Pseudomonas aeruginosa is the most common species in the Pseudomonas genus. It thrives in moist conditions, and is found on bar soaps, distilled water, saunas, soil and in contaminated eye drops and solutions.
P. aeruginosa is the most common cause of contact lens-associated keratitis. It invades tissue compromised by trauma or long-term hypoxia. These Gram-negative rods exist in two forms: the motile swimming form possesses one or more flagella, while the second form is a non-motile microcolony encased in a slimy glycocalyx that protects the
organism, and is thought to facilitate adherence for initiating colonization. Adherence of bacteria to the cornea is directly related to the extent of debris on the lens.
Pseudomonas produces destructive extracellular enzymes. Exotoxin A prevents host cell protein synthesis, leading to necrosis and death. Elastease and collagenase melt and destroy corneal tissue, enhancing the progression of infection through the tissue. For many years, these attributes were credited with the destruction and scarring caused by Pseudomonas.
The body's immune response also contributes significantly to the ulceration process. Polymorphonuclear neutrophils (PMNs) migrate to the site and release powerful enzymes that destroy bacteria. Collagenase and other proleolytic enzymes can cause permanent and extensive damage to epithelium and stromal cells.
In 1977, Kessler et al showed that enzymes produced by PMNs played an important role in the destruction of corneal tissue in P. aeruginosa keratitis. The majority of tissue damage is, in fact, due to leukocyte release of lysosomal enzymes. More recently, Schmut et al showed that PMN elastase was present in tissue long after the active infection caused by P. aeruginosa was gone. They postulated that PMNs cause a significant part of corneal inflammation and destruction in bacterial keratitis.
Our first priority must be to halt and eliminate all infection. The complex nature of P. aeruginosa's genetic makeup renders it prone to acquired resistance. A few years ago, monotherapy using fluoroquinolones was touted as the best approach for treating bacterial keratitis. In Ophthalmology July 1999, Garg et al found ciprofloxacin resistance in 22 of 141 patients treated for P. aeruginosa keratitis, and gentamicin resistance in 63 percent of isolates.
The next level of care in treating corneal ulcers has been fortified aminoglycosides and
cefazolin. This "standard" may need to be changed; Robinson et al demonstrated that strains of P. aeruginosa highly resistant to fortified cefazolin and aminoglycosides responded when ceftazidime was substituted for cefazolin.
Once the infection is controlled, some corneal specialists advocate treating the inflammatory portion of the disease with topical corticosteroids. Another possible approach is the use of other agents to block the deleterious effects of the immune system. Matsumoto et al found that superoxide dismutase can prevent excessive tissue destruction caused by infiltrating PMNs in P. aeruginosa corneal ulcers.
As we better understand the exact process by which tissue damage occurs, we may be able to prevent some of the vision loss caused by this opportunistic bacteria.
Dr. Townsend is in private practice in Canyon, Texas, and is a consultant at the Amarillo VA Medical Center.
Contact Lens Spectrum, Issue: June 2000