Endophthalmitis Caused by Mycobacterium chelonae: Selection of Antibiotics and Outcomes of Treatment

Mycobacterium chelonae is a rapidly growing acid-fast bacterium that has been reported to cause keratitis, ¹ interface infection after laser in situ keratomileusis, ^2,3 scleral buckle infection, ⁴ keratitis in a corneal graft, ⁵ and periocular infection after dacryocystorhinostomy and ptosis repair.⁶ In a review of the literature, a total of 4 cases of endophthalmitis caused by M chelonae have been reported.^7-10 The current study reports 5 cases of culture-proved endophthalmitis caused by M chelonae at Bascom Palmer Eye Institute, Miami, Fla, between January 1, 1980, and December 31, 2001.

Case 1. A 62-year-old man received an intravitreal injection of triamcinolone acetonide (4 mg/0.1 mL) in October 2001 for clinically significant macular edema reducing visual acuity to 20/70 OD. In November 2001, the patient returned with blurry vision and pain in the right eye. Results of examination demonstrated a visual acuity of hand motions, anterior chamber cells, and dense vitritis in the right eye. The eye was treated with a vitreous tap and injection of intravitreal antibiotics. Vitreous cultures were negative. Because of persistent vitreous inflammation, a pars plana vitrectomy was performed in the right eye in December 2001. Vitreous cultures were again negative.

On initial examination by our group, the patient had a visual acuity of hand motions, 2+ corneal edema, 2+ cell and flare in the anterior chamber, and opacification of the vitreous cavity in the right eye. Ultrasonography showed diffuse vitreous opacities, 360° choroidal detachment, and no retinal detachment. A pars plana vitrectomy and lensectomy were performed. Injections of amphotericin B, 0.01 mg, ceftazidime, 2.25 mg, and vancomycin, 1.0 mg, were given. Cultures of the vitreous cavity yielded M chelonae, sensitive to clarithromycin and amikacin; intermediately sensitive to tobramycin, imipenem, and cefoxitin; and resistant to ciprofloxacin, doxycycline, and sulfamethoxazole-trimethoprim. Despite 3 months of treatment with topical fortified amikacin sulfate and 4 intravitreal injections of 0.4 mg of amikacin sulfate, the visual acuity progressed to no light perception in February 2002. In each of 4 separate vitreous cultures, growth of M chelonae was documented, but the final culture, taken when the visual acuity was no light perception, showed no growth. The eye was enucleated in April 2002, and histopathologic examination demonstrated persistent acid-fast organisms in multiple intraocular tissues.

Case 2. A 76-year-old man underwent uncomplicated extracapsular cataract extraction and intraocular lens (IOL) implantation in the left eye in September 1992. In May 1994, the patient was referred with a complaint of 4 months of pain and decreased vision in the left eye.

On initial examination by our group, the patient had visual acuity of 20/300, a hypopyon smaller than 1 mm with anterior chamber cellular reaction, a posterior capsular plaque, and diffuse vitreous cells in the left eye. Pars plana vitrectomy and injection of intravitreal antibiotics were performed in May 1994. A second pars plana vitrectomy and injection of intraocular antiobiotics, as well as an IOL exchange, were performed in August 1994. In October 1994, the patient returned with visual acuity of 1/200 and a hypopyon in the left eye; a fluid-air exchange was perfomed, and vitreous cultures yielded M chelonae, which was sensitive to erythromycin, intermediately sensitive to ciprofloxacin, and resistant to tetracycline, sulfamethoxazole-trimethoprim, cefoxitin, and amikacin. Treatment with topical amikacin and oral rifampin was initiated, and smoldering inflammation with intermittent hypopyon formation persisted. In April 1995, the patient underwent a third pars plana vitrectomy, with further removal of residual lens capsule, vitreous culture, and injection of intravitreal erythromycin lactobionate, 0.5 mg, and imipenem, 0.5 mg. Vitreous cultures showed growth of M chelonae. Intraocular inflammation resolved. In July 1995, final visual acuity was 5/200 OS.

Case 3. A 77-year-old man underwent intracapsular cataract extraction without IOL in the left eye in 1979. A secondary IOL was placed in the left eye in December 1985 without complication. Four weeks postoperatively, pain and blurry vision developed in that eye.

On initial examination by our group, the patient had a visual acuity of 20/100 OS with a 10% hypopyon, and fluffy white infiltrates on the anterior hyaloid face (Figure 1, A). Possible fungal endophthalmitis was diagnosed. The patient was treated with an anterior chamber tap, anterior vitrectomy, and intravitreal injection of gentamicin sulfate, 0.1 mg, and amphotericin B, 0.01 mg. Anterior chamber cultures yielded M chelonae sensitive to clarithromycin, amikacin, kanamycin, and tobramycin, and resistant to ofloxacin and ciprofloxacin. Despite 3 intravitreal injections of amikacin sulfate (0.25 mg) and 2 months of topical fortified amikacin and prednisolone acetate, in December 1986, final visual acuity was hand motions and the intraocular pressure was 0 mmHg by applanation tonometry(Figure 1, B).

Case 4. A 70-year-old woman underwent complicated cataract extraction in the right eye in February 1995, with anterior chamber IOL implantation, 2 penetrating keratoplasties for pseudophakic bullous keratopathy and failed graft, and 2 Baerveldt implantations for elevated intraocular pressure. In December 1998, the patient complained of pain and decreased vision in the right eye. On initial examination by our group, the patient's right eye had a visual acuity of hand motions, an exposed Baerveldt glaucoma drainage device, a flat anterior chamber, and peripheral choroidal detachment. The Baerveldt tube was removed and the fistula tract was closed. Postoperatively, dense intraocular inflammation was noted, and an anterior vitrectomy with vitreous culture was performed. Intravitreal injections of cefazolin, 2.25 mg, ceftazidime, 1.0 mg, and dexamethasone sodium phosphate, 0.4 mg, were administered at the conclusion of the procedure. Intraocular cultures yielded M chelonae, sensitive to clarithromycin, intermediately sensitive to ciprofloxacin and amikacin, and resistant to tobramycin, doxycycline, and tetracycline. Postoperatively, a 2-month course of fortified amikacin, atropine, and prednisolone acetate, and oral clarithromycin, resulted in resolution of smoldering intraocular inflammation. At last follow-up in April 2000, visual acuity was 3/200 OD.

Case 5. A 73-year-old man was examined in March 1990 complaining of pain and discharge in the right eye for 1 week. A tarsorrhaphy had been performed in February 1990 for a neurotrophic corneal ulcer.

On initial examination by our group, the patient had a visual acuity of light perception, a 70% lateral tarsorrhaphy, a central corneal infiltrate with perforation plugged by a fibrin plaque, and dense anterior chamber fibrin. A penetrating keratoplasty with extracapsular cataract extraction, peripheral iridectomy, and conjunctival flap was performed, and treatment was initiated with topical amikacin and oral ciprofloxacin. Culture of the anterior chamber yielded M chelonae sensitive to erythromycin, azithromycin, and clarithromycin, and resistant to cefoxitin and ciprofloxacin. One month postoperatively, the patient did not complain of pain in the right eye, and visual acuity was light perception. A vascularized cornea prevented further examination.

In the present series, several categories of endophthalmitis are represented:(1) acute-onset postoperative endophthalmitis, (2) chronic or delayed-onset postoperative endophthalmitis, (3) endophthalmitis associated with glaucoma surgery, (4) endophthalmitis associated with a perforated corneal ulcer, and(5) intravitreal injection of triamcinolone. The 2 cases that occurred after anterior segment surgery each were notable for the presence of white opacifications of the capsular bag or anterior vitreous face, leading to initial misdiagnosis as Propionibacterium acnes or fungal endophthalmitis. Other authors have noted white opacities of the lens capsule or vitreous in cases of M chelonae endophthalmitis.^7,8

Mycobacterium chelonae endophthalmitis is generally associated with poor visual acuity outcomes (Table 1). No patients in previous reports or the current series achieved visual acuity of 20/400 or better. Many eyes developed chronic hypotony or underwent enucleation or evisceration.^7-10

The preferred antibiotic for M chelonae remains uncertain, but amikacin is usually considered as the first-line antibiotic of choice⁷ (Table 2). In the present series, the cultured organism was sensitive to macrolide antibiotics (sensitivity was tested to clarithromycin in 4 cases and to erythromycin in 2 cases). However, the cultured organism was sensitive to amikacin in only 2 cases, was intermediately sensitive in 1 case, and was resistant in 1 case (sensitivity to amikacin was not tested in 1 case). In a recent case series of nontuberculous mycobacterial keratitis, 70% of isolates were sensitive to amikacin, while 100% of isolates were sensitive to clarithromycin.¹ Clinical resolution of infection may not occur despite appropriate antibiotic therapy.¹ Intravitreal clarithromycin has been reported to be nontoxic to rabbit eyes up to a dose of 1.0 mg¹³; to our knowledge, the use of intravitreal clarithromycin in humans has not been reported.

In summary, M chelonae is an uncommon cause of endophthalmitis. It is associated with a chronic course of marked intraocular inflammation and, in some cases, a white plaque inside the capsular bag in eyes after cataract surgery. While macrolide antibiotics may show good in vitro efficacy against M chelonae, endophthalmitis caused by this organism has generally poor visual acuity outcomes.

This study was supported in part by Research to Prevent Blindness Inc, New York, NY.

Corresponding author: Ingrid U. Scott, MD, MPH, Bascom Palmer Eye Institute, PO Box 016880, Miami, FL 33101.