Endophthalmitis can occur following glaucoma drainage implant surgery, with an estimated incidence of less than 2%.1
Although the major risk factor for endophthalmitis in glaucoma drainage implant surgery is tube exposure,2
endophthalmitis has been reported in cases with no tube exposure or obvious external risk factors.3
Endophthalmitis secondary to Serratia marcescens is uncommon and has been described following endogenous seeding4
as well as ocular surgery.5
We describe the case of an elderly woman using contaminated eye drops who developed S. marcescens keratitis in the right eye and simultaneous endophthalmitis in the left eye with the glaucoma drainage implant.
A 90-year-old Caucasian woman with pseudoexfoliative glaucoma presented with a 1-day history of pain and decreased vision in the right eye and a 3-day history of photophobia and vision loss in the left eye. She had undergone a trabeculectomy in the right eye and Baerveldt implant placement in the left eye 13 and 3.5 years prior to presentation, respectively. At the time of presentation, she had been using timolol 0.5%, prednisolone 1%, and nepafenac 0.1%, all twice daily in both eyes.
Best corrected visual acuity at presentation was 20/400 in the right eye and light perception in the left eye. Intraocular pressure was 8 mm Hg in the right eye and 14 mm Hg in the left eye. The patient was pseudophakic in both eyes. Anterior segment examination in the right eye revealed 1+ conjunctival injection with a 3-mm paracentral corneal ulcer (Figure 1A
). A superior bleb was present in the right eye, which was clear and Seidel-negative. Dilated fundus examination revealed a cupped optic nerve in the right eye. The anterior chamber in the left eye was formed with 4+ cell, a 2-mm hypopyon, moderate fibrin, an edematous hazy cornea, and a patent glaucoma drainage implant in the supratemporal quadrant (Figure 1B
). No areas of tube or plate exposure were noted, and Seidel testing yielded a negative result (Figure 1C
). There was a bare orange reflex with 4+ vitreous cells and haze that obscured visualization of the retina in the left eye.
Figure 1. (A) Paracentral corneal ulcer and stromal thickening in the right eye at presentation. (B) Left eye on postoperative day 1 after pars plana vitrectomy and intravitreal antibiotics. Fibrin and hemorrhage remain present within the anterior chamber. The hypopyon has completely resolved. (C) Photo of supratemporal quadrant of the left eye demonstrates that the tube shunt is covered with an intact conjunctival epithelium.
The patient was diagnosed with a corneal ulcer in the right eye and delayed-onset endophthalmitis in the left eye. She underwent a limited 23-gauge vitrectomy in the left eye with culture of the vitreous aspirate and injection of intravitreal 0.1 cc vancomycin (1 mg/mL) and 0.1 cc ceftazadime (2.25 mg/mL). Additionally, the corneal ulcer in the right eye was cultured and treated with hourly fortified topical to-bramycin (14 mg/mL) and vancomycin (50 mg/mL). The corneal culture in the right eye and the aqueous/vitreous cultures in the left eye grew S. marcescens on chocolate, blood, and thioglycolate media. For each of the patient’s presurgical topical medications, the bottle tip, cap, and solution were plated individually and all yielded positive cultures of S. marcescens.
At the 2-month visit, the patient’s vision had improved to 20/400 in both eyes. The corneal ulcer in the right eye had healed into a vascularized stromal scar (Figure 2A
). In the left eye, the cornea remained thickened with few Descemet’s folds; the anterior chamber was deep and quiet, and the retina was flat, with only mild vitreous cavity haze (Figure 2B
Figure 2. Two-month follow-up. (A) The corneal ulcer in the right eye has completely healed into a vascularized paracentral scar. (B) The left eye is quiet and void of any signs of inflammation or infection. Mild corneal haze and thickening persist.
Serratia marcescens is a gram-negative coccobacillus that can cause a variety of ocular infections. Although most commonly implicated in anterior segment infections, it has also been isolated in cases of both endogenous4
and exogenous endophthalmitis,5
with outcomes that are generally poor.4
This concurrent presentation of S. marcescens endophthalmitis and keratitis is unique in a few respects. S. marcescens endophthalmitis following glaucoma drainage implant placement has not been previously reported in the literature. The patient’s topical medications (ie, topical beta blocker, non-steroidal anti-inflammatory agent, and steroid) may have disturbed the ocular surface and are known risk factors for keratitis. Similarly, these medications may have led to breakdown of surface defenses, facilitating organism entry to the tube or plate. S. marcescens has been shown to produce proteases that have a number of biological roles, including the degradation of tissue integrity and lysis of host defense proteins,6
thereby increasing the risk of endophthalmitis in spite of no apparent tube or plate exposure. The mechanism of bilateral infection in this case is not completely clear. One possibility is that the drops served as a source or conduit of infection for at least one of the eyes. Alternatively, there may have been another source of both ocular infections concurrently, with the eye drops only becoming secondarily contaminated. In patients presenting with bilateral ocular infections, exploration of in-use eye drops as a possible source or conduit of infection should be strongly considered. Suspicion of contaminated eye drops serving as a conduit for ocular infections should be particularly high in patients who reside in nursing or convalescent facilities, where nosocomial infections and bacterial colonization are generally more prevalent and multiple caretakers handle medications. S. marcescens is highly destructive to ocular tissues, and endophthalmitis from this organism generally carries a poor visual prognosis. Prompt cultures with sensitivity should be performed, and suspected endophthalmitis should be treated immediately with intravitreal antibiotics (eg, aminoglycosides or newer-generation cephalosporins such as ceftazidime) and possible concomitant vitrectomy.
- Morad Y, Donaldson CE, Kim YM, Abdolel M, Levin AV. The Ahmed drainage implant in the treatment of pediatric glaucoma. Am J Ophthalmol. 2003;135(6):821–829 doi:10.1016/S0002-9394(02)02274-2 [CrossRef] .
- Gedde SJ, Scott IU, Tabandeh H, et al. Late endophthalmitis associated with glaucoma drainage implants. Ophthalmology. 2001;108(7):1323–1327 doi:10.1016/S0161-6420(01)00598-X [CrossRef] .
- Nguyen QH, Budenz DL, Parrish RK 2nd, . Complications of Baerveldt glaucoma drainage implants. Arch Ophthalmol. 1998;116(5):571–575.
- Equi RA, Green WR. Endogenous Serratia marcescens endophthalmitis with dark hypopyon: case report and review. Surv Ophthalmol. 2001;46(3):259–268 doi:10.1016/S0039-6257(01)00263-6 [CrossRef] .
- Cohen SM, Flynn HW Jr, Miller D. Endophthalmitis caused by Serratia marcescens. Ophthalmic Surg Lasers. 1997;28(3):195–200.
- Matsumoto K. Role of bacterial proteases in pseudomonal and serratial keratitis. Biol Chem. 2004;385(11):1007–1016 doi:10.1515/BC.2004.131 [CrossRef] .