Endophthalmitis is a rare but well known complication of ocular surgery and is caused by various organisms involving different mechanisms.1,2 Recurrent postoperative endophthalmitis can occur rarely, especially when the initial treatment was a vitreous tap and injection.3,4 Bacterial cultures persistently positive for indolent organisms in eyes after intravitreal antimicrobial therapy for endophthalmitis have been reported.5 However, to the best of our knowledge, there are only four prior publications in the English language literature of chronic persistent postoperative endophthalmitis with apparent clinical resolution between episodes caused by the typically virulent organism Enterococcus faecalis.2,4,6,7 The following is a case report of E. faecalis endophthalmitis that occurred 3 days, 78 months, and 80 months after cataract surgery. Electron microscopy indicated that the organisms had been sequestered in the surgically removed capsular bag, escaping total eradication despite repeated examinations indicating apparent clinical recovery.
A 77-year-old man with open-angle glaucoma underwent an uncomplicated trabeculectomy. Five years after the trabeculectomy, clear corneal phacoemulsification and implantation of an intraocular lens was performed in the right eye with a corneal suture placed close to the wound. Three days postoperatively, the patient reported pain and decreased vision. His visual acuity was 20/100 in the right eye with 3+ conjunctival injection and 3+ cell and flare in the anterior chamber and +1 cells in the anterior vitreous. He was diagnosed as having endophthalmitis based on his clinical features and underwent a vitreous tap and injection of vancomycin and ceftazidime. Vitreous cultures were negative but symptoms resolved after a prolonged course of topical fortified vancomycin drops (25 mg/mL). His visual acuity recovered to 20/25 and the anterior chamber was quiet.
Three months postoperatively, the patient was referred to the Bascom Palmer Eye Institute for a corneal wound infection at the site of his temporal clear corneal cataract incision. Several corneal cultures were negative but the patient slowly responded to fortified vancomycin (25 mg/mL) and oral doxycycline 100 mg twice daily over the course of 1 year. The patient’s visual acuity recovered to 20/30 and remained stable.
Six years later, the patient was re-referred to the Bascom Palmer Eye Institute for persistent hypotony, which responded to topical steroids but recurred on withdrawal of the eye drops. On presentation, his visual acuity was 20/40 in the right eye with an intraocular pressure of 6 mm Hg, and no bleb leak was identified. There was no evidence of inflammation or infection in the anterior or posterior segment. A slow steroid taper was initiated.
One month later, the patient presented with severe pain and hand motions visual acuity. The cornea was hazy with 2+ microcystic edema and a 2-mm hypopyon (Figure 1). Ultrasound demonstrated dense vitreous membranes consistent with endophthalmitis. A vitreous tap and injection was performed with intravitreal vancomycin (1 mg/0.1 mL), ceftazidime (2.25 mg/0.1 mL), and dexamethasone (0.4 mg/0.1 mL). Fortified vancomycin topical eye drops were initiated. The vitreous culture yielded E. faecalis.
Figure 1. Slit-lamp photograph on presentation with endophthalmitis demonstrating severe corneal edema, conjunctival injection, hypopyon, and involvement of the trabeculectomy site.
Approximately 24 hours after the vitreous tap and injection, the patient’s visual acuity deteriorated to light perception. The patient underwent a 23-gauge pars plana vitrectomy with repeat injection of intravitreal antibiotics. E. faecalis was recovered in the vitreous cassette and was sensitive to vancomycin. Two weeks later, the inflammation had resolved and the vitreous was clear (Figure 2). The patient’s visual acuity remained counting fingers secondary to severe optic and foveal atrophy.
Figure 2. (A) Slit-lamp photograph demonstrating apparent resolution of conjunctival injection and anterior segment inflammation after the first pars plana vitrectomy. (B) Fundus photograph 2 months after initial pars plana injection demonstrating optic nerve pallor, sclerotic vessels, and intraretinal hemorrhages with a clear vitreous.
Six weeks later, the patient returned with onset of pain and reduced vision. His visual acuity was light perception. On examination, intraocular pressure was 38 mm Hg with a 2-mm hypopyon, corneal edema, and no view to the posterior pole. Vitreous tap and injection revealed E. faecalis again. The next day, the patient underwent pars plana vitrectomy, air–fluid exchange, intravitreal injection of vancomycin and dexamethasone, removal of the intraocular lens and capsular bag (Figure 3), and silicone oil injection in the right eye. A capsular bag abscess was noted at vitrectomy. Two weeks later, the patient’s visual acuity was counting fingers at 1 foot. His intraocular pressure was 7 mm Hg, the conjunctiva was clear, and there was a good view of the retina, which remained attached under oil. Two months later, the patient’s condition remained stable with visual acuity of counting fingers and an intraocular pressure of 12 mm Hg.
Figure 3. (A) Low magnification of scanning electron micrograph (SEM) demonstrating Enterococcus faecalis on the intraocular lens. (B) High-magnification SEM of several E. faecalis organisms along with debris scattered over the lens capsule. (C) High-magnification SEM of E. faecalis within a dense mix of cellular debris. (D) Ultrahigh magnification SEM of E. faecalis secreting biofilm.
Postoperative endophthalmitis is a rare but devastating complication of ocular surgery, occurring after 0.05% to 2% of cataract surgeries.8 Only 40% of patients recover visual acuity better than 20/100 and more than half of patients have no light perception even after the infection resolves.9
Enterococcus is a virulent organism that causes postoperative endophthalmitis in 2% to 8% of endophthalmitis cases.10Enterococcus, previously classified as group D streptococcus, is a gram-positive diplococcus associated with urinary or gastrointestinal tract infections. However, it can also be part of the normal oral and intestinal flora. Although organisms of low virulence, such as Propionibacterium acnes, tend to cause indolent or recurrent endophthalmitis, Enterococcus classically causes a more fulminant infection. To our knowledge, there are only four other cases of recurrent E. faecalis endophthalmitis in the English language literature (Table 1).2,4,6,7 In general, recurrent endophthalmitis is postulated to be the result of limited antibiotic action and/or sequestration of the organism in biofilms in the capsular bag behind the intraocular lens. Biofilm production, a process not unique to Enterococcus species, provides an environment that impedes the effectiveness of antimicrobial and immune-mediated microbial killing.11,12
Table 1: Cases of Recurrent Enterococcus faecalis in the English Language Literature
In the current patient, electron microscopy performed on the surgically removed capsular bag confirmed the presence of sequestered Enterococcus organisms (Figure 3). Based on this finding, we hypothesize that the initial episode of endophthalmitis 3 days after cataract surgery and the corneal wound infection, which were culture negative, were likely due to E. faecalis and the two culture-positive episodes. Enterococcus organisms can sometimes require multiple attempts at culture before growth, which may have accounted for the lack of growth in the first two episodes.13
Silicone oil was used because of its antimicrobial properties against common endophthalmitis-causing agents. A study performed by Parsek and Singh14 showed greater decrease in the colony-forming units of bacterial and fungal species in silicone oil when compared with physiologic saline and brain–heart infusion. Enterococcus species were not among the tested organisms in this study, but our use of silicone oil was empiric. Furthermore, we anticipated that the silicone oil would help prevent postoperative hypotony in this patient, a concern after severe endophthalmitis.15
Our patient demonstrates that even virulent bacteria may present with an atypical late-onset relapse of severe inflammation. The current study suggests that recurrences may occur months after apparently successful initial therapy. Based on this case and our review of the literature, we recommend that clinicians consider removal of the capsular bag and intraocular lens in cases of E. faecalis to prevent recurrences.
- Song A, Scott IU, Flynn HW Jr, Budenz DL. Delayed-onset bleb-associated endophthalmitis: clinical features and visual acuity outcomes. Ophthalmology. 2002;109:985–991. doi:10.1016/S0161-6420(02)00965-X [CrossRef]
- Stern GA, Engel HM, Driebe WT Jr, . Recurrent postoperative endophthalmitis. Cornea. 1990;9:102–107. doi:10.1097/00003226-199004000-00004 [CrossRef]
- Leng T, Miller D, Flynn HW Jr, Jacobs DJ, Gedde SJ. Delayed-onset bleb-associated endophthalmitis (1996–2008): causative organisms and visual acuity outcomes. Retina. 2011;31:344–352. doi:10.1097/IAE.0b013e3181e09810 [CrossRef]
- Teoh SC, Lee JJ, Chee CK, Au Eong KG. Recurrent Enterococcus faecalis endophthalmitis after phacoemulsification. J Cataract Refract Surg. 2005;31:622–626. doi:10.1016/j.jcrs.2004.06.047 [CrossRef]
- Shaarawy A, Grand MG, Meredith TA, Ibanez HE. Persistent endophthalmitis after intravitreal antimicrobial therapy. Ophthalmology. 1995;102:382–387.
- Nasrallah FP, Desai SA. Recurrent enterococcal endophthalmitis following cataract surgery: a case report. Ophthalmic Surg Lasers Imaging. 1999;30:481–482.
- Miller KV, Eisley KM, Shanks RM, et al. Recurrent enterococcal endophthalmitis seeded by an intraocular lens biofilm. J Cataract Refract Surg. 2011;37:1355–1359. doi:10.1016/j.jcrs.2011.04.014 [CrossRef]
- Flynn HW Jr, Scott IU. Legacy of the endophthalmitis vitrectomy study. Arch Ophthalmol. 2008;126:559–561. doi:10.1001/archopht.126.4.559 [CrossRef]
- Lalwani GA, Flynn HW Jr, Scott IU, et al. Acute-onset endophthalmitis after clear corneal cataract surgery (1996–2005): clinical features, causative organisms, and visual acuity outcomes. Ophthalmology. 2008;115:473–476. doi:10.1016/j.ophtha.2007.06.006 [CrossRef]
- Scott IU, Loo RH, Flynn HW Jr, Miller D. Endophthalmitis caused by enterococcus faecalis: antibiotic selection and treatment outcomes. Ophthalmology. 2003;110:1573–1577. doi:10.1016/S0161-6420(03)00502-5 [CrossRef]
- Ozdamar A, Aras C, Ozturk R, Akin E, Karacorlu M, Ercikan C. In vitro antimicrobial activity of silicone oil against endophthalmitis-causing agents. Retina. 1999;19:122–126. doi:10.1097/00006982-199902000-00006 [CrossRef]
- Kapur R, Birnbaum AD, Goldstein DA, et al. Treating uveitis-associated hypotony with pars plana vitrectomy and silicone oil injection. Retina. 2010;30:140–145. doi:10.1097/IAE.0b013e3181b32f06 [CrossRef]
- Fraser SG, Ohri R. Endophthalmitis caused by enterococcus faecalis. Eye (Lond). 1995;9:535–536. doi:10.1038/eye.1995.124 [CrossRef]
- Parsek MR, Singh PK. Bacterial biofilms: an emerging link to disease pathogenesis. Annu Rev Microbiol. 2003;57:677–701. doi:10.1146/annurev.micro.57.030502.090720 [CrossRef]
- Chuang-Smith ON, Wells CL, Henry-Stanley MJ, Dunny GM. Acceleration of enterococcus faecalis biofilm formation by aggregation substance expression in an ex vivo model of cardiac valve colonization. PLoS One. 2010;30;5:e15798. doi:10.1371/journal.pone.0015798 [CrossRef]
Cases of Recurrent Enterococcus faecalis in the English Language Literature
|Author||Cases ofE. faecalisin Series||No. of Culture-Positive Episodes||No. of Clinically Apparent Episodes||Surgeries Performed||Final Visual Outcome After Each Episode|
|Current case||1||1st: Negative; 2nd: VSEF; 3rd:VSEF||3||1st: Intravitreal vancomycin, intravitreal ceftazidime, and topical vancomycin. 2nd: Same as first surgery with intravitreal dexamethasone and PPV. 3rd: Same as first surgery. PPV replaced with silicone. Capsule and IOL removal.||1st: 20/25; 2nd: CF; 3rd: CF|
|Miller et al. (2011)||1||1st: VSEF; 2nd: VSEF||2||1st: Intravitreal vancomycin, intravitreal ceftazidime, oral moxifloxacin and topical vancomycin, and topical gentamicin. 2nd: Same first surgery. Also topical prednisolone. Capsule and IOL removal. Anterior vitrectomy.||1st: 20/25; 2nd: No mention; 3rd: CF|
|Teoh et al. (2005)||1||1st: Positive; 2nd: No mention; 3rd: Positive||3||1st: Intravitreal vancomycin, intravitreal amikacin, subconjunctival vancomycin, subconjunctival amikacin, topical vancomycin, and topical gentamicin. 2nd: Intravitreal vancomycin, topical vancomycin, topical prednisolone. 3rd: Intravitreal vancomycin, intravitreal cefuroxime. PPV, AC washout, and removal of IOL and bag.||1st: 20/25; 2nd: 20/60; 3rd: NLP|
|Nasrallah & Desai (1999)||1||1st: EF; 2nd: EF; 3rd: EF||3||1st: Intravitreal vancomycin, intravitreal amikacin, intravitreal dexamethasone. 2nd: Same as first surgery. 3rd: Same as first surgery. Also PPV and removal of IOL and bag.||1st: 20/100; 2nd: No mention; 3rd: No mention|
|Stern et al. (1990)||1 (4 non EF)||1st: EF; 2nd: Negative; 3rd: EF||3||1st: Intravitreal methicillin, intravitreal gentamycin, subconjunctival methicillin, subconjunctival gentamycin, intravenous cefazolin, intravenous gentamicin, topical prednisolone, and oral prednisone. 2nd: Same as first surgery with intravitreal dexamethasone, intravitreal vancomycin, topical prednisolone, and oral prednisone. 3rd: PPV.||1st: No mention; 2nd: 6/30; 3rd: CF|