Initial Presentation of Cutibacterium (Formerly Propionibacterium) acnes Endophthalmitis Twenty-One Years After Cataract Surgery

Introduction

Cutibacterium acnes (C. acnes, formerly known as Propionibacterium acnes or P. acnes) has been implicated in chronic endophthalmitis following intraocular lens (IOL) surgery.¹ Although typical postoperative endophthalmitis presents acutely with eye pain, conjunctival injection, and chemosis, chronic endophthalmitis may involve persistent low-grade inflammation, often with delayed onset and absence of these hallmark symptoms.¹ This is attributed to the relatively low virulence of C. acnes, and sequestration within capsular remnants after IOL surgery.² Without capsulectomy and IOL removal, C. acnes activity often recurs despite treatment of flares with intravitreal antibiotics and corticosteroids.¹

Case Report

An 81-year-old woman with a history of bilateral cataract surgery and intraocular lens (IOL) placement (1996 in the left eye [OS], 2001 in the right eye [OD]), retinal detachment (RD) (OD, status post scleral buckle in 1985), and peripheral retinal tears (OS, status post laser retinopexy), presented in November 2016 with sudden onset of light perception vision in the left eye (Figure 1). At presentation, the left eye showed 3+ conjunctival injection, diffuse anterior chamber fibrin, and a layered hypopyon. No white plaque was observed on the IOL or lens capsule. Dilated fundus exam revealed an attached retina. She had no recent or intervening history of ocular trauma, intraocular surgery, or intravitreal injection. She received intravitreal vancomycin (1 mg/0.10 mL), ceftazidime (2.25 mg/0.10 mL), and topical corticosteroids. An aqueous humor sample showed 1+ leukocytes without bacterial growth. To assess possible endogenous endophthalmitis, a blood culture was obtained, which showed no growth.

Figure 1. Clinical images of the left eye in an 81-year-old female who presented in November 2016 with 1 day of sudden-onset vision loss (light perception visual acuity on presentation) and evidence of intraocular inflammation. Slit-lamp photography (A) showed evidence of a hypopyon, anterior chamber fibrin, and diffuse conjunctival injection. B-scan ultrasonography showed dense vitreous opacities and membrane formation (B), as well as dispersed anterior chamber opacities with a dense collection of tissue near the angle (C), best visualized in Panel D.

One month later, the patient developed total RD in the left eye with tractional membranes. Examination showed improved anterior chamber inflammation, but significant vitreous debris remained. She underwent a diagnostic pars plana vitrectomy (PPV) prior to RD repair in order to determine the cause of endophthalmitis (December 2016). Vitreous biopsy from this PPV did not grow pathogens. The patient subsequently underwent RD repair (Figure 2). Multiple postoperative follow-up examinations revealed persistent mild inflammation with varying degrees fibrin or hypopyon.

Figure 2. Clinical images representing complications and follow-up for an 81-year-old female with suspected Cutibacterium acnes endophthalmitis 21 years after initial cataract surgery. The patient developed a total retinal detachment 3 weeks after presentation (December 2016), as noted on B-scan ultrasonography (A). The patient underwent retinal detachment repair, and postoperative imaging showed an attached retina under silicone oil 2 weeks after surgery (B). In late January 2017, an aqueous tap was positive for C. acnes. In February 2017, 3 months after initial presentation, the patient developed punctate deposits on the lens (C). Subsequently, a total capsulectomy and intraocular lens removal was performed in April 2017 and led to resolution of chronic intraocular inflammation.

Six weeks after RD repair and PPV, the patient presented again with acute vision loss in the left eye (counting fingers at 4 feet) with a 1-mm hypopyon. She received intravitreal vancomycin (1 mg/0.10 mL) and an aqueous tap grew C. acnes after 1 week (February 2017). Two months later, the patient underwent IOL removal and total capsulectomy. IOL/capsule culture grew only Staphylococcus epidermidis, a presumed contaminant. She was scheduled for earlier surgery but missed preoperative appointments due to hospitalization for community-acquired pneumonia. Following these interventions, her inflammatory symptoms resolved without recurrence.

Discussion

Although the literature often describes C. acnes as a common cause of chronic post-cataract endophthalmitis, cases are often indolent and marked by recurrent inflammatory episodes.^1–3 The patient in this report had an interval of 252 months (21 years) without inflammation, reported trauma, or other known invasive intraocular procedure that could have introduced C. acnes into the eye between her cataract surgery and eventual presentation with endophthalmitis. This duration from surgery to symptom onset is substantially longer than that of previously documented cases of chronic post-IOL C. acnes endophthalmitis.^1,2,4–6 Chien et al. reported one case with a 2-year delay between cataract surgery and onset of inflammatory symptoms.⁴ Aldave et al. reported 25 cases of C. acnes endophthalmitis, for which the average interval between cataract surgery and presentation for endophthalmitis was 4.5 months (range: 2 days to 16 months).¹ Zambrano et al. reported nine cases with an interval of 4 months on average (range: 0.25 months to 12 months) between cataract surgery date and onset of endophthalmitis symptoms; the longest duration between surgery date and microbiologic confirmation was 38 months.⁶ The 36-patient cohort of post-IOL C. acnes endophthalmitis patients studied by Clark et al. had an average duration of 9 months between cataract surgery and first treatment; the longest such interval was 40 months.²

Given the atypical nature of a 21-year delay from surgery to presentation for a case of chronic post-IOL C. acnes endophthalmitis, other possible etiologies for this presentation are worth consideration. Although C. acnes could be a rare contaminant of microbiological sampling, it was felt that C. acnes was indeed the causative organism. The numerous C. acnes-negative cultures obtained throughout this patient's course may be due to the inherent difficulty in culturing this particular microorganism as a result of its relatively low virulence, slow growth rate, and sequestration within capsular remnants.^7,8 Moreover, capsulectomy and lens removal, the typical definitive treatment for C. acnes chronic endophthalmitis, led to resolution of the patient's inflammation, further suggesting that C. acnes was indeed the most likely causative organism.¹

Although the culture of the removed IOL and capsule remnants did grow Staphylococcus epidermidis, it is unlikely that this pathogen would explain the patients' episodes of inflammation over the months preceding definitive intervention or the initial presentation in the absence of recent intraocular surgical history and is most likely a contaminant in this case.

Clinicians should be aware that C. acnes may rarely cause a delayed acute and severe endophthalmitis. In our patient, C. acnes contributed to the development of a total RD in the setting of prior peripheral retinal tears. In this case, we demonstrate an atypical C. acnes endophthalmitis presentation; as such, clinicians should be vigilant in suspecting, diagnosing, and appropriately managing these cases.