Propionibacterium acnes Endophthalmitis after Intracapsular Cataract Extraction

Ann M. Chien, MD,1 Irving M. Raber, MD,1 David H. Fischer, MD,z Ralph C. Eagle, Jr., MD,3 Michael A. Naidoff, MDI

The authors report a case of Propionibacterium acnes endophthalmitis after intra­capsular cataract extraction with implantation of an anterior chamber intraocular

lens. The patient's chronic inflammation persisted for 5 years after cataract surgery despite treatment with pars plana vitrectomy, intraocular lens removal, topical and oral steroids, and topical fortified antibiotics. Fluctuations in the inflammation were paralleled by changes in the size and appearance of a white plaque on the posterior corneal surface. Anterior chamber tap cultures were positive for P. acnes after 8 days of in­cubation under anaerobic conditions. The inflammation was not controlled until the posterior corneal plaque, which was the presumed nidus of the chronic infection, was removed and the patient was treated with intravitreal and oral antibiotics. Ophthalmology 1992;99:487-490

Propionibacterium acnes has become a well-recognized cause of chronic, delayed postoperative endophthalmitis. All 27 previously reported cases of culture-positive post­operative endophthalmitis associated with P. acnes have occurred after extracapsular cataract extraction. 1-12 Most of these case reports describe a white plaque situated within residual lens remnants or between the intraocular lens optic and the posterior capsule. 1,2,4,9,11,12 The asso­ciation of P. acnes endophthalmitis with extracapsular cataract surgery has been attributed to the tendency of the organism to loculate in the capsular bag. In addition, P. acnes has been postulated as having adjuvant qualities that promote hypersensitivity to lens protein. 13 We report the first case of culture-proven P. acnes endophthalmitis in a patient who had intracapsular surgery with p.o residual lens material, which was associated with a fluctuating white plaque on the posterior corneal surface.

Originally received: July 29, 1991. Manuscript accepted: November 4, 1991.

From the Cornea Service,l Uveitis Service,2 and Pathology Department,3 Wills Eye Hospital, Thomas Jefferson University, Philadelphia.

Reprint requests to Ann M. Chien, MD, Wills Eye Hospital, Ninth and Walnut Sts, Philadelphia, PA 19107.

Case Report

A 73-year-old woman underwent intracapsular cataract extrac­tion with implantation of a Choyce anterior chamber intraocular lens in the right eye in 1983 with uneventful visual recovery. She then underwent intracapsular cataract extraction with im­plantation of an anterior chamber intraocular lens in the left eye in November 1984. After surgery in the left eye, she com­plained of poor vision and was noted to have vitreous to the wound and chronic cystoid macular edema. She subsequently underwent a pars plana vitrectomy in October 1985 with no improvement in vision.

Over the next 3 years, she manifested chronic recurrent in­flammation in her left eye, which was partially controlled by topical steroids and atropine. She developed increased intraocular pressure in her left eye while receiving topical steroids and was treated with supplemental topical beta-blockers. The patient's past medical history was notable for rheumatoid arthritis, for which she was taking oral prednisone, 10 mg daily. Evaluation for associated systemic inflammatory processes was unrevealing.

In November 1987, examination showed best corrected visual acuity of 20/40 in the right eye and counting fingers at 6 feet in the left. Laser interferometry measured 20/50 in the left eye. Slit-lamp biomicroscopy showed an area of stromal thinning and scarring in the superior periphery of the left cornea. A small discrete yellow-white plaque was noted on the superocentral endothelial surface, just below the area of thinning. Greasy ker-

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atic precipitates and a moderate anterior chamber reaction were present. Cells also were noted in the anterior vitreous. A Choyce anterior chamber lens was in stable position well back from the corneal endothelium in the left eye. Gonioscopy showed that the superior foot of the lens was embedded in the peripheral iris distorting the superior iris. Peripheral anterior synechiae were noted superiorly. The view of the left fundus was hazy, but the optic nerve appeared healthy. There was no gross macular pa­thology or evidence of vasculitis or choroiditis. Examination of the right eye was notable for a Choyce anterior chamber intra­ocular lens, but was otherwise unremarkable. The intraocular pressure was 20 mmHg in each eye.

In December 1987, the vertically oriented anterior chamber lens was removed from the patient's left eye on the premise that the implant and/or the iris tuck might be contributing to the chronic inflammation. The lens was removed via an inferior approach to avoid the area of superior corneal thinning and scarring, which was presumed to be secondary to the rheumatoid arthritis. The patient continued to manifest low-grade anterior chamber inflammation despite the chronic use of topical steroids.

In April 1988, the patient presented with an acute flare-up of iridocyclitis in her left eye. The superior posterior corneal

plaque was larger and fluffier, and a small layered hypopyon was present in the inferior angle. An anterior chamber paracen­tesis was performed with the bevel ofthe needle placed adjacent to the white plaque. Cultures for anaerobic, aerobic, and fungal organisms were reported as negative at 1 week. Treatment with topical fortified antibiotics and steroids decreased the inflam­mation and the size of the posterior corneal plaque, which sub­sequently resumed a quiescent, scarred appearance.

In August 1989, the patient was referred to the Wills Eye Hospital Uveitis Service because of persistent uveitis in her left eye. Results of examination showed recurrence of the white pos­terior corneal inflammatory mass (Figs I and 2) and a moderate anterior chamber reaction. In September 1989, a pars plana vi­trectomy and evacuation ofthe endothelial mass were performed using an automated vitrectomy instrument. No residual lens remnants were noted during surgery. Intravitreal cefazolin and gentamicin were given.

Histopathologic evaluation of the specimen showed inflam­matory cells, consisting mostly of epithelioid histiocytes, as well as some polymorphonuclear leukocytes, foamy macrophages, and inflammatory giant cells (Fig 3). No lens remnants or Des­cemet's membrane were evident in the specimen. Gram stain

Top left, Figure 1. Slit-lamp photograph of left eye shows large white inflammatory posterior corneal plaque.

Top right, Figure 2. Slit-beam illumination shows area of stromal thinning superiorly and posterior corneal plaque.

Bottom left, Figure 3. Photomicrograph of granulomatous inflammatory tissue from posterior cornea shows epithelioid histiocytes, a multinucleated giant cell (arrow), and large quantities of mildly basophilic granular material identified as bacteria in Figure 4. Some of the bacteria appear to be intracellular (hematoxylin-eosin; original magnification, X250).

Bottom right, Figure 4. The tissue gram stain confirms that myriad pleomorphic gram-positive bacteria consistent with Propionibacterium acnes constitute the granular material seen in Figure 3 (Brown and Hopps; original magnification, X250).

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Chien et al . Propionibacterium acnes Endophthalmitis

showed multiple pleomorphic gram-positive rods, some of which were intracellular, consistent with P. acnes (Fig 4). Unfortunately, the entire vitrectomy specimen was inadvertently submitted to pathology, and no specimen was submitted for culture and sen­sitivity. However, on review ofthe culture reports from the orig­inal paracentesis specimen obtained in April 1988, it became apparent that a light growth of P. acnes had been noted on the anaerobic culture after 8 days. A negative verbal report had been issued from the laboratory at 7 days. The final culture report had been misfiled, and the attending ophthalmologist had not been notified.

The patient was treated with a 3-week course of oral anti­biotics (cephalexin 250 mg 4 times daily) in addition to topical antibiotics and beta-blockers. She also was being treated with oral steroids (prednisone 15 mg every day) for rheumatoid ar­thritis. After 9 months of follow-up, there has been no recurrence of inflammation in the left eye, and the white posterior corneal plaque has not reappeared. Her vision remains decreased due to diffuse corneal edema and probable chronic cystoid macular edema. She requires levobunolol (l drop twice daily in her left eye) and methazolamide (50 mg twice daily) to control elevated intraocular pressure because of angle-closure glaucoma.

Discussion

P. acnes endophthalmitis after extracapsular cataract ex­traction has been well described over the past several years. Including Meisler's initial report in 1986, 27 cases of cul­ture-positive P. acnes infections have been reported. 1-12 P. acnes endophthalmitis is characterized by a chronic, indolent course that responds transiently to steroids. Clinical findings suggestive of P. acnes endophthalmitis include granulomatous inflammatory precipitates on the corneal endothelium or intraocular implant surface and white plaques on the posterior capsule. Histopathologic studies of lens capsular remnants4-7 suggest that these plaques represent colonies of organisms sequestered within residual lens material. The prognosis is much more fa­vorable than other forms of postoperative endophthalmitis in which the eye is often rapidly and permanently de­stroyed.

All previously reported cases of P. acnes endophthal­mitis have occurred after extracapsular cataract extraction. To our knowledge, the patient reported here is the first case of chronic postoperative P. acnes infection that has developed after intracapsular cataract extraction. Chronic P. acnes endophthalmitis was diagnosed in our patient after 5 years of chronic uveitis after intracapsular cataract surgery and anterior chamber intraocular lens implan­tation.

P. acnes is a pleomorphic gram-positive rod with a cell wall that is not broken down by macrophages or poly­morphonuclear leukocytes. The enhanced ability of the organism to remain viable in the eye as well as its tendency to loculate in lens capsular remnants may account for the stuttering, persistent course of the infection if there is in­termittent release of sequestered organisms either spon­taneously, as postulated by Meisler and Mandelbaum, 10

or after Nd:YAG laser posterior capsulotomy, as reported in four cases. 1.5-7

The Propionibacterium is known to stimulate inflam­mation, activate complement, and trigger release of poly­morphonuclear chemotactic factors and hydrolytic en­zymes in vitro. 14- 16 Studies using animal models of lens­induced hypersensitivity have suggested that P. acnes may in fact act as an adjuvant in promoting hypersensitivity to lens protein. 13 These findings and the characteristics of previously reported cases have led some to presume that the presence of lens capsular remnants and/or lens ma­terial are prerequisite for the development of P. acnes endophthalmitis.

Our case is similar to those previously reported in its chronicity and clinical presentation with granulomatous keratic precipitates, hypopyon, and white plaque. The latter, however, was on the posterior corneal surface rather than posterior capsule. Our patient had intracapsular sur­gery and the inflammation persisted in the absence of residual lens capsular or cortical remnants. The white posterior corneal plaque that fluctuated along with the intraocular inflammation consisted of P. acnes bacteria and inflammatory cells. Because Descemet's membrane, corneal stroma, or corneal endothelial cells were not identified on the diagnostic vitrectomy specimen, it is im­possible to determine if the inflammatory mass was in­terposed between the stroma and the corneal endothelium or was situated on the posterior surface of the endothe­lium. However, the persistence of the plaque attests to the ability ofthe organisms to survive without loculation in the lens capsule, and to be associated with persistent inflammation without interaction with lens cortical ma­terial.

To identify P. acnes when it is suspected, the impor­tance of obtaining anaerobic cultures and holding them for at least 14 days must be stressed. Two previously re­ported cases required incubation of anaerobic cultures for 9 days before growth of P. acnes was noted,6,1l and 14 days of incubation were required in another case. 12 In our case,the organism did not grow out until 8 days of in­cubation.

A variety of treatment modalities have been recom­mended for P. acnes endophthalmitis, including pars plana vitrectomy, intraocular lens removal, complete capsulectomy, and injection of intravitreal antibiotics. Five cases have responded successfully to purely nonsur­gical therapy using combinations of topical, intraocular, and systemic antibiotics.9,12 Zambrano et al12 have pro­posed a management approach for cases of suspected P. acnes endophthalmitis. For mild cases, cultures are ob­tained and intravitreal antibiotics are injected, with or without topical and intravenous antibiotics. If the intra­ocular antibiotics fail to cure the endophthalmitis or if the case is especially severe, excision of any white capsular plaque, or total capsulectomy combined with intravitreal antibiotics, with or without intraocular lens removal or exchange, are advocated.

Our patient was successfully treated by the removal of the plaque from the posterior corneal surface combined with intravitreal and oral antibiotics. No lens capsular or cortical remnants were present.

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It is now well accepted that P. acnes is a cause of delayed onset, persistent inflammation after extracapsular cataract extraction. Our case in a patient who had intracapsular cataract extraction with no retained lens material raises questions concerning the theory that lens capsule or cor­tical remnants are necessary for this clinical entity and also identifies the cornea as a new site where the Pro­pionibacterium organism can be sequestered and remain viable for an extended period of time.

References

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2. Jaffe GJ, Whitcher JP, Biswell R, Irvine AR. Propionibac­terium acnes endophthalmitis seven months after extracap­sular cataract extraction and intraocular lens implantation. Ophthalmic Surg 1986; 17:791-3.

3. Ormerod LD, Paton BF, Haaf J, et al. Anaerobic bacterial endophthalmitis. Ophthalmology 1987;94:799-808.

4. Roussel TJ, Culbertson WW, Jaffe NS. Chronic postoper­ative endophthalmitis associated with Propionibacterium acnes. Arch Ophthalmol 1987;105: 1199-1201.

5. Piest KL, Kincaid MC, Tetz MR, et al. Localized endoph­thalmitis: a newly described cause of the so-called toxic lens syndrome. J Cataract Refract Surg 1987;13:498-510.

6. Meisler DM, Zakov ZN, Bruner WE, et al. Endophthalmitis associated with sequestered intraocular Propionibacterium acnes [letter]. Am J Ophthalmol 1987;104:428-9.

7. Tetz MR, Apple DJ, Price FW Jr, et al. A newly described

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complication of Neodymium-Y AG laser posterior capsu­lotomy: exacerbation of an intraocular infection [letter]. Arch Ophthalmol 1987;105:1324-5.

8. Carlson AN, Koch DD. Endophthalmitis following Nd:YAG laser posterior capsulotomy. Ophthalmic Surg 1988; 19: 168-70.

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11. Sawusch MR, Michels RG, Stark WJ, et al. Endophthalmitis due to Propionibacterium acnes sequestered between IOL optic and posterior capsule. Ophthalmic Surg 1989; 20:90-2.

12. Zambrano W, Flynn HW Jr, Pflugfelder SC, et al. Man­agement options for Propionibacterium acnes endophthal­mitis. Ophthalmology 1989;96: 1100-5.

13. Maguire HC Jr, Cipriano D. Immunopotentiation of cell­mediated hypersensitivity by Corynebacterium parvum (Propionibacterium acnes). Int Arch Allergy Appl Immunol 1983;70:34-9.

14. Webster GF, Leyden 11, Norman ME, Nilsson UR. Com­plement activation in acne vulgaris: in vitro studies with Propionibacterium acnes and Propionibacterium granu­losum. Infect Immun 1978;22:523-9.

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16. Webster GF, Leyden 11. Characterization of serum-inde­pendent polymorphonuclear leukocyte chemotactic factors produced by Propionibacterium acnes. Inflammation 1980;4:261-9.