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Postoperative Vancomycin-Resistant Enterococcus faecium Endophthalmitis
Harshivinderjit S. Bains, MD, PhD;
David V. Weinberg, MD;
Robert S. Feder, MD;
Gary A. Noskin, MD
Arch Ophthalmol. 2007;125(9):1292-1293.
Enterococci are normal flora in the human gastrointestinal tract. They are intrinsically resistant to many antibiotic agents and may acquire resistance to almost all available antibiotics, including vancomycin. Vancomycin-resistant enterococci (VRE) have emerged as serious nosocomial pathogens. More than 28% of enterococcal infections in US intensive care units are resistant to vancomycin and many more patients become colonized than infected with these organisms.1 Despite the increasing incidence of infection with this organism, ophthalmologic infections are rare. We report the first case, to our knowledge, of postoperative VRE endophthalmitis. The infection occurred as a result of colonized donor corneal tissue.
Report of a Case
A 73-year-old woman with a history of Fuchs dystrophy underwent penetrating keratoplasty. On the first postoperative morning, she reported eye pain. Visual acuity was light perception. There was moderate conjunctival hyperemia. Fibrin and a small hypopyon were present in the anterior chamber. The patient underwent immediate pars plana vitrectomy and intravitreal injections of 1 mg of vancomycin hydrochloride and 400 µg of amikacin sulfate. Frequent topical fortified vancomycin and gentamicin sulfate, as well as topical and oral steroid agents, were used during the early postoperative period. Cultures of the aqueous, the vitreous, and the donor corneal rim yielded vancomycin-resistant (minimum inhibitory concentration >64 µg/mL) Enterococcus faecium. Restriction endonuclease analysis of genomic DNA confirmed that the isolates from the 3 sources were genetically identical. The organism was susceptible to linezolid (minimum inhibitory concentration 1 µg/mL), and 600 mg of linezolid was administered intravenously twice daily. Additional intravitreal injections of 1 mg of vancomycin and 500 µg of ampicillin sodium were given. Signs and symptoms of infection improved steadily. The patient received a 2-week course of oral linezolid after discharge from the hospital. Two years after surgery, visual acuity was 20/80. The graft was thin and clear. There was pallor of the optic nerve and attenuation of the retinal vessels.
Comment
A case of endogenous endophthalmitis caused by VRE in an immunocompromised patient has been reported; the outcome was poor, resulting in enucleation.2 Postoperative enterococcal endophthalmitis is relatively rare but associated with a poor prognosis. In 2 large series of postcataract endophthalmitis, only 2% to 4% of positive isolates yielded enterococcal organisms; all were susceptible to vancomycin.3-4 In addition, vancomycin-susceptible enterococcal endophthalmitis has been reported after penetrating keratoplasty.5 A MEDLINE search of the literature from January 1966 to October 2005 revealed no cases of postoperative VRE endophthalmitis. Genetic analysis of specimens identified the corneal donor tissue as the source of infection.
The organism was resistant to vancomycin and to all other antibiotics on the panel with known intraocular safety. The patient was reinjected with intravitreal vancomycin in an attempt to achieve levels in excess of the minimum inhibitory concentration. Systemic treatment with linezolid, an oxazolidinone with potent activity against VRE,6 was added to intravitreal and topical antibiotic therapy. At the time we treated our patient, the ocular penetration of linezolid was unknown. Subsequent investigation has shown effective intraocular concentrations after oral dosing.7 The infection was successfully eradicated with preservation of ambulatory vision.
This first case of postoperative VRE endophthalmitis is an unfortunate milestone in ophthalmic surgery. Future cases are probably inevitable given the trends in the epidemiology of VRE infection and colonization, especially in patients with compromised immunity. Colonized donor corneal tissue is a potential source. While optimal treatment of this infection is unknown, the favorable outcome in our patient may have been the result of early intervention and the use of linezolid.
AUTHOR INFORMATION
Correspondence: Dr Weinberg, Department of Ophthalmology, Medical College of Wisconsin, 925 N 87th St, Milwaukee, WI 53226 (dweinber{at}mcw.edu).
Financial Disclosure: None reported.
Funding/Support: This study was supported in part by an unrestricted grant from Research to Prevent Blindness Inc.
REFERENCES
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1. Tenover FC, McDonald LC. Vancomycin-resistant staphylococci and enterococci: epidemiology and control. Curr Opin Infect Dis. 2005;18(4):300-305.
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2. Esmaeli B, Holtz ER, Ahmadi MA, Krathen RA, Raad II. Endogenous endophthalmitis secondary to vancomycin-resistant enterococci infection. Retina. 2003;23(1):118-119.
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3. Han DP, Wisniewski SR, Wilson LA; et al. Spectrum and susceptibilities of microbiologic isolates in the Endophthalmitis Vitrectomy Study [published correction appears in Am J Ophthalmol. 1996;122(6):920]. Am J Ophthalmol. 1996;122(1):1-17.
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4. Recchia FM, Busbee BG, Pearlman RB, Carvalho-Recchia CA, Ho AC. Changing trends in microbiologic aspects of postcataract endophthalmitis. Arch Ophthalmol. 2005;123(3):341-346.
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6. Noskin GA, Siddiqui F, Stosor F, Hacek D, Peterson LR. In vitro activities of linezolid against important gram-positive bacterial pathogens including vancomycin resistant enterococci. Antimicrob Agents Chemother. 1999;43(8):2059-2062.
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7. Fiscella RG, Lai WW, Burek B; et al. Aqueous and vitreous penetration of linezolid (Zyvox) after oral administration. Ophthalmology. 2004;111(6):1191-1195.
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SECTION EDITOR: W. RICHARD GREEN, MD
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