Endophthalmitis — Diagnosis & Microbiology

Clinical Presentation

Pain, decreased vision, and hypopyon, a layered collection of white blood cells settling in the anterior chamber, make up the classic triad suggestive of endophthalmitis. This combination, appearing after intraocular surgery or an intravitreal injection, warrants urgent evaluation rather than a routine postoperative visit.

Diagnostic Sampling

Vitreous tap and biopsy is the primary diagnostic procedure for confirming suspected endophthalmitis and obtaining culture material. The vitreous cavity is the primary site of infection, so a vitreous sample yields a diagnosis far more reliably than an anterior chamber paracentesis or a conjunctival swab. The sample goes for Gram stain, culture, and sensitivity testing: the first two identify the likely organism class quickly, and sensitivity results then guide antibiotic selection once the specific pathogen and its resistance pattern are known.

Empiric intravitreal antibiotics are given immediately after sampling, before culture results return. Treatment delay measurably worsens visual outcomes, so therapy is never held pending a lab report (see the companion page on endophthalmitis management for the specific regimen and the trial evidence behind it).

Acute Postoperative Endophthalmitis

Coagulase-negative staphylococci, particularly Staphylococcus epidermidis, cause most acute postoperative endophthalmitis after cataract surgery. These organisms come from the patient's own periocular and conjunctival flora rather than an outside source, which is why perioperative antisepsis (povidone-iodine prep, sterile technique) is the primary defense, not postoperative antibiotics alone. Gram-positive organisms predominate overall in this setting.

Chronic Delayed-Onset Postoperative Endophthalmitis

A distinct pattern presents months, not days, after uneventful cataract surgery, with a low-grade, indolent course rather than the explosive onset of acute infection. Cutibacterium acnes (formerly Propionibacterium acnes) is the organism most classically responsible. It produces low-grade granulomatous inflammation, often with a white plaque sequestered within the capsular bag. The organism's indolent growth and its protected niche behind the intraocular lens let it smolder for weeks to months before becoming clinically apparent.

Endogenous (Metastatic) Endophthalmitis

Endogenous endophthalmitis arises from hematogenous seeding of the eye rather than direct inoculation during surgery or trauma. Candida species are the most commonly reported overall cause, typically in patients with candidemia, indwelling catheters, or immunosuppression. Klebsiella pneumoniae, often originating from a liver abscess, is a common cause in Asian populations and tends to run a particularly fulminant course.

Fulminant Bacillus cereus endophthalmitis is a separate, far more destructive pattern: severe pain, a ring corneal infiltrate, and hypopyon develop within 24 hours, classically after trauma or intravenous drug use. B. cereus produces potent exotoxins that drive an explosive inflammatory response. Its speed demands urgent, aggressive intravitreal and systemic therapy, often with early vitrectomy, rather than the more measured tap-and-inject approach suited to a typical postoperative case.

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