Sir,

Clostridium perfringens, a toxin-producing Gram-positive anaerobic bacillus, is a rare cause of fulminating suppurative endophthalmitis or panophthalmitis with grave visual outcomes. It has typically been reported after penetrating eye injuries and rarely after invasive surgeries. To our knowledge, there have been only three reported cases of C. perfringens endogenous endophthalmitis (EE) all in association with underlying enteric diseases. We present the first case of C. perfringens endophthalmitis rapidly progressing to panophthalmitis in an intravenous drug abuser (IVDA).

Case report

A 28-year-old IVDA presented with 24-h history of headache and left visual acuity of perception of light. He was apyrexial and had no gastrointestinal symptoms and ocular trauma. He had erythematous eyelid swelling, conjunctival injection, severe uveitis, no hypopyon, fixed constricted pupil, and absent red reflex. Intra-ocular pressure was 26 mmHg. White cell count was 15.7 × 109/l. Diagnosis of EE was made. He underwent vitreous tap and intravitreal injection of vancomycin (2.0 mg), amikacin (0.4 mg), and amphoteracin (0.005 mg) on the same day. Unfortunately, he absconded after the procedure.

Microscopy showed Gram-positive and -negative bacilli in the vitreous sample. C. perfringens was the only isolate, sensitive to metronidazole. Blood culture grew coagulase-negative staphylococcus, reported to be of doubtful significance.

He returned on day 3 with hypopyon, superonasal scleral abscess, and proptosis, confirming panophthalmitis (Figure 1). Computed tomography of the orbit (Figure 2) did not reveal bony erosion or sinus involvement. Despite treatment with intravenous metronidazole and cefuroxime, the eye perforated at the limbus, requiring evisceration.

Figure 1
figure 1

Severe panophthalmitis with superonasal scleral abscess, and extrusion of pus from the limbus.

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Figure 2
figure 2

Axial section of MRI head scan showing proptosis, enlargement of the globe, posterior dislocation of the lens, thickening of the peri-orbital soft tissue, and posterior wall of the globe in the left eye.

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Comment

Rapidity of ocular destruction in C. perfringens infection is related to massive necrosis of ocular structures by potent exotoxins; therefore, antibiotics are unlikely to prevent this process once the infection is well established.1 Although there is one documented case of successful prevention of exogenous C. perfringens endophthalmitis by early vitrectomy and intravitreal antibiotics,2 the fulminating nature of this infection along with systemic co-morbidity often precludes operative intervention.

Blood cultures alone cannot be relied upon to establish the diagnosis of EE.3 Blood culture in our patient did not isolate C. perfringens. We suspected the source of infection in our case to be either the contaminated needle or the access sites for intravenous injection.

There is well-known association of endogenous fungal endophthalmitis in IVDA. Our case highlights the importance of considering C. perfringens as a cause of endophthalmitis in an IVDA.