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Purpose. To report a rapid endogenous fulminating panophthalmitis from Clostridium perfringens in a patient with diverticulitis and proliferative diabetic retinopathy. Methods. A 61-year-old female with poorly controlled diabetes mellitus, active proliferative diabetic retinopathy, and recent diverticulitis presented with conjunctival injection, ocular discharge, and sudden onset of painful vision loss of the left eye. Patient denied history of ocular trauma, intraocular surgery, or intravenous drug abuse. Examination revealed an erythematous, proptotic eye with restricted extraocular movements, mucopurulent discharge, diffuse corneal edema, and vitreous haze and cell. Orbital computed tomography (CT) confirmed no retained intraocular foreign body. Results. Despite 48 hours of treatment with systemic broad spectrum antimicrobial therapy (vancomycin, meropenem, and amphotericin B), patient underwent enucleation due to declined condition and progressive infection. Patient’s culture revealed gram-positive bacillus microbes (Clostridium perfringens). Patient’s subsequent CT abdomen showed resolved diverticulitis after antimicrobial therapy. Conclusion. Although rare, Clostridium perfringens infection can be a cause of rapid loss of vision from fulminate endogenous panophthalmitis. Urgent extensive systemic work-up to identify potential port of entry from visceral pathology and rapid removal of source of infection are pivotal to avoid high rate of mortality.

TO THE EDITOR:— I would like to comment on a recent editorial, "Carbohydrate Intolerance in Post-gastrectomy Patients" (197:918, 1966). We have observed results of oral glucose tolerance tests done on 34 gastrectomized patients.1 Twenty-one of these exhibited the characteristic pattern of initial hyperglycemia followed by sharp descent to hypoglycemic levels. Six of these subjects underwent an intravenous glucose tolerance test. The subsequent one-, two-, and three-hour levels were within normal limits. No hypoglycemia was noted in reaction to the sharp rise in the systemic level of blood sugar, produced by the administration of glucose intravenously. None of these patients to date (and some have been observed for as long as 20 years), has exhibited clinical evidence of diabetes mellitus. To consider these patients as potential diabetics is, in my opinion, erroneous. Diabetes mellitus is a genetic disorder, exhibiting, in addition to the carbohydrate disturbance, accelerated atherosclerosis, microangiopathy (involving