“…The characteristic lesion begins as an erythematous nodule, vesicle, or bulla, and progresses rapidly to necrotic ulceration with a black eschar and erythematous rim. 1,2 Local infarction is due to arterial and venous thrombosis during bacterial multiplication. 1 Although P. aeruginosa is the most common pathogen causing EG, other bacteria (Staphylococcus aureus, Streptococcus, Aeromonas hydrophila, Serratia marcescens, Escherichia coli, Klebsiella, Neisseria meningitidis, Pseudomonas maltophilia, and Stenotrophomonas maltophilia) and some fungi (Aspergillus, Candida, Fusarium, and Rhizopus) can also cause EG-like lesions.…”