764 Letters © 2005 European Academy of Dermatology and Venereology JEADV (2005) 19, 763– 784 known that clindamycin can inactivate toxin production from β -haemolytic streptococci. We suppose that the same pathogenesis is implicated in inactivation of enterotoxic haemo- lysin from enterobacter. Dermatologists should be able to differentiate haemorrhagic cellulitis from more serious and often fatal necrotizing fasciitis, which both commonly begin with cellulitis and blisters and are very painful conditions with the potential for rapid evolution into necrosis and gangrene. The source of the Enterobacter infection in our case is unknown. We can not rule out that patient exposure to the micro- organism occurred while he soaked his leg in a contaminated antiseptic solution. 6 P Dyachenko,*† M Ziv,† S Kamil,† R Dodiuk-Gad,† B Chazan,‡ D Rozenman† †Department of Dermatology, Ha’emek Medical Center, Afula, ‡Infectious Diseases Unit, Ha’emek Medical Center, Afula, Israel. *Corresponding author: Haagana 60, Afula-Ilit, Israel, 18580, tel. +972 4 6421472, fax +972 4 6494255; E-mail: pavela4@hotmail.com References 1 Livingston W, Grossman ME, Garvey G. Hemorrhagic bullae in association with Enterobacter cloacae septicemia. J Am Acad Dermatol 1992; 27: 637 – 638. 2 Wickboldt LG, Sanders CV. Vibrio vulnificus infection. J Am Acad Dermatol 1983; 9: 243 – 251. 3 Burchard KW, Barroll DT, Reed M et al. Enterobacter bacteremia in surgical patients. Surgery 1986; 100: 857 – 861. 4 Chow JW, Fine MJ, Schlaes DM et al. Enterobacter bacteremia: clinical features and emergence of antibiotic resistance during therapy. Ann Intern Med 1991; 115: 585 – 590. 5 Simi S, Carbonell GV, Falcon RM et al. A low weight enterotoxic hemolysin from clinical Enterobacter cloacae. Can J Microbiol 2003; 49: 479. 6 Harbarth S, Sudre P, Dharan S, Cadenas M, Pitted D. Outbreak of Enterobacter cloacae related to understaffing, overcrowding, and poor hygiene practices. Infect Control Hosp Epidemiol 1999; 9: 598 – 603. DOI: 10.1111/j.1468-3083.2005.01246.x ? 2005 19 ? Letters Letters Letters LETTERS Atrophia maculosa varioliformis cutis: a case with extrafacial involvement and familial facial lesions To the Editor Atrophia maculosa varioliformis cutis (AMVC) is a rare and curious form of idiopathic facial, macular, non-inflammatory atrophy. 1 This rare disorder was first reported by Heidingsfeld in 1918 when spontaneous atrophic scars developed on the cheeks of a young adult. 2 Since then only 16 cases have been re- ported in the literature 1,3 and there is only one description about extrafacial lesions. 4 We describe such a case in a 22-year-old man. A 22-year-old man visited our hospital because of facial and extrafacial atrophic lesions. The patient had first noticed some atrophic lesions on his cheeks, arms, forearms, thighs and legs which had occurred at 14 years of age and gradually developed, slowly increasing in size and number over time. Familial history of a similar disorder was positive in a 19-year-old sister and in an 8-year-old nephew. Their past medical history was not sig- nificant for varicella-zoster infection, molluscum contagiosum, or psychiatric or internal illnesses. Our patient had had very mild acne lesions since the age of 16. The following comple- mentary examinations in both patients demonstrated normal or negative results: total blood count cells, fasting blood sugar and syphilis (VDRL and FTA-abs). A dermatological examination revealed a bilateral distribution of a number of lenticular and linear depressed lesions on his cheeks (fig. 1) and limbs (fig. 2). The depressed sites were fig. 1 Twenty-two-year-old man with depressed, linear and lenticular scars on right cheek.