No abstract

Necrotizing fasciitis has conventionally been associated with the streptococci, and when it is caused by other organisms, it is most often the result of a polymicrobial infection. We report on two cases of fatal monomicrobial necrotizing fasciitis due to Acinetobacter baumannii, an unusual finding that may be an indication of enhanced virulence of the organism. CASE REPORTS Case 1. Patient X was a 21-year-old male with multiple medical problems, including end-stage renal disease secondary to systemic lupus erythematosus, thrombotic thrombocytopenic purpura, and mesenteric vasculitis. The patient had been treated with prolonged courses of systemic corticosteroids and intermittently with rituximab and had undergone multiple courses of treatment consisting of plasmapheresis, blood transfusions, and hemodialysis. In August 2007, he was admitted to the hospital for pulmonary edema and bright red blood from the rectum. At that time, blood cultures grew vancomycinresistant Enterococcus faecium and Candida albicans. He was treated with daptomycin and fluconazole, and all blood cultures subsequently became negative. Days later, he tested positive for Clostridium difficile-associated colitis; therefore, metronidazole was added to his antibiotic regimen.Despite embolization of the vessels of the terminal ileum, the patient continued to experience gastrointestinal bleeding. He therefore underwent an exploratory laparotomy, ileocecal resection, and ileostomy 3 weeks after admission. He appeared to be recovering until 5 days later, when he developed bacteremia caused by the gram-negative organisms Klebsiella pneumoniae and Citrobacter freundii, for which he was treated with imipenem and was continued on metronidazole.Two weeks after the ileocecectomy, at approximately 2 a.m., the patient noted pain along his left flank and thigh. Physical examination revealed faint erythema and tenderness. By 11 a.m. of the same day, there were marked increases in the levels of erythema, edema, and pain. The erythema extended beyond a marked line by greater than 2 cm in 1 h. It extended from flank to flank across the patient's back and thighs bilaterally. Bullae appeared on the skin over a similar distribution. An incision was performed at the bedside, and a frozen section revealed inflamed and necrotic fibroconnective tissue and muscle, with quantitative biopsy specimens revealing Ͼ100,000 gram-negative rods. The patient gave consent for and underwent an emergent debridement in the operating room for suspected necrotizing fasciitis. Amikacin, vancomycin, and clindamycin were empirically added to his existing antibiotic regimen of imipenem and metronidazole, pending culture and susceptibility testing results.

We have investigated whether by introducing a mutated p21 cyclin-dependent kinase inhibitor through a standard type 5 adenovirus (Ad), it would be possible to interfere with restenosis in hypercholesterolemic apolipoprotein E knockout mice. Restenosis is a clinically relevant, undesired effect of percutaneous transluminal coronary angioplasty (PTCA). A critical event underlying restenosis is smooth muscle cell (SMC) proliferation leading to neointimal formation and vessel reocclusion. Recent data demonstrated that it is possible to reduce restenosis by introducing various genes blocking the cell cycle through Ad vectors. Nonetheless, most experiments were conducted in the healthy carotid artery of rat, which is far from the condition of human disease. Therefore, we investigated whether antiproliferative or proapoptotic genes affect restenosis in a model of atherosclerosis closer to clinical settings. Ad-mutated(m)-p21WAF/CIP1 transgene overexpression induces a significant reduction of restenosis in hypercholesterolemic apolipoprotein E knockout mice subjected to injury of common carotid artery. This was associated with reduced SMC density and proliferation, macrophage deposition, and oxidation-sensitive mechanisms. Treatment with p21/WAF also enhanced TUNEL positivity of arterial cells. We show that in an experimental model of atherosclerosis, braking the cell proliferation through increased vascular apoptosis and reduced oxidation-sensitive signal transduction and macrophage accumulation can significantly ameliorate the deleterious effects of vascular injuries similar to those that occur during PTCA and related procedures.

Transfer to a burn intensive care unit and initiation of critical care and wound protocols similar to those used for burn patients are recommended for patients with toxic epidermal necrolysis syndrome. Antishear wound care provides an effective alternative wound care approach with equivalent mortality rates.