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464 SHORT COMMUNICATION Severe Septic Vasculitis Preceding Thoracic Empyema: Staphylococcus aureus Enterotoxin Deposition in Vessel Walls as a Possible Pathomechanism Yasuyuki YAMAGUCHI 1 , Yasuyuki FUJITA 1 *, Tetsuya IKEDA 2 , Yosuke MAI 1 , Hajime MIYAZAWA 1 , Wakana MATSUMURA 1 , Toshifumi NOMURA 1 and Hiroshi SHIMIZU 1 1 Department of Dermatology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, N15 W7, Kita-ku, Sapporo 060- 8638, and 2 Department of Bacteriology, Hokkaido Institute of Public Health, Sapporo, Japan. *E-mail: [email protected] CASE REPORT Septic vasculitis or septic vasculopathy is defined as vascular changes occurring in patients with sepsis (1). Although the process whereby the cutaneous changes de- velop has yet to be fully clarified, several complex patho- genic mechanisms of septic vasculitis are assumed, such as disseminated intravascular coagulation, direct vessel wall invasion by the microorganism, immune-mediated vasculitis and septic embolism (2). Although these have been observed histopathologically, there have been no investigations of whether the toxins directly affect skin vessels (1). We present here a case of septic vasculitis that preceded thoracic empyema, in which deposition of Staphylococcus aureus enterotoxin (SE) on the vessel walls was a factor in the severe cutaneous manifestations. This case suggests that SE plays a significant role in the pathogenesis of septic vasculitis. Accepted Jan 16, 2019; E-published Jan 17, 2019 An 82-year-old Japanese woman was referred to our department with a 1-week history of necrolytic ulcers on the lower legs. Physical examination revealed reddish-violaceous ulcers, 15 cm in size, with yellow or black necrolytic tissue surrounded by disseminated blood blisters and purpura on the flexor surfaces of the lower legs (Fig. 1a, b). A biopsy specimen obtained from purpura showed interface changes, dermal neutrophilic infiltrates, extravasated erythrocytes and small blood vessel thrombi (Fig. 1c). Ziehl-Neelsen, Periodic acid–Schiff, Grocott and Gram-staining were all negative. The patient’s vital signs at administration (day 0) were as follows: body temperature 38.1°C, heart rate 115 beats per min, blood pressure 129/76 mmHg, respiratory rate 16 breaths per min and oxygen saturation as detected by the pulse oximeter (SpO 2 ) 93% in room air. The patient’s subjective symptoms were unremarkable. She had a medical history of dementia. Labora- tory examinations revealed a white blood cell count of 13,800 mm 3 (88% neutrophils) and C-reactive protein of 20.43 mg/dl (normal range 0–0.39). All antibodies were negative, including anti-glomerular basement membrane antibodies, anti-neutrophil cytoplasmic antibodies, anti-desmoglein 1/3 antibodies and anti- BP180 antibodies. A chest X-ray showed mild infiltrates in the left lower lung (Fig. 1d). A transthoracic echocardiogram showed no vegetation. Intravenous ceftriaxone (1 g every 24 h) was administe- red after blood culture. On day 2, methicillin-susceptible S. aureus (MSSA) was identified from blood samples, and the antibiotics were switched to ampicillin/sulbactam (3 g every 12 h). However, her respiratory condition worsened in 3 days. Chest X-ray on day 5 showed massive pleural effusion in the left lower lung (Fig. 1e), which led to chest tube insertion to treat thoracic empyema. Since the culture from the pleural effusion also yielded MSSA, the time interval of antibiotics administration was shortened to every 6 h. Thereafter, the drainage volume decreased and ulcers on the lower legs gradually epithelized, and the patient was discharged on day 30. From this disease course, the diagnosis of septic vasculitis that preceded thoracic empyema was made. To investigate the pathogenesis of the cutaneous lesions, we analysed the biological properties of MSSA colonies obtained from 2 independent blood cultures and 2 independent pleural ef- fusion cultures. PCR detecting genes encoding SE serotypes A-R, performed according to the method of Omoe et al. (3), identified staphylococcal enterotoxin-like toxin type P (SElP) in all speci- mens (Fig. 2a). Sandwich enzyme-linked immunosorbent assays from SE strains confirmed the production of SElP (16.1 ng/ml, 16.6 ng/ml from 2 independent blood cultures and 18.1 ng/ml, 18.3 ng/ml from 2 independent pleural effusion cultures, negative control <0.25 ng/ml) (4). Reverse passive latex agglutination reac- tion assays specific for toxic shock syndrome toxin 1 (TSST-1), exfoliative toxin and Panton-Valentine leucocidin (PVL) were negative (5–7) (data not shown). Since the histopathology showed no microorganisms, it was suspected that MSSA toxins directly affected the vessels in the Fig. 1. (a) Erythematous-violaceous ulcers, 15 cm in size, with yellow or black necrolytic tissue surrounded by disseminated multiple blood blisters and purpura on the flexor surfaces of both lower legs. (b) Many blood blisters of various size on the right ankle. (c) A biopsy specimen obtained from purpura shows interface changes, dermal neutrophilic infiltrates, extravasated erythrocytes and small blood vessel thrombi (haematoxylin and eosin staining, original magnification ×40). (d) A chest X-ray at admission shows infiltrates in the left lower lung. (e) A chest X-ray shows massive pleural effusion in the left lower lung 5 days after admission. doi: 10.2340/00015555-3122 Acta Derm Venereol 2019; 99: 464–465 This is an open access article under the CC BY-NC license. www.medicaljournals.se/acta Journal Compilation © 2019 Acta Dermato-Venereologica.