Cutaneous Coinfection of Cytomegalovirus and Mycobacterium chelonae Accelerated by Immunosuppression.

IF 0.7 Q4 PATHOLOGY
Case Reports in Pathology Pub Date : 2021-01-29 eCollection Date: 2021-01-01 DOI:10.1155/2021/8819560
Yutaka Tsutsumi, Kentaro Odani, Yasuhito Kaneko, Hideo Hashizume, Mitsuhiro Tachibana
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引用次数: 2

Abstract

A mildly diabetic 58-year-old male had traumatic ulceration on the left popliteal fossa, and the lesion progressed to a painful 6 cm deep ulcer. After surgical debridement and skin grafting, ulceration recurred. Pyoderma gangrenosum was clinically diagnosed after the first biopsy, indicating a noninfective ulcer. Immunosuppressive therapy (prednisolone and cyclosporine A) induced complete epithelialization in three months. Four months later, subcutaneous nonulcerated nodules appeared on the anterior area of the left lower leg. Subcutaneous induration progressed and ulceration recurred, so that immunosuppressive therapy continued for one year. Cytomegalovirus (CMV) viremia was detected, and the second biopsy demonstrated CMV inclusions of endothelial and perivascular cells in fibrosing septolobular panniculitis. Cyclosporine A was cancelled, prednisolone was tapered, and ganciclovir started. Viremia soon disappeared, but the lesion progressed to large induration with multiple ulcers measuring up to 3 cm. The third biopsy disclosed infection of Gram-positive mycobacteria, accompanying fat droplet-centered suppurative granulomas without CMV infection. Microbial culture identified Mycobacterium chelonae. Clarithromycin with thermotherapy was effective. A review of the second biopsy confirmed coinfection of CMV and Gram-positive mycobacteria. Immunostaining using a panel of anti-bacterial antibodies visualized the mycobacteria in the lesion. Positive findings were obtained with antibodies to Bacillus Calmette-Guérin, Bacillus cereus, MPT64 (Mycobacterium tuberculosis-specific 24 kDa secretory antigen), LAM (Mycobacterium tuberculosis-related lipoarabinomannan), and PAB (Propionibacterium acnes-specific lipoteichoic acid).

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免疫抑制加速巨细胞病毒和龟分枝杆菌皮肤共感染。
轻度糖尿病患者,58岁男性,左腘窝创伤性溃疡,病变进展为疼痛的6厘米深溃疡。手术清创和植皮后,溃疡复发。坏疽性脓皮病在第一次活检后被临床诊断为非感染性溃疡。免疫抑制治疗(强的松龙和环孢素A)在三个月内诱导完全上皮化。4个月后,左小腿前侧出现皮下无溃疡性结节。皮下硬化进展和溃疡复发,因此免疫抑制治疗持续了一年。检测到巨细胞病毒(CMV)病毒血症,第二次活检显示纤维化性中隔小叶泛膜炎的内皮细胞和血管周围细胞有巨细胞病毒包涵体。停用环孢素A,逐渐减少泼尼松龙,并开始使用更昔洛韦。病毒血症很快消失,但病变进展为大硬化,并发多处溃疡,最大可达3厘米。第三次活检显示革兰氏阳性分枝杆菌感染,伴脂肪滴中心化脓性肉芽肿,无巨细胞病毒感染。微生物培养鉴定出龟分枝杆菌。克拉霉素热疗有效。复查第二次活检证实巨细胞病毒和革兰氏阳性分枝杆菌合并感染。使用一组抗细菌抗体进行免疫染色,可见病变中的分枝杆菌。卡介苗芽孢杆菌、蜡样芽孢杆菌、MPT64(结核分枝杆菌特异性24 kDa分泌抗原)、LAM(结核分枝杆菌相关脂阿拉伯糖甘露聚糖)和PAB(痤疮丙酸杆菌特异性脂磷壁酸)抗体均呈阳性。
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