一例胸膜结核分枝杆菌感染病例,Quantiferon Gold Plus 结果由阳性转为阴性。

Access microbiology Pub Date : 2024-09-05 eCollection Date: 2024-01-01 DOI:10.1099/acmi.0.000737.v3
N Goire, M S Suchard, A Barling, R Fernando, L Dreyer, A A Mahony
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摘要

导言。在全球范围内,结核分枝杆菌(MTB)感染继续造成很高的死亡率和发病率。γ干扰素释放测定(如Quantiferon Gold Plus (QFG-Plus))有助于诊断潜伏肺结核,但胸膜肺结核的诊断仍具有挑战性。我们介绍了一例活动性胸膜 MTB 感染病例,其 IGRA 结果由阳性转为阴性,胸膜活检组织的 Xpert MTB/RIF Ultra PCR 结果也为阴性。病例摘要。一名 52 岁的健康男性于 2022 年 8 月就诊,胸膜炎性胸痛病史 2 周,伴有炎症标记物轻度升高。患者曾在 2018 年出现过 QFG-Plus 阳性结果,但此次入院时 QFG-Plus 为阴性。计算机断层扫描肺血管造影和针刺胸腔穿刺术显示左侧胸腔渗出液以淋巴细胞为主。患者的症状在接受社区获得性肺炎的经验性抗菌治疗后未能缓解。支气管肺泡灌洗以及通过视频辅助胸腔镜手术从左下叶对胸膜组织进行活检的常规微生物培养和 Xpert Ultra PCR 结果均为阴性。胸膜组织的分枝杆菌培养中发现了酸性耐酸杆菌的生长,经鉴定为 MTB。结论。尽管技术取得了重大进步,但 MTB 感染的微生物学诊断仍具有挑战性。我们记录了 QFG-Plus 在胸膜结核病从潜伏期发展到活动期过程中的逆转。CD4+ 和 CD8+ T 细胞对结核抗原(ESAT-6 和 CFP-10)产生γ干扰素的能力下降可能与宿主失去对潜伏 MTB 的控制有关。这个病例提醒我们,尽管使用最先进的诊断平台进行了详尽的检测,但 MTB 感染仍有可能不被发现。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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A case of pleural Mycobacterium tuberculosis infection with reversion of Quantiferon Gold Plus results from positive to negative.

Introduction. Mycobacterium tuberculosis (MTB) infections continue to have a high mortality and morbidity burden globally. Interferon-gamma release assays such as Quantiferon Gold Plus (QFG-Plus) aid in diagnosis of latent TB but diagnosis of pleural TB remains challenging. We present a case of active pleural MTB infection with reversion from positive to negative of IGRA result as well as negative Xpert MTB/RIF Ultra PCR result from tissues obtained from pleural biopsy. Case summary. A 52-year-old otherwise healthy male presented in August 2022 with a 2 week history of pleuritic chest pain associated with modest elevation in inflammatory markers. The patient had had a positive QFG-Plus result in 2018, however QFG-Plus during this admission was negative. Computed-tomography pulmonary angiogram and needle thoracocentesis showed an exudative left pleural effusion with predominant lymphocytes. The patient's symptoms failed to resolve with empiric antimicrobial therapy for community-acquired pneumonia. Broncho-alveolar lavage as well as biopsies of pleural tissues via video-assisted thoracoscopic surgery from the left lower lobe yielded negative results on routine microbiological culture as well as Xpert Ultra PCR. Growth of acid-fast bacilli was noted from mycobacterial cultures of pleural tissues which was identified as MTB. Conclusion. Despite significant technological advances, microbiological diagnosis of MTB infections remains challenging. We document QFG-Plus reversion during development from latent to active pleural TB. Decline in the ability of CD4+ and CD8+ T cells to produce interferon gamma in response to TB antigens (ESAT-6 and CFP-10) was likely associated with loss of host control of latent MTB. This case serves as a reminder that despite exhaustive testing with state-of-art diagnostic platforms, MTB infections can still elude discovery.

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