Invasive pulmonary mucormycosis: rare presentation with pulmonary eosinophilia.

Invasive pulmonary mucormycosis: rare presentation with pulmonary eosinophilia.
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DOI:
10.1186/s12890-017-0419-1
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发表时间:
2017-04-28
影响因子:
3.1
通讯作者:
Ichinose M
Ichinose M
中科院分区:
医学3区
文献类型:
--
作者:
Hirano T;Yamada M;Sato K;Murakami K;Tamai T;Mitsuhashi Y;Tamada T;Sugiura H;Sato N;Saito R;Tominaga J;Watanabe A;Ichinose M

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真菌可引起多种感染性疾病,包括侵袭性真菌病和非侵袭性真菌病,以及过敏性疾病。不同形式的真菌病通常被描述为相互排斥的独立实体,很少有重叠病例的描述。在这里,我们描述了第一次报告的情况下,患者的并发症肺嗜酸性粒细胞增多症的过程中侵袭性毛霉菌病。一名74岁的日本男性患有哮喘-COPD重叠,因腹主动脉瘤破裂接受了急诊手术。手术成功,但出现发热和呼吸困难恶化,并从术后第10天(POD)开始持续。全血细胞计数显示白细胞增多伴嗜中性粒细胞增多和嗜酸性粒细胞增多,胸部X线检查显示POD 15时左上肺实变。我们怀疑院内感染性肺炎合并哮喘-COPD重叠加重,并开始抗生素和支气管扩张剂治疗。然而,症状、嗜酸性粒细胞增多和影像学表现恶化。然后我们进行了支气管镜检查,支气管肺泡灌洗液(BAL)分析显示嗜酸性粒细胞(82%的全细胞)以及丝状真菌的百分比增加。我们首先怀疑这是一例由曲霉菌感染引起的过敏性支气管肺真菌病(ABPM),并在术后第27天开始静脉注射伏立康唑进行皮质类固醇治疗。然而,BAL液的真菌培养检查显示毛霉菌,随后通过PCR和DNA测序鉴定为Cunninghamella bertholletiae。然后,我们在POD 29时将抗真菌剂转换为脂质体阿替霉素B用于治疗肺毛霉菌病。尽管用脂质体阿替霉素B替代伏立康唑,患者仍发生败血性休克,并在术后第39天死亡。尸检显示丝状真菌已侵入肺、心脏、甲状腺、肾和脾,表明发生了播散性毛霉菌病。我们描述了第一个报告的情况下,肺毛霉菌病与肺嗜酸性粒细胞增多症引起的小克银汉菌bertholletiae,导致播散性毛霉菌病。虽然这是一个相当罕见的情况下,可以得出两个重要的结论:i)真菌病可以同时引起侵袭性感染和宿主过敏反应,和ii)小克银汉霉bertholletiae很少感染免疫功能正常的患者。
Fungi can cause a variety of infectious diseases, including invasive mycosis and non-invasive mycosis, as well as allergic diseases. The different forms of mycosis usually have been described as mutually exclusive, independent entities, with few descriptions of overlapping cases. Here, we describe the first reported case of a patient with the complication of pulmonary eosinophilia in the course of invasive mucormycosis. A 74-year-old Japanese man with asthma-COPD overlap underwent emergency surgery for a ruptured abdominal aortic aneurysm. The surgery was successful, but fever and worsening dyspnea appeared and continued from postoperative day (POD) 10. A complete blood count showed leukocytosis with neutrophilia and eosinophilia, and the chest X-ray showed consolidation of the left upper lung at POD 15. We suspected nosocomial pneumonia together with an exacerbation of the asthma-COPD overlap, and both antibiotics and bronchodilator therapy were initiated. However, the symptoms, eosinophilia and imaging findings deteriorated. We then performed a bronchoscopy, and bronchoalveolar lavage (BAL) fluid analysis revealed an increased percentage of eosinophils (82% of whole cells) as well as filamentous fungi. We first suspected that this was a case of allergic bronchopulmonary mycosis (ABPM) caused by Aspergillus infection and began corticosteroid therapy with an intravenous administration of voriconazole at POD 27. However, the fungal culture examination of the BAL fluid revealed mucormycetes, which were later identified as Cunninghamella bertholletiae by PCR and DNA sequencing. We then switched the antifungal agent to liposomal amphotericin B for the treatment of the pulmonary mucormycosis at POD 29. Despite replacing voriconazole with liposomal amphotericin B, the patient developed septic shock and died at POD 39. The autopsy revealed that filamentous fungi had invaded the lung, heart, thyroid glands, kidneys, and spleen, suggesting that disseminated mucormycosis had occurred. We describe the first reported case of pulmonary mucormycosis with pulmonary eosinophilia caused by Cunninghamella bertholletiae, which resulted in disseminated mucormycosis. Although it is a rather rare case, two important conclusions can be drawn: i) mycosis can simultaneously cause both invasive infection and a host allergic reaction, and ii) Cunninghamella bertholletiae rarely infects immunocompetent patients.