Ureaplasma and Lung Transplantation: A Pinch of Prophylaxis May Mollify a Not so Cute Infection.
Ureaplasma and Lung Transplantation: A Pinch of Prophylaxis May Mollify a Not so Cute Infection.
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解脲支原体和肺移植：一点预防措施可能会缓解不那么可爱的感染。
DOI：
10.1097/tp.0000000000003541
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发表时间：
2020
期刊：
影响因子：
6.2
通讯作者：
A. Glanville
中科院分区：
文献类型：
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作者：
A. Glanville
M是支原体科的一类，包括支原体和脲原体，两者都是泌尿生殖道中常见的无症状居民。成年女性下生殖道标本中人支原体的检出率为21% ~ 53%，脲原体的检出率为40% ~ 80%。男性的发病率被认为较低，但在无症状的普通人群中，数据并不全面。关于不孕症的风险和非特异性尿道炎的发病率的争论仍在继续，但口咽定植有充分的记录，可能是短暂的，并取决于性伴侣的数量和特定的活动。因此，健康个体睡眠期间口咽内容物的吸入，甚至是微小的吸入，特别是在潜在供体插管期间，都是下呼吸道被分子菌定植的危险因素。事实上，在一个系列中，莫里特阳性的肺供者是年轻的，主要是男性，并且有多个性伴侣。胸外科手术后弥散性感染，受者常规留置导尿管，这是血源性感染的潜在门户，多年来已经被认识到，肺移植术后“培养阴性”伤口破裂，包括支气管吻合口裂开。最初的报告显示，联合心肺移植的受者更容易发生这种情况，这可能反映了当时选择的方式或移植的组织更大。有趣的是，胸膜和心包表面经常受累，导致积液。与此同时，高氨血症综合征（HS）是一种罕见但通常致命的并发症，不仅在LTX术后早期发生，而且在一些其他形式的实体器官移植（SOT）和骨髓移植后也主要发生。在这种情况下，它最初被称为“特发性HS”，以区别于急性和慢性肝功能衰竭、先天性肝代谢错误、药物作用和其他已知原因。一些病例很可能被误诊为后可逆脑病综合征（PRES）在没有简单的权宜之计检查氨水平。PRES和HS都表现为精神状态的改变，通常在没有低氧血症的情况下，并可能发展为癫痫持续状态和昏迷，并因脑水肿而死亡。视觉障碍和高血压是PRES发展的早期线索，呼吸性碱中毒常见于HS。积累的SOT后HS的经验也证明了LTX接受者中HS的发病率更高。Krutsinger等人描述了LTX受体的发生率为3.9%，而其他SOT受体的发生率为0.1% （P = 0.004）。他们的文献综述发现81%的报告病例发生在LTX接受者中，其中69%死亡，而Chen等人在一项单中心回顾性综述中描述了807例LTX中的8例，其中7例死亡。迄今为止，HS的治疗一直是复杂和昂贵的，重症监护病房和住院治疗的时间延长，包括血液透析、机械通气支持、体外膜氧合和实验性治疗，如使用人工肝脏，这些治疗只是偶尔有效。移植社区和受者群体在很大程度上归功于当前研究的作者，他们孜孜不业地追求一种有洞察力和分析性的方法来研究供体源性脲原体感染的起源和预防，目的是根除ltx后HS的幽灵。他们在这一期《移植》杂志上报道的结果既简单又令人信服，并且建立在从实验室得出的可靠的科学证据之上，尽管在小鼠模型中，Fernandez等人能够满足Koch关于HS和尿原体因果关系的一些假设，以支持Wang等人的开创性工作。问题是为什么以及如何花了这么多年才达到这个关键的决策点。很简单，这些感染有些挑剔；即使在特殊培养基上，菌落也非常小（“针尖”），可能需要更长的时间才能生长。脲原体16S核糖体RNA测序的明确诊断测试至今尚未普遍可用。要了解莫里特感染的恶性潜能，需要对泌尿生殖健康有更广泛深入的了解，而这种技能在肺和心脏移植临床医生和外科医生中可能有些不常见。强调了与能够在这些领域提供丰富经验和支持的传染病同事密切合作的重要性。评论
M are a class of the Mycoplasmataceae family, which includes Mycoplasma and Ureaplasma spp., both of which are not infrequent asymptomatic inhabitants of the urogenital tract. Mycoplasma hominis may be detected in 21%–53% of lower genital tract specimens of adult women, while Ureaplasma spp. can be found in 40%–80%. The rate in men is thought to be lower, but data are not as comprehensive in the asymptomatic general population. Debate continues regarding the risks of infertility and the rate of nonspecific urethritis, but oropharyngeal colonization is well documented, may be transient, and depends on the number of sexual partners and specific activities. Aspiration of oropharyngeal contents, even microaspiration during sleep in healthy individuals, and especially during intubation of potential donors, are therefore risk factors for lower respiratory tract colonization with mollicutes. Indeed in one series, lung donors who were positive for mollicutes were younger, predominantly male individuals, and sexually active with multiple partners. Disseminated infection with mollicutes after cardiothoracic surgery, where recipients routinely have an indwelling urinary catheter, which is a potential portal for blood-borne infection, has been recognized for many years, as has “culture-negative” wound breakdown, including bronchial anastomotic dehiscence, after lung transplantation (LTX). Initial reports suggested a greater predisposition in recipients of combined heartlung transplants, which may have reflected the choice of modality at the time or the greater bulk of tissue transplanted. Interestingly, pleural and pericardial surfaces were often involved leading to effusions. In temporal parallel, the hyperammonemia syndrome (HS), an infrequent but commonly fatal complication, was described as occurring predominantly early not only after LTX but also after some other forms of solid organ transplantation (SOT) and bone marrow transplantation. In this context, it was originally termed “idiopathic HS” to differentiate it from acute and chronic liver failure, inborn errors of hepatic metabolism, drug effects, and other known causes. Some cases may well have been misdiagnosed as posterior reversible encephalopathy syndrome (PRES) in the absence of the simple expediency of checking an ammonia level. Both PRES and HS present with changes in the mental state, usually in the absence of hypoxemia, and may progress to status epilepticus and coma with death from cerebral edema. Visual disturbance and hypertension are early clues to the development of PRES, and respiratory alkalosis is often seen in HS. Accumulating experience with HS after SOT also demonstrated a higher incidence of HS among LTX recipients. Krutsinger et al described an incidence of 3.9% in LTX recipients versus 0.1% in other SOT (P = 0.004). Their literature review found that 81% of all reported cases occurred in LTX recipients, of whom 69% died, while Chen et al in a single-center retrospective review described 8 cases from 807 LTX, of whom 7 died. Therapy to date for HS has been complex and expensive with prolongation of intensive care unit stays and inpatient care following a raft of treatments including hemodialysis, mechanical ventilatory support, extracorporeal membrane oxygenation, and experimental therapies such as the use of an artificial liver, which were only occasionally effective. The transplant community at large and the recipient population owe much to the authors of the current study, who have assiduously pursued an insightful and analytical approach to the origins and prevention of donor-derived Ureaplasma infections with the aim of eradicating the specter of HS post-LTX. Their results reported in this issue of Transplantation are at once simple and compelling and build on sound scientific evidence drawn from the laboratory, albeit in murine models, where Fernandez et al were able to fulfill some of Koch’s postulates regarding causality of HS and Ureaplasma to support the seminal work of Wang et al. The question arises as to why and how it has taken so many years to arrive at this nodal decision point. Quite simply, these infections are somewhat fastidious; even on special media, colonies are extremely small (“pinpoint”) and may take longer to grow. Definitive diagnostic testing for Ureaplasma spp. with 16S ribosomal RNA sequencing is not available universally to date. Understanding the malignant potential of mollicute infections requires a broader in-depth understanding of urogenital health, which skill is arguably somewhat uncommon in lung and heart transplant clinicians and surgeons. The importance of working closely with our infectious disease colleagues who can provide a wealth of experience and support in these areas is emphasized. Commentary