成人社区获得性肺炎概述 - UpToDate

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成人社区获得性肺炎概述
AUTHOR: Julio A Ramirez, MD, FACP
SECTION EDITOR: Thomas M File, Jr, MD
DEPUTY E D I T O R : Sheila Bond, MD
翻译: 韩锋锋, 主任医师，教授
我们的所有专题都会依据新发表的证据和同行评议过程而更新。
文献评审有效期至： 2023-07.
专题最后更新日期： 2023-04-13.
There is a newer version of this topic available in English. 该主题有一个新的英文版

本。
引言
社区获得性肺炎(community-acquired pneumonia, CAP)是全球发病和死亡的主要原因。CAP患者的临床

表现不一，可为发热和咳痰为特征的轻症肺炎，也可为呼吸窘迫和脓毒症为特征的重症肺炎。由于CAP
的临床表现广泛，所以几乎所有呼吸道疾病的鉴别诊断均包括CAP。
本专题将概述免疫功能正常成人中CAP的流行病学、微生物学、发病机制、临床特征、诊断和管理。这
些问题均在其他专题详细讨论，相关链接见下文。
定义
肺炎常根据获得场所分类( 表 1)。
● 社区获得性肺炎(community-acquired pneumonia, CAP)指在医院外获得的肺实质急性感染。
● 医院内肺炎是指在医院发生的急性肺实质感染，包括医院获得性肺炎(hospital-acquired
pneumonia, HAP)和呼吸机相关肺炎(ventilator-associated pneumonia, VAP)。
new.migangpro.com/contents/zh-Hans/overview-of-community-acquired-pneumonia-in-adults/print?search=肺炎&source=search_result&selectedTitle… 1/72
• HAP是指在入院≥48小时之后发生的肺炎。
• VAP是指在气管插管≥48小时之后发生的肺炎。
健康护理相关肺炎(health care-associated pneumonia, HCAP)这个术语已不再使用，指的是在医疗保

健机构(例如，疗养院、血液透析中心)以及近期住院后发生的肺炎。过去使用HCAP一词是为了识别存在
多药耐药病原体感染风险的患者。然而，这一分类可能过于敏感，导致了抗生素滥用增加，因此已经淘
汰。一般而言，之前归类为HCAP的患者应接受与CAP患者类似的治疗。(参见 “成人医院获得性肺炎和
呼吸机相关肺炎的流行病学、发病机制、微生物学和诊断”)
流行病学
发病率 — CAP是临床中最常见且最严重的疾病之一[1-3]。在美国，每年的CAP门急诊就诊数超过
450万，约占0.4%[4]。CAP是住院的第二大原因，并且是最常见的感染性死因[5,6]。在美国，每年每10
万成年人中约有650人因CAP住院，相当于每年有150万成人因CAP住院(同一患者只计算1次)[7]。近9%的
CAP住院患者将在一年内因新发CAP而再次入院。
危险因素
● 高龄–CAP的风险随着年龄的增长而上升[7,8]。在美国，年龄≥65岁的人群中，CAP的年住院率
约为2000/100,000[7,9]。这大约是一般人群的3倍，表明每年有2%的老年人因CAP住院
( 图 1)。
● 慢性共存疾病–慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)患者因CAP

住院的风险最高，在美国COPD患者中CAP住院的年发生率为5832/100,000[7]。使CAP发病率增加的
其他共存疾病包括其他慢性肺病(如支气管扩张和哮喘)、慢性心脏病(特别是充血性心力衰竭)、
脑卒中、糖尿病、营养不良和损害免疫功能的疾病( 图 2)[7,10,11]。
● 病毒性呼吸道感染–病毒性呼吸道感染可导致原发性病毒性肺炎，也使患者易继发细菌性肺炎。
这种情况在流感病毒感染时最明显。(参见 “成人季节性流感的临床表现和诊断”，关于‘肺
炎’一节)
● 气道保护受损–一些疾病可增加胃内容物大量误吸和/或上呼吸道分泌物微量误吸的风险，这些
疾病会使患者易发生CAP，例如，意识改变(如，脑卒中、癫痫、麻醉、药物或酒精使用所致)或吞
咽困难(食道病变或动力障碍引起)。
● 吸烟和酗酒–吸烟、酗酒(例如，＞80g/d)和使用阿片类物质是CAP重要的可纠正行为危险因素
[7,10,12,13]。
● 其他生活方式因素–与CAP风险增加相关的其他因素包括拥挤的生活条件(例如，监狱、收容
所)、居住于经济条件较差的地区，以及暴露于环境毒素(例如，溶剂、油漆或汽油)
[7,10,11,14]。
同时存在多种危险因素会使风险累加，例如，同时存在吸烟、COPD和充血性心力衰竭[15]。这些危险因
素和CAP的其他易感因素详见其他专题。(参见 “成人社区获得性肺炎的流行病学、发病机制和微生物
学”，关于‘宿主易感因素’一节)
微生物学
常见病因 — 肺炎链球菌(Streptococcus pneumoniae，又叫肺炎球菌)和呼吸道病毒是CAP患者中最
常检出的病原体[8,16]。然而，在很大一部分病例中(在医院进行的一些研究中高达62%)，尽管进行了
广泛的微生物学评估，还是没有发现病原体[8,17,18]。
最常检出的导致CAP的病原体可分为3类：
● 典型细菌
• 肺炎链球菌(最常见的CAP致病细菌)
• 流感嗜血杆菌(Haemophilus influenzae)
• 卡他莫拉菌(Moraxella catarrhalis)
• 金黄色葡萄球菌(Staphylococcus aureus)
• A组链球菌
• 革兰阴性需氧菌，例如肠杆菌科的克雷伯菌属(Klebsiella)或大肠埃希菌(Escherichia coli)
• 微需氧菌和厌氧菌(与误吸有关)
● 非典型细菌(“非典型”是指这些细菌对β-内酰胺类药物存在固有耐药性，以及革兰染色或传统
技术培养无法发现)
• 军团菌(Legionella)
• 肺炎支原体(Mycoplasma pneumoniae)
• 肺炎衣原体(Chlamydia pneumoniae)
• 鹦鹉热衣原体(Chlamydia psittaci)
• 贝纳柯克斯体(Coxiella burnetii)
● 呼吸道病毒
• 甲型和乙型流感病毒
• 严重急性呼吸综合征冠状病毒2型(severe acute respiratory syndrome coronavirus 2,
SARS-CoV-2)
• 其他冠状病毒(如CoV-229E、CoV-NL63、CoV-OC43、CoV-HKU1)
• 鼻病毒
• 副流感病毒
• 腺病毒
• 呼吸道合胞病毒
• 人类偏肺病毒
• 人博卡病毒
这些病原体所致病例的相对比例因地理位置、肺炎球菌疫苗接种率、宿主危险因素(如吸烟)、季节和肺
炎严重程度的不同而有所差异( 表 2)。
某些流行病学接触也会增加感染特定病原体的可能性( 表 3)。例如，接触受污染的水是军团菌感染
的危险因素，接触鸟类会增加鹦鹉热衣原体感染的可能性，对美国西南部旅行或居住者应怀疑球孢子菌
病，不良的口腔卫生可能使患者易发生口腔菌群或厌氧菌引起的肺炎。在免疫功能低下的患者中，可能
的病原体范围也扩大到包括真菌和寄生虫，以及不常见的细菌和病毒病原体。(参见 “免疫功能受损患
者肺部感染的流行病学”和 “免疫功能受损患者发热伴肺部浸润的概述”)
虽然上面详细列出了一些导致CAP的最常见病因，但研究报道有超过100种细菌、病毒、真菌和寄生虫可
导致CAP。(参见 “成人社区获得性肺炎的流行病学、发病机制和微生物学”，关于‘微生物学’一节)
重要趋势 — CAP病原体的分布和我们对这些病原体的认识都在不断变化。一些关键的发现改变了我
们对CAP的理解，并影响了我们的治疗策略，包括：
● 肺炎链球菌发病率下降–虽然在大多数研究中肺炎链球菌(肺炎球菌)是最常见的CAP致病菌，但
肺炎球菌肺炎的总体发病率正在下降。这在一定程度上是由于肺炎球菌疫苗的广泛使用，使得肺
炎球菌肺炎个体发生率下降以及群体免疫形成。(参见 “需住院治疗患者的肺炎球菌性肺炎”，
关于‘患病率’一节)
肺炎球菌疫苗接种率有地区差异，因此肺炎链球菌感染率也有差异。例如，在欧洲估计约30%的
CAP病例是肺炎链球菌所致，但在美国只有10%-15%，而美国的人群肺炎球菌疫苗接种率更高[8]。
● COVID-19大流行–SARS-CoV-2是CAP的重要病因，详见其他专题。(参见 “2019冠状病毒病
(COVID-19)的流行病学、病毒学和预防”)
● 其他呼吸道病毒检出增加–使用分子学方法，在大约1/3的成人CAP病例中检测到了呼吸道病毒
[8]。呼吸道病毒在以下方面的作用尚不确定：作为单一病原体，作为发生细菌性CAP的辅助因
素，或触发宿主免疫应答失调。
● 病原体总体检出率低–尽管使用分子诊断和其他微生物学检测方法进行广泛评估，仍仅有一半
的CAP病例可以确定病原体。这表明我们对CAP发病机制的理解还不充分。随着分子诊断技术的发
展和应用范围的扩大，我们对CAP的认识将不断提高。
● 肺部微生物群的发现–以前认为肺部是无菌的。然而，非培养技术(即高通量16S rRNA基因测
序)已在肺泡内发现复杂多样的微生物群落[19-21]。这一发现表明，肺泡常驻微生物在肺炎的发
生中起一定作用，其机制可能是调节宿主对感染病原体的免疫应答，或肺泡微生物群内特定病原
体直接过度生长。(参见下文‘发病机制’)
抗生素耐药性 — 了解抗生素耐药模式和感染耐药病原体的危险因素，有助于选择CAP经验性治疗的
抗生素( 表 4)。
● 肺炎链球菌可能对一种或多种常用于CAP经验性治疗的抗生素耐药。
• 大环内酯类的耐药率在不同地区有所差异，但在美国、亚洲和南欧通常较高(＞25%)。北欧的
耐药率倾向于较低。(参见 “肺炎链球菌对大环内酯类、氮杂内酯类、林可酰胺类和酮内酯类
药物的耐药性”)
• 多西环素的耐药率尚不确定，在世界各地差异很大。在美国，耐药率往往低于20%，但可能在
逐渐上升。(参见 “肺炎链球菌对氟喹诺酮类、多西环素和复方磺胺甲噁唑的耐药性”)
• 不同区域的β-内酰胺类药物耐药率也不同，但其地区差异小于大环内酯类和多西环素耐药
率。在美国，＜20%的分离株对青霉素耐药，＜1%的分离株对头孢菌素类耐药。(参见 “肺炎
链球菌对β-内酰胺类抗生素的耐药性”)
• 在美国，氟喹诺酮耐药率往往小于2%，但因地区和特定危险因素(如近期使用抗生素或住院)的
不同而有所差异。(参见 “肺炎链球菌对氟喹诺酮类、多西环素和复方磺胺甲噁唑的耐药
性”)
耐药率甚至在同一地区也存在差异，所以如果条件允许，临床医生应参考当地抗菌谱来选择抗生
素。一般流行病学数据可通过一些资源获得，例如疾病动态、经济与政策中心( Center for
Disease Dynamics, Economics & Policy)。
● 耐甲氧西林金黄色葡萄球菌(Methicillin-resistant S. aureus, MRSA)也可导致CAP但不常见。

感染MRSA的危险因素分为两类：医疗保健相关和社区获得性。发生MRSA肺炎的最强危险因素包括
已知有MRSA定植或曾感染MRSA，尤其是呼吸道。痰革兰染色示革兰阳性球菌也可预测MRSA感染。
其他提示应考虑MRSA感染的因素包括：近期用过抗生素(尤其是过去3个月内接受过抗生素静脉给
药)，近期发生过流感样疾病，存在脓胸、坏死性/空洞性肺炎，以及免疫抑制( 表 4)。
与医疗保健相关的MRSA感染相比，社区获得性MRSA(community-acquired MRSA, CA-MRSA)感染往

往发生在年轻的健康人群[22]。CA-MRSA感染的危险因素包括MRSA皮损病史、参与身体接触性运
动、注射吸毒、拥挤的生活条件以及男男性行为。(参见 “成人耐甲氧西林金黄色葡萄球菌感染
的流行病学”)
由CA-MRSA引起的CAP可能很严重，可导致坏死和/或空洞性肺炎、脓胸、明显咯血(gross
hemoptysis)、脓毒性休克和呼吸衰竭。这些症状可归因于产毒素CA-MRSA菌株感染。在美国，这
些菌株往往对甲氧西林耐药，属于流行株USA300。(参见 “社区获得性耐甲氧西林金黄色葡萄球
菌的毒力决定因子”)
● 假单胞菌属(Pseudomonas)也是CAP的不常见病因，往往更常见于有以下因素的患者：已知定植
或曾感染假单胞菌属，近期住院或使用抗生素，存在基础结构性肺病[如囊性纤维化或晚期
COPD(支气管扩张)]，或者存在免疫抑制。抗生素耐药在假单胞菌属菌株中很常见，对于有风险的
中至重度CAP患者，给予经验性治疗时需要使用超过1种针对假单胞菌属的药物( 表 4)。(参见
“铜绿假单胞菌肺炎”和‘住院抗生素治疗’)
发病机制
传统上将CAP视为肺实质感染，主要由细菌性或病毒性呼吸道病原体引起。在相关发病机制模型中，呼
吸道病原体通过飞沫在人与人之间传播，有时通过气溶胶吸入传播[例如军团菌或柯克斯体属
(Coxiella)]。吸入后，病原体定植于鼻咽部，然后通过微量误吸到达肺泡。当接种量足够和/或宿主免
疫防御能力受损时，就会发生感染。病原体复制、致病因子产生和宿主免疫应答会导致肺实质炎症和损
伤，最终引起肺炎( 图 3)。
随着肺部微生物群的鉴定，发病机制模型发生了变化[19-21]。虽然肺炎的发病机制可能仍涉及呼吸道
病原体进入肺泡，但感染病原体可能必须与常驻微生物竞争才能复制。此外，常驻微生物也可能影响或
调节宿主对感染病原体的免疫应答。如果确实如此，则肺泡微生物群改变(肺泡生态失调)可能是肺炎的
易感因素。
在某些病例中，肺泡内的常驻微生物不受控制的复制也可能引起CAP。肺泡微生物群与口腔菌群相似，
其组成主要为厌氧菌[如普氏菌(Prevotella)和韦荣球菌(Veillonella)]以及微需氧性链球菌[19-21]。
有研究者提出以下假设：病毒感染或烟雾暴露等外源性损伤可能改变肺泡微生物群的组成，并触发某些
微生物的过度生长。由于构成肺泡微生物群的微生物通常不能采用标准培养方法来培养，上述假设可能
解释了为什么CAP患者中病原体检出率低。
在任何情况下，宿主对肺泡内微生物复制的免疫应答都对疾病的严重程度有重要决定作用。对于某些患
者，肺部的局部炎症反应占主导，并可能足以控制感染。对于其他患者，需要全身反应才能控制感染和
防止播散或发生并发症，如菌血症。在少数患者中，全身反应可能失调，导致组织损伤、脓毒症、急性
呼吸窘迫综合征和/或多器官功能障碍。
CAP的发病机制详见其他专题。(参见 “成人社区获得性肺炎的流行病学、发病机制和微生物学”)
临床表现
CAP的临床表现差异很大，可为发热、咳嗽和呼吸急促为特征的轻症肺炎，也可为脓毒症和呼吸窘迫为
特征的重症肺炎。症状的严重程度与患者个体的局部和全身免疫应答的强度直接相关。
● 肺部症状和体征–干咳或咳痰、呼吸困难和胸膜炎性胸痛是CAP的最常见症状。肺炎的体征包括
呼吸过速、呼吸功增加，以及附加呼吸音，包括湿啰音和干啰音。触觉震颤、羊鸣音和叩诊呈浊
音也提示肺炎。这些体征和症状是白细胞、液体和蛋白质在肺泡腔内积聚造成的。随后的肺泡气
体交换受损可导致低氧血症。在胸片上，肺泡内白细胞和液体积聚表现为肺不透光
( 影像 1A-B)。
● 全身症状和体征–绝大多数CAP患者会出现发热。其他全身症状也很常见，如寒战、疲劳、不
适、胸痛(可能是胸膜炎性)和厌食。全身炎症反应还可导致心动过速、白细胞增多及核左移或白
细胞减少。炎症标志物可能升高，例如，红细胞沉降率(erythrocyte sedimentation rate,
ESR)、C反应蛋白(C-reactive protein, CRP)和前降钙素，但前降钙素升高大多提示细菌感染。
CAP也是脓毒症的主要原因，因此初始特征可能为低血压、神志改变，以及器官功能障碍的其他表
现，如肾功能障碍、肝功能障碍和/或血小板减少[23]。
尽管某些症状和体征在CAP患者中很常见，如发热、咳嗽、心动过速和啰音，但这些表现终究无特异
性，在许多呼吸系统疾病中均可出现(参见下文‘鉴别诊断’)。不进行胸部影像学检查的情况下，任何
单独症状或症状集合都不足以进行诊断。例如，在初级保健机构就诊且诉呼吸系统症状的患者中，以胸
片作为参考标准，发热、心动过速、啰音和缺氧(氧饱和度＜95%)联合表现的阳性预测值＜60%[24]。
在高龄和/或免疫系统受损的患者中肺炎的症状和体征也可能不明显，可能需要高度警惕才能诊断。例
如，老年患者可能出现神志改变，但没有发热和白细胞增多[25]。在免疫功能低下的患者中，胸片可能
无法检测到肺浸润，但CT可以。
CAP和脓毒症的临床表现和诊断特点详见其他专题。(参见 “成人社区获得性肺炎的临床评估和诊断性
检测”和 “成人脓毒症综合征的流行病学、定义、临床表现、诊断和预后”，关于‘临床表现’一节)
诊断
诊断 — 诊断CAP通常需要满足以下条件：胸部影像学检查证实肺部浸润，且患者有临床符合的综合
征(例如，发热、呼吸困难、咳嗽和咳痰)[26]。
● 对于大多数疑似CAP患者，通常拍摄后前位和侧位胸片。与CAP诊断一致的影像学检查结果包括：
肺叶实变( 影像 1A, 1C)、间质浸润( 影像 1B, 1D-E)和/或空洞形成( 影像 2)。尽管某
些影像学特征提示肺炎的特定病因(例如，肺叶实变提示典型细菌感染)，但仅凭影像学表现不能
可靠地区分病因。
● 对于胸片阴性但根据临床特征仍怀疑CAP的特定患者，我们会进行胸部CT检查，包括：免疫功能低
下的患者，他们可能不产生强烈的炎症反应，因此胸片呈阴性；已知暴露于肺炎流行病原体(如军
团菌)的患者。由于没有直接证据表明CT扫描能改善大多数患者的结局，而且检查成本很高，我们
在评估CAP时，通常不会进行CT扫描。
有相符的临床综合征，并且影像学检查结果符合肺炎，则足以做出CAP的初步临床诊断。但这些表现组
合不具有特异性，在许多心肺疾病中都会出现。因此，随着患者病程的发展，仍需要继续关注其他可能
的诊断，这对治疗很重要。(参见下文‘鉴别诊断’)
确定严重程度和治疗地点 — 对于最可能的诊断为CAP的患者，下一步是确定疾病的严重程度和确
定最合适的治疗点。根据临床判断确定疾病的严重程度，可使用严重程度评分作为辅助
( 流程图 1)。
最常用的严重程度评分是肺炎严重程度指数(Pneumonia Severity Index, PSI)和CURB-65[27,28]。我

们通常首选PSI，也叫PORT评分(计算器 1)，因为其最准确，并且用于指导临床决策的安全性和效果已
得到验证[29-32]。但也可选择CURB-65评分，其使用更简便，因而成为许多医生的首选(计算器 2)。
通常3个等级的严重程度(轻、中和重)对应3个等级的治疗：
● 门诊治疗–大多数其他方面健康、生命征正常(除发热外)且无并发症的患者考虑为轻症肺炎，可
在门诊治疗。这些患者通常PSI评分为Ⅰ-Ⅱ，CURB-65评分为0(如果年龄＞65岁，则CURB-65评分
为1)。
● 住院治疗–呼吸室内空气的情况下，外周血氧饱和度＜92%且与基线相比有显著变化的患者应住
院治疗。此外，PSI评分≥Ⅲ、CURB-65评分≥1时(如果年龄＞65岁，则CURB-65评分≥2)，患者一
般也应住院治疗。
有脓毒症早期征象、病情快速进展或疑似感染侵袭性病原体的患者在严重程度评分系统中未充分
体现，因此这些患者可能也需要住院，以便密切监测对治疗的反应。
可能造成患者需要住院的现实问题包括：无法口服药物，认知或功能受损，或其他可能降低药物
依从性或导致无法在临床恶化时复诊的社会因素(例如，物质滥用、无家可归或住所远离医疗机
构)。
● 入住ICU–符合以下任一主要标准的患者为重症CAP，应收入ICU[26]：
• 因呼吸衰竭而需要机械通气
• 需要血管加压药支持的脓毒症
这两个ICU入住标准的识别相对简单。困难的是，如何在已发展为脓毒症的重症CAP患者发生器官
衰竭前将其识别出来。对于这些患者，早期入住ICU并使用适当的抗生素可改善结局。为了在发生
器官衰竭前识别重症CAP患者，美国胸科学会(American Thoracic Society, ATS)和美国感染病学
会(Infectious Diseases Society of America, IDSA)提出了一些次要标准[1,26]。
符合以下标准中的3项即需收治ICU：
• 神志改变
• 需要液体支持的低血压
• 体温＜36℃(96.8°F)
• 呼吸频率≥30次/分钟
• 动脉血氧分压(arterial partial pressure of oxygen, PaO2)与吸入氧分数(fraction of
inspired oxygen, FiO2)的比值≤250
• BUN≥20mg/dL(7mmol/L)
• 白细胞计数＜4000/μL
• 血小板计数＜100,000/mL
• 多肺叶浸润
虽然已经制定了一些其他评分系统来识别重症CAP和/或收治ICU，但我们通常使用ATS/IDSA主要和次要
标准，因为它们经过了充分验证[33-35]。
评估CAP严重程度和确定治疗地点的相关内容详见其他专题。(参见 “成人社区获得性肺炎：评估严重
程度和确定恰当的治疗场所”)
确诊或疑似COVID-19患者的分诊也见其他专题。
微生物学检测 — 对于每一名患者，都应权衡微生物学诊断的益处与全面评估耗费的时间和费用。
我们一般根据CAP的严重程度和治疗地点，采用分级的方法来进行微生物学评估( 表 5)：
● 门诊患者−对于大多数在门诊接受治疗的轻度CAP患者，除大流行期间的SARS-CoV-2检测外，无需
其他微生物学检查。经验性抗生素治疗通常有效，识别感染病原体一般不能进一步改善结局。
● 收入普通内科的中度CAP患者−对于大多数收入普通内科的中度CAP患者，我们进行以下检查：
• 血培养
• 痰革兰染色和培养
• 肺炎链球菌尿抗原检测
• 军团菌检测，如有条件可进行PCR检查，否则可用尿抗原检测作为替代
• SARS-CoV-2检测
在大流行期间，我们对所有患者检测COVID-19。在呼吸道病毒流行季节(如北半球的深秋至早
春)，我们还检测其他呼吸道病毒，如流感病毒、腺病毒、副流感病毒、呼吸道合胞病毒和人类偏
肺病毒。检测流感病毒时，PCR优于快速抗原检测。(参见 “成人季节性流感的临床表现和诊
断”)
对于这些患者，做出微生物学诊断则可进行针对性治疗，这有助于限制抗生素滥用、防止抗生素
耐药以及减少不必要的并发症，如艰难梭菌(Clostridioides difficile)感染。
● 重症CAP(包括收入ICU)患者−对于大多数重症CAP住院患者，包括收入ICU的患者，我们行血培
养、痰培养、尿链球菌抗原检测和军团菌检测。此外，如果可行，我们会用支气管镜采样进行微
生物学检测，但要根据个体情况权衡获得微生物学诊断的益处与该操作的风险(例如，需要插管、
出血、支气管痉挛、气胸)。在进行支气管镜检查时，我们通常取样进行需氧菌培养、军团菌培
养、真菌染色和培养，以及呼吸道病毒检测。
不同机构使用的病毒诊断性检测方法不同(例如，PCR、血清学、培养)。有时会使用可检测多种病
毒和细菌病原体的多重PCR。虽然我们通常赞同使用这些方法检查重症肺炎患者，但我们会谨慎地
解读这些检测结果，因为大多数多重分析尚未批准用于下呼吸道标本。应注意，单检出病毒病原
体不能确诊为病毒性肺炎，因为病毒可为细菌性CAP发病的辅助因素，或者存在于患者体内而不引
起症状。
对于所有病例，无论CAP严重程度如何或在何处治疗，我们都会根据流行病学暴露、患者危险因素和临
床特征调整微生物学检测方法( 表 3)。例如：
● 对于已知或可能暴露于流行病原体(如军团菌或流行的冠状病毒)的患者，可扩大评估范围，将这
些病原体纳入检测。(参见 “成人社区获得性肺炎的临床评估和诊断性检测”，关于‘重要病原
体’一节)
● 对于空洞性肺炎患者，我们可能还要检测结核病、真菌病原体和诺卡菌属(Nocardia)。
● 对于免疫功能低下的患者，我们会扩大鉴别诊断以包括机会致病菌[如耶氏肺孢子菌
(Pneumocystis jirovecii)]、真菌病原体、寄生虫，以及不常见的病毒病原体(如巨细胞病毒)。
应根据免疫功能低下的类型和程度以及其他患者特有因素调整诊断性试验方法。(参见 “免疫功
能受损患者发热伴肺部浸润的概述”和 “免疫功能受损患者肺部感染的流行病学”)
在确定微生物学评估范围时，我们还会考虑CAP诊断的确定性。由于初始临床诊断为CAP的住院患者中有
很大一部分最终发现为其他疾病[17]，因此进行全面的微生物学评估有助于获得最终诊断(例如，将血
培养纳入CAP评估可能有助于最终诊断出心内膜炎)。
CAP的微生物学评估详见其他专题。(参见 “成人社区获得性肺炎的临床评估和诊断性检测”和 “痰培

养对评估细菌性肺炎的作用”)
大流行期间COVID-19的诊断也详见其他专题。(参见 “COVID-19的诊断”)
鉴别诊断
new.migangpro.com/contents/zh-Hans/overview-of-community-acquired-pneumonia-in-adults/print?search=肺炎&source=search_result&selectedTitl… 10/72
对于表现为肺浸润和咳嗽的患者、呼吸道感染者和脓毒症患者，CAP是最可能的诊断，鉴别诊断中往往
需予以考虑。(参见 “成人社区获得性肺炎的临床评估和诊断性检测”，关于‘鉴别诊断’一节)
与CAP相似或与CAP共存且表现为肺浸润和咳嗽的非感染性疾病包括：
• 充血性心力衰竭伴肺水肿
• 肺栓塞
• 肺出血
• 肺不张
• 误吸或化学性肺炎
• 药物反应
• 肺癌
• 胶原血管病
• 血管炎
• 支气管扩张急性加重
• 间质性肺疾病，如结节病、石棉肺、过敏性肺炎或隐源性机化性肺炎
对于初始临床诊断为CAP但肺浸润迅速消散的患者，应考虑其他诊断。CAP患者的肺浸润主要由肺泡腔中
白细胞累积引起，通常需要数周才消散。在1-2日内消散的肺浸润可能由肺泡内积液(即肺水肿)或肺泡
塌陷(即肺不张)引起，而不是由于白细胞累积。
与CAP相似或与CAP共存的呼吸系统疾病包括：
• COPD急性加重
• 流感和其他呼吸道病毒感染
• 急性支气管炎( 图 4)
• 哮喘发作
发热性疾病和/或脓毒症也可能是CAP患者的起病综合征；这些综合征的其他常见病因包括泌尿道感染、
腹腔感染和心内膜炎。
治疗
大多数已排除COVID-19的CAP患者在诊断时尚未确定病因，可针对最可能的病原体进行经验性抗生素治
疗。最可能引起CAP的病原体因疾病严重程度、当地流行病学和感染耐药微生物的患者危险因素不同而
有所差异。
例如，对于大多数在门诊治疗且其他方面健康的轻症CAP患者，可能的病原体范围有限。而对于病情严
重到需要住院治疗的CAP患者，可能的病原体更为多样，初始治疗方案通常覆盖范围较广。
COVID-19的处理详见其他专题。(参见 “COVID-19：住院成人患者的处理”和 “COVID-19的疗养院管

理”和 “COVID-19：成人急性患者的门诊管理”)
门诊抗生素治疗 — 所有CAP患者的经验性治疗方案都要覆盖肺炎链球菌(最常见、毒力最强的致CAP
细菌)和非典型病原体。若门诊治疗患者有共存疾病、吸烟或者近期用过抗生素，则要扩大覆盖范围以
包含或更好地治疗产β-内酰胺酶流感嗜血杆菌、卡他莫拉菌和甲氧西林敏感性金黄色葡萄球菌。若患
者有结构性肺病，我们会进一步扩大覆盖范围以包含肠杆菌科细菌，例如大肠埃希菌和克雷伯菌属
( 流程图 2)。
初始方案的选择取决于下列因素：现有药物的不良反应、潜在药物相互作用、患者过敏情况及其他患者
特有因素。
● 对于大多数65岁以下、平素体健且近期没有用过抗生素的患者，我们通常使用口服阿莫西林(一次
1g、一日3次)，加上大环内酯类抗生素(如阿奇霉素或克拉霉素)或多西环素。相比多西环素，我
们一般首选大环内酯类。
ATS/IDSA的推荐则不同：对于这类患者，一线治疗采用阿莫西林单药治疗，而将多西环素或大环
内酯类(当地耐药率＜25%的情况下，例如美国以外某些地区)单药治疗作为备选方案[26]。使用每
种方案的理由详见其他专题。(参见 “成人社区获得性肺炎的门诊治疗”，关于‘经验性抗生素
治疗’一节)
● 对于以下患者，我们建议口服阿莫西林克拉维酸(875mg、一日2次，或缓释剂型2g、一日2次)，加
上大环内酯类(首选)或多西环素：有重大共存疾病(如慢性心、肺、肾或肝脏疾病，糖尿病，酒精
依赖，免疫抑制)、吸烟和/或过去3个月内用过抗生素。
上述基于阿莫西林方案的替代方案包括头孢菌素与大环内酯类或多西环素的联合治疗，或者来法莫林
(lefamulin)单药治疗。
● 若患者可使用头孢菌素类，我们采用第三代头孢菌素(如头孢泊肟)加大环内酯类或多西环素。
● 若患者不能使用β-内酰胺类药物，我们选择针对呼吸系统感染的氟喹诺酮类(如左氧氟沙星、莫
西沙星或吉米沙星)或来法莫林。对于有结构性肺病的患者，我们首选针对呼吸系统感染的氟喹诺
酮类，因为可覆盖肠杆菌科细菌。
对于其他大多数患者，没有肝功能损害或药物相互作用的情况下，来法莫林或许可替代氟喹诺酮
类。但是，临床上使用该药的经验有限。以下情况应避免使用来法莫林：患者有中至重度肝功能
障碍；存在长QT综合征或者在使用延长QT间期的药物；妊娠期和哺乳期女性；没有使用避孕措施
的有生育潜能女性。来法莫林与CYP3A4和P-gp诱导剂及底物可发生药物相互作用；此外，来法莫
林片剂禁止与可延长QT间期的CYP3A4底物一起使用。具体参见UpToDate的Lexicomp药物相互作用
工具。
奥玛环素(omadacycline)是另一种对大多数CAP病原体(包括肠杆菌科)有活性的新药。对于不能耐
受β-内酰胺类(或其他药物)且想要避免使用氟喹诺酮类的患者，也许可改用奥玛环素。(参见
“需住院的成人社区获得性肺炎的治疗”，关于‘新型抗生素’一节)
若存在抗生素过敏、药物相互作用、特定暴露情况和其他患者特有因素，可能需要调整这些治疗方案。
尤其是在流感季节，有流感结局不良高风险的患者可能需要抗病毒治疗( 表 6)。
我们对大多数患者治疗5日。然而，我们通常会确保所有患者在停用抗生素前症状在改善，并至少保持
48小时无发热。一般而言，延长疗程至超过7日不会增加获益。支持上述方法的研究详见其他专题。(参
见 “成人社区获得性肺炎的门诊治疗”，关于‘疗程’一节)
门诊环境下治疗CAP的详细讨论，包括抗生素疗效数据，详见其他专题。(参见 “成人社区获得性肺炎
的门诊治疗”)
住院抗生素治疗
普通内科病房 — 对于收入内科病房的CAP患者，经验性抗生素治疗方案不仅要覆盖典型病原体(如
肺炎链球菌、流感嗜血杆菌和卡他莫拉菌)和非典型病原体[如嗜肺军团菌(Legionella
pneumophilia)、肺炎支原体和肺炎衣原体]，还要覆盖金黄色葡萄球菌和革兰阴性肠杆菌[如肺炎克雷
伯杆菌(Klebsiella pneumoniae)]。
我们通常在确定CAP是最可能的诊断后立即开始抗生素治疗，最好在就诊后4小时内开始。就诊4小时后
才开始恰当的抗生素治疗与死亡率增加有关[36]。
为住院CAP患者选择初始治疗方案的关键因素是感染假单胞菌属和/或MRSA的风险：感染MRSA或假单胞菌
属的最强危险因素是已知定植或曾感染这些病原体，尤其是如果这些情况是从呼吸道标本发现。近期住
院(即过去3个月内)接受了抗生素静脉给药也是危险因素，尤其是感染假单胞菌属的危险因素。怀疑这
些病原体感染还应考虑当地流行情况、其他患者特有危险因素以及总体临床评估结果( 流程图 3和
表 4)：
● 若不考虑MRSA或假单胞菌属感染，我们一般采用以下两种方案之一：β-内酰胺类与大环内酯类
联用，或者针对呼吸系统感染的氟喹诺酮类单药治疗[26]。由于这两种方案具有相似的临床疗
效，我们通常根据其他因素(例如，抗生素过敏、药物相互作用)进行选择。对于大环内酯类和氟
喹诺酮类均不能使用的患者，我们使用β-内酰胺类加多西环素。
● 若患者已知定植或曾感染假单胞菌属、近期住院接受了抗生素静脉给药或存在其他强烈提示
假单胞菌属感染的因素，我们通常使用联合治疗，即抗假单胞菌β-内酰胺类(如哌拉西林/他唑
巴坦、头孢吡肟、头孢他啶、美罗培南或亚胺培南)加上抗假单胞菌氟喹诺酮类(如环丙沙星或左
氧氟沙星)。选择经验性治疗方案时还应考虑既往分离株的药敏模式。
● 若患者已知定植或曾感染MRSA或者有其他强烈提示MRSA感染的因素，除了上述方案，我们还
加用具有抗MRSA活性的药物，如万古霉素或利奈唑胺。怀疑社区获得性MRSA感染时(例如参加身体
接触性运动、表现为坏死性肺炎的平素体健年轻患者)，我们通常首选利奈唑胺而不是万古霉素，
因其可抑制细菌产生毒素[37]。头孢洛林可能是治疗MRSA的备选药物，但尚未得到美国FDA批准。
(参见 “需住院的成人社区获得性肺炎的治疗”，关于‘社区获得性MRSA’一节)
可能需要根据以下情况调整初始经验性治疗方案：抗生素过敏、潜在药物相互作用、当前流行情况、特
定暴露情况、已知的定植微生物或以往感染分离出的微生物的耐药模式，以及其他患者特有因素。尤其
是对任何已知或疑似流感的住院患者，应尽快进行抗病毒治疗(如奥司他韦)。(参见 “非妊娠成人季节
性流感的治疗”)
收入普通内科病房患者的抗生素治疗，包括新药的使用(如来法莫林和奥玛环素)，详见其他专题。(参
见 “需住院的成人社区获得性肺炎的治疗”)
入住ICU
抗生素选择 — 对于收入ICU的CAP患者，我们选择抗生素的方法与收入普通内科病房的患者相
似。然而，由于该人群病情较严重，我们不使用单药疗法( 流程图 4)。此外，我们在危重患者就诊
后1小时内就开始抗生素治疗。
对于存在假单胞菌属感染或MRSA感染危险因素的患者，应扩大经验性治疗方案的抗菌范围( 表 4)。
● 对于大多数不考虑MRSA或假单胞菌属感染的患者，我们使用β-内酰胺类(如头孢曲松、头孢噻
肟、头孢洛林、氨苄西林-舒巴坦或厄他培南)，加上大环内酯类(如阿奇霉素或克拉霉素)或者针
对呼吸系统感染的氟喹诺酮类(如左氧氟沙星或莫西沙星)[26]。
对于青霉素过敏患者，我们根据过敏反应类型和严重程度选择合适的药物(例如，新一代头孢菌
素、卡巴培南或β-内酰胺类替代药物)( 流程图 5)。对于不能使用任何β-内酰胺类药物(即，
青霉素类、头孢菌素类和碳青霉烯类)的患者，我们通常使用针对呼吸系统感染的氟喹诺酮和氨曲
南进行联合治疗。
● 若患者已知定植或曾感染MRSA、近期住院接受了抗生素静脉给药或有其他强烈提示MRSA感
染的因素，除了上述方案，我们还加用具有抗MRSA活性的药物，如万古霉素或利奈唑胺[26]。
● 若患者已知定植或曾感染假单胞菌属、近期住院接受了抗生素静脉给药或有其他强烈提示假
单胞菌属感染的因素，经验性治疗我们通常采用联合治疗，即抗假单胞菌的β-内酰胺类(如哌
拉西林/他唑巴坦、头孢吡肟、头孢他啶、美罗培南或亚胺培南)加抗假单胞菌的氟喹诺酮类(如环
丙沙星或左氧氟沙星)[26]。
对于青霉素过敏患者，我们根据青霉素过敏反应的类型和严重程度( 流程图 5)及先前的假单胞

菌药敏试验结果选择合适药物。
可能需要根据以下情况调整初始经验性治疗方案：抗生素过敏、潜在药物相互作用、当前流行情况、特
定暴露情况、定植细菌或以往感染分离出的细菌的耐药模式，以及其他患者特有因素。尤其是对任何已
知或疑似流感的住院患者，应尽快进行抗病毒治疗(如奥司他韦)。(参见 “非妊娠成人季节性流感的治
疗”)
入住ICU的CAP患者以及出现脓毒症和/或呼吸衰竭患者的抗生素治疗详见其他专题。(参见 “需住院的
成人社区获得性肺炎的治疗”，关于‘ICU’一节和 “成人疑似脓毒症及脓毒性休克的评估和治疗”)
糖皮质激素辅助治疗 — 糖皮质激素用于CAP辅助治疗尚有争议，我们与ATS/IDSA一样，不推
荐对大多数CAP患者常规采用此法[26,38,39]。糖皮质激素治疗CAP患者的基本原理是缓解全身炎症反应
失调，这种失调会促进并发症和死亡的发生。然而，尚不清楚该治疗对哪些人群最有益，而且不良反应
可能很严重。
● 如果CAP患者有宿主炎症反应过度或失调的证据，即存在液体复苏和血管加压药无效的脓毒性休
克，或者出现需要吸入氧分数＞50%的呼吸衰竭并存在以下1项或多项：动脉血pH＜7.3的代谢性酸
中毒、乳酸＞4mmol/L或CRP＞150mg/L，我们建议给予糖皮质激素辅助治疗。
● 我们进行糖皮质激素辅助治疗的疗程为5日。如果患者不能口服药物，我们会静脉给予甲泼尼龙，
一次0.5mg/kg、每12小时1次。对于可以口服药物的患者，我们给予泼尼松，口服，50mg/d。对于
流感患者或有曲霉菌病风险的患者，我们不使用辅助性糖皮质激素。
糖皮质激素在重症CAP中的应用详见其他专题。对于非危重病患者，使用糖皮质激素治疗CAP的作用有
限。(参见 “需住院的成人社区获得性肺炎的治疗”，关于‘糖皮质激素辅助治疗’一节)
COVID-19患者中糖皮质激素的应用也见其他专题。(参见 “COVID-19：住院成人患者的处理”，关
于‘地塞米松和其他糖皮质激素’一节)
患者处置 — 一旦CAP患者住院，进一步处理取决于对初始经验性治疗的反应。每日查房时应评估
临床反应。虽然已有研究提出了评估临床反应的各种标准[40-42]，但我们通常评估咳嗽、咳痰、呼吸
困难和胸痛的主观改善。评估的客观指标包括退热情况，以及心率、呼吸频率、氧合和白细胞计数是否
恢复正常。一般来说，患者会在48-72小时内出现一些临床改善( 表 7)。
抗生素降阶治疗 — 对于已确定致病病原体的患者，我们针对病原体进行治疗[43]。如果经
验性加用覆盖MRSA的治疗，但未将MRSA确定为病原体也未在鼻拭子筛查中发现MRSA，且患者病情不断改
善，我们通常会停用抗MRSA药物(如万古霉素)。然而，大多数CAP住院患者无法识别致病病原体。对于
这些患者，如果病情在改善，我们会在整个治疗期间继续采用经验性治疗。随着患者病情好转，静脉抗
生素治疗方案可以换为具有类似抗菌谱的口服药物方案( 流程图 6)[44,45]。
疗程 — 我们通常根据患者对治疗的临床反应来确定治疗持续时间。
对于所有患者，我们都会治疗到退热至少48小时并且临床情况稳定至少5日。轻度感染的患者通常需要
治疗5-7日。严重感染或存在慢性共存疾病的患者通常需要治疗7-10日。若患者免疫功能低下、感染由
特定病原体引起[如铜绿假单胞菌(P. aeruginosa)]或有并发症，则可能需要延长疗程。(参见 “需住
院的成人社区获得性肺炎的治疗”，关于‘治疗时长’一节)
与ATS/IDSA的意见一致，我们不采用前降钙素帮助确定是否开始使用抗生素[26]。不过，我们有时使用
前降钙素阈值辅助临床判断，以帮助指导临床稳定患者的抗生素停用。我们通常在诊断时检测该指标，
并且在临床稳定后每1-2日重复检测。我们根据临床改善情况和连续的前降钙素检测结果来确定是否有
必要继续抗生素治疗( 流程图 7)。(参见 “前降钙素在下呼吸道感染中的应用”)
出院 — 当患者临床情况稳定，可以口服药物，当前没有其他医学问题，并有安全的继续治疗
环境时，可出院。转为口服治疗后，患者无需继续住院观察一夜。鼓励根据临床稳定情况和转为口服治
疗的标准让患者提早出院，以减少长期住院相关风险和不必要的费用。
免疫功能低下的患者 — 免疫功能低下患者的潜在病原体范围明显扩大，包括侵袭性真菌感染、较
少见的病毒感染(如巨细胞病毒)和寄生虫感染(如弓形虫病)[46]。
具体感染的发生风险取决于免疫抑制的类型和程度，以及患者是否在使用预防性抗生素。例如，长期中
性粒细胞减少、T细胞免疫抑制和使用TNF-α抑制剂会使患者易发生侵袭性真菌感染(例如，曲霉菌病、
毛霉菌病)和分枝杆菌感染。若患者存在晚期HIV感染(如CD4细胞计数<200/μL)、长期使用糖皮质激素
(尤其是与某些化疗药物合用)或存在淋巴细胞减少，都应考虑到肺孢子菌肺炎。该人群可能同时发生多
重感染，发生播散性感染的可能性也增大。由于免疫功能低下患者的感染症状和体征可能不明显且无特
异性，诊断存在困难，常需要实施侵入性操作才能做出微生物学诊断。获得具体微生物学诊断之前可能
需要进行广谱经验性治疗。
由于治疗复杂、药物相互作用常见、可能需要调整免疫抑制治疗方案，并且可选经验性治疗(如两性霉
素B)可能伴有显著毒性，我们通常由多学科专家团队治疗免疫功能低下的肺炎患者。(参见 “免疫功能
受损患者肺部感染的流行病学”和 “免疫功能受损患者发热伴肺部浸润的概述”和 “肿瘤坏死因子-
α抑制剂：细菌、病毒和真菌感染”)
影像学随访
治疗后临床缓解的患者大多不需要复查胸片，因为影像学缓解比临床缓解滞后。但门诊随访是基于年
龄、吸烟史和近期影像学检查结果评估患者肺癌风险的良好机会( 流程图 8)。
这与ATS/IDSA提出的方法相似，其推荐不对症状在5-7日内消退的患者复查胸片[26]。(参见 “需住院
的成人社区获得性肺炎的治疗”，关于‘随访胸片’一节)
并发症和预后
虽然大多数CAP患者经适当抗生素治疗可恢复，但有些患者即使给予适当治疗也会进展和/或出现并发症
(即临床治疗失败)，而有些患者症状无改变(即非消散性肺炎)。
临床治疗失败 — 临床治疗失败的明确指标包括尽管有适当的抗生素治疗和呼吸支持，仍发展为脓
毒症和/或呼吸衰竭。其他指标包括主观症状(例如，咳嗽、呼吸困难)加重，通常结合客观标准(例如，
氧合下降、持续发热或白细胞升高)。有研究提出多种定义临床治疗失败的标准，但均没有得到广泛采
用[47-49]。
临床治疗失败的原因一般分为以下类别：
● 初始感染进展–一些患者尽管进行了适当的抗生素治疗，CAP仍可能导致凶险性感染。在某些患
者中这表明宿主免疫应答失调。在其他病例中，这可能表明感染已经扩散到肺实质以外(例如，脓
胸、肺脓肿、菌血症、心内膜炎)。
其他的可能原因包括耐药病原体感染，或初始经验性抗生素治疗方案未覆盖的罕见病原体感染。
此外，治疗失败可能意味着存在免疫缺陷(例如，新诊断HIV感染)。
● 发生并发症–并发症可能是感染性的或非感染性的。医院感染，尤其是HAP，是临床治疗失败的
常见原因。除HAP外，并发症还包括导管相关血行感染、泌尿道感染和艰难梭菌感染[50]。
心血管事件也是常见的并发症，包括急性心肌梗死、心律失常、充血性心力衰竭、肺栓塞和脑卒
中[51-53]。年龄较大、已有心血管疾病、重症肺炎以及感染某些病原体(即肺炎链球菌和流感病
毒)均与发生心血管事件的风险增加相关[51,54-56]。认识到在CAP急性期可能发生心血管事件和
其他系统性并发症，这也转变了我们对CAP的看法：过去认为它是急性肺疾病，现在认为是急性系
统性疾病。(参见 “成人社区获得性肺炎相关并发症及死亡”，关于‘心脏并发症’一节)
由于存在这些可能性，对经过适当经验性治疗病情仍在进展的患者，我们通常扩大初始抗生素治疗方
案，并评估是否为其他诊断、少见或耐药病原体感染，以及/或感染性心血管并发症。(参见上文‘鉴别
诊断’和 “成人社区获得性肺炎相关并发症及死亡”)
非消散性CAP — 对于某些患者，经过至少7日的适当经验性抗生素治疗后，初始症状既不会进展也
不会改善。我们一般认为这些患者存在非消散性肺炎。非消散性CAP的可能原因包括：
● 临床缓解延迟–对于某些患者，尤其是有多种共存疾病、重症肺炎、菌血症或者感染某些病原体
(如肺炎链球菌)的患者，治疗可能起效较慢。可能需要治疗8-9日才会出现临床改善。
● 包裹性感染–尽管选择了适当的抗生素，存在并发症(例如，肺脓肿、脓胸或其他封闭间隙感染)
的患者仍有可能无法获得临床改善。这些感染可能需要引流和/或长期抗生素治疗。(参见 “成人
肺脓肿”和 “成人肺炎旁胸腔积液和脓胸的流行病学、临床表现和诊断性评估”)
● 支气管阻塞–支气管阻塞(如被肿瘤阻塞)可导致阻塞性肺炎，可能对CAP的标准经验性抗生素治
疗无反应或反应缓慢。
● 引起亚急性/慢性CAP的病原体–以下病原体可引起亚急性或慢性肺炎，并且采用CAP的标准经验
性抗生素方案可能无效或效果不足：结核分枝杆菌(Mycobacterium tuberculosis)，非结核分枝
杆菌如堪萨斯分枝杆菌(Mycobacterium kansasii)，真菌如荚膜组织胞浆菌(Histoplasma
capsulatum)和皮炎芽生菌(Blastomyces dermatitidis)，或者不常见细菌如诺卡菌属和衣氏放线
菌(Actinomyces israelii)。
● 不正确的初始诊断–治疗7日仍无改善，也提示可能为其他诊断(例如，恶性肿瘤或炎症性肺
病)。(参见上文‘鉴别诊断’)
一旦发现患者存在非消散性CAP的特征，就需要重新进行全面体格检查、实验室评估、影像学检查和微
生物学诊断性检查，以确定非消散性CAP的病因[50]。对非消散性CAP进行诊断性检查并不一定会改变初
始经验性抗生素治疗。(参见 “非消散性肺炎”)
长期并发症和死亡率 — 尽管大多数CAP患者康复且无并发症，但CAP是一种严重的疾病，在全世界
都是死亡的主要原因之一。死亡可直接由CAP导致(例如，极重度脓毒症或呼吸衰竭)，也可间接由心血
管事件或其他共存疾病(如COPD)引起[57]。
人们对肺炎所致长期并发症的认识逐渐增加，医学界偏向将肺炎界定为可导致慢性疾病的全身性疾病
[58]。虽然长期并发症的确切发生率不明，但较常见的长期后遗症涉及呼吸道和心血管系统[59]。
在美国，肺炎加流感是十大最常见的死亡原因之一[5]。30日死亡率因疾病严重程度不同而有所差异，
在门诊患者中＜1%，在重症CAP患者中为20%-25%。除疾病严重程度外，高龄、共存疾病(例如，COPD、
糖尿病、心血管疾病)、感染某些病原体(如肺炎链球菌)和急性心脏并发症均与短期死亡率增加有关
[51,60,61]。
CAP还与远期死亡率增加相关[7,62-64]。一项人群研究对7449例因CAP住院的患者进行了评估，发现住
院期间死亡率为6.5%，入院起30日为13%，入院起6个月为23%，入院起1年为31%[7]。在该研究的同一
年，估计美国有1,581,860名患者住院。将死亡率数据外推至这些患者，则住院期间的死亡人数为
102,821人，30日时为205,642人，6个月时为370,156人，1年时为484,050人[7]。远期死亡主要与共存
疾病相关，包括恶性肿瘤、COPD和心血管疾病[57]。
CAP远期死亡率相关数据表明，CAP不仅是急性发病和死亡的常见原因，而且有重要长期健康结局。
预防
预防CAP的3个主要措施是[65-67]：
● 戒烟
● 为所有患者接种流感疫苗
● 为有风险患者接种肺炎球菌疫苗
各项措施详见其他专题。(参见 “成人戒烟管理概述”和 “成人季节性流感疫苗接种”和 “成人肺炎

球菌疫苗接种”)
学会指南链接
部分国家及地区的学会指南和政府指南的链接参见其他专题。(参见 “学会指南链接：成人社区获得性
肺炎”)
患者教育
UpToDate提供两种类型的患者教育资料：“基础篇”和“高级篇”。基础篇通俗易懂，相当于5-6年级
阅读水平(美国)，可以解答关于某种疾病患者可能想了解的4-5个关键问题；基础篇更适合想了解疾病
概况且喜欢阅读简短易读资料的患者。高级篇篇幅较长，内容更深入详尽；相当于10-12年级阅读水平
(美国)，适合想深入了解并且能接受一些医学术语的患者。
以下是与此专题相关的患者教育资料。我们建议您以打印或电子邮件的方式给予患者。(您也可以通过
检索“患者教育”和关键词找到更多相关专题内容。)
● 基础篇(参见 “患者教育：成人肺炎(基础篇)”)
● 高级篇(参见 “Patient education: Pneumonia in adults (Beyond the Basics)”)
总结与推荐
● 背景−社区获得性肺炎(CAP)是全球发病和死亡的主要原因。(参见上文‘发病率’)
● 危险因素−危险因素包括年龄≥65岁、慢性共存疾病、合并或前驱呼吸道病毒感染、气道保护受
损、吸烟、酗酒和其他生活方式因素(如拥挤的生活条件)。(参见上文‘危险因素’)
● 微生物学−最常见的CAP病原体包括呼吸道病毒(特别是大流行期间的SARS-CoV-2)，典型细菌(如
肺炎链球菌、流感嗜血杆菌、卡他莫拉菌)，以及非典型细菌(如军团菌属、肺炎支原体、肺炎衣
原体)。假单胞菌属和耐甲氧西林金黄色葡萄球菌(MRSA)是不常见病因，主要见于具有特定危险因
素的患者。(参见上文‘微生物学’和‘发病机制’)
● 诊断−诊断要求患者有临床相符的综合征(如发热、呼吸困难、咳嗽和白细胞增多)，同时胸部影
像学检查显示肺部浸润。大多数患者拍摄后前位和侧位胸片即足够。CT仅用于特定患者。(参见上
文‘临床表现’和‘诊断’)
● 替代和并存诊断−尽管相符的临床综合征结合胸部影像学检查发现肺部浸润足以做出CAP的初步
临床诊断，但这些发现不具特异性。随着患者病程发展，仍需继续关注可能的替代或并存诊断，
这对治疗十分重要。(参见上文‘鉴别诊断’)
● 确定疾病严重程度−若最可能的诊断为CAP，初始处理步骤是确定疾病严重程度，并决定最合适
的治疗场所( 流程图 1)。对于大多数患者，我们会根据该评估确定微生物学检测方法
( 表 5)。(参见上文‘微生物学检测’)
● 经验性抗生素选择−经验性抗生素治疗方案的选择取决于病情严重程度、治疗场所和最可能的病
原体。我们通常在确定CAP是最可能的诊断后立即开始抗生素治疗，最好在住院患者就诊4小时
内，在危重患者就诊1小时内开始(参见上文‘治疗’)：
• 对于大多数门诊患者，我们倾向于联用β内酰胺类与大环内酯类(首选)或多西环素。基于β-
内酰胺类的方案可用以下单药治疗替代：氟喹诺酮类、来法莫林或奥玛环素(新药)。根据患者
共存疾病、药物相互作用、是否过敏和其他导致不耐受的情况做出选择。临床上使用来法莫林
和奥玛环素的经验有限，有一些注意事项和禁忌证( 流程图 2)。
美国胸科学会(ATS)/美国感染病学会(IDSA)的推荐则不同：对于这类患者，一线治疗采用阿莫
西林单药治疗，而多西环素或大环内酯类(当地耐药率<25%的情况下，如美国以外某些地区)单
药治疗作为备选方案。
• 对于大多数收入普通内科病房的患者，治疗选择包括β-内酰胺类加大环内酯类或加多西环素
的静脉联合治疗，或针对呼吸系统感染的氟喹诺酮类单药治疗( 流程图 3)。对于存在假单
胞菌属或MRSA感染危险因素的患者，应扩大覆盖范围( 表 4)。
• 对于大多数收入ICU的患者，治疗选择包括静脉用β-内酰胺类加大环内酯类，或β-内酰胺类
加针对呼吸系统感染的氟喹诺酮类( 流程图 4)。与其他住院患者一样，对于存在假单胞菌
属或MRSA感染危险因素的患者，应扩大治疗方案( 表 4)。
● 针对性治疗−对于已确定致病病原体的患者，我们针对病原体进行治疗。(参见上文‘抗生素降
阶治疗’)
● 抗生素疗程−对于所有患者，我们治疗至退热至少48小时且临床情况稳定至少5日。轻度感染患
者通常需要治疗5-7日；严重感染或有慢性共存疾病的患者通常需要治疗7-10日。(参见上文‘疗
程’)
● 抗生素治疗无效−如果在抗生素治疗72小时内病情无改善，应重新考虑诊断和经验性治疗方案，
并评估并发症。(参见上文‘临床治疗失败’和‘非消散性CAP’)
● 预防−关键预防措施包括戒烟(若恰当)、一般人群接种流感疫苗和风险人群接种肺炎球菌疫苗。
(参见上文‘预防’)
致谢
我们沉痛悼念于2021年1月去世的John G Bartlett, MD。UpToDate衷心感谢Dr. John G Bartlett担任

UpToDate感染病学创始主编和长期参与UpToDate项目所做的贡献。
使用UpToDate临床顾问须遵循使用条款.
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专题 117561 版本 28.0.zh-Hans.1.0
图表
Pneumonia terminology
Term Definition
Classification by site of acquisition
Community-acquired An acute infection of the pulmonary parenchyma acquired outside of

pneumonia (CAP) health care settings
Nosocomial pneumonia An acute infection of the pulmonary parenchyma acquired in hospital

settings, which encompasses hospital-acquired pneumonia and
ventilator-associated pneumonia
Hospital-acquired Pneumonia acquired ≥48 hours after hospital admission; includes

pneumonia (HAP) both HAP and VAP
Ventilator-associated Pneumonia acquired ≥48 hours after endotracheal intubation

pneumonia (VAP)
Health care-associated Retired term, which referred to pneumonia acquired in health care
pneumonia (HCAP) facilities (eg, nursing homes, hemodialysis centers) or after recent
hospitalization*
Classification by etiology
Atypical pneumonia Pneumonia caused by "atypical" ¶ bacterial pathogens including

Legionella spp, Mycoplasma pneumoniae, Chlamydia pneumoniae,
Chlamydia psittaci, and Coxiella burnetii
Aspiration pneumonia Pneumonia resulting from entry of gastric or oropharyngeal fluid,

which may contain bacteria and/or be of low pH, or exogenous
substances (eg, ingested food particles or liquids, mineral oil, salt or
fresh water) into the lower airways
Chemical pneumonitis Aspiration of substances (eg, acidic gastric fluid) that cause an
inflammatory reaction in the lower airways, independent of bacterial
infection
Bacterial aspiration An active infection caused by inoculation of large amounts of bacteria

pneumonia into the lungs via orogastric contents
* The term HCAP was used to identify patients at risk for infection with multidrug-resistant
pathogens. This categorization may have been overly sensitive, leading to increased, inappropriately
broad antibiotic use.
¶ The origin of the term "atypical" is a matter of debate. The term may refer to the fact that these
organisms are not "typical" bacteria, which cannot be identified by standard microbiologic
techniques. Others suggest that atypical refers to the mild nature of the pneumonia caused by some
of these organisms compared with pneumonia caused by Streptococcus pneumoniae.
Graphic 130821 Version 3.0
The impact of age on the incidence of patients hospitalized with community-ac

pneumonia in the United States
Reproduced from: Ramirez JA, Wiemken TL, Peyrani P, et al. Adults hospitalized with pneumonia in the United States: Incidence,
epidemiology, and mortality. Clin Infect Dis 2017; 65(11):1806-1812. By permission of Oxford University Press on behalf of the Infectio
Diseases Society of America. Copyright © 2017.
The impact of comorbid conditions on the incidence of patients hospitalized wi

community-acquired pneumonia in the United States
CHF: congestive heart failure; COPD: chronic obstructive pulmonary disease.
Reproduced from: Ramirez JA, Wiemken TL, Peyrani P, et al. Adults hospitalized with pneumonia in the United States: Incidence,
epidemiology, and mortality. Clin Infect Dis 2017; 65(11):1806-1812. By permission of Oxford University Press on behalf of the Infectio
Diseases Society of America. Copyright © 2017.
Microbial etiology of community-acquired pneumonia by site of care*
Outpatients Ward patients Inte

United
Spain [1 ] Canada [2] Spain [1] S
States [3]
Total patients 514 507 2521 585 488

evaluated
Patients in whom 161 (31.3) 244 (48.1) 1042 (41) 120 (21) 260 (53
a pathogen was
identified
Patients in whom 353 (68.7) 263 (51.9) 1479 (59) 465 (79) 228 (47
no pathogen was
identified
Pathogen ¶
Streptococcus 56 (10.9) 30 (5.9) 447 (17.7) 38 (6.5) 110 (22

pneumoniae
Other 0 5 (1.0) 0 0 0
Streptococcus
spp
Haemophilus 8 (1.6) 25 (4.9) 54 (2.1) 16 (2.7) 8 (1.6)

influenzae
Haemophilus 0 10 (2.0) 0 0 0
parainfluenzae
Moraxella 0 6 (1.2) 4 (0.2) 0 1 (0.2)

catarrhalis
Legionella 10 (1.9) Δ 87 (3.5) ◊ 21 (4.3

pneumophila
Mycoplasma 27 (5.3) § 87 (17.2) § 32 (1.3) § ¥ 6 (1.2) §

pneumoniae
Chlamydia 10 (1.9) § 72 (14.2) § 32 (1.3) § ¥ 8 (1.6) §

pneumoniae
Coxiella 11 (2.1) § Δ 17 (0.7) § ¥ 2 (0.4) §

burnetii
Staphylococcus 1 (0.2) 6 (1.2) 18 (0.7) 25 (4.3) 6 (1.2)

aureus
MSSA 1 (0.2) NR 9 (0.4) 18 (3.1) 4 (0.8)
MRSA 0 NR 9 (0.4) 7 (1.2) 2 (0.4)
Gram- 1 (0.2) 2 (0.4) 23 (0.9) 15 (2.6) 3 (0.6)

negative
enteric bacilli
Pseudomonas 1 (0.2) 1 (0.2) 37 (1.5) 12 (2.1) 12 (2.5

aeruginosa
Respiratory 15 (2.9) § † 123 (4.9) § † 10 (2.0

viruses ‡
Other 6 (1.2) 14 (2.8) 33 (1.3) 8 (1.4) 15 (3.1

pathogen
>1 pathogen 15 (2.9) ** 135 (5.4) 6 (1.0) 58 (11.
Diagnostic methods
Cultures (sputum, Cultures Cultures (sputum, Cultures Culture

blood, transthoracic (sputum, blood, transthoracic (blood, blood,
needle aspirate, blood), needle aspirate, endotracheal needle
transbronchial serologic transbronchial aspirates, transb
aspirates, BAL fluid, testing (for aspirates, BAL fluid, protected aspirat
protected specimen M. protected specimen specimen protect
brush respiratory pneumoniae, brush respiratory brush brush r
samples, pleural C. samples, pleural respiratory sample
fluid), serologic pneumoniae) fluid), serologic samples, fluid), s
testing (for M. testing (for M. BAL fluid, testing
pneumoniae, C. pneumoniae, C. pleural fluid), pneum
pneumoniae, L. pneumoniae, L. urinary pneum
pneumophila, C. pneumophila, C. antigen (for pneum
burnetti, influenza A burnetti, influenza A L. burnett
and B, parainfluenza and B, parainfluenza pneumophila) and B,
viruses 1 to 3, viruses 1 to 3, viruses
respiratory syncytial respiratory syncytial respira
virus, adenovirus), virus, adenovirus), virus, a
urinary antigen urinary antigen urinary
testing (for S. testing (for S. testing
pneumoniae and L. pneumoniae and L. pneum
pneumophila), pneumophila), pneum
immunofluorescence immunofluorescence immun
assay plus virus assay plus virus assay p
isolation or reverse isolation or reverse isolatio
transcriptase PCR for transcriptase PCR for transcr
influenza A and B, influenza A and B, influen
parainfluenza parainfluenza parainf
viruses 1 to 3, viruses 1 to 3, viruses
respiratory syncytial respiratory syncytial respira
virus, adenovirus virus, adenovirus virus, a
MSSA: methicillin-susceptible Staphylococcus aureus; MRSA: methicillin-resistant Staphylococcus

aureus; NR: not reported; BAL: bronchoalveolar lavage; PCR: polymerase chain reaction.
* Results are reported as number of patients (percent). Different methods were used for diagnosis in
each study, as described in the row on diagnostic methods.
¶ Results are reported as the number of patients with a given pathogen, followed by the percentage
of patients in whom the pathogen was identified out of all of the patients in the study. For example,
in the first column, S. pneumoniae was detected in 30 of 507 patients in the study (5.9%). Among the
244 patients in whom a pathogen was identified, S. pneumoniae was detected in 12.3%.
Δ Testing for Legionella spp and C. burnetti was not performed.
◊ Legionella urinary antigen testing was performed in 35 ward patients and 26 intensive care unit
patients, but all results were negative. Legionella culture was not performed.
§ Pathogens detected by serologic methods may represent recent infection rather than active
infection.
¥ Testing for M. pneumoniae, C. pneumoniae, and C. burnetii was not performed.
‡ Influenza viruses A or B, parainfluenza viruses 1 to 3, respiratory syncytial virus, adenovirus.
† Testing for viruses was not performed.
** Some patients had >1 pathogen isolated, but the details were not reported.
References:
1. Cillóniz C, Ewig S, Polverino E, et al. Microbial aetiology of community-acquired pneumonia and its relation to
severity. Thorax 2011; 66:340.
2. Marrie TJ, Poulin-Costello M, Beecroft MD, Herman-Bnjidic Z. Etiology of community-acquired pneumonia treated in
an ambulatory setting. Resp Medicine 2005; 99:60.
3. Restrepo MI, Mortensen EM, Velez JA, et al. A comparative study of community-acquired pneumonia patients admitted
to the ward and the ICU. Chest 2008; 133:610.
Community-acquired pneumonia: Risk factors for specific pathogens in

adults
Condition Commonly encountered pathogen(s)
Alcohol use disorder Streptococcus pneumoniae, oral anaerobes, Klebsiella pneumoniae,

Acinetobacter species, Mycobacterium tuberculosis
COPD and/or smoking Haemophilus influenzae, Pseudomonas aeruginosa, Legionella species, S.

pneumoniae, Moraxella catarrhalis, Chlamydia pneumoniae
Aspiration Gram-negative enteric pathogens, oral anaerobes
Lung abscess CA-MRSA, oral anaerobes, endemic fungal pneumonia, M. tuberculosis,

atypical mycobacteria
Exposure to bat or bird Histoplasma capsulatum

droppings
Exposure to birds Chlamydia psittaci (if poultry: avian influenza)
Exposure to rabbits Francisella tularensis
Exposure to farm animals or Coxiella burnetti (Q fever)

parturient cats
HIV infection (early) S. pneumoniae, H. influenzae, M. tuberculosis
HIV infection (late) The pathogens listed for early infection plus Pneumocystis jirovecii,
Cryptococcus, Histoplasma, Aspergillus, atypical mycobacteria (especially
Mycobacterium kansasii), P. aeruginosa, H. influenzae
Hotel or cruise ship stay in Legionella species

previous two weeks
Travel to or residence in Coccidioides species, hantavirus

southwestern United States
Travel to or residence in Burkholderia pseudomallei, avian (H5N1, H7N9) influenza, SARS

Southeast and East Asia coronavirus
Travel to or residence in the Middle East respiratory syndrome coronavirus

Arabian peninsula
Influenza active in Influenza, S. pneumoniae, Staphylococcus aureus, H. influenzae

community
Cough >2 weeks with whoop Bordetella pertussis

or posttussive vomiting
Structural lung disease (eg, P. aeruginosa, Burkholderia cepacia, S. aureus

bronchiectasis)
Injection drug use S. aureus, anaerobes, M. tuberculosis, S. pneumoniae
Endobronchial obstruction Anaerobes, S. pneumoniae, H. influenzae, S. aureus
In context of bioterrorism Bacillus anthracis (anthrax), Yersinia pestis (plague), Francisella tularensis
(tularemia)
The most commonly identified causes of community-acquired pneumonia include respiratory

viruses (particularly SARS coronavirus 2 during the pandemic), typical bacteria (eg, S. pneumoniae, H.
influenzae, M. catarrhalis), and atypical bacteria (eg, Legionella spp, Mycoplasma pneumoniae, C.
pneumoniae). The relative prevalence of these pathogens varies with geography, pneumococcal
vaccination rates, patient risk factors, season, and pneumonia severity. Certain epidemiologic
exposures, like those listed above, also raise the likelihood of infection with a particular pathogen.
COPD: chronic obstructive pulmonary disease; CA-MRSA: community-acquired methicillin-resistant

Staphylococcus aureus; HIV: human immunodeficiency virus; SARS: severe acute respiratory
syndrome.
Adapted with permission from: Mandell, LA, Wunderink, RG, Anzueto, A, et al. Infectious Diseases Society of
America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults.
Clin Infect Dis 2007; 44:S27. Copyright © 2007 University of Chicago Press.
Community-acquired pneumonia: Risk factors for MRSA and Pseudomonas in

adults
MRSA Pseudomonas
Strong risk Known MRSA colonization Known Pseudomonas colonization

factors*
Prior MRSA infection Prior Pseudomonas infection
Detection of gram-positive cocci in Detection of gram-negative rods on a

clusters on a good-quality sputum good-quality sputum Gram stain
Gram stain
Hospitalization with receipt of IV
antibiotics in the prior 3 months
Other factors Recent hospitalization or antibiotic Recent hospitalization or stay in a

that should raise use, particularly hospitalization with long-term care facility
suspicion for receipt of IV antibiotics in the prior 3
infection ¶ months
Recent influenza-like illness Recent antibiotic use of any kind
Necrotizing or cavitary pneumonia Frequent COPD exacerbations

requiring glucocorticoid and/or
antibiotic use
Empyema Δ Other structural lung diseases (eg,

bronchiectasis, cystic fibrosis)
Immunosuppression Immunosuppression
Risk factors for MRSA colonization,

including:
End-stage kidney disease
Crowded living conditions (eg,
incarceration) Δ
Injection drug use Δ
Contact sports participation Δ
Men who have sex with men Δ
CAP: community-acquired pneumonia; MRSA: methicillin-resistant Staphylococcus aureus; IV:

intravenous; COPD: chronic obstructive pulmonary disease.
* The presence of these risk factors generally warrant empiric treatment in patients with CAP of any
severity.
¶ The presence of these factors should raise suspicion for MRSA or Pseudomonas infection and
generally warrants treatment in those who are severely ill; in others, the need for empiric treatment
should take into account local prevalence, severity of illness, and overall clinical assessment.
Δ This factor is associated with community-acquired MRSA infection, which can cause severe toxin-
mediated infection. Refer to the UpToDate topic on MRSA infections and treatment of CAP in
patients with risk factors for MRSA infection for further detail.
Community-acquired pneumonia (CAP) pathogenesis
Traditionally, CAP is thought to be caused by inhalation or aspiration of a respiratory

pathogen into an otherwise sterile alveoli. The local inflammatory response to the
pathogen results in pulmonary signs and symptoms such as cough, sputum production,
dyspnea, crackles, and hypoxemia. Release of cytokines into the bloodstream leads to the
systemic signs or symptoms of pneumonia, which often include fever, fatigue,
tachycardia, and leukocytosis.
With the discovery of the lung microbiome, the traditional model has evolved. When a
respiratory pathogen arrives in the alveolar space, it likely has to compete with resident
microbes to replicate. Additionally, resident microbes may also modulate the host
immune response to the infecting pathogen. Hypothetically, CAP might also arise from
uncontrolled replication of microbes that normally reside in the alveoli.
Pneumococcal pneumonia: Chest radiograph
64-year-old male with insulin-dependent diabetes mellitus. He was

admitted with bacteremic pneumococcal pneumonia. Note the left
lower lobe opacity.
Courtesy of Thomas J Marrie, MD.
Mycoplasma pneumoniae pneumonia: Chest radiograph
Diffuse bilateral interstitial infiltrates with M. pneumoniae infection.
Courtesy of Dwight A Powell, MD.
Pneumococcal pneumonia: Lateral chest

radiograph
Chest radiograph from a 55-year-old female with bacteremic

pneumococcal pneumonia. Shows a dense left lower lobe opacity
with a bulging fissure.
Courtesy of Thomas J Marrie, MD.
Chest radiograph of Pneumocystis jirovecii pneumonia with ground-glass opacif
Chest radiograph in patients with Pneumocystis jirovecii pneumonia, one that shows perihilar ground-glass
opacification with early consolidation (A) and the other that shows left-sided ground-glass opacification and
sided early consolidation (B).
Mycoplasma pneumonia: Chest imaging
Chest radiograph (A) shows a bilateral reticulonodular pattern. High-resolution

computed tomography (CT) image at the level of the main bronchi (B) demonstrates
bilateral ground-glass opacities and centrilobular nodules (arrows). High-resolution CT
scan at the level of the basal segmental bronchi (C) shows centrilobular nodules
(straight arrows), branching opacities (tree-in-bud pattern; curved arrow), ground-glass
opacities, small foci of consolidation, and mild thickening of the interlobular septa
(arrowheads). The patient was a 20-year-old man with Mycoplasma pneumoniae
pneumonia.
Reproduced with permission from: Viruses, Mycoplasma, and Chlamydia. In: Imaging of Pulmonary
Infections, Müller NL, Franquet T, Lee KS (Eds), Lippincott Williams & Wilkins, Philadelphia 2007. Copyright ©
2007 Lippincott Williams & Wilkins. www.lww.com.
Pneumococcal pneumonia: Complications
Radiographic images of the complications of pneumococcal

pneumonia.
(Left panel) Lung abscess with an air-fluid level in the right lung.
Abscess cavity material is nearly always culture positive, and patients
commonly defervesce within 48 hours of interventional drainage.
(Right panel) Radiograph of necrotizing pneumonia in the left lung.
Community-acquired pneumonia: Determining the appropriate site of treatme
ICU: intensive care unit; ED: emergency department; PSI: Pneumonia Severity Index; PaO2: partial pressure o
oxygen; CURB-65: confusion, uremia, respiratory rate, blood pressure, age ≥ 65 years; CAP: community-acq
* Among the available scoring systems for determining the need for admission in patients with CAP, we pref
and validated. If a less complex scoring system is desired, the CURB-65 score is a reasonable alternative, alt
guiding the initial site of treatment have not been empirically assessed. Refer to the UpToDate topic on asse
appropriate site of care in patients with CAP for additional details and to access PSI and CURB-65 calculators
¶ Scoring systems, such as the PSI and CURB-65, and clinical criteria are intended to supplement rather than
physician. Factors other than the predictors included in the rules and the clinical criteria may be important w
selecting the site of inpatient care. As examples, patients with early signs of sepsis or rapidly progressive illn
scores. Patients with these features may warrant hospitalization and/or ICU admission regardless of score. C
overrepresented in severity scores; this should be taken into account when determining site of care.
Δ Using the CURB-65 score, if the patient has a score of 1 because he or she is ≥65 years of age and he or sh
admission is not necessarily indicated.
◊ Although a definitive etiologic diagnosis is often not established until after the site of treatment decision
epidemiologic evidence favoring pathogens associated with rapidly progressive forms of pneumonia (eg, po
severe acute respiratory syndrome, Middle East respiratory syndrome, avian influenza [eg, H5N1, H7N9], Leg
2019) indicate a need to perform close clinical follow-up to monitor severity of illness particularly for patient
presentation and treated outside of the hospital setting.
§ Some PSI class II and III patients may benefit from in-home health care support, also termed "hospital-at-
fluids, intravenous antibiotics).
Community-acquired pneumonia: Initial evaluation and site of care based

on severity assessment in adults
Microbiologic
Severity score* Site of care
evaluation
Mild PSI: I or II Ambulatory care COVID-19 testing

or during the pandemic
Influenza testing
CURB-65: 0 ¶
(when incidence is
high and results
would change
management) Δ
Otherwise, testing is
usually not needed
Moderate PSI: III or IV General medical ward Blood cultures

or Sputum Gram stain
and culture
CURB-65: 1 ¶ to 2
Urine streptococcal
antigen
Legionella testing ◊
Respiratory viral
panel during
respiratory virus
season §
COVID-19 testing ¥
HIV screening ‡
Severe PSI: IV or V ICU Blood cultures

or Sputum Gram stain
and culture
CURB-65: ≥3
Urine streptococcal
and/or antigen test
Fulfillment of ATS/IDSA Legionella testing ◊
criteria for ICU Respiratory viral
admission † panel §
Bronchoscopy
specimens for Gram
stain, fungal stain,
aerobic, fungal
culture, and
molecular testing
(when feasible)**
COVID-19 testing ¥
HIV screening ‡
CAP presents along a continuum of severity. For practical purposes, we typically categorize CAP as
mild, moderate, or severe. Severity assessment is based on clinical judgement and can be aided by
severity scores, such as the PSI or the CURB-65 score. We generally prefer the PSI as it is better
validated; however, many clinicians prefer the CURB-65 as it is easier to use. The three levels of
severity correspond to the three levels of care (ambulatory care, hospital admission to the general
medical ward, and ICU). The severity assessment and site of care each inform the initial
microbiologic evaluation and empiric antibiotic selection. For all patients, we modify our approach
based on patient-specific factors such as epidemiologic exposures and ability to care for oneself at
home. Refer to the UpToDate topic on the treatment of CAP for further detail.
PSI: Pneumonia Severity Index; COVID-19: coronavirus disease 2019; ATS: American Thoracic Society;
IDSA: Infectious Diseases Society of America; ICU: intensive care unit; CAP: community-acquired
pneumonia; PCR: polymerase chain reaction; PaO2/FiO2: arterial oxygen tension to fraction of
inspired oxygen.
* Severity scores should be used as an adjunct to clinical judgment. Patients with early signs of
sepsis (eg, patients fulfilling minor ATS/IDSA criteria) or rapidly progressive illness are not well
represented in severity scoring systems. Patients with these features may warrant hospitalization
and/or ICU admission regardless of score. Conversely, older age may be overrepresented in severity
scores; this should be taken into account when determining site of care.
¶ Because age >65 years is a criterion in the CURB-65 score, patients with CURB-65 scores of 1 who
are older than 65 years may also be reasonably treated in the ambulatory setting.
Δ Refer to the UpToDate content on the diagnosis of influenza for detail.
◊ PCR on sputum sample is preferred for the diagnosis of Legionella spp because it detects most
clinically relevant Legionella spp. The urine antigen test is an acceptable alternative when PCR is not
available but is specific for Legionella pneumophila serogroup 1.
§ The approach to testing for respiratory viruses varies among institutions. At a minimum, testing
for influenza by PCR should be performed. However, testing is often expanded to include
adenovirus, parainfluenza, respiratory syncytial virus, and human metapneumovirus. The
specific assay used (eg, PCR, serology, culture) may also vary among institutions. Results from
multiplex PCR assays should be interpreted with caution because most multiplex PCR assays have
not been approved for use on lower respiratory tract specimens.
¥ Testing for COVID-19 is recommended for all patients during the pandemic. Refer to the related
UpToDate content on the approach to testing.
‡ Refer to UpToDate content on screening and diagnosis of HIV infection for detail.
† ATS and IDSA major criteria for ICU admission include either septic shock with need for
vasopressor support and/or respiratory failure with need for mechanical ventilation. If major criteria
are not met, patients should also be considered for ICU admission if 3 or more of the following
minor criteria are present: altered mental status, hypotension requiring fluid support, temperature
<36°C/96.8°F, respiratory rate ≥30 breaths/minute, PaO2/FiO2 ratio ≤250, blood urea nitrogen ≥20
mg/dL (7 mmol/L), leukocyte count <4000 cells/microL, platelet count <100,000/mL, or multilobar
infiltrates.
** We generally weigh the benefits of obtaining a microbiologic diagnosis against the risks of the
bronchoscopy (eg, need for intubation, bleeding, bronchospasm, pneumothorax) on a case-by-case
basis. When pursuing bronchoscopy, we usually send specimens for aerobic and anaerobic culture,
Legionella culture, fungal stain and culture, and testing for viral pathogens (influenza, adenovirus,
parainfluenza, respiratory syncytial virus, and human metapneumovirus).
Distinguishing acute bronchitis from pneumonia in adults
Community-acquired pneumonia: Empiric outpatient antibiotic selection in adu
For all patients, our empiric regimens are designed to target: ◊

Streptococcus pneumoniae (most common bacterial CAP pathogen)
Atypical pathogens (eg, Legionella spp, Mycoplasma pneumoniae, Chlamydia pneumoniae)

Coverage is expanded in those with comorbidities, older age, or recent antibiotic use to include or better tre
Beta-lactamase-producing Haemophilus influenzae
Moraxella catarrhalis
Methicillin-susceptible Staphylococcus aureus
For patients with structural lung disease (eg, advanced COPD), coverage is further expanded to include Ente
Escherichia coli and Klebsiella spp.
ATS/IDSA: American Thoracic Society/Infectious Diseases Society of America; COPD: chronic obstructive pulm
community-acquired pneumonia; IgE: immunoglobulin E.
* Major comorbidities include but are not limited to chronic heart, renal, or liver disease, diabetes mellitus, a
immunosuppression.
¶ Patients with mild non-IgE-mediated reactions (eg, maculopapular rash) to penicillin or known cephalospo
later-generation cephalosporins safely. Patients with IgE-mediated reactions (hives, angioedema, anaphylax
should generally use other agents. Refer to the UpToDate text on penicillin hypersensitivity reactions for det
Δ Reasons to avoid macrolides include baseline prolonged QTc interval or risk for QTc prolongation (eg, hypo
clinically significant bradycardia, or use of other QT-prolonging agents).
◊ Our approach differs from the ATS/IDSA, which recommend monotherapy with amoxicillin, doxycycline, o
macrolide resistance is low) as options for patients without comorbidities or risk factors for drug-resistant S
prefer to treat all patients with a regimen that treats most strains of drug-resistant S. pneumoniae and atypic
because the potential to reduce morbidity is high and the downside of a short course of therapy for most pa
UpToDate text for detail.
§ For macrolides, resistance rates among S. pneumoniae are often >30% in the United States and typically >2
apart from some regions in Northern Europe. For doxycycline, resistance rates are less well established but
the United States and likely rising.
¥ Lefamulin is a newer agent that is active against most CAP pathogens including S. pneumoniae, H. influenza
atypical pathogens. Although lefamulin lacks activity against Enterobacteriaceae (eg, Klebsiella spp and E. co
for patients with structural lung disease, its more targeted spectrum makes it less disruptive to the microbio
lefamulin is limited, and it is not recommended in moderate to severe hepatic dysfunction, pregnancy, brea
syndrome, or with concomitant QT-prolonging agents. There are drug interactions with CYP3A4 and P-gp in
addition, lefamulin tablets are contraindicated with QT-prolonging CYP3A4 substrates. Refer to the Lexicom
UpToDate text for detail.
‡ Omadacycline is another newer agent that is active against most CAP pathogens, including Enterobacteria
for patients who cannot tolerate beta-lactams (or other agents) and want to avoid fluoroquinolones.
Groups at higher risk for influenza complications
Children <5 years, but especially <2 years*
Adults ≥65 years of age
People who are pregnant or up to 2 weeks postpartum
Residents of nursing homes and long-term care facilities
Non-Hispanic Black persons, Hispanic or Latino persons, and American Indian or Alaska Native
persons ¶
People with medical conditions including:

Asthma
Neurologic and neurodevelopmental conditions (including disorders of the brain, spinal cord,
and peripheral nerve and muscle such as cerebral palsy, epilepsy, stroke, intellectual disability,
moderate-to-severe developmental delay, muscular dystrophy, and spinal cord injury)
Chronic lung disease (eg, chronic obstructive pulmonary disease, cystic fibrosis)
Heart disease (eg, congenital heart disease, congestive heart failure, coronary artery disease)
Blood disorders (eg, sickle cell disease)
Endocrine disorders (eg, diabetes mellitus)
Kidney diseases
Liver disorders
Metabolic disorders (eg, inherited metabolic disorders and mitochondrial disorders)
Weakened immune system due to disease (eg, HIV, AIDS, cancer) or medication (eg,
chemotherapy or radiation therapy, chronic glucocorticoids)
Children <19 years of age who are receiving long-term aspirin therapy
People with Class III obesity (body mass index [BMI] ≥40 or ≥140% of the 95 th percentile value)
* In young children, rates of hospitalization and mortality are greatest among those <6 months of
age.
¶ Possibly related to economic and social conditions (eg, poverty, multigenerational households,
limited access or barriers to influenza vaccination).
Adapted from: Influenza: People at higher risk of flu complications. Centers for Disease Control and Prevention. Available at:
cdc.gov/flu/highrisk/index.htm (Accessed on September 2, 2022).
Community-acquired pneumonia: Empiric antibiotic selection for adults admitt
CAP: community-acquired pneumonia; MRSA: methicillin-resistant Staphylococcus aureus; PCR: polymerase c
* This algorithm is intended for patients in whom admission to a general medical ward is considered approp
be administered as soon as possible after diagnosing CAP. If the etiology of CAP has been identified based u
evidence of coinfection, treatment regimens should be simplified and directed to that pathogen.
¶ Individuals with a past reaction to penicillin that was mild (not Stevens Johnson syndrome, toxic epiderma
not have features of an immunoglobulin (Ig)E-mediated reaction can receive a broad-spectrum (third- or fou
Δ Empiric therapy with aztreonam plus levofloxacin plus an aminoglycoside is generally appropriate for pati
preclude the use of penicillins, cephalosporins, and carbapenems. However, patients with a prior life-threate
evaluated by an allergy specialist because of the possibility of cross-reactivity. Such patients can receive levo
◊ Combination therapy with a beta-lactam plus a macrolide and monotherapy with a respiratory fluoroquin
studies have suggested that beta-lactam plus macrolide combination regimens are associated with better c
effects of macrolides. Furthermore, the severity of adverse effects (including the risk for Clostridioides [form
organisms are generally thought to be greater with fluoroquinolones than with the combination therapy reg
lactam plus a macrolide rather than monotherapy with a fluoroquinolone. Nevertheless, cephalosporins and
use should also inform the decision about the most appropriate regimen; if the patient has used a beta-lact
versa.
§ Omadacycline and lefamulin are newer agents and potential alternatives for patients who cannot tolerate
be limited by availability and/or insurance coverage.
¥ Examples of contraindications include increased risk for a prolonged QT interval and allergy.
‡ Doxycycline should not be used in pregnant women.
† The combination of vancomycin and piperacillin-tazobactam has been associated with acute kidney injury.
antipseudomonal/antipneumococcal beta-lactam, options include using a beta-lactam other than piperacilli
using linezolid instead of vancomycin.
** Ceftaroline has activity against MRSA but not Pseudomonas; because of its extended spectrum, it is often
Community-acquired pneumonia: Empiric antibiotic selection for adults admitt
CAP: community-acquired pneumonia; MRSA: methicillin-resistant Staphylococcus aureus; PCR: polymerase c

* This algorithm is intended for patients in whom admission to an intensive care unit is considered appropr
be administered as soon as possible after diagnosing CAP. If the etiology of CAP has been identified based u
evidence of coinfection, treatment regimens should be simplified and directed to that pathogen.
¶ Individuals with a past reaction to penicillin that was mild (not Stevens Johnson syndrome, toxic epiderma
did not have features of an immunoglobulin (Ig)E-mediated reaction can receive a broad-spectrum (third- or
Δ Empiric therapy with aztreonam plus levofloxacin plus an aminoglycoside is generally appropriate for pati
preclude the use of penicillins, cephalosporins, and carbapenems. However, patients with a prior life-threate
evaluated by an allergy specialist because of the possibility of cross-reactivity. Such patients can receive levo
◊ Regimens containing either a macrolide or fluoroquinolone have been generally comparable in clinical tri
regimens are associated with better clinical outcomes for patients with severe CAP, possibly due to the imm
(including the risk for Clostridioides [formerly Clostridium] difficile infection) and the risk of selection for resist
fluoroquinolones than with other antibiotic classes. For this reason, we generally favor a macrolide-containi
patient allergy or intolerance. Recent antibiotic use should also inform the decision about the most appropr
fluoroquinolone should be chosen if possible, and vice versa.
§ The combination of vancomycin and piperacillin-tazobactam has been associated with acute kidney injury.
antipseudomonal/antipneumococcal beta-lactam, options include using a beta-lactam other than piperacilli
using linezolid instead of vancomycin.
¥ Ceftaroline has activity against MRSA but not Pseudomonas; because of its extended spectrum, it is often
Approach to the patient with a past penicillin reaction who requires antibiotics
This algorithm is intended for use in conjunction with the UpToDate content on choice of antibiotics in penic
but also applies to outpatients if test dose procedures can be performed in an appropriately monitored sett
including anaphylaxis.
IgE: immunoglobulin E.
* Ask the following:

1. What exactly were the symptoms?
Raised, red, itchy spots with each lesion lasting less than 24 hours (hives/urticaria)?
Swelling of the mouth, eyes, lips, or tongue (angioedema)?
Blisters or ulcers involving the lips, mouth, eyes, urethra, vagina, or peeling skin (seen in SJS, T
Respiratory or hemodynamic changes (anaphylaxis)?
Joint pains (seen in serum sickness)?
Did the reaction involve organs like the kidneys, lungs, or liver (seen in DRESS, other severe typ
2. What was the timing of the reaction after taking penicillin: Minutes, hours, or days later? Was it after t
3. How long ago did the reaction happen? (After 10 years of avoidance, only 20% of patients with IgE-me
4. How was the reaction treated? Was there a need for urgent care or was adrenaline/epinephrine admi
5. Has the patient tolerated similar medications, such as ampicillin, amoxicillin, or cephalexin since the p
¶ Isolated mild hives, without other symptoms of an IgE-mediated reaction, can often occur in the setting o
or >10 years ago, may also be considered to be at minimal risk for a recurrent serious reaction.
Δ This algorithm is intended for use in conjunction with additional UpToDate content. For a description of ho
on choice of antibiotics in penicillin-allergic hospitalized patients.
◊ Consult allergist to perform skin testing. If skin testing is not possible, patient may still be able to receive
desensitization (also known as tolerance induction) procedure. Refer to the UpToDate topic on rapid drug de
Original figure modified for this publication. Blumenthal KG, Shenoy ES, Varughese CA, et al. Impact of a clinical guideline for prescrib
Immunol 2015; 115:294. Illustration used with the permission of Elsevier Inc. All rights reserved.
Usual duration of findings in treated community-acquired pneumonia
Abnormality Duration (days)
Tachycardia and hypotension 2
Fever, tachypnea, and hypoxia 3
Cough 14
Fatigue 14
Infiltrates on chest radiograph 30
References:
1. Marrie TJ, Beecroft MD, Herman-Gnjidic Z. Resolution of symptoms in patients with community-acquired pneumonia
treated on an ambulatory basis. J Infect 2004; 49:302.
2. Metlay JP, Atlas SJ, Borowsky LH, Singer DE. Time course of symptom resolution in patients with community-acquired
pneumonia. Respir Med 1998; 92:1137.
3. Fine MJ, Stone RA, Singer DE, et al. Processes and outcomes of care for patients with community-acquired pneumonia:
results from the Pneumonia Patient Outcomes Research Team (PORT) cohort study. Arch Intern Med 1999; 159:970.
Transitioning inpatients with community-acquired pneumonia from IV to

oral antibiotics
IV: intravenous.
* Patients should show some clinical response before switching to oral medications. Fever may
persist with lobar pneumonia. Cough from pneumococcal pneumonia may not clear for a week;
abnormal chest radiograph findings usually clear within 4 weeks but may persist for 12 weeks in
older individuals and those with underlying pulmonary disease.
¶ Generally avoid in patients with known QT interval prolongation or risk factors for QT interval
prolongation.
Δ Dose adjustment is necessary in patients with renal insufficiency.
◊ Cefpodoxime has similar coverage to ceftriaxone and cefotaxime and is generally preferred
for patients with structural lung disease and others at risk for infection with Enterobacteriaceae
(eg, Escherichia coli, Klebsiella spp).
§ If the patient has already received 1.5 g of azithromycin, atypical coverage can be
discontinued.
Algorithm for procalcitonin-guided antibiotic discontinuation in clinically stabl

patients with known or suspected community-acquired pneumonia*
CAP: community-acquired pneumonia.
* Procalcitonin has not been well studied in immunocompromised patients, trauma or surgery patients, pre
women, patients with cystic fibrosis, and patients with chronic kidney disease. The algorithm may not be ap
these populations or other patients with complex comorbidities.
¶ Optimal thresholds have not been precisely determined. Some experts use a lower threshold, typically 0.1
deciding to discontinue antibiotics.
Δ Decisions to stop antibiotics should be made in combination with clinical judgment and presume that the
stable and that a bacterial infection that requires a longer course of therapy, such as CAP complicated by ba
was not identified.
◊ Systemic inflammation due to other causes, such as burns, trauma, surgery, pancreatitis, malaria, or inva
candidiasis can also lead to elevated procalcitonin levels.
§ Reaching a procalcitonin level of <0.25 ng/mL is not a requirement for antibiotic discontinuation. For patie
clinically resolved pneumonia and levels >0.25 ng/mL, clinical judgment alone is adequate.
Follow-up imaging for immunocompetent adults

who have recovered from community-acquired
pneumonia
Follow-up imaging is not needed for most patients who have

promptly recovered from CAP (eg, within 5 to 7 days for an
otherwise healthy person). However, follow-up clinic visits are good
opportunities to review the patient's risk for lung cancer based on
age, smoking history, and recent imaging findings.
CT: computed tomography; CAP: community-acquired pneumonia.
* Criteria for lung cancer screening vary among clinical practice

guidelines (eg, thresholds for age and duration of smoking therapy).
Refer to UpToDate text for detail.
¶ Exceptions include patients who are followed radiographically for

other reasons (eg, selected patients with advanced structural lung
disease). Whether patients with small pleural effusions require
follow-up is an open question. We generally do not obtain follow-up
imagining unless the patient is slow to recover or develops new
systemic or respiratory symptoms.
Contributor Disclosures
Julio A Ramirez, MD, FACP Grant/Research/Clinical Trial Support: Eli Lilly [Monoclonal antibodies];
Janssen [Vaccines]; Pfizer [Vaccines]. Consultant/Advisory Boards: Dompe [Infectious diseases]; Nabriva
[Respiratory infections]; Paratek [Respiratory infections]; Pfizer [Vaccines]. All of the relevant financial
relationships listed have been mitigated. Thomas M File, Jr, MD Consultant/Advisory Boards:
HealthTrackRX [Diagnostic for respiratory infections (provided input into study design but did not receive
payment but did receive reimbursement for traveling to a study development meeting)]; Nabriva
Therapeutics [Community-acquired pneumonia]; ThermoFisher [Biomarker for infection]. Other Financial
Interest: Board of Directors of Infectious Diseases Society of America (2017-2022) [Infections Diseases];
Wolters Kluwer-Editor-in-Chief, Infectious Diseases in Clinical Practice [Infections Diseases]. All of the
relevant financial relationships listed have been mitigated. Sheila Bond, MD No relevant financial
relationship(s) with ineligible companies to disclose.
编辑组会认真审核作者的声明。之间的利益冲突将会通过编辑组对文章以及参考文献的多级审评来解决。所有的
作者都必须提供与文章相关的文献，文章以及文献须严格依循UpToDate 的相关的标准。
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成人社区获得性肺炎概述 - UpToDate

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成人社区获得性肺炎概述 - UpToDate

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8/2/23, 6:51 PM 成人社区获得性肺炎概述 - UpToDate

Official reprint from UpToDate®

翻译: 韩锋锋, 主任医师，教授

There is a newer version of this topic available in English. 该主题有一个新的英文版

社区获得性肺炎(community-acquired pneumonia, CAP)是全球发病和死亡的主要原因。CAP患者的临床

● 社区获得性肺炎(community-acquired pneumonia, CAP)指在医院外获得的肺实质急性感染。

健康护理相关肺炎(health care-associated pneumonia, HCAP)这个术语已不再使用，指的是在医疗保

● 慢性共存疾病–慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)患者因CAP

● 耐甲氧西林金黄色葡萄球菌(Methicillin-resistant S. aureus, MRSA)也可导致CAP但不常见。

与医疗保健相关的MRSA感染相比，社区获得性MRSA(community-acquired MRSA, CA-MRSA)感染往

最常用的严重程度评分是肺炎严重程度指数(Pneumonia Severity Index, PSI)和CURB-65[27,28]。我

CAP的微生物学评估详见其他专题。(参见 “成人社区获得性肺炎的临床评估和诊断性检测”和 “痰培

COVID-19的处理详见其他专题。(参见 “COVID-19：住院成人患者的处理”和 “COVID-19的疗养院管

对于青霉素过敏患者，我们根据青霉素过敏反应的类型和严重程度( 流程图 5)及先前的假单胞

各项措施详见其他专题。(参见 “成人戒烟管理概述”和 “成人季节性流感疫苗接种”和 “成人肺炎

● 高级篇(参见 “Patient education: Pneumonia in adults (Beyond the Basics)”)

我们沉痛悼念于2021年1月去世的John G Bartlett, MD。UpToDate衷心感谢Dr. John G Bartlett担任

1. Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society of

2. File TM. Community-acquired pneumonia. Lancet 2003; 362:1991.

23. Annane D, Renault A, Brun-Buisson C, et al. Hydrocortisone plus Fludrocortisone for

24. Moore M, Stuart B, Little P, et al. Predictors of pneumonia in lower respiratory

31. Carratalà J, Fernández-Sabé N, Ortega L, et al. Outpatient care compared with

admission in community-acquired pneumonia patients without major criteria or

38. Briel M, Spoorenberg SMC, Snijders D, et al. Corticosteroids in Patients Hospitalized

47. Menéndez R, Torres A, Zalacaín R, et al. Risk factors of treatment failure in

Classification by site of acquisition

Community-acquired An acute infection of the pulmonary parenchyma acquired outside of

Nosocomial pneumonia An acute infection of the pulmonary parenchyma acquired in hospital

Hospital-acquired Pneumonia acquired ≥48 hours after hospital admission; includes

Ventilator-associated Pneumonia acquired ≥48 hours after endotracheal intubation

Atypical pneumonia Pneumonia caused by "atypical" ¶ bacterial pathogens including

Aspiration pneumonia Pneumonia resulting from entry of gastric or oropharyngeal fluid,

Bacterial aspiration An active infection caused by inoculation of large amounts of bacteria

Graphic 130821 Version 3.0

The impact of age on the incidence of patients hospitalized with community-ac

Graphic 118032 Version 11.0

The impact of comorbid conditions on the incidence of patients hospitalized wi

CHF: congestive heart failure; COPD: chronic obstructive pulmonary disease.

Graphic 118033 Version 10.0

Microbial etiology of community-acquired pneumonia by site of care*

Outpatients Ward patients Inte

Total patients 514 507 2521 585 488

Streptococcus 56 (10.9) 30 (5.9) 447 (17.7) 38 (6.5) 110 (22

Haemophilus 8 (1.6) 25 (4.9) 54 (2.1) 16 (2.7) 8 (1.6)

Moraxella 0 6 (1.2) 4 (0.2) 0 1 (0.2)

Legionella 10 (1.9) Δ 87 (3.5) ◊ 21 (4.3

Mycoplasma 27 (5.3) § 87 (17.2) § 32 (1.3) § ¥ 6 (1.2) §

Chlamydia 10 (1.9) § 72 (14.2) § 32 (1.3) § ¥ 8 (1.6) §

Coxiella 11 (2.1) § Δ 17 (0.7) § ¥ 2 (0.4) §

Staphylococcus 1 (0.2) 6 (1.2) 18 (0.7) 25 (4.3) 6 (1.2)

MSSA 1 (0.2) NR 9 (0.4) 18 (3.1) 4 (0.8)

MRSA 0 NR 9 (0.4) 7 (1.2) 2 (0.4)

Gram- 1 (0.2) 2 (0.4) 23 (0.9) 15 (2.6) 3 (0.6)

Pseudomonas 1 (0.2) 1 (0.2) 37 (1.5) 12 (2.1) 12 (2.5

Respiratory 15 (2.9) § † 123 (4.9) § † 10 (2.0

Other 6 (1.2) 14 (2.8) 33 (1.3) 8 (1.4) 15 (3.1

>1 pathogen 15 (2.9) ** 135 (5.4) 6 (1.0) 58 (11.

Cultures (sputum, Cultures Cultures (sputum, Cultures Culture

MSSA: methicillin-susceptible Staphylococcus aureus; MRSA: methicillin-resistant Staphylococcus

Δ Testing for Legionella spp and C. burnetti was not performed.

¥ Testing for M. pneumoniae, C. pneumoniae, and C. burnetii was not performed.

‡ Influenza viruses A or B, parainfluenza viruses 1 to 3, respiratory syncytial virus, adenovirus.

† Testing for viruses was not performed.

Graphic 72014 Version 14.0