肺炎克雷伯细菌及其荚膜

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新生儿肺炎克雷伯菌脓毒症的护理

新生儿肺炎克雷伯菌脓毒症的护理

新生儿肺炎克雷伯菌脓毒症的护理一、新生儿肺炎克雷伯菌脓毒症概述1.肺炎克雷伯菌的生物学特性肺炎克雷伯菌是肠杆菌科克雷伯氏菌属中最为重要的一类细菌,革兰氏阴性杆菌,无芽孢,无鞭毛,有较厚的荚膜。

它在自然界广泛存在,如土壤、水、农产品等,同时也是人和动物肠道内的正常菌群之一。

然而,在特定条件下,如新生儿免疫力低下时,它可能会成为致病菌,引发严重的感染。

2.新生儿易感染的原因新生儿由于其免疫系统尚未完全发育成熟,皮肤和黏膜屏障功能较弱,容易受到病原体的侵袭。

此外,新生儿的肠道菌群尚未稳定建立,正常菌群的定植和抵抗病原体的能力相对不足。

再加上住院期间可能接触到各种医疗器械和医护人员的操作,增加了感染的风险。

3.肺炎克雷伯菌脓毒症的临床表现新生儿肺炎克雷伯菌脓毒症的临床表现可能不典型,常见的症状包括体温不稳定(发热或低体温)、呼吸急促或呼吸困难、心率增快、精神萎靡、食欲减退、黄疸加重等。

在严重情况下,可能会出现休克、多器官功能衰竭等危及生命的并发症。

二、新生儿肺炎克雷伯菌脓毒症的发病机制1.细菌侵入途径肺炎克雷伯菌可以通过多种途径侵入新生儿体内,如呼吸道吸入、皮肤破损处感染、胃肠道定植后移位、血行感染等。

其中,呼吸道和胃肠道是较为常见的侵入部位。

2.免疫反应失调新生儿的免疫系统在应对病原体感染时,可能会出现免疫反应失调的情况。

一方面,免疫细胞的数量和功能相对不足,导致对病原体的清除能力下降;另一方面,过度的炎症反应可能会导致组织损伤和器官功能障碍。

3.细菌毒素的作用肺炎克雷伯菌可以产生多种毒素,如内毒素、外毒素等。

这些毒素可以直接损伤细胞,破坏组织和器官的正常功能,从而加重病情。

三、新生儿肺炎克雷伯菌脓毒症的诊断方法1.临床症状和体征评估医生会仔细观察新生儿的体温、呼吸、心率、精神状态、皮肤颜色等症状和体征,结合病史进行初步判断。

2.实验室检查(1)血常规:白细胞计数升高或降低,中性粒细胞比例异常,血小板减少等。

克雷伯菌属优秀课件

克雷伯菌属优秀课件
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初步鉴定 • 氧化酶(-) • 葡萄糖(+) • 动力(-) • 吲哚(-):产酸克雷伯(+) • 尿素酶(+)
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基本生化
• TSI:⊕/⊕, • 枸(+) • 尿素酶(+), • 吲哚(-) • V-P(+) • 动力(-) • 鸟氨酸(-) • 丙二酸盐(+)
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亚种鉴别
• 肺炎克雷伯菌三个亚种的鉴别关键是 IMViC试验;
所致疾病:肺炎、脑膜炎、腹膜炎、 泌尿系统感染、败血症
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四、微生物学检验
(一)检验程序 (二)标本采集 (三)检验方法 (四)耐药性 (五)结果分析与报告
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微生物检验
1、标本直接检验 2、分离培养与鉴定
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标本的采集
• 肺部感染:采集痰液 • 肠炎采集粪便, • 败血症者采集血液, • 其他根据病症分别采集尿液、脓汁、脑
克雷伯菌属
一、分类 二、细菌特性 三、临床意义 四、微生物学检验
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一、克雷伯菌属分类 肺炎克雷伯菌 臭鼻克雷伯菌 鼻硬结克雷伯菌 产酸克雷伯菌 解鸟氨酸克雷伯菌 植生克雷伯菌 土壤克雷伯菌
最常见:肺炎克雷伯菌
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二、细菌特性
• 形态与染色
较短粗的杆菌,大小0.5~0.8×1~2um, 单独、成双或短链状排列。无芽胞,无 鞭毛,有较厚的荚膜,多数有菌毛。
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• 抗原构造 具有O抗原与K抗原,后者用以分型。 利用荚膜肿胀试验,本属K抗原可分为82型。 肺炎克氏菌大多属3型和12型; 臭鼻克氏菌主要属4型,少数为5型或6型; 鼻硬结克氏菌一般属3型,但并非所有3型均为
该菌。
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三、临床意义
克雷伯菌属的细菌多感染免疫力低 下的人群,是医院感染中最重要的条件 致病菌。

肺炎克雷伯杆菌肺炎

肺炎克雷伯杆菌肺炎

克雷白杆菌肺炎(Klebsiella pneumonia):近20余年来,该菌已成为院内获得性肺炎得主要致病菌,耐药株不断增加,且产生超广谱酶,成为防治中得难点、本病多见于中年以上男性,起病急、高热、咳嗽、痰多及胸痛,可有发绀、气急、心悸,约半数患者有畏寒,可早期出现休克。

临床表现类似因为得肺炎球菌肺炎,但其痰常呈粘稠脓性,量多、带血,灰绿色或砖红色、胶冻状,但此类典型得痰液并不多见。

胸部X线表现常呈多样性,包括大叶实变,好发于右肺上叶、双肺下叶,有多发性蜂窝状肺脓肿、叶间隙下坠、严重病例有呼吸衰竭、周围循环衰竭。

慢性病程者表现为咳嗽、咳痰、衰弱、贫血等、克雷白杆菌肺炎得预后较差,病死率高。

临床表现:①发病骤起,出现呼吸困难;②年长儿有大量黏稠血性痰,但婴儿少见;③由于气道被黏液梗阻,肺部体征较少或完全缺乏;④病情极为严重,发展迅速,患儿常呈休克状态;⑤X线胸片示肺段或大叶性致密实变阴影,其边缘往往膨胀凸出、可迅速发展到邻近肺段,以上叶后段及下叶前段较多见;⑥常见并发症为肺脓肿,可呈多房性蜂窝状,日后形成纤维性变;其次为脓胸及胸膜肥厚。

治疗尚缺乏有效抗菌药物。

临床病理:肺炎克雷白杆菌为革兰阴性杆菌,常存在于人体上呼吸道与肠道,当机体抵抗力降低时,便经呼吸道进入肺内而引起大叶或小叶融合性实变,以上叶较为多见。

病变中渗出液粘稠而重,致使叶间隙下坠、细菌具有荚膜,在肺泡内生长繁殖时,引起组织坏死、液化、形成单个或多发性脓肿。

病变累及胸膜、心包时,可引起渗出性或脓性积液。

病灶纤维组织增生活跃,易于机化;纤维素性胸腔积液可早期出现粘连。

在院内感染得败血症中,克雷白杆菌以及绿脓杆菌与沙雷菌等均为重要病原菌,病死率较高。

老年体弱患者有急性肺炎、中毒症状严重、且有血性粘稠痰者,应考虑本病。

确诊有赖于痰细菌学检查,并与葡萄球菌、结核菌或其她革兰阴性杆菌所致肺炎相鉴别。

年老、白细胞减少、菌血症及原有严重疾病者预后较差、与支气管扩张症区别支气管扩张症就是常见得慢性支气管化脓性疾病,大多数继发于呼吸道感染与支气管阻塞,尤其就是儿童与青年时期麻疹、百日咳后得支气管肺炎,由于破环支气管管壁,形成管腔扩张与变形。

肺炎克雷伯菌

肺炎克雷伯菌

肺炎克雷伯菌
肺炎克雷伯菌存在于人体上呼吸道和肠道,当机体抵抗力降低时,便经呼吸道进入肺内而引起大叶或小叶融合性实变,以上叶较为多见。

为革兰阴性杆菌,病变中渗出液粘稠而重,致使叶间隙下坠。

细菌具有荚膜,在肺泡内生长繁殖时,引起组织坏死、液化、形成单个或多发性脓肿。

病变累及胸膜、心包时,可引起渗出性或脓性积液。

病灶纤维组织增生活跃,易于机化;纤维素性胸腔积液可早期出现粘连。

在院内感染的败血症中,克雷白杆菌以及绿脓杆菌和沙雷菌等均为重要病原菌,病死率较高。

及早使用有效抗生素是治愈的关键。

首选氨基甙类抗生素,如庆大霉素、卡那霉素、妥布霉素、丁胺卡那霉素,可肌注、静滴或管腔内用药。

重症宜加用头孢菌素如头孢孟多、头孢西丁、头孢噻肟等。

哌拉西林,美洛西林与氨基甙类联用、以及氧氟沙星疗效亦佳。

部分病例使用氯霉素、四环素及SMZ-TMP亦有效。

重症多有肺组织损伤,慢性病例有时需行肺叶切除。

耐药机制:肺炎克雷伯菌(KNP)是临床分离及医院感染的重要致病菌之一,随着β-内酰胺类及氨基糖苷类等广谱抗菌素的广泛使用,细菌易产生超广谱β-内酰胺酶(ESBLs)和头孢菌素酶(AmpC酶)以及氨基糖苷类修饰酶(AMEs),对常用药物包括第三代头孢菌素和氨基糖苷类呈现出严重的多重耐药性。

肺炎克雷伯菌引起的医院感染率近期逐年增高,且多耐药性菌株的不断增加常导致临床抗菌药物治疗的失败和病程迁延。

肺炎克雷伯菌耐药机制主要包括产生β-内酰胺酶、生物被膜的形成、外膜孔蛋白的缺失。

抗菌药物主动外排等,抗菌药物耐药基因水平播散是多药耐药菌株临床加剧的重要原因。

微生物肺炎克雷伯

微生物肺炎克雷伯
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固定:手执玻片一端,有菌膜的一面朝上,通过微火三次(手指触摸反面不烫手为宜)疑菌落涂在干净的玻片上自然晾干,用结晶紫(1液)覆盖细菌初染1min,清水冲洗干净玻片再滴加革兰染液(2液)媒染1min,清水冲去表面的染液,用95﹪乙醇(3液)脱洗约30s(以乙醇不再有颜色为好),最后用稀释的复红(4液)复染30s。自然晾干后在显微镜下观察形态。
定科:氧化酶试验(-)、IMViC(- - ++) 定属:KIA(AA+ -)、MIU(- - +)、
O/F(F)、鸟氨酸脱羧酶试验(-)
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I(吲哚):有些细菌具有色氨酸酶,能分解蛋白胨中的色氨酸产生吲哚,与对甲基氨基苯甲醛结合,生成红色化合物玫瑰吲哚。主要用于肠杆菌科细菌的鉴定。 M(甲基红):某些细菌分解葡萄糖产生丙酮酸,丙酮酸可进一步分解为甲酸、乙酸等酸性物质,不再继续分解,故培养基pH在4.5以下,加入甲基红指示剂后呈紫红色(阳性)。有些细菌将分解葡萄糖产生的酸进一步转化为醇酮等非酸性物质,使培养基pH在6.2以上,加入甲基红试剂成橘黄色(阴性)。一般用于肠杆菌科各菌属的鉴别。 Vi:某些细菌分解葡萄糖生成丙酮酸,丙酮酸可进一步脱羧生成乙酰甲基甲醇,乙酰甲基甲醇在碱性环境下被氧化成二乙酰,后者与蛋白胨中的精氨酸所含的胍基起作用,生成红色胍缩二乙酰,为VP试验阳性。若培养基中胍基含量少,加入少量含胍基的化合物如肌酸肌酐,可加速其反应。一般用于肠杆菌科各菌属的鉴别。 C(枸橼酸盐)枸橼酸盐培养基中不含任何糖类,枸橼酸盐为唯一碳源,磷酸二氢铵为唯一氮源。如果细菌能利用铵盐作为唯一氮源,并能利用枸橼酸盐作为唯一碳源,在枸橼酸盐培养基上生长,并分解枸橼酸盐为碳酸盐,使培养基变碱,指示剂溴麝香草酚蓝由绿色变为深蓝色,为枸橼酸盐利用实验阳性。若细菌不能利用枸橼酸盐为碳源,则细菌不能生长,培养基不变色。 back

肺炎克雷伯菌乳房炎的致病机理及其耐药性分析

肺炎克雷伯菌乳房炎的致病机理及其耐药性分析

肺炎克雷伯菌乳房炎的致病机理及其耐药性分析李海源莘县畜牧兽医事业发展中心,山东聊城 252400摘 要:肺炎克雷伯菌是引起奶牛乳房炎的重要病原微生物之一。

奶牛场通常用抗生素对其进行治疗。

但抗生素的大量使用,使得肺炎克雷伯菌的耐药性越来越高,给疾病治疗造成了不利影响。

因此,为了更好地应对由肺炎克雷伯菌引起的乳房炎,本文对肺炎克雷伯菌的生物学特性进行了阐述,特别对生长特性、基因编码和种属等进行了介绍,同时对肺炎克雷伯菌目前的危害情况进行了概要,对其毒力因子中的荚膜多糖、脂多糖、黏附因子、铁载体和外排泵等进行了综合分析,概述了肺炎克雷伯菌对不同抗生素的耐药性特点。

只有加深对肺炎克雷伯菌的了解,才能够有效降低该病菌引起的乳房炎发病率,促进奶牛养殖业的绿色健康发展。

关键词:乳房炎;肺炎克雷伯菌;耐药性;毒力因子文章编号:1671-4393(2023)11-0039-06 DOI:10.12377/1671-4393.23.11.080 引言奶牛乳房炎是奶牛在养殖过程中乳腺部位受到外部物理、化学或病原微生物的入侵而导致炎症反应的一种常见疾病。

患病乳房内部会发生病理变化,主要表现为乳汁中体细胞数量增多、pH值大于7.0,NaCl的含量增高,电导率上升,细菌学鉴定为阳性等[1]。

奶牛乳房炎是一种危害牛群范围广的疾病,国外发病率可达25%~60%,国内的平均发病率可达33.4%[2]。

我国每年由于乳房炎而淘汰的奶牛占总淘汰奶牛数的10%,经济损失高达6 亿元人民币[3]。

奶牛乳房炎致病微生物主要分为传染性病原微生物和环境型病原微生物,其中环境型病原微生物占主要地位[4],主要包括大肠杆菌、乳房链球菌、停乳链球菌、沙雷氏菌、肠球菌和肺炎克雷伯菌等。

它们广泛存在于垫料等牛舍环境中,感染细菌后,可引起乳房部位发生急性红肿,坚硬且有触痛,乳汁呈絮状或水样,严重者产奶量显著下降[5]。

其中的肺炎克雷伯菌还能进一步感染奶牛尿作者简介:李海源(1973-),男,山东莘县人,本科,高级兽医师,研究方向为畜禽屠宰检疫技术。

微生物肺炎克雷伯讲义

微生物肺炎克雷伯讲义
微生物肺炎克雷伯还能通过改变自身抗原性,使免疫系统无法识别和攻击病菌, 从而逃避免疫系统的清除。
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微生物肺炎克雷伯的诊断 与治疗
微生物肺炎克雷伯的诊断方法
临床表现
观察患者是否有咳嗽、咳痰、 呼吸困难等症状,以及是否有
发热、胸痛等体征。
实验室检查
通过血液检查、痰液检查等手 段,检测白细胞计数、C反应蛋 白等指标,以辅助诊断。
微生物肺炎克雷伯主要通过呼吸作用 进行代谢,利用氧气的氧化作用产生 能量。
微生物肺炎克雷伯的基因组与变异
微生物肺炎克雷伯的基因组较大,含有多个质粒和转座子, 容易发生变异。
微生物肺炎克雷伯的变异类型包括抗药性变异、毒力变异和 表型变异等,这些变异使得肺炎克雷伯具有更强的适应性和 生存能力。
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微生物肺炎克雷伯的致病 性
对于呼吸困难的患者,给予吸氧、机械通 气等支持治疗措施,以改善呼吸功能。
并发症处理
预防复发
针对肺炎克雷伯菌感染可能引起的并发症 ,如心内膜炎、脑膜炎等,采取相应的治 疗措施。
对于高危人群或易感人群,采取预防措施 ,如加强免疫接种、改善生活方式等,以 降低复发风险。
微生物肺炎克雷伯的预防措施
加强卫生宣传
微生物肺炎克雷伯的感染机制
微生物肺炎克雷伯通过空气传播进入人体,首先在呼吸道定植,然后通过血液传播 至肺部,引起感染。
微生物肺炎克雷伯在人体内繁殖,破坏肺部组织,引发炎症反应,导致肺炎。
微生物肺炎克雷伯的感染机制还包括对呼吸道上皮细胞的粘附作用和对免疫系统的 逃避。
微生物肺炎克雷伯的毒力因子
微生物肺炎克雷伯产生多种毒力因子 ,如荚膜、外毒素和溶血素等,这些 毒力因子可导致肺部炎症、组织损伤 和免疫逃避。

肺炎克雷伯杆菌肺炎

肺炎克雷伯杆菌肺炎

克雷白杆菌肺炎(Klebsiella pneumonia):近20余年来,该菌已成为院内获得性肺炎得主要致病菌,耐药株不断增加,且产生超广谱酶,成为防治中得难点。

本病多见于中年以上男性,起病急、高热、咳嗽、痰多及胸痛,可有发绀、气急、心悸,约半数患者有畏寒,可早期出现休克。

临床表现类似因为得肺炎球菌肺炎,但其痰常呈粘稠脓性,量多、带血,灰绿色或砖红色、胶冻状,但此类典型得痰液并不多见、胸部X线表现常呈多样性,包括大叶实变,好发于右肺上叶、双肺下叶,有多发性蜂窝状肺脓肿、叶间隙下坠。

严重病例有呼吸衰竭、周围循环衰竭、慢性病程者表现为咳嗽、咳痰、衰弱、贫血等。

克雷白杆菌肺炎得预后较差,病死率高、临床表现:①发病骤起,出现呼吸困难;②年长儿有大量黏稠血性痰,但婴儿少见;③由于气道被黏液梗阻,肺部体征较少或完全缺乏;④病情极为严重,发展迅速,患儿常呈休克状态;⑤X线胸片示肺段或大叶性致密实变阴影,其边缘往往膨胀凸出、可迅速发展到邻近肺段,以上叶后段及下叶前段较多见;⑥常见并发症为肺脓肿,可呈多房性蜂窝状,日后形成纤维性变;其次为脓胸及胸膜肥厚、治疗尚缺乏有效抗菌药物。

临床病理:肺炎克雷白杆菌为革兰阴性杆菌,常存在于人体上呼吸道与肠道,当机体抵抗力降低时,便经呼吸道进入肺内而引起大叶或小叶融合性实变,以上叶较为多见。

病变中渗出液粘稠而重,致使叶间隙下坠。

细菌具有荚膜,在肺泡内生长繁殖时,引起组织坏死、液化、形成单个或多发性脓肿、病变累及胸膜、心包时,可引起渗出性或脓性积液。

病灶纤维组织增生活跃,易于机化;纤维素性胸腔积液可早期出现粘连、在院内感染得败血症中,克雷白杆菌以及绿脓杆菌与沙雷菌等均为重要病原菌,病死率较高、老年体弱患者有急性肺炎、中毒症状严重、且有血性粘稠痰者,应考虑本病。

确诊有赖于痰细菌学检查,并与葡萄球菌、结核菌或其她革兰阴性杆菌所致肺炎相鉴别。

年老、白细胞减少、菌血症及原有严重疾病者预后较差。

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Klebsiella pneumoniae Bacteremia and Capsular Serotypes, Taiwan Chun-Hsing Liao, Yu-Tsung Huang, Chih-Cheng Lai, Cheng-Yu Chang, Fang-Yeh Chu, Meng-Shiuan Hsu, Hsin-Sui Hsu, and Po-Ren HsuehCapsular serotypes of 225 Klebsiella pneumoniae isolates in Taiwan were identi fi ed by using PCR. Patients infected with K1 serotypes (41 isolates) had increased community-onset bacteremia, more nonfatal diseases and liver abscesses, lower Pittsburgh bacteremia scores and mortality rates, and fewer urinary tract infections than patients infected with non–K1/K2 serotypes (147 isolates).Klebsiella pneumoniae bacteria cause a variety of infections (1,2). Geographic differences in this organism have been recognized, and a high prevalence of liver abscesses has been observed for >20 years in persons in Taiwan infected with K . pneumoniae (3,4). K1 and K2 are the major capsular serotypes that cause liver abscesses and have increased virulence (4–7). In contrast, only limited information is available about serotypes causing K. pneumoniae bacteremia (3,5).Yu et al. grouped K1 and K2 serotypes and compared clinical characteristics for patients with K. pneumoniae bacteremia with those for patients infected with non–K1/K2 serotypes (3). Recent evidence suggests that K1 is a major cause of primary liver abscesses and has greater potential for causing metastasis, and that K2 is a major cause of secondary liver abscesses (6,8). We examined the distribution and clinical characteristics of serotypes that cause K. pneumoniae bacteremia from 225 patients (9) and performed PCR-based genotyping to identify capsular serotypes (10).The StudyThe study was conducted at Far-Eastern Memorial Hospital in Taipei, Taiwan. Patients with K . pneumoniae bacteremia were identi fi ed during January 1–December31, 2007. Identi fi cation of K . pneumoniae was based oncolony morphologic features and biochemical reactions(11). Data on time until positive blood culture results wereobtained from the automated blood culture system at the hospital. Data for each patient were included only once (atthe time of the fi rst detection of bacteremia). Patients <18years of age and those not admitted to our hospital wereexcluded. Inactive malignancy was not included as anunderlying illness. In-hospital and 14-day mortality rateswere assessed. For 225 available bacterial isolates, cps genotyping was performed (10).A total of 231 patients with K . pneumoniae bacteremia were observed at the hospital during the study; 225 isolates from 225 patients were used. A total of 133 (59%) of these patients had community-onset bacteremia (bacteremia identi fi ed in an emergency department). The in-hospital mortality rate was 32.4%. Among 225 isolates, 41 (18.2%) were identi fi ed as K1 serotype, 37 (16.4%) as K2, 15 (6.7%) as K57, and 8 (3.6%) as K54. The K1 serotype was found predominantly in community-onset infections (36 [87.8%] of 41 patients compared with 75 [51.0%] of 147 patients infected with non–K1/K2 serotypes; odds ratio [OR] 6.91, 95% con fi dence interval [CI] 2.57–18.60) (online Appendix Table 1, /EID/content/17/6/1113-appT1.htm).Underlying illness was classi fi ed as nonfatal in 75.6% of patients with K1 bacteremia (53.7% of patients with non–K1/K2 bacteremia; OR 2.67, 95% CI 1.22–5.84). A lower percentage of patients with K1 bacteremia had surgery in the previous 3 months (9.8% vs. 30.6%; OR 0.25, 95% CI 0.09–0.73). Patients with K1 bacteremia had lower mean ± SD Pittsburgh bacteremia scores than those with non–K1/K2 bacteremia (2.7 ± 3.1 vs. 4.4 ± 4.7; OR 0.90, 95% CI 0.81–0.99), but the time until a positive blood culture was obtained was not different. K1 serotype was more common in patients with liver abscesses (46.3% vs. 4.1%; OR 20.3, 95% CI 7.31–56.40) and less common in patients with urinary tract infections (UTIs) (4.9% vs. 20.4%; OR 0.20, 95% CI 0.05–0.88). The in-hospital mortality rate for patients with K1 bacteremia was lower that that for patients with non–K1/K2 bacteremia (14.6% vs. 34.7%; OR 0.32, 95% CI 0.13–0.82).No differences were found in clinical characteristics for patients with K2 bacteremia and those with non–K1/K2 bacteremia except for a higher frequency of liver abscesses in patients with K2 bacteremia (13.5% vs. 4.1%; OR 3.67, 95% CI 1.06–12.8). For patients infected with K54 and K57 serotypes, 1 K57 serotype caused liver abscesses; no abscesses were found in patients infected with a K54 serotype. The in-hospital mortality rate was 50% (4/8) for patients with K54 bacteremia and 53.3% (8/15) for patients with K57 bacteremia.Patients infected with a K1 serotype had lower mean ± SD Pittsburgh bacteremia scores (2.7 ± 3.1 vs. 5.0 ± 5.3;Emerging Infectious Diseases • /eid • Vol. 17, No. 6, June 20111113Author af fi liations: Far Eastern Memorial Hospital, Taipei, Taiwan (C.-H. Liao, C.-C. Lai, C.-Y . Chang, F.-Y . Chu, M.-S. Hsu, H.-S. Hsu); and National Taiwan University College of Medicine, Taipei (Y .-T. Huang, P .-R. Hsueh)DOI: 10.3201/eid1706.100811OR 0.88, 95% CI 0.78–0.98, p = 0.002) and lower 14-day and in-hospital mortality rates (9.8% vs. 27.0%; OR 0.29, 95% CI 0.08–1.03, p = 0.06; and 14.6% vs. 43.2%; OR 0.23, 95% CI 0.08–0.67, p = 0.007) than patients infected with K2 serotypes. A higher percentage of patients with K1 bacteremia had liver abscesses at the site of infection (46.3% vs. 13.5%; OR 5.53, 95% CI 1.80–17.02, p = 0.003).Characteristics of patients with community-onset K. pneumoniae bacteremia were also analyzed (online Appendix Table 2, /EID/content/17/6/1113-appT2.htm). Patients infected with a K1 serotype were more likely to have liver abscesses and less likely to have UTIs or biliary tract infections (OR 11.5, 95% CI 3.99–33.20; OR 0.20, 95% CI 0.04–0.92; and OR 0.25, 95% CI 0.07–0.91, respectively).In our patients, K1 and K2 serotypes were found at similar frequencies (18.2% and 16.4%, respectively), which differs from results of Fung et al., in which the K1 serotype was more common (K1 30.8% and K2 5.1%) (12). Despite reported virulence of the K1 serotype, it was primarily responsible for community-onset bacteremia in patients with less severe underlying illness and associated with lower mortality rates. Moreover, the K1 serotype is associated with liver abscesses and lower mortality rates (2–7). Liver abscesses were found in 46% of patients with K1 bacteremia, and a K1 serotype was found in 63.3% of patients with liver abscesses.ConclusionsManagement of liver abscesses has improved in Taiwan because of increased physician awareness (13). Mortality rates for patients with K. pneumoniae bacteremia were lower in patients with UTIs or biliary tract infections (5,14), which were less common in patients infected with a K1 serotype. Thus, patient outcomes depend more on underlying conditions and severity of sepsis than on bacterial serotypes (5,9,14).In our previous study of the interval until a positive blood culture for K. pneumoniae bacteremia was obtained(9), we found that higher Pittsburgh bacteremia scores,a time until a positive blood culture <7 hours, and active malignancy were associated with death. In this study, we found no difference in time until a positive blood culture was obtained for patients infected with different serotypes. This interval for patients infected with K1 serotypes was slightly longer than that for patients infected with K2 and non–K1/K2 serotypes. This finding may have resulted from a higher percentage of community-onset infections and liver abscesses and less severe underlying illness in patients infected with a K1 serotype.Studies investigating K. pneumoniae bacteremia have grouped K1 and K2 serotypes (3,7). However, such grouping may be problematic because evidence suggests that the K1 serotype is the major cause of primary liver abscesses (6). Another report showed that the genetic background of serotype K2 is diversifi ed, and only 1 of the 2 major K2 clones was highly virulent in mice (15). These findings are consistent with our clinical observations. Differences in symptoms of patients infected with K2 and non–K1/K2 serotypes were minimal, despite slightly more liver abscesses among patients infected with K2 serotypes, which was lower than for patients infected with K1 serotypes. Because of different serotyping methods used (3,5,15), caution is required when interpreting data from various studies.Despite greater virulence of the K1 serotype, it is predominant in patients with community-onset infections and in those with less severe underlying illness. Although the K1 serotype is the major cause of liver abscesses, it results in a lower mortality rate, which can be attributed to host factors.Dr Liao is an infectious diseases specialist in the Department of Internal Medicine, Far-Eastern Memorial Hospital, Taipei, Taiwan. His research interests are clinical characteristics, epidemiology, and pathogenesis of bacterial infections, particularly methicillin-resistant Staphylococcus aureus and Klebsiella pneumoniae.References1. 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J Clin Microbiol. 2004;42:3388–98. doi:10.1128/JCM.42.8.3388-3398.2004Address for correspondence: Po-Ren Hsueh, Departments of Laboratory Medicine and Internal Medicine, National Taiwan University Hospital, No. 7, Chung-Shan South Rd, Taipei, Taiwan; email: hsporen@.twEmerging Infectious Diseases • /eid • Vol. 17, No. 6, June 20111115。

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