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1、金黄色葡萄球菌脑炎病例讨论,南华大学附二医院神经内科 魏麓云主任医师,病例简介,李军 男 62岁，因“四肢乏力、肌肉痛4天”于2012-1-17日17：52入院。患者入院4天前渐觉肢体无力，双下肢无力明显，尚能行走，无特殊诊治，17日自觉无力、肌痛症状加重，不能站立，急诊入院。既往：近2月来发现右侧颈部肿块，有心脏病、高血压病、脑外伤史，入院10天前有受凉感冒，自服感冒药。入院时查体：体温37.90C，血压150/100mmHg，血糖7.5 mmol/l，神清、语言可，双侧瞳孔等大、等圆，对光反应灵敏，瞳孔直径3毫米，眼球运动正常，伸舌居中，颈抗阴性，双上肢肌力4级，双下肢肌力3级，病理征阴性
2、，四肢肌肉压痛明显，心尖区吹风样杂音。有胸闷，吸氧，血氧饱和度正常。右侧颈部可扪及到一肿块，大约3X4cm大小，质地中等,实验室检查：急诊查（1月17号）血钾4.49 mmol/l 钠135.6 mmol/l；白细胞7.05 X109/L,中性粒82.3%，血小板74 X109/L 血沉37s,血红蛋白128 g/l,。1月17日晚查 血钾4.14 mmol/l 钠135 mmol/l；1月18号：血常规 白细胞7.2 X109/L，中性粒79.6%；血小板60 X 109/L，血红蛋白132 g/l，抽血查血培养。乳酸脱氢酶325 U/L 肌酸激酶161.3 U/L;尿素氮11.2 mmol
3、/l 肌酐131.7 umol/l 血糖6.98 mmol/l 白蛋白34.7 g/l 总胆27.3 umol/l 直胆8.9 umol/l 间胆18.4 umol/l 谷丙48 u/l 谷草60 u/l。FT3 1.92 pg/ml FT4 1.37 ng/dl TSH 0.12 uIU/ml。头颅颈椎MRI：1.左颞叶脑软化灶形成；2.双侧半卵圆中心多发腔梗；3.大脑萎缩，脑白质疏松；4.颈3/4、4/5、5/6、6/7椎间盘膨出并向后方轻度突出；5.颈椎退行性变；6.甲状腺体积明显增大且信号不均匀，性质待定，,腰穿：脑脊液清亮,压力240mmH2O,蛋白547 mg/l,氯113 mmo
4、l/l,糖4.10 mmol/l,白细胞10 X106/L,红细胞0.5 X109/L。1月18日查体较前无明显变化，自诉无力稍好转，仍有肌痛，发热，38度左右；1月19日体温37.7-38度，血压136/98 mmHg，神志欠清、夜间有讲胡话，双侧瞳孔等大、等圆，对光反应灵敏，瞳孔直径3毫米，水平眼震阳性，伸舌居中，颈抗弱阳性，双上肢肌力3级，双下肢肌力3级，肌肉压痛明显，病理征阴性。心尖区吹风样杂音。20日 体温37.2度，血压110/70 mmHg，神志模糊、夜间有讲胡话，问话不能准确应答，双侧瞳孔等大、等圆，对光反应灵敏，瞳孔直径3毫米，眼球固定，左右及上下视不能，眼睑闭合不全，张口费
5、力，伸舌不能，咽反射减退，声嘶，颈抗阳性，左侧肢体肌力3级，右侧肢体肌力0级，病理征阴性，四肢肌肉压痛明显，心尖区吹风样杂音。周身散在出血点，前胸及双侧大腿内侧明显。,1月19号血钾4.28 mmol/l 钠135.5 mmol/l；血常规 白细胞18.2 X109/L，中性粒80.7%；血小板41 X109/L，红细胞3.84 X1012/L,血红蛋白124 g/l,结核抗体阴性。20日转入ICU治疗，20日上午血培养报告：金黄色葡萄球菌感染，尿素氮19.0mmol/l，肌酐214.5umol/l，白蛋白27.5 g/l，总胆53.8 umol/l，直胆27.3 umol/l，间胆26.5
6、umol/l，谷丙51.6 u/l，谷草95.1 u/l，复查腰穿脑脊液蛋白614 mg/l,氯117 mmol/l,糖3.8 mmol/l,白细胞75 X106/L,红细胞0.5 X109/L；CSF压力?头颅MRI 示脑内多发病变并部分出血合并脑梗死可能；左颞叶软化灶，脑白质疏松、脑萎缩同前。颈部CT示甲状腺右叶改变性质待定：结节型甲状腺肿？腺瘤？腺癌？建议进一步检查；肺部CT双侧胸腔积液；心脏增大（左房、左室增大为主），请结合临床；腹部CT两肺感染；胆囊多发结石；肝及左肾低密度灶性质待定，建议上腹部CT增强扫描；肝多发钙化灶。头颅CT示双侧额叶、左侧顶、枕叶及右侧小脑半球病变，结合临床考
7、虑脑炎并出血可能性大，不除外合并部分脑梗死，建议治疗后复查。,病例特点,1 中老年男性病人，突发四肢无力、疼痛，以下肢无力明显，进行性加重，发展到眼球固定、双眼睑下垂，声音嘶哑，吞咽困难，左侧肢体瘫痪。2 发病前有感冒病史，既往有脑外伤、高血压病史3 胸腹部、大腿内侧、脚趾有散在的、大小不等出血瘀斑、疱疹。4 甲状腺肿块已有2个月，甲状腺功能示甲减5 实验室检查：入院时白细胞总数7.05 X109/L,中性粒82.3%，随着病情发展，白细胞总数增加，中性粒细胞数增加；入院时血小板减少血小板74 X109/L，第二天血小板60 X 109/L，第三天血小板41 X109/L,5 血培养示金黄色葡
8、萄球菌感染，以后在尿液、多次血培养均发现金黄色葡萄球菌感染，痰培养克雷柏氏菌。6 肾功能逐渐加重1月18号尿素氮11.2 mmol/l 肌酐131.7 umol/l，19号尿素氮19.0mmol/l，肌酐214.5umol/l，20号7 脑脊液：1月18号压力240mmH20,白细胞10 X106/L,19号压力？白细胞75 X106/L8 TSH受体抗体（+）GAD抗体（-）丙肝抗体（+）TF3,2.02,TSH 0.05,D二聚体（+）FDP(+)TG-G(-)C反应蛋白156.40，肌钙蛋白17.99ABO血型 A型，RH血型（+）,头部CT,MRI演变,头部CT,MRI演变,头部CT,
9、MRI演变,头部CT,MRI演变,头部CT,MRI演变,头部CT,MRI演变,头部CT,MRI演变,头部CT,MRI演变,甲状腺CT,强化的MRI,强化的MRI,神经影像学点评,该病例神经影像学演变有以下几个特点：1 由于病情发展快，神经影像学变化大，做到实时跟踪。2 发病第五天第一次头部MRI平扫，除左侧颞叶因脑外伤所致脑软化灶外，可见右侧额叶散在的大小不一类似脑梗死灶。如图所示。未见出血等其他病灶。,3 发病第七天头部MRI平扫，DWI,CT显示病灶播散、广泛，小脑、双侧大脑半球白质、灰质均有病灶，出血与类似梗死灶同时存在。但是，中线结构没有移位，脑室系统内未见出血。脑干未见明显病灶，与临
10、床表现不符（眼球固定、双眼睑下垂、声音嘶哑）。此时，已有胸、腹部、大腿内侧散在暗红色疱疹。在ICU抢救后，病情一度有好转。,4 发病后第十天，头部CT示脑出血，脑室内出血。但是，中线结构仍然没有移位。病情进行性加重，出现昏迷。,5 发病第十三天，头部CT没有很大变化（与23号比较），病情有所好转，皮疹消退，输血小板后，血小板有所恢复。但是，神经系统状况无好转。,结合文献讨论,金黄色葡萄球菌简介,金黄色葡萄球菌(Staphyloccocus aureus Rosenbach)是人类的一种重要病原菌，隶属于葡萄球菌属（Staphylococcus），有“嗜肉菌”的别称，是革兰氏阳性菌的代表，可引起
11、许多严重感染。金黄色葡萄球菌细胞壁含90%的肽聚糖和10%的磷壁酸。其肽聚糖的网状结构比革兰氏阴性菌致密，染色时结晶紫附着后不被酒精脱色故而呈现紫色，相反，阴性菌没有细胞壁结构，所以紫色被酒精冲掉然后附着了沙黄的红色。新出现的耐甲氧西林金黄色葡萄球菌，被称作超级细菌，几乎能抵抗人类现在所有的药物，但是万古霉素可以对付它。典型的金黄色葡萄球菌为球型，直径0.8m左右，显微镜下排列成葡萄串状。金黄色葡萄球菌无芽胞、鞭毛，大多数无荚膜，革兰氏染色阳性。金黄色葡萄球菌营养要求不高，在普通培养基上生长良好，需氧或兼性厌氧，最适生长温度37C，最适生长pH7.4,干燥环境下可存活数周。平板上菌落厚、有光泽
12、、圆形凸起，直径12mm。血平板菌落周围形成透明的溶血环。金黄色葡萄球菌有高度的耐盐性，可在1015%NaCl肉汤中生长。可分解葡萄糖、麦芽糖、乳糖、蔗糖，产酸不产气。甲基红反应阳性，VP反应弱阳性。许多菌株可分解精氨酸，水解尿素，还原硝酸盐，液化明胶。金黄色葡萄球菌具有较强的抵抗力，对磺胺类药物敏感性低，但对青霉素、红霉素等高度敏感。对碱性染料敏感，十万分之一的龙胆紫液即可抑制其生长。,流行病学,金黄色葡萄球菌在自然界中无处不在，空气、水、灰尘及人和动物的排泄物中都可找到。因而，食品受其污染的机会很多。美国疾病控制中心报告，由金黄色葡萄球菌引起的感染占第二位，仅次于大肠杆菌。金黄色葡萄球菌肠
13、毒素是个世界性卫生难题，在美国由金黄色葡萄球菌肠毒素引起的食物中毒，占整个细菌性食物中毒的33%，加拿大则更多，占到45%，我国每年发生的此类中毒事件也非常多。金黄色葡萄球菌的流行病学一般有如下特点：季节分布，多见于春夏季；中毒食品种类多，如奶、肉、蛋、鱼及其制品。此外，剩饭、油煎蛋、糯米糕及凉粉等引起的中毒事件也有报道。上呼吸道感染患者鼻腔带菌率83%，所以人畜化脓性感染部位，常成为污染源。一般说，金黄色葡萄球菌可通过以下途径污染食品：食品加工人员、炊事员或销售人员带菌，造成食品污染；食品在加工前本身带菌，或在加工过程中受到了污染，产生了肠毒素，引起食物中毒；熟食制品包装不密封，运输过程中受
14、到污染；奶牛患化脓性乳腺炎或禽畜局部化脓时，对肉体其他部位的污染。金黄色葡萄球菌是人类化脓感染中最常见的病原菌，可引起局部化脓感染，也可引起肺炎、伪膜性肠炎、心包炎等，甚至败血症、脓毒症等全身感染。金葡菌还是医源性感染原因之一金黄色葡萄球菌的致病力强弱主要取决于其产生的毒素和侵袭性酶：,a.溶血毒素：外毒素，分、四种，能损伤血小板，破坏溶酶体，引起肌体局部缺血和坏死 b.杀死白细胞素：可破坏人的白细胞和巨噬细胞 c.血浆凝固酶：当金黄色葡萄球菌侵入人体时，该酶使血液或血浆中的纤维蛋白沉积于菌体表面或凝固，阻碍吞噬细胞的吞噬作用。葡萄球菌形成的感染易局部化与此酶有关 d.脱氧核糖核酸酶：金黄色葡
15、萄球菌产生的脱氧核糖核酸酶能耐受高温，可用来作为依据鉴定金黄色葡萄球菌 e.肠毒素：金黄色葡萄球菌能产生数种引起急性胃肠炎的蛋白质性肠毒素，分为A、B、C1、C2、C3、D、E及F八种血清型。肠毒素可耐受100C煮沸30分钟而不被破坏。它引起的食物中毒症状是呕吐和腹泻。此外，金黄色葡萄球菌还产生溶表皮素、明胶酶、蛋白酶、脂肪酶、肽酶等。,金葡菌引发各种疾病,1 肠炎：多因原发疾病长期用抗生素引起肠道菌群失调所致（如感冒），抗生素敏感菌株受到抑制，耐药的金黄色葡萄球菌株趁机繁殖。金黄色葡萄球菌为侵袭性细菌，能产生毒素，对肠道破坏性大，所以金黄色葡萄球菌肠炎起病急，中毒症状严重，主要表现为呕吐、发
16、热、腹泻。呕吐常在发热前出现，发热很高。轻症大便次数稍多，为黄绿色糊状便；重症大便次数频数，每日可达数十次，大便呈暗绿色水样便，外观像海水，所以叫海水样便。粘液多，有腥臭味，有时可排出片状伪膜，将伪膜放入生理水，脱落的肠粘膜即漂在水面上，对诊断帮助很大。体液损失多，患儿脱水、电解质紊乱和酸中毒严重，可发生休克。挑选大便粘液部分涂片，在显微镜下检查可见大量脓细胞，如经革兰氏染色，显微镜检查可见成堆的大量革兰氏阳性球菌。大便培养金黄色葡萄球菌生长，即可明确诊断。,2 亚急性细菌性心内膜炎：病因：1，病原体侵入血流：引起菌血症败血症或脓毒血症并侵袭心内膜；2，心瓣膜异常：有利于病原微生物的寄居繁殖；
17、3，防御机制的抑制：例如肿瘤患者使用细胞毒性药物和器官移植患者用免疫抑制剂时病因包括各种细菌真菌及贝纳特考克斯体（coxiella burnettii）等。,临床症状亚急性感染性心内膜炎：较急性者为常见且重要（1）一般表现：大多数病例起病缓慢，低热、乏力疲倦、少数起病急，有寒战、高热，或栓塞现象；部分患者起病前有口腔手术史，呼吸道感染、流产或分娩的病史。（2）发热：伴全身性感染时，发热最常见，常呈原因不明的持续发热一周以上，不规则低热多在38.540之间，也可为间歇热或弛张热伴有乏力盗汗，进行性贫血，脾肿大，晚期可有杵状指（3）精神障碍：患者可伴有轻微的精神症状，但极少出现严重的精神错乱或谵妄
18、，若心内膜炎并发蛛网膜下腔出血或脑膜炎，则常会出现激越行为，精神错乱和意识障碍，亦可伴有局灶性的神经系统体征 未治疗的急性患者几乎均在4周内死亡，亚急性者的自然史一般6个月。预后不良因素中以心力衰竭最为严重。除耐药的格兰阴性杆菌和真菌所致的心内膜炎者外，大多数患者可获细菌学治愈。但本病的近期和远期病死率仍较高。,体证：原有心脏病杂音，相当一部分的病例在病程中杂音的性质及强度发生改变。部分病例有欧氏小结，也可有詹恩威结。后期可见脑、脾、肾等器官栓塞相应体征。,Toxic Shock Syndrome（TSS)Author:Ramesh Venkataraman,MBBS;Chief Editor
19、:Michael R Pinsky,MD,CM,FCCP,FCCM 定义：Toxic shock syndrome(TSS)is a toxin-mediated acute life-threatening illness,usually precipitated by infection with either Staphylococcus aureus or group A Streptococcus(GAS),also called Streptococcus pyogenes,临床表现：It is characterized by high fever,rash,hypotensio
20、n,multiorgan failure(involving at least 3 or more organ systems),and desquamation,typically of the palms and soles,1-2 weeks after the onset of acute illness.The clinical syndrome can also include severe myalgia,vomiting,diarrhea,headache,and nonfocal neurologic abnormalities.,金黄色葡萄球菌脑膜炎,一、病因 主要是亚细，
21、其次颅脑损伤、颅脑手术后及腰椎穿刺时消毒不严也可并发脑膜炎。脑膜附近的感染病灶如中耳炎、乳突炎、鼻窦炎等亦可引起该病。新生儿脐带和皮肤的金葡菌感染也可继发脑膜炎，发病时间多在产后2周左右。其他易患因素为：糖尿病、静脉滥用毒品、血液透析及恶性肿瘤等。二、发病机制 细菌侵入脑膜可有多种途径：血源性：经血循环进入脑膜；直接扩散：可以是颅脑外伤从颅外如耳部或鼻部感染向颅内扩散；逆行性血栓性脉管炎；医源性通路：颅脑手术的污染、脑室引流及造影而将化脓菌直接接种于蛛网膜下腔。细菌抵达脑膜引起化脑，其致病机制和病理改变与脑膜炎球菌脑膜炎相似,三、临床表现 起病不太急，常于原发化脓性感染数天或数周后发病，多有全
22、身感染中毒症状。畏寒发热，伴持久而剧烈的头痛，颈强直较一般脑膜炎明显。除有脑膜炎症状外，尚有局部感染病灶，败血症患者还可有其他迁徙性病灶。还可出现皮疹，如荨麻疹样、猩红热样皮疹或小脓疱疹。皮肤可见出血点，但很少融合成片，与脑膜炎球菌脑膜炎不同。如败血症过程中出现头痛、呕吐、神志改变、脑膜刺激征等表现，应及时地进行脑脊液检查。病变以蛛网膜下腔为主，额叶、颞叶、顶叶部位较明显，病程中可出现硬膜下积液、积脓，颅底粘连，可致脑神经损害。并发脑脓肿者，可发生肢体瘫痪。,ThyroiditisAuthor:Robert P Hoffman,MD;Chief Editor:Stephen Kemp,MD,P
23、hD,Medscape The broad category of thyroiditis includes the following inflammatory diseases of the thyroid gland:(1)acute suppurative thyroiditis,which is due to bacterial infection;(2)subacute thyroiditis,which results from a viral infection of the gland;and(3)chronic thyroiditis,which is usually au
24、toimmune in nature,Acute suppurative thyroiditis is rare in childhood because the thyroid is remarkably resistant to hematogenously spread infection.Most cases of acute thyroiditis involve the left lobe of the thyroid and are associated with a developmental abnormality of thyroid migration and the p
25、ersistence of a pyriform sinus from the pharynx to the thyroid capsule.The usual organisms responsible include Staphylococcus aureus,Streptococcus hemolyticus,and pneumococcus.Other aerobic or anaerobic bacteria may also be involved.,History A history of acute illness,including fever,chills,neck pai
26、n,sore throat,hoarseness,and dysphagia,is common.Neck pain is frequently unilateral and radiates to the mandible,ears,or occiput.Neck flexion reduces the severity of the pain.The pain worsens with neck hyperextension.Physical Acute thyroiditis The patient may have a fever of 38-40C.Acute illness may
27、 be evident.Neck tenderness is present,and the swollen thyroid gland is tender.The swelling and tenderness may be unilateral.Erythemas develop over the gland,and regional lymphadenopathy may develop as the disease progresses.Abscess formation may occur,Laboratory Studies Acute thyroiditis Laboratory
28、 abnormalities in acute thyroiditis reflect the acute systemic illness.Findings include leukocytosis with a left shift and an increased sedimentation rate.Thyroid function test results are within the reference range,Subacute thyroiditis is generally thought to be due to viral processes and usually f
29、ollows a prodromal viral illness.Various viral illnesses may precede the disease,including mumps,measles,influenza,infectious mononucleosis,adenoviral or Coxsackievirus infections,myocarditis,or the common cold.Other illnesses or situations associated with subacute thyroiditis include catscratch fev
30、er,sarcoidosis,Q fever,malaria,emotional crisis,or dental work.The disease is more common in individuals with human leukocyte antigen(HLA)Bw35.,History Subacute thyroiditis Neck tenderness and swelling may occur.Occasionally,the initial symptoms are those of hyperthyroidism.Systemic symptoms such as
31、 weakness,fatigue,malaise,and fever are usually low grade.Physical Subacute thyroiditis The patient may have signs of systemic illness,such as low-grade fever and weakness.Signs of hyperthyroidism,including increased pulse rate,widened pulse pressure,fidgeting,tremor,nervousness,tongue fasciculation
32、s,brisk reflexes(possibly with clonus),weight loss,and warm moist skin,may be present.The thyroid gland may be enlarged and tender,with tenderness exacerbated by neck extension.,Laboratory Studies Subacute thyroiditis The primary laboratory abnormalities are consistent with abnormal thyroid function
33、.Initially,the thyroid-stimulating hormone(TSH)level is suppressed,and the free thyroxine(T4)level is increased.As the disorder progresses,transient or sometimes permanent hypothyroidism may develop.The WBC count is usually within the reference range but may be mildly elevated.High-sensitivity C-rea
34、ctive protein levels are usually elevated in subacute thyroiditis.,Because chronic thyroiditis in children is usually due to an autoimmune process,it is HLA-associated,similar to other autoimmune endocrine diseases.The specific alleles in the atrophic and goitrous forms of the disease vary.The histo
35、logic disease picture varies,but lymphocytic thyroid infiltration is the hallmark of the disease and frequently obliterates much of the normal thyroid tissue.Follicular thyroid cells may be small or hyperplastic.The degree of fibrosis among patients also widely varies.Children usually have hyperplas
36、ia with minimal fibrosis.The blood contains autoantibodies to thyroid peroxidase and,frequently,autoantibodies to thyroglobulin.Autoimmune thyroiditis is also frequently part of the polyglandular autoimmune syndromes.,History Chronic autoimmune thyroiditis is observed in the following 3 patterns:Goi
37、ter that is usually diffuse and nontender:Systemic illness is not evident.The thyroid gland is frequently 2-3 times its normal size and may be larger.The patient,parent,or physician may discover the goiter.Symptoms of hypothyroidism:In children,this frequently includes poor growth or short stature.A
38、dolescent girls may have primary or secondary amenorrhea.Boys may have delayed puberty.Because the disease develops slowly,the patient or parent may not notice other signs of hypothyroidism,including constipation,lethargy,and cold intolerance.The child with diabetes may have decreasing insulin requi
39、rement.Symptoms of hyperthyroidism:These may include poor attention span,hyperactivity,restlessness,heat intolerance,or loose stools.,Physical Chronic autoimmune thyroiditis Initially,an enlarged,lumpy,bumpy,and nontender thyroid is often present.The gland may not be enlarged,particularly in childre
40、n who have profound hypothyroidism.Signs of hypothyroidism include slow growth rate,weight gain,slow pulse,cold dry skin,coarse hair and facial features,edema,and delayed relaxation of the deep tendon reflexes.Signs of hyperthyroidism are occasionally present early in the disease,Laboratory Studies
41、Chronic thyroiditis Laboratory abnormalities reflect thyroid function abnormality and evidence of autoimmunity.TSH levels are increased in children with subclinical and overt hypothyroidism.Free T4 levels are within the reference range in the former and low in the latter.In children with hyperthyroi
42、dism,TSH levels are suppressed.Many children have normal thyroid function and normal TSH levels.Antithyroid peroxidase(antithyrocellular,antimicrosomal)antibody levels elevated above the reference range are the most sensitive indicator of thyroid autoimmunity.Many children also have antithyroglobuli
43、n antibodies,although this is less sensitive and less specific.,staphylococcus aureus encephalitis,After acute development of a left sided palsy a 57-year-old Caucasian German woman was referred to us with a preceding 4-day history of high-grade fever,coughing andgeneral weakness.Due to mechanical r
44、eplacement of theaortic valve 11 months ago,ampicillin and sulbactam hadbeen selected for antibiotic treatment.Initial chest X-ray,transthoracic echocardiography,abdominal ultrasound,and cultures of blood and urine had all been negative forsigns of infection.,The neurological exam revealed left faci
45、al weakness,slurriness of speech,left-sided hemi-paresis and hemihypaesthesia whereas clinical examina-tion was normal apart from minor respiratory distress.Blood tests showed a normal white cell count,a lowplatelet count(60 109/l),elevations of creatine kinase(466 U/l),serum troponin T(0.04 g/l),an
46、d an elevatedCRP(471 mg/l)while coagulation tests demonstrated anINR of 2.4(under coumarine treatment)that was normal-ized rapidly thereafter.,The initial brain CT and MRI revealed two secondarily haemorrhaged infarcted areas(Figure 1).The analysis of the cerebrospinal fluid displayed a cell count o
47、f 127/l,a total protein of 1.36 g/l and lactate concentration of 3.5 mmol/l.Because of the severe septic clinical course antibiotic therapy was changed to ceftriax-one,gentamicin and linezolid.Complementary transoeso-phageal echocardiography showed two major vegetations on the mechanical aortic valv
48、e and the development of an aortic ring abscess(Figure 1,I+J).These findings pointedconclusively to a septic embolic encephalitis due to IE.,A severe deterioration of the patient s clinical conditioncaused by additional intracranial bleedings four days later(Figure 1,C+D)prevented a surgical replace
49、ment of theaortic valve.All blood cultures revealed a Staphylococcusaureus bacteriaemia resistant to the formerly appliedampicillin but sensitive to gentamicine and linezolid.Although medical therapy was intensified,the patientfinally died from cardiac failure.,Figure 1.Axial cNECT and cMR images on
50、 admission(A+B,E-H)and 4 days after onset of neurological symptoms(C+D).(A+B)NECT images show initially small cortical bleedings left frontal and right occipital and swollen cortex sections right occipital.(C+D)4 days later the haemorrhage is enlarged,and multiple zones of infarction are visible.(E+
