神经型布氏杆菌病(特选材料)
6例神经型布氏杆菌病临床特点与分析
6例神经型布氏杆菌病临床特点与分析张丹【摘要】目的:分析探讨神经型布氏杆菌病的临床特点.方法:回顾性分析本院自2009年1月～2012年1月收治的6例神经型布氏杆菌病病例.结果:经临床对症治疗,4例治愈,2例好转.结论:神经型布氏杆菌病传播途径复杂,临床表现多样,易导致误诊；治疗需早期、联合用药、足够疗程治疗方可改善预后.【期刊名称】《内蒙古医学杂志》【年(卷),期】2012(044)011【总页数】2页(P1334-1335)【关键词】布氏杆菌病;布氏杆菌;药物【作者】张丹【作者单位】赤峰市医院神经内科,内蒙古赤峰024000【正文语种】中文【中图分类】R517.9布氏杆菌病是人畜共患的传染性疾病,在我国主要流行于内蒙古自治区、吉林省、黑龙江省和新疆维吾尔自治区等地,其致病菌为布氏杆菌。
当患者以神经系统局部症状为首发症状就诊时,如临床医师对本病表现认识不足,极易造成误诊,因此本文就我院2009～2012年收治的6例神经型布氏杆菌病患者的临床特点进行详细的解析,以使临床医师获得较全面的认识。
1 资料及方法1.1 临床资料6例均为住院患者,男性 4例,女性2例;年龄29～45岁,平均年龄34.5岁;病程15～60 d,所有患者均符合神经型布氏杆菌病的诊断标准。
1.2 神经型布氏杆菌病的诊断标准[1]①流行病学接触史:密切接触家畜、野生动物(包括观赏动物)、畜产品、布氏杆菌培养物等,或生活在疫区;②出现神经系统的相关临床表现;③脑脊液改变早期类似病毒性脑膜炎,后期类似于结核性脑膜炎;④从患者血、脊髓或脑脊液中分离出布氏杆菌,或者血清学凝集试验效价＞1:160,或者脑脊液布氏杆菌抗体阳性;⑤经针对布氏杆菌的有效治疗后病情好转;⑥除外其他相似疾病。
1.3 临床表现神经系统损害表现:头痛3例,脑膜刺激征阳性2例,手足麻木2例,双下肢无力1例,面神经瘫痪1例,听力减退1例。
全身系统损害表现:发热2例,淋巴结肿大3例,肝脾肿大3例,食欲不振、腹痛、腹泻 2例,关节痛1例。
布氏杆菌病ppt课件
病原学（Etiology）
布氏杆菌-- G-阴性多形性球杆状细菌，无鞭毛，无芽孢，无荚膜，不运动 根据储存宿主菌种的不同分6个种： 羊布氏杆菌 （马尔他布氏杆菌） 致病力最强 牛布氏杆菌 （流产布氏杆菌） 致病力最弱 猪布氏杆菌 致病力次强 犬布氏杆菌 隐匿发病，复发/慢性化 绵羊附睾布氏杆菌 沙林鼠布氏杆菌
流行病学 （Epidemiology）
传染源（source of infection） ： 病畜，以羊为主，包括绵羊、山羊、其次为牛（黄牛、水牛、奶牛）及猪。我国主要为羊布氏杆菌病 传播途径（route of transmission）： 主要经皮肤黏膜接触传播，亦可经消化道、呼吸道传播。 易感人群（susceptible population）： 普遍易感，病后有一定免疫力，再次感染发病率2%-7%。
发病机制复杂，细菌、毒素和变态反应均参与 累及范围广，以单核巨噬细胞系统、骨关节系统、神经系统最常见 机体免疫功能正常，可通过细胞免疫和体液免疫清除病菌而痊愈 机体免疫功能低下/感染菌量大、毒力强，则部分细菌逃逸免疫，被吞噬细胞带入新的组织器官形成新感染灶--多发性病灶阶段。感染灶的细菌再次入血导致复发。
世界各地均有发病 WHO统计：>50万人/年 中国： 地区分布： －常见于牧区，20~60年代，6000人次/年 －近年增多，主要在内蒙、新疆、青海、甘肃、宁夏、山东等地有流行区 主要流行类型： －羊型，其次为牛型，少数为猪型。 流产布氏杆菌、马尔他布氏杆菌为主要病原体
地区性: 牧区最多，半农半牧区次之， 农业区又次之，城市最低 职业性：兽医、畜牧者、屠宰工人 季节性：春末夏初，家畜流产高峰后 1-2个月最多。
流行特点 （epidemic characteristics）
神经布鲁氏菌病
１４（６）：１７
福平。 ３．２预后
Ａｌ Ｄｅｅｄ等治疗１３例神经布病患者元１例复发，由急性
脑膜脑炎和乳头状水肿而迅速恢复的病人均无后遗症。脑膜
９杨忠礼译．酷似偏头痛的神经布氏菌病．地方病译丛，１９９３，１４（６）：
神经系统发生病变的患者中，中枢神经系统的损害占３０％， 周围神经损害占６０％，植物神经损害占１０％。中枢神经系统 的损害多表现为脑膜炎、脑炎和脊髓炎，由于脑膜感染，致使
经系统损害。神经系统的病理变化为退行性、渗出性、增殖一
肉芽肿性和硬化性改变，除炎症外，还常见有中枢神经系统的 营养不良性改变。Ｓｈｅｈａｂｉ等对约旦大学医院１０６例布病患者 进行检测【６Ｊ，发现有６例病人有脑膜炎。日］阻ｚａＩ【报道ｌ例１３ 岁女孩左眼急性失明Ｌ＿川，并伴有双侧视神经乳头水肿，眼眶计 算机断层扫描显示视神经增厚和不规则。Ｍｄｅ觚等报道了１８
１临床特征
神经布病的临床表现是多种多样的，且易与许多神经系
侧小脑征候和双侧视乳头水肿。对中枢神经系统实际侵犯的
频率可能不同，姚等认为３％～５％，Ｓｐｉｎｋ认为是１０％，
址哪吣ｌ（ｙ认为是２５％。ｎｎｃｈ锄等从临床病理学观点将神经
布病分为急性或慢性脑膜炎、多数神经根炎和播散性中枢神
统性疾病（如神梅毒、神经官能症等）相混淆。据统计…，在
发电位（ＢＪ旧）检测听神经等均可作为神经布病的辅助诊断
方法。
３治疗及预后
３．１
在１：６４０、１：１ ２８０以上；（４）对化疗有一定的临床反应。Ｍｄｅａｎ 等认为神经性布病者应符合下列标准：（１）神经症状和体征不 能用其他疾病解释；（２）布氏菌凝集滴度＞ｌ：１６０；（３）若患者 尚未治疗，则脑脊液淋巴细胞增多；（４）经特异性治疗临床情 况改善。还有人认为，当具备下列至少一条标准应考虑脑膜
布氏杆菌病的症状及治疗方法
布氏杆菌病的症状及治疗方法章节安排：1. 引言：介绍布氏杆菌病的背景和概述2. 症状：详细描述布氏杆菌病的常见症状3. 治疗方法：介绍常用的治疗布氏杆菌病的方法4. 结论：总结布氏杆菌病的症状及治疗方法布氏杆菌病的症状及治疗方法引言布氏杆菌病是一种由布氏杆菌（Brucella）引起的人畜共患传染病，是一种世界范围内的重要公共卫生问题。
本论文旨在概述布氏杆菌病的症状及治疗方法，为广大读者提供了解和认识这种疾病的基础。
症状布氏杆菌病的症状多样，主要包括以下几个方面：1. 发热：高热是布氏杆菌病的典型症状，持续数天至几周不等。
2. 寒战：患者常伴有明显的寒战症状，特别是在发热初期。
3. 乏力：布氏杆菌病会引起患者持续乏力，使其无法进行正常工作和日常活动。
4. 头痛：部分患者会出现不同程度的头痛，可伴随着眼部不适或视力模糊等症状。
5. 关节疼痛：布氏杆菌病可引发关节疼痛，多为多关节受累，甚至导致关节肿胀、功能损害。
6. 肝脾肿大：约有一半患者可出现肝脾肿大现象，患者常伴有食欲不振、腹胀等相关症状。
7. 精神障碍：在慢性布氏杆菌病的患者中，约有1/3会出现神经精神症状，如抑郁、焦虑和睡眠障碍等。
治疗方法布氏杆菌病的治疗主要包括药物治疗和支持治疗两个方面：1. 药物治疗：常用的治疗布氏杆菌病的药物包括多西环素、链霉素、氟喹诺酮类药物等。
根据患者的病情和病程，医生会根据具体情况确定药物的剂量和疗程。
2. 支持治疗：在治疗布氏杆菌病的过程中，患者需要适当的休息和调整饮食。
对于合并其他症状的患者，医生会针对性地进行相应的治疗，比如给予镇痛药物或抗抑郁药物等。
结论布氏杆菌病是一种严重危害人畜健康的传染病。
通过对布氏杆菌病的症状和治疗方法的论述，我们了解到早期诊断和治疗对于提高患者的治愈率至关重要。
在布氏杆菌病的治疗中，合理使用抗生素药物是至关重要的，同时还需配合适宜的支持治疗，以提高治疗效果。
为了遏制布氏杆菌病的传播，加强公众的健康教育和卫生常识普及也非常重要，增强人们对布氏杆菌病的认识，减少患病风险。
神经型布氏杆菌病
NeurobrucellosisOsman Kizilkilic,MD a,*,Cem Calli,MD bBrucellosis is a multisystem infection that can involve any organ system and may present with a broad spectrum of clinical presentations.Nervous system involvement of brucellosis is known as neurobrucellosis (NB).The nervous system may be one of several systems involved in chronic diffuse brucellosis 1or,rarely,neurologic findings may be the only signs of brucellosis.1–4NB has neither a typical clinical picture nor specific CSF findings.In endemic areas,NB must be considered in the differential diagnosis of patients presented with neurologic symptoms and concomitant fever.PHYSIOPATHOLOGY OF NEUROBRUCELLOSIS The exact mechanism by which the organism rea-ches nervous system is uncertain but,after gaining entry into the body,it invades the reticuloendo-thelial system from where it reaches the blood stream,causing bacteremia,and later reaches the meninges.When host immunity declines,the or-ganism proliferates and invades other nervous system structures.5,6The occurrence of NB during the acute phase of illness may be due to direct deleterious effects oforganisms invading nervous tissues,to the releaseof circulating endotoxins,or to the immunologic and inflammatory reactions of the host to the presence of these organisms within the nervous system or within other tissues of the body.1Brucella bacteria may affect the nervous system directly or indirectly as a result of cytokine or endotoxin on the neural tissue.Cytotoxic lympho-cytes and microglia activation play an immunopatho-logic role in this disease.A depressed immune status is believed to be a risk factor for developing NB.1Nervous system involvement in brucellosis might be due to the persisting intracellular micro-organisms or,perhaps,the infection triggers an immune mechanism leading to neuropathology.7,8In an experimental animal model,the ganglioside-like molecules expressed on the surface of Brucella melitensis were found to induce anti-ganglioside membrane 1(GM1)ganglioside antibodies,result-ing in flaccid limb weakness and ataxia-like symptoms.7,9Involvement of the CNS in brucellosis has been reported with the incidence varying between 0.5%and 25%in different series.10–16Neurologiccomplications of Brucella are rarely seen in chil-dren 17–22;the rate of neurologic complications is0.8%of children affected with systemic brucel-losis.22NB is categorized according to the clinical manifestation,which is CNS or peripheral nervous system involvement,or a combination.23Some immunologic mechanisms operate to produce the demyelinating lesions in the cerebral and spinal cord white matter.13,20,24Although the NB is not very common,it has marked clinical importance for its severity and morbidity.CLINICAL PRESENTATION OFNEUROBRUCELLOSISClinical presentations of NB vary widely because Brucella exhibits a great affinity for the meninges.Brucella enters the CNS during the first stage of the disease by hematogenous spread;then,latent or clinical meningitis occur,from which microor-ganisms may eventually invade the neighboring nervous structures.17The early manifestations appear during the course of the septicemia or a Department of Radiology,Cerrahpasa Medical Faculty,University of Istanbul,34300Kocamustafapasa,Istanbulb Department of Radiology,Medical Faculty,Ege University,35100Bornova,Izmir,Turkey*Corresponding author.E-mail address:ebos90@KEYWORDSNeurobrucellosis Brucellosis NeuropathologyNeuroimag Clin N Am 21(2011)927–937doi:10.1016/j.nic.2011.07.0081052-5149/11/$–see front matter Ó2011Elsevier Inc.All rights reserved.ne u r o i m a g i n g .t h e c l i n i c s .c o mshortly after its termination,whereas the late ones, which are more frequent,may last months or years after having occurred in the septicemic period, which many times are subclinical.17NB can present at any stage of systemic brucel-losis and several clinical forms,such as meningi-tis,meningoencephalitis,brain abscess,epidural abscess,myelitis,radiculoneuritis,cranial nerve involvement,or demyelinating or vascular disease, may be seen.10,13,15,25The clinical manifestation in this group included fever,headache,sweating, weight loss,and neurologic manifestations,such as papilledema,seizures,confusion,polyradicul-opathy,and lymphocytic meningitis.7,26Headache and psychiatric symptoms may develop owing to the toxic effect of NB.20The most common clinical form is meningitis or meningoencephalitis,occurring in50%of the cases(Figs.1and2).Development of basal menin-gitis may lead to lymphocytic pleocytosis,cranial nerve enhancement,and intracranial hypertension. It is characterized by CSF pleocytosis and high protein levels.1,12,27In cases with brucellosis,other possible causes of infection of inflammatory dis-ease such as tuberculosis,fungal infection,or sarcoidosis can be ruled out by the negative culture of CSF or granuloma,and the high index of suspi-cion of brucellosis with positive Brucella titers and marked improvement with adequate treatment. Various chronic manifestations are perhaps best divided into those presenting with peripheral neuropathy or radiculopathy and those presenting with more diffuse CNS involvement including myelitis with cranial nerve involvement and a syn-drome of parenchymatous dysfunction.1,2,15 Symptoms of peripheral neuropathy and radi-culopathy include back pain,areflexia,and para-paresis with involvement of the proximal nerve radicals.In patients with diffuse CNS involvement, myelitis is evidenced by back pain,spastic para-paresis,and demyelination and can also occur with cerebellar dysfunction.The syndrome of parenchymatous dysfunction can occur at any point in the CNS but it most commonly affects the cerebellum,spinal cord and cerebral white matter.Meningovascular complica-tions,in particular mycotic aneurysms,ischemic strokes,and subarachnoid hemorrhage are relatively common.1–3NB can present with other rare neuro-logic manifestations including isolated intracranial hypertension,Guillain-Barre syndrome,solitary ex-traaxial posterior fossa abscess,cerebral venous thrombosis,and subdural hemorrhage.1,28–31Both pseudotumor cerebri and papillitis(optic neuritis)have been implicated in the pathophysi-ology of papilledema.11,32,33Pseudotumor cerebri is characterized by increased CSF pressure,papilledema,but with generally preserved vision, and pupillary reflexes.Papillitis(optic neuritis) presents as pain on movement of the eyes,papil-ledema,rapidly occurring visual loss and relative afferent pupillary defect.32Spinal granuloma or abscess because of brucel-losis may cause an upper motor neuron-type lesion,whereas brucellar spinal root involvement may cause a lower motor neuron-type lesion.34 All these manifestations can lead to confusion and delay in diagnosis.It may also lead to difficulty in differentiating NB from other chronic infections, especially tuberculosis and syphilis.35 DIAGNOSIS OF NEUROBRUCELLOSISNB has neither a typical clinical picture nor specific CSF findings.36The diagnosis of NB is based on the existence of a neurologic picture not explained by any other neurologic disease,evidenced by systemic brucellar infection,and the presence of inflammatory alteration in CSF.37Examination of CSF typically reveals an elevated protein concentration,a depressed glucose con-centration,and a moderate leukocytosis composed mainly of lymphocytes.2,15,38The exception is the cerebellar syndrome,in which the protein concen-tration is elevated but there is no leukocytosis.1,39 Blood culture is not an ideal test for diagnosis of NB because of low yield and long time it req-uires.1,40As a result of low rate of Brucella isolation from CSF(<20%),the diagnosis of NB mainly depends on the detection of specific antibodies in CSF.1,15,41Although the positive culture is the gold standard for diagnosis,it has been thought to be suboptimal.37,42Neuroimaging and neurophysiologic evaluation combined with the microbiological diagnostic tools is useful for both diagnosis and detection of complications.Accurate diagnosis and proper management of central nervous system brucel-losis appears to be fundamental since it is a very subtle disease.7IMAGING OF NEUROBRUCELLOSISMagnetic resonance imaging(MRI)is the imaging modality with capability to show both parenchymal lesions,and cranial nerve involvement;contrast administration is mandatory for the evaluation of leptomeningeal involvement.Although the imaging methods are important for the diagnosis of neurobrucellosis,the test results must be in accordance with the patient’s clin-ical condition to have diagnostic value.A focal cortical cerebral lesion with nodular enhancement and surrounding edema,increase in perivascularKizilkilic&Calli 928Fig.1.MR images of a51-year-old female with NB(A)Axial T2weighted and T1weighted(B)images show supra-sellar cistern located extraaxial lesion,hypointense on both sequences.Contrast enhanced T1weighted image(C) shows slight leptomeningeal contrast enhancement consistent with inflammation.Axial T2weighted superior section image(D)shows diffuse increased white matter intensity,secondary to white matter involvement3 months post medication MR images obtained show:(E)Axial T2weighted image,contrast enhanced T1weighted image(F)show resolution of suprasellar cistern lesion and leptomeningeal contrast enhancement.929vascularization and generalized inflammation of the white matter can be seen on CT and MRI.17Imaging abnormalities in NB are variable and may mimic other infectious or inflammatory conditions.Imaging appearance reflects inflam-matory or demyelinating processes or vascular insult and does not always correlate with clinical situation.1,26According to the Al Sous and colleagues 26imaging findings of NB are divided into 4categories:normal,inflammation (recog-nized by granulomas,abnormal enhancement of the meninges,perivascular space,or lumbar nerve roots),white matter changes and vascular changes.INFLAMMATION AND IMAGING FEATURES Involvement of one or more cranial nerves is seen in more than 50%of the cases with NB,this is mostly a result of basal meningitis.In cases with Brucellosis the causes of cranial nerve involve-ment include extension of meningeal infection,possible vasculitic processes,pseudotumor cere-bri and side effect of tetracycline which is com-monly used for the treatment of Brucellosis (see Figs.1and 2;Fig.3).Cranial nerve paralyses are seen more frequently during the acute/subacute disease course associated with CNS involve-ment.2,20,22The vestibulocochlear nerve is the most common affected cranial nerve in NB.On the other hand isolated involvement of cranial nerve is a very rare.23,27,33,43Brucellar cranial nerve palsies usually resolve completely with the administration of antibiotics,whereas those withchronic CNS infections often have permanentneurologic deficits.7,8,20,44The abducens nerve has the longest intracranialcourse and is therefore susceptible to direct and indirect insults like microvascular infarction or direct compression.7,45Fig.2.MR images of 24-year-old female presented with headache andfever,CSF examination revealed neurobrucellosis.(A )Axial T2weighted,(B )FLAIR,and (C )T1weighted images,show leptomeningeal thickeningin the right half of prepontine cistern that shows leptomeningeal thick-ening and contrast enhancement in the same location on postcontrastT1weighted image (D ).Kizilkilic &Calli930The pathogenesis of optic neuritis and abdu-cens nerve palsy is speculative.Possible mecha-nisms include extension of meningeal infection secondary to an inflammation of the meninges in the subarachnoid cistern and microorganism reaching the neuroaxis via the bloodstream or lym-phatic system.It attacks the Schwann cells and leads to demyelination.Another theory is a vas-culitic process.The bacterial antigen,antibody,and complement complex are deposited in the vasa nervosum with vascular and perivascular infiltrates.23,46,47Although formation of the granulomas results from inflammation that is relevant to infection,it is a rare manifestation in NB.Brucella meningitis may behave as an exclusively neurologic disease mimicking vascular accidents that are frequently paroxysmal and recurrent.3Computed tomography and MR studies in uncomplicated meningitis are usually normal or some enhancement of the meninges is seen on post contrast images.In granulomatous menin-gitis,enhancement is typically seen in basal meninges,whereas bacterial meningitistypically Fig.3.MR images of a 18-year-old female presented with malasia,fever and headcahe.Physical examination re-vealed nuchal rigidity,microbiological examinations were consistent with NB and meningitis.(A )Axial T2weighted,(B )T1weighted images,show subdural collection on the left side and leptomeningeal thickening.Post contrast Axial (C )and Coronal (D )T1weighted image shows diffuse leptomeningeal thickening,contrast enhancement and subdural effusion (empyema).Neurobrucellosis931shows enhancement over the cerebral convexi-ties.In all types of meningitis contrast MR ismore sensitive than CT.Contrast enhanced FLAIR sequence may be even more sensitive in detecting enhancement.Extension of enhancing subarach-noid exudates deep into the sulci can be seen in severe cases.Imaging of the affected patients is not per-formed routinely other than to ensure the absence of hydrocephalus or abscess before a lumbar puncture is performed.Neuroimaging is indicated if the clinical diagnosis is unclear,if neurologic deterioration occurs secondary to increased intra-cranial pressure or if patients’recovery from the disease is slow.Cortical lesions with surrounding edema show a characteristic enhancement consisting of a cen-tral nodular intense enhancement and a faint peripheral enhancement (target sign)that might reflect diverse stages of brain inflammation,similar to those reported in chronic brain abscess,such as tuberculosis.17,47Early stage of the parenchymal infection is the cerebritis stage.In the cerebritis stage,an ill-defined subcortical hyperintense lesion can be seen in T2W images.During the late stage the central necrotic area is hyperintense on T2W images and show restricted diffusion on diffusion weighted imaging.The thick,somewhat irregularly marginated rim appears iso to mildly hyperintense on T1W images and enhances after administration of contrast media.Peripheral vasogenic edema is always present.Despite its rareness,brucellosis should be consid-ered in the differential diagnosis of focal brain lesionsor leptomeningeal enhancing lesions,especially in the patients with a history of contact with domestic animals,consumption of non-pasteurized lactic pro-ducts or previous brucellosis.17WHITE MATTER INVOLVEMENTThree patterns of white matter involvement that manifests as hyperintense lesions on T2weigh-ted images have been noted.The first pattern is a diffuse appearance affecting the arcuate fibers region,the second pattern is periventricular,and the third pattern is a focal demyelinating appearance.Brain MRI shows extensive bilateral high signal abnormalities in the periventricular white matter on T2-weighted and FLAIR images.MR angiog-raphy could be normal (see Fig.1;Fig.4).Imaging of multifocal white matter hyperintensities on T2W and FLAIR MR Images are nonspecific,and the differential diagnosis of these lesions is very broad.The nature and cause of white matter abnormali-ties are not known,but they may be due to an auto-immune reaction.The white matter involvement may mimic other inflammatory or infectious disease,such as multiple sclerosis,acute disseminated encephalomyelitis,or Lyme disease.11,26,36,48–51In contrast multiple sclerosis these white matter lesions do no tend to locate in the callosomarginal region and they do not enhance.MRI features consisting of high-intensity con-fluent areas in the white matter of the brain around the lateral ventricles are in favor of a demyelinating process.In the presence of any posterior fossa or brain stem lesion highly probable diagnosis will be multiple sclerosis.VASCULAR INVOLVEMENTBrucella infection by itself triggers the immune mechanism leading to a demyelinating state.As the disease gets more chronic,theimmune Fig.4.MR images of a 37-year-old female.(A )Coronal FLAIR,Axial T2(B )weighted images show millimetric hyperintense lesion in the periventricular white matter in both cerebral hemispheres.Axial post contrast T1weighted image (C )shows lack of enhancement of periventricular lesions.Kizilkilic &Calli932mechanism processes increase.20,24This disease does not show predilection of size or location of vascular structure.20The vascular insult is likely due to one of the following two mechanisms.In the first,an inflam-matory process of the small vessels or venous sys-tem causes lacunar infarcts,small hemorrhages,or venous thrombosis.2,26,52–55Brucella can cause vasculitis;it has no predilection of size or location of vascular structure.Arterial and/or venous struc-tures may be affected.56,57Vascular involvement may result in lacunar infarcts,small hemorrhages or venous thrombosis.10The second possible mechanism is hemorrhagic stroke caused by rupture of a mycotic aneurysm,a likely sequel of embolic stroke from brucellar endocarditis.2,26,58,59 The pathogenesis of TIA and ischemic stroke in brucellosis still remains uncertain.Transient cerebral ischemic attacks can be seen secondary to the vascular-perivascular inflammatory reaction or vascular rge vessel involvement is rare in NB.1,7,10Most likely,ischemic stroke in NB is a consequence of an accompanying vascu-litis.2,25Various degrees of vascular inflammation ranging from acute to chronic with the possibility of necrosis and aneurysmal formation have been described in NB.25,60It has been proposed that TIA in brucellosis may be related to infectious vasculitis,cerebral vasospasm or cardioembo-lism.11,60,61Vessel involvement in Brucella may also develop secondary to cardiac embolization leading to necrosis of the occluded vessel and formation of mycotic aneurysm that may rupture and lead to subarachnoid or cerebral hemorrhage.55 Carotid angiograms may disclose diffuse vas-cular spasm in the territory of the affected artery. Most of the patients with ischemic cerebral symp-toms in the literature have normal cerebral angio-grams.61Normal appearance of cerebral vessels in DSA is considered consistent with vasculitis of deep penetrating arteries.11Diffusion weighted imaging is useful in the setting of acute ischemia,as it will detect infarc-tions earlier than conventional MR sequences or FLAIR sequence.Frequently multiple lacunar type infarcts are seen in the distribution of perforating vessels in the brainstem,basal ganglia,and white matter as a result of involvement of basal cisterns and vessels contained therein.Myelitis is generally evidenced by back pain,ataxia, paresthesia,paraplegia and sphincter abnormalities.7 Since NB mimics peripheral and central nervous system pathologies,differential diagnosis is important in probable patients.MR examination shows thick-ening of the spinal roots and diffuse enhancement along the distal cord and caudaequina.Fig.5.MR images of21-year-male with NB and meningitis(A)Sagittal T2weighted image of cervical regionshows intradural-extramedullary hypointense nodular lesions(consistent with granuloma formation).Sagittal postcontrast T1weighted(B)cervical region image shows peripheral enhancement of the spinal cord,and lackof contrast enhancement of intradural-extramedullary lesions.(C)Sagittal and axial(D)postcontrast T1weightedlumbar images show contrast enhancement of the cauda equina and thickening of the filum terminale roots.Imaging following medical treatment show:(E)Sagittal T2weighted cervical MR image shows resolution of intradural-extramedullary lesions.Sagittal contrast enhanced T1weighted image(F)shows resolution of samelesions and lack of contrast enhancement of cervical spinal cord.Sagittal T1weighted postcontrast MR image(G)of lumbar region shows absence of contrast enhancement of the cauda equina.Neurobrucellosis933MR imaging of focal brain involvement by NB is scant,and no specific reports in pediatric patients has been made to date.MYELOPATY AND SPINAL DISEASE Myelopathy may result from different mecha-nisms.Acute transvers myelitis,spinal cord infarc-tion,adhesive arachnoiditis,compression from epidural abscess or from brucellar spondylitis may occur.Brucella spondylitis affects the lumbo-sacral and lower thoracic region most frequently,causing erosion and vertebral collapse leading tocord or cauda equina compression.35The major role of neuroimaging is to identifytreatable conditions that can mimic myelopathy.These include acute disk herniation,hematoma,epidural abscess,or compressive myelopathy.During the acute phase of the myelopathy,MR images are normal in half of the patientsand Fig.6.MR images of a patient presented with acute neurologic deficit and headache.(A )Axial T2weighted,(B )FLAIR images shows hyperintens lesion in the left half of pons.Diffusion weighted image (C )with b 51000sec/mm 2with corresponding ADC map (D )shows restricted diffusion of the same lesion consistent with acute ischemic lesion.Sagittal T1weighted postcontrast image (E )shows thrombosis of the right transvers sinus (filling defect-empty delta sign).MR angiography,MIP image (F )shows normal intracranial arteries.Imaging of the patient after success full medical treatment clinical recovery shows:(G )Axial T2weighted,(H )FLAIR and (I )T1weighted images show lesion on the left side of the pons with CSF-like signal intensity on all images,consistent with chronic lacune.MR venography MIP image (J )shows patency and recanalizationof the right transvers sinus.Kizilkilic &Calli934nonspecific in the other half.Focal cord expan-sion,poorly delineated increased signal in the spinal cord on T2W images may seen.Varying degree of contrast enhancement occurs in some of the cases(Fig.5).CEREBRAL VENOUS THROMBOSIS AND VENOUS INFARCTCerebral venous thrombosis may occur as a complication of certain infections during preg-nancy or postpartum,with contraceptives,in Beh-cet’s disease or systemic lupus erythematosus, and in several coagulopathies including protein C and S antithrombin III deficiency,and in antiphos-pholipid antibody syndrome.62In the acute phase(when the clot is dense), thrombus can be seen on CT as hyperdense in the sinus on non contrast CT.In the subacute phase of the thrombosis,contrast enhanced images show filling defect within the sinus.MR imaging is very helpful for the diagnosis and is the best method of noninvasive investigation. The acutely thrombosed sinus is isointense to the brain parenchyma on T1W images and hypoin-tense to brain on T2W images.This appearance cannot be distinguished from slow flow.When the thrombus is subacute and hyperintens on T1W images it is very easy to recognize(Fig.6). Advances in MR venography have greatly aided the diagnosis of venous sinus thrombosis by MR imaging.Two-dimensional time-of-flight MR ven-ography or phase contrast MR venography can be used to make the diagnosis.Since time-of-flight MR angiography is acquired using T1W images,both moving blood and subacute thrombus may be seen equivocal.CT venography is also a fast and reliable way of making the diagnosis.The MR differential diagnosis of dural sinus thro-mbosis is primarily imaging artifacts that can mimic intravascular clot.These include contrast enhanced scans with flow compensation meth-ods,unenhanced scans with inflow of fully un-saturated spins into the imaged slice(entry phenomena),incorrect pulse sequence selection or misplaced saturation bands,incorporation of hyperintense clot.On CT,venous infarcts are usually poorly de-limited,hypodense or mixed attenuation areas involving the subcortical white matter and causing a slight mass effect on ventricles.On MR,early venous infarcts may be identified by prolongation of T1and T2W images.Reduced diffusion is not an early sign of venous infarction;diffusion appears to be heterogenous with areas of in-creased,normal and decreased diffusion.Some of the venous infarct may be hemorrhagic or maycause hematoma.SUMMARYNB has neither a typical clinical picture nor specificCSF findings and its diagnosis is based on the existence of a neurologic picture not explainedby any other neurologic disease,evidenced by systemic brucellar infection,and the presence of inflammatory alteration in CSF,especially in patients living in endemic areas for the infection. Neuroimaging and neurophysiologic evaluation combined with the microbiological diagnostictools is useful for both diagnosis and detection of complications.Magnetic resonance imaging isthe imaging modality,which may show both parenchymal lesions,and cranial nerve involve-ment;contrast administration is mandatory forthe evaluation of leptomeningeal involvement. 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【精品】特种经济动物题库(1)
特种经济动物题库(1)填空题A1. 特种经济动物：是指家畜、家禽以外被人工驯养的，具有特殊用途和功效，经济价值较高的一类动物。
2. 鹿的配种方法包括自然交配、人工授精两种。
3. 特种经济动物按自然属性分类中，其中特种兽类主要包括其药用价值和皮用价值比较高的哺乳类动物；特种珍禽主要包括其肉用价值、蛋用价值或观赏价值比较高的鸟类动物。
4. 公麝的饲养目的是获得高产、优质的麝香和种用价值较高的公麝，其中麝香和精液产生以蛋白质、矿物质和维生素为物质基础5. 雉鸡的饲养分为育雏期、育成期、种用期三个阶段。
B1. 特种经济动物按用途分为毛皮动物、药用动物、观赏动物、肉用动物、实验动物和伴侣动物六类。
2. 举出7种鹿的常见品种：梅花鹿、马鹿、白唇鹿、坡鹿、黑麂、水鹿和驼鹿。
3. 乌骨鸡的四种常见传染病是新城疫、马立克氏病、传染性法氏囊病和禽流感。
4. 鹿的配种方法包括自然交配和人工授精两种，其中自然交配的最佳配种方式是单公群母。
5. 幼鹿的饲养目的是提高仔鹿成活率，减少疾病发生，加快育成鹿的生长。
C1. 特种经济动物按自然属性分为特种兽类、特种珍禽、特种水产和特种昆虫四类。
2. 麝香和精液产生以蛋白质、矿物质和维生素为物质基础，公麝在泌香期和配种期特别需要甘氨酸、蛋氨酸和含硫氨基酸。
3. 在公鹿繁殖过程中，分别包括配种期、越冬期和生茸期三个重要时期。
4. 雉鸡的常见普通病有鸡白痢、禽巴氏杆菌病、曲霉菌病、硒缺乏症和生物素缺乏症。
5. 麝香具有通诸窍、开经络和透肌骨等药用价值。
D1. 我国麝共有5种，包括林麝、马麝、原麝、黑麝和喜马拉雅麝，其中林麝是饲养的主要品种，其次是马麝。
2. 在母鹿在繁殖过程中，包括配种期、妊娠期和产仔哺乳期三个重要时期。
3. 公鹿的饲养目的是获得高产、优质的鹿茸和种用价值较高的种公鹿。
母鹿的饲养目的是保证母鹿健康，提高繁殖力。
4. 难产的治疗方法有充气助产法、按摩挤压法和破卵助产法三种5. 根据鸡马立克氏病病变发生部位和临床症状，分为神经型、内脏型、眼型和皮肤型。
布氏杆菌病的诊断与治疗
01
02
03
抗生素治疗
急性期布氏杆菌病需要使 用抗生素进行治疗，常用 的抗生素有链霉素、四环 素、磺胺类药物等。
症状缓解
急性期治疗的主要目的是 缓解症状，减轻患者的痛 苦，同时防止疾病进一步 恶化。
预防并发症
急性期治疗过程中，应密 切关注患者病情变化，及 时处理并发症，如心脏疾 病、神经系统疾病等。
血清学检查
检测患者血清中抗布氏杆菌抗体，如酶联免疫吸附试验（ELISA） 和凝集试验等。
鉴别诊断
风湿性疾病
布氏杆菌病与风湿性疾病有相似的关 节痛症状，需要进行鉴别。可通过血 清学检查和细菌学检查进行鉴别。
其他感染性疾病
布氏杆菌病与其他感染性疾病有相似 的发热等症状，需要进行鉴别。可通 过临床表现、实验室检查和病原学检 查进行鉴别。
和预防措施。
疫苗接种与科研进展
疫苗种类
目前市面上主要有单价疫苗、多价疫苗和基因工 程疫苗等。
科研进展
科研人员正在不断探索新型疫苗和治疗手段，以 提高预防和治疗效果。
疫苗接种情况
全球范围内，不同国家和地区的疫苗接种策略和 覆盖率存在差异，需要加强国际合作与交流。
05 布氏杆菌病的康复与预后
康复期护理
定期复查
在康复期间，患者应定期进行身体检查，以便及时发现并处理可 能出现的复发症状。
生活方式调整
保持健康的生活方式，包括规律的作息、均衡的饮食和适量的运动， 有助于提高康复效果。
避免感染
避免接触可能引起感染的环境和人群，以防再次感染布氏杆菌。
预后评估
1 2
评估指标
预后评估的指标包括病情严重程度、治疗方式、 并发症情况以及患者的年龄、身体状况等。
布氏杆菌病临床表现
布⽒杆菌病临床表现 很多患者去医院检查后被确诊为布⽒杆菌病后，都会感到很困惑，会觉得：我就是有点重感冒，怎么就成了布⽒杆菌病呢?在此我想说：那并不是重感冒，只是它的症状跟重感冒很相似，很多⼈都会混淆，误以为⾃⼰只是得了感冒。
那么布⽒杆菌病临床表现有什么呢?下⾯和⼩编来看看吧! 布⽒杆菌病临床表现： 1.急性期患者⼤多起病缓慢，常有前驱症状，如全⾝不适、疲乏⽆⼒、⾷欲不振、肌⾁痛疼、头晕头痛等类似重感冒的症状。
时间持续约3～5天。
但也有约10%～27%的病⼈呈急骤起病，表现为寒战、⾼热、多汗、关节疼痛等。
本病急性期的主要症状有： ①发热典型病例热型呈波浪状，体温逐⽇升⾼，达⾼峰后缓慢下降，热程约2～3周，间歇数⽇⾄2周，⼜发热再起，如此反复数次。
但据统计如此典型热型者仅占15%左右。
其他可表现为低热约占42%、不规则热约占15%。
另外较少见的热型有弛张热、稽留热等。
发热前多伴有畏寒或寒战。
⾼热病⼈神志多清楚，部分病⼈还可下床活动，热退后反觉症状加重，抑郁寡欢，软弱⽆⼒。
②多汗为本病突出的症状，多与发热相伴，亦有部分病⼈处于间歇期时出现此症状。
⼤汗多于夜间或凌晨热退时出现，汗味酸臭，浸湿⾐裤，甚⾄影响睡眠。
⼤多数病⼈感汗后体温下降，体弱⽆⼒，有虚脱感，尤其是⼤汗后。
③关节痛约76%的患者出现关节痛，也是患者最痛苦的症状。
急性期与风湿热相类似，可出现于⼀个或⼏个关节，呈游⾛性，受累者主要为髋、膝、肩、腕、肘等⼤关节。
⾮对称性，局部可有红肿，偶有化脓。
疼痛呈锥刺样、或钝痛，剧烈时患者辗转不安，服⼀般镇痛药不能奏效。
此外尚可见局限性肿胀如滑囊炎、腱鞘炎、关节周围炎等。
在慢性期病变多局限，疼痛固定于某⼀关节。
肌⾁尤其是下肢肌⾁及臀部肌⾁疼痛明显，重者呈痉挛性痛。
④泌尿⽣殖系症状男性患者常有睾丸炎、附睾炎，⽽出现睾丸肿痛，多为单侧。
个别病⼈可有鞘膜积液、肾盂肾炎。
⼥性病⼈可表现为卵巢炎、⼦宫内膜炎及乳房肿痛。
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辅助检查 MRI
• 白质损害： 1、弥散性弓状纤维损害 2、脑室旁病变 3、局灶性脱髓鞘（可及大脑、小脑、脑干、 脊髓） 病灶可类似MS、ADEM、Lyme影像表现。
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辅助检查 MRI
• 血管损害 少见，可见小血管损害
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辅助检查 神经电生理
• 可有正中神经、尺神经、胫神经、腓神经 的运动和（或）感觉传导速度减慢。
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病例汇报
辅助检查： 2015年8月14日肌电图：右侧正中神经（指
1、3）感觉传导波幅减低，余未见异常。F波、H 反射：右胫神经潜伏期延长，右胫前肌重收缩呈 单混相，余未见异常。 诱发电位：VEP双侧P100潜伏期及波形未见异常 。BAEP：听阈L70dB,双侧1波潜伏期正常，双侧3 、5波均未引出肯定波形；SEP：左上肢N9潜伏期 正常，N13、P15、N20、P25未引出肯定波形，左 下肢N8潜伏期正常；N18、P40未引出肯定波形。 提示：中枢性传导异常。
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病例汇报
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病例汇报
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病例汇报
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病例汇报
辅助检查： 2014年3月，肌电图：EMG：双侧股四头肌
、股二头肌自发纤颤电位改变；IP单混相；NCV ：双侧腓总神经、胫神经、坐骨神经运动传导略 减慢，神经传导阻滞，腓肠神经传导、股神经运 动传导正常。F波：左侧腰3-5、右侧腰4-骶1出 现率下降，神经根性传导阻滞。VEP：视觉诱发 电位双侧正常。AEP:脑干听觉神经传导双侧1-5 潜伏期延长，听神经病损。
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诊断
• 无典型临床表现
• 无特异性的CSF和影像特征
• 金标准：脑脊液布氏杆菌培养，阳性率低 ，耗时（6周），目前多采用血清凝集试验 ，1天出结果。
• 无法用神经系统其他疾病解释
• 感染证据，脑脊液感染相（蛋白高，细胞 多，糖可降低），疫区生活史
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鉴别
• 炎症：中枢结核、真菌感染、结节病 **位听神经损害相对特异 血清凝集试验阳性 脑脊液相似
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• 本例为神经型布氏杆菌病，无其他系统损 害证据
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神经型布氏杆菌病
• 传染源：牛羊 • 传播途径：肺、消化道、结膜、破损皮肤 • 发病机制：菌血症--脑膜--免疫低下时进入
中枢神经系统 • 免疫病理：免疫抑制，细胞毒性淋巴细胞
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辅助检查： MRI：2014-1-9日颞骨及内听道MRI可见
桥脑异常信号；2014-3-11胸腰段显示：胸12 可见脊髓水肿；2014-3-14头双侧小脑中脚、 桥脑、颞叶、双侧侧脑室旁白质多发异常信号 。2014-12-2头同3月份，脑白质旁病灶略有增 加。2015-8-13脑桥、双侧侧脑室周围及额颞 叶深部脑白质异常信号；2015-8-17部分马尾 神经强化改变，马尾神经炎？
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鉴别
• 白质病变： MS、ADEM、Lyme病 CSF单核多，蛋白高，血清凝集试验阳性
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治疗
• 多数建议多西环素和利福平两药联用。 • 治疗复查以腰穿阴性为标准，尤其细胞数
和糖正常，蛋白回复正常需要时间长。
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神经型布氏杆菌病
病例汇报学习
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主因：耳鸣3年，听力下降1年半
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现病史：3年前，患者感冒、受凉发热，在当地诊 所治疗过程后期，患者逐渐感觉耳鸣，为风声或下 小雨的沙沙声，伴有听力下降。未在意。2年前（ 2013-10月），患者逐渐感觉大小便排出困难，伴 有双侧小腿疼痛，不受活动影响。18月前（2014-2 月），患者出现双下肢无力，抬小腿和向上勾脚更 明显，双侧小腿疼痛同时明显减轻。并出现大便费 力，小便困难同前。在当地医院治疗，具体方案后 显示，中间应用激素冲击、异烟肼等无改善。
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临床表现
• 颅底脑膜炎 如果影响颅底部，可致1-？个颅神经受累 1、位听神经（为脑干内损害可能大） 2、外展神经（因其走行长，故此，结核颅底 脑膜炎、血管压迫，外伤牵拉等均容易损害 ） 3、面神经损害。
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临床表现
• 急性起病：多为脑膜炎，提醒我们急性脑 膜炎需要想到布氏杆菌病（尤其牛羊接触 史者），可有急性上呼吸道感染表现。
2015年8月14日，脑电图：轻微异常脑电图
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病例汇报
实验室检查：入院后血尿有机酸和血尿毒物筛 查均未见异常。 血液常规检查未见异常。 脑脊液免疫球蛋白：IgG、IgA、IgM均明显升 高。肿瘤标记物、细菌、病毒、结核、脱髓鞘 等检查均阴性，寄生虫检查协和布氏杆菌凝集 试验阳性。
脑脊液检查共六次：均有异常（见图）
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查体：皮层功能正常。颅神经有双眼双向水 平凝视细小眼震，余无异常。运动系统：双 上肢正常，双下肢髋、膝关节5-级，踝关节 肌力5级，右侧膝、踝反射活跃，左侧正常 ，右侧病理征阳性。痛觉双侧L2以下痛觉减 退。肛门反射阴性。
• 慢性时期或慢性起病表现：周围神经（包 括神经根）受累常见，或弥散的中枢神经 受累（常见于小脑、脊髓和脑白质）。
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实验室检查 主要为脑脊液
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辅助检查 MRI
• MRI炎性反应 脑膜增厚、神经根增粗，增强可强化，严重 病例有脑脓肿改变。
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临床表现
• 特点：复杂多样，可及神经系统的所有部 位，或其中几个部位。
• 硬膜外--脑膜--脑--脑干--脊髓--颅神经--脊神 经。可以为血管病、脱髓鞘、脓肿表现
• 可表现症状：精神、情感、认知、意识、 椎体系、锥体外系损害。
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临床表现
• 常见5种： 1、脑膜脑炎 2、脑膜血管病变 3、中枢神经系统脱髓鞘 4、周围神经病 5、颅内压升高