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首页> 外文期刊>The Internet Journal of Tropical Medicine >Acute Meningococcemia Complicating Epidemic Meningitis In Zaria, Nigeria
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Acute Meningococcemia Complicating Epidemic Meningitis In Zaria, Nigeria

机译：尼日利亚扎里亚的急性脑膜炎球菌血症并发流行性脑膜炎

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Neisseria meningitidis is a bacterium known to cause 5-10 years cyclical epidemic meningitis in the meningitic belt of Africa. In these case reports, we highlight the multi-systemic manifestations and management challenges of acute meningococcemia, a rare life threatening complication of epidemic meningitis. Introduction Neisseria meningitidis is a bacterium known to cause 5-10 years cyclical epidemic meningitis or cerebrospinal meningitis (CSM) in the meningitic belt of Africa (1). Acute meningococcemia is a rare life threatening complication of this infection. We highlight the multi-systemic manifestations and clinical sequelae of acute meningococcemia in 3 young patients who were referred to our centre during the 2009 CSM epidemic in Nigeria. All patients were residents of overcrowded rural settlements. Case Histories A 20year old male petty trader (Case 1), a 13year old female pupil (Case 2) and a 16yr old female student (Case 3) each, presented with acute symptoms of headache, fever, vomiting and neck pain associated with microscopic haematuria, haemorrhagic skin lesions, meningeal irritation, oliguria as well as hypotension and altered consciousness. Case 1 had petechaie and purpuric lesions on the right foot while Case 2 had similar lesions on her upper and lower limbs. Both of these patients had mild thrombocytopenia and prolonged international normalised ratio of 2.0. Case 3 had different degrees of purpura, blisters and ulcers all over the body, in addition to recurrent generalized seizures, papilloedema, coma and septic shock. She was bleeding from mucosal orifices with laboratory features of disseminated intravascular coagulation (DIC) (platelet counts of 62 X 109/L, normal range 100-400 X 109/L, prolonged prothrombin time by 8s above control and prolonged Kaolin cephalin clotting time by 17s above control). Gram negative intracellular diploccoci were identified from the cerebrospinal fluids (CSFs) of the patients but Neisseria meningitides was not isolated from CSF and blood cultures, probably because all patients were referred from secondary health facilities where they had received antibiotics. Antigenic detection could not be done due to absence of facilities. Investigations were negative for sickle cell disease and HIV-1/2 infections. Spleen sizes, by abdominal ultrasound, were normal in all patients. Patients were treated with intravenous fluids, dexamethasone 24mg/day in divided doses, and ceftriaxone 2g daily for 3 weeks. While Cases 1 and 2 recovered in the general ward and were discharged without sequelae up to 3 months of follow-up, Case 3 had to be managed in intensive care unit (ICU) with additional transfusions of two units of fresh whole blood. On the 10th day of treatment, she developed bilateral sterile knee arthritis. However, she recovered after 86 days of hospital care and was discharged with residual bilateral knee arthralgia which persisted 3 months post-discharge. The features of hemorrhagic skin lesions, septic shock, DIC and acute renal failure seen in these patients with meningitis are consistent with acute meningococcemia (1). Endothelial dysfunction, vasculitis, and capillary leakage due to the effects of meningococci endotoxin and endotoxin-induced cytokines such as tumour necrosis factor α and interferon γ, underlie these manifestations (1, 2). The occurrence of sterile arthritis in one of the patients may be due to immune complex deposition as suggested by an earlier study from Zaria, Nigeria (3) All the patients reported lived in overcrowded poor rural environment which are known risk factors for epidemic meningitis. While some of the risk factors for meningococcemia, such as sickle cell disease, asplenia and HIV infection, were excluded in our patients, investigations for the role of other risk factors, such as complement deficiency, properdin deficiency and polymorphisms of various inflammatory mediators (1, 2), were limited by the absence of facilities. Acute meningococcemia is a
机译：脑膜炎奈瑟氏球菌是一种细菌，已知会在非洲的脑膜炎带引起5-10年的周期性流行性脑膜炎。在这些病例报告中，我们强调了急性脑膜炎球菌血症的多系统表现和管理挑战，这是一种罕见的威胁生命的流行性脑膜炎并发症。前言脑膜炎奈瑟氏球菌是一种细菌，已知会在非洲的脑膜炎带引起5-10年的周期性流行性脑膜炎或脑脊髓膜炎（CSM）（1）。急性脑膜炎球菌血症是这种感染罕见的威胁生命的并发症。我们重点介绍了在2009年CSM尼日利亚流行期间转诊到我们中心的3例年轻患者的急性脑膜炎球菌血症的多系统表现和临床后遗症。所有患者都是拥挤的农村住区的居民。案例历史一名20岁的男性小商人（案例1），一名13岁的女学生（案例2）和一名16岁的女学生（案例3），均表现出头痛，发烧，呕吐和颈部疼痛等微观症状的急性症状血尿，出血性皮肤病变，脑膜刺激，少尿以及低血压和意识改变。病例1的右脚有petechaie和紫癜性病变，而病例2的上，下肢也有类似的病变。这两名患者均患有轻度血小板减少症，国际标准化比率延长至2.0。案例3的全身性紫癜，水疱和溃疡除了反复发作的全身性癫痫，乳头水肿，昏迷和败血性休克外，其他情况也不同。她因具有弥散性血管内凝血（DIC）实验室特征而从粘膜孔口流血（血小板计数为62 X 109 / L，正常范围为100-400 X 109 / L，凝血酶原时间比对照延长了8s，高岭土脑梗塞时间延长了8s）。超出控制17秒）。从患者的脑脊液（CSF）中鉴定出革兰氏阴性细胞内双球菌，但脑膜炎奈瑟氏球菌并未从CSF和血液培养物中分离出来，可能是因为所有患者均从接受抗生素的二级医疗机构转诊。由于缺少设备，无法进行抗原检测。镰状细胞病和HIV-1 / 2感染调查为阴性。通过腹部超声检查，所有患者的脾脏大小均正常。患者接受静脉输液，地塞米松24毫克/天（分剂量）和头孢曲松钠2克/天治疗3周。病例1和2在普通病房中康复，并且在没有后遗症的情况下出院，长达3个月的随访，而病例3必须在重症监护病房（ICU）进行管理，并另外输注两个单位的新鲜全血。在治疗的第10天，她患上了双侧无菌性膝关节炎。但是，她在住院86天后康复，并因残留的双侧膝关节痛出院，出院后持续3个月。这些脑膜炎患者的出血性皮肤病变，败血性休克，DIC和急性肾功能衰竭的特征与急性脑膜炎球菌血症一致（1）。这些表现是脑膜炎球菌内毒素和内毒素诱导的细胞因子如肿瘤坏死因子α和干扰素γ引起的内皮功能障碍，血管炎和毛细血管渗漏（1、2）。一名患者发生无菌性关节炎的原因可能是免疫复合物沉积所致，这是尼日利亚Zaria较早的一项研究表明的（3）所有患者均报告居住在人满为患的恶劣农村环境中，这是流行性脑膜炎的危险因素。虽然我们的患者中排除了一些脑膜炎球菌血症的危险因素，例如镰状细胞病，无精子症和HIV感染，但调查了其他危险因素的作用，例如补体缺乏症，备解素缺乏症和各种炎症介质的多态性（1 ，2），由于缺少设施而受到限制。急性脑膜炎球菌血症是一种

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