Chikungunya is a vector-borne zoonosis caused by the chikungunya virus (CHIKV) and transmitted by mosquitoes of the genus Aedes. An outbreak of the disease occurred in Brazil from 2015 to 2017, causing multiple deaths and severe consequences for survivors. Little is known of the potential psychiatric sequelae of CHIKV infection, but studies have demonstrated that depressive episodes, anxiety, and somatoform disorders may occur during infection and may strongly affect patient quality of life. A significant elevation of pro-inflammatory cytokine levels (interleukin [IL]-6, IL-1b, IL-2, and tumor necrosis factor [TNF]-a), both circulating and within the central nervous system (CNS), has been identified in patients with bipolar disorder, especially during depressive and manic episodes. Excessive cytokine production in the CNS may lead to apoptosis of neurons in vital neural pathways, including those involved in mood. We report the case of a 53-year-old homemaker with no personal or familial psychiatric history who presented with sudden onset of fever, skin rash, and right ankle edema. Acute CHIKV infection was diagnosed by serologic testing (IgM) in the emergency department (ED). Inflammatory markers, including C-reactive protein and erythrocyte sedimentation rate (ESR), were elevated. After 5 days, she developed manic symptoms, including decreased need for sleep, logorrhea, psychomotor agitation, excessive energy, irritation, racing thoughts, and grandiosity. She returned to the ED with a chief complaint of sudden change of behavior, agitation, and disinhibition. General blood tests were negative, and computed tomography (CT) of the head was within normal limits. She denied use of any drugs or medicines other than those prescribed during her previous ED visit, and a toxicology panel was negative. There were no hallucinations, delusions, or depressive symptoms. Thirty days after onset of mania, she was admitted to our outpatient psychiatric clinic and olanzapine 10 mg/day was initiated. Manic symptoms persisted for 45 days after onset of CHIKV symptoms. A comprehensive laboratory workup, which included antinuclear factor, anti-SSA, antiSSB, rheumatoid factor, serologies for HIV, hepatitis B and C virus, toxoplasmosis, cytomegalovirus, and venereal disease research laboratory (VDRL), was negative. IgG antibodies to CHIKV were detected. Brain magnetic resonance imaging (MRI) showed no relevant alterations. The patient continues to receive follow-up at our service, and has been in remission for 2 years. To our knowledge, there is no report in the scientific literature of a manic episode induced by chikungunya in a patient with no previous psychiatric history. Like bipolar disorder, CHIKV infection leads to significant cytokine overproduction and CNS inflammation. Both Th1 and Th2 immune responses are activated during the infection, which may trigger mood episodes. IL-6 has been proposed as a key factor in the pathogenesis of CNS immune response to CHIKV, and is known to be elevated in patients with depressive and manic episodes, indicating a possible link between this infection and mood disorders. Therefore, we hypothesize that the inflammatory response generated by the viral infection may have triggered a manic episode in the patient reported herein. Considering the magnitude of the chikungunya epidemic and its consequences to public health, describing and presenting instances of CHIKV-induced mania may be of pivotal importance for identification and treatment of future cases.

中文翻译：

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无精神病史患者基孔肯雅热引起的躁狂发作：病例报告

基孔肯雅热是由基孔肯雅病毒 (CHIKV) 引起的一种媒介传播的人畜共患病，由伊蚊属的蚊子传播。该病于 2015 年至 2017 年在巴西爆发，造成多人死亡和对幸存者的严重后果。对 CHIKV 感染的潜在精神后遗症知之甚少，但研究表明，感染期间可能会出现抑郁发作、焦虑和躯体形式障碍，并可能严重影响患者的生活质量。循环中和中枢神经系统 (CNS) 内的促炎细胞因子水平（白介素 [IL]-6、IL-1b、IL-2 和肿瘤坏死因子 [TNF]-a）显着升高。在双相情感障碍患者中发现，尤其是在抑郁和躁狂发作期间。中枢神经系统中过量的细胞因子产生可能导致重要神经通路中神经元的凋亡，包括与情绪有关的神经通路。我们报告了一个没有个人或家族精神病史的 53 岁家庭主妇的病例，她突然出现发烧、皮疹和右脚踝水肿。急诊科 (ED) 通过血清学检测 (IgM) 诊断出急性 CHIKV 感染。炎症标志物，包括 C 反应蛋白和红细胞沉降率 (ESR) 升高。5 天后，她出现了躁狂症状，包括睡眠需求减少、多语、精神运动性激动、过度精力、烦躁、思绪奔腾和自大。她回到急诊室，主诉行为突然改变、激动和去抑制。一般血液检查呈阴性，头部计算机断层扫描（CT）在正常范围内。她否认使用任何药物或药物，而不是在她之前的 ED 访问期间规定的药物，并且毒理学小组为阴性。没有幻觉、妄想或抑郁症状。躁狂发作 30 天后，她被收入我们的精神科门诊并开始服用奥氮平 10 毫克/天。在 CHIKV 症状出现后，躁狂症状持续了 45 天。包括抗核因子、抗 SSA、抗 SSB、类风湿因子、HIV 血清学、乙型和丙型肝炎病毒、弓形体病、巨细胞病毒和性病研究实验室 (VDRL) 在内的综合实验室检查结果为阴性。检测到 CHIKV 的 IgG 抗体。脑磁共振成像 (MRI) 未显示相关改变。患者继续在我们的服务处接受随访，并且已经缓解了 2 年。据我们所知，科学文献中没有关于基孔肯雅热在没有精神病史的患者中引起躁狂发作的报道。与双相情感障碍一样，CHIKV 感染会导致显着的细胞因子过度产生和中枢神经系统炎症。Th1 和 Th2 免疫反应在感染期间都被激活，这可能会引发情绪发作。IL-6 已被认为是 CNS 免疫反应对 CHIKV 的发病机制的关键因素，并且已知在患有抑郁症和躁狂发作的患者中升高，表明这种感染与情绪障碍之间可能存在联系。所以，我们假设病毒感染产生的炎症反应可能引发了本文报道的患者的躁狂发作。考虑到基孔肯雅热流行的严重程度及其对公共健康的影响，描述和展示 CHIKV 诱发的躁狂症实例对于识别和治疗未来病例可能至关重要。