Valkov Trifon, Argirova Radka, Dimitrov George
Department of Infectious Diseases, Medical University of Sofia, Prof. Ivan Kirov hospital, 1431 Sofia, Bulgaria.
Department of Clinical Laboratory, Acibadem City Clinic Tokuda Hospital, 1407 Sofia, Bulgaria.
Viruses. 2024 Dec 21;16(12):1962. doi: 10.3390/v16121962.
Central nervous system (CNS) infections caused by SARS-CoV-2 are uncommon. This case report describes the clinical progression of a 92-year-old female who developed a persistent neuroinfection associated with SARS-CoV-2. The patient initially presented with progressive fatigue, catarrhal symptoms, and a fever (38.6 °C). Initial laboratory findings revealed hypoxemia (O saturation 79.8%), acidosis (pH 7.3), an elevated C-reactive protein (CRP) level of 14.8 mg/L, and a high D-dimer level (2.15 µg/mL). Nasopharyngeal (NP) antigen and RT-PCR tests confirmed SARS-CoV-2 infection, and an NP swab also detected penicillin- and ampicillin-resistant Staphylococcus aureus. She was admitted for conservative management, including oxygen supplementation, IV fluids, and prophylactic anticoagulation. Subsequently, she developed neurological symptoms-lethargy, discoordination, and impaired communication-without signs of meningism. Cerebrospinal fluid (CSF) analysis identified SARS-CoV-2 RNA (Ct = 29) on RT-PCR, while bacterial cultures remained negative. Treatment was intensified to include 10% mannitol, dexamethasone, and empiric ceftriaxone. Despite these interventions, the patient remained somnolent, with a Glasgow Coma Scale (GCS) score of 10. Upon discharge, her GCS had improved to 14; however, she continued to experience lethargy and cognitive issues, commonly described as "brain fog". Inflammatory markers remained elevated (CRP 23 mg/L) and repeat RT-PCR of CSF confirmed a persistent SARS-CoV-2 presence (Ct = 31). This case underscores the potential for SARS-CoV-2 to cause prolonged CNS involvement, leading to persistent neurological impairment despite standard therapy. Further research is essential to clarify the pathophysiology of and determine optimal management for SARS-CoV-2 neuroinfections.
由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引起的中枢神经系统(CNS)感染并不常见。本病例报告描述了一名92岁女性患者的临床病程,该患者发生了与SARS-CoV-2相关的持续性神经感染。患者最初表现为进行性疲劳、卡他症状和发热(38.6℃)。初始实验室检查结果显示低氧血症(氧饱和度79.8%)、酸中毒(pH 7.3)、C反应蛋白(CRP)水平升高至14.8mg/L以及D-二聚体水平升高(2.15μg/mL)。鼻咽(NP)抗原和逆转录聚合酶链反应(RT-PCR)检测确诊为SARS-CoV-2感染,NP拭子还检测到耐青霉素和氨苄西林的金黄色葡萄球菌。她因保守治疗入院,包括吸氧、静脉输液和预防性抗凝。随后,她出现了神经症状——嗜睡、共济失调和沟通障碍,无脑膜刺激征迹象。脑脊液(CSF)分析在RT-PCR检测中发现了SARS-CoV-2 RNA(Ct=29),而细菌培养仍为阴性。治疗加强,包括使用10%甘露醇、地塞米松和经验性头孢曲松。尽管采取了这些干预措施,患者仍处于嗜睡状态,格拉斯哥昏迷量表(GCS)评分为10分。出院时,她的GCS评分提高到了14分;然而,她仍持续存在嗜睡和认知问题,通常被称为“脑雾”。炎症标志物仍升高(CRP 23mg/L),脑脊液重复RT-PCR证实仍存在持续性SARS-CoV-2(Ct=31)。本病例强调了SARS-CoV-2导致中枢神经系统长期受累的可能性,尽管进行了标准治疗仍会导致持续性神经功能损害。进一步的研究对于阐明SARS-CoV-2神经感染的病理生理学并确定最佳治疗方案至关重要。