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Elevated lumbar puncture opening pressure (ELPOP) is a reported but understudied phenomenon in aseptic meningitis. This study aimed to characterize the features of ELPOP in aseptic meningitis patients.An observational, retrospective, single-center study was conducted. We included all adult patients diagnosed with aseptic meningitis or meningoencephalitis from October 2015 to May 2017, for whom lumbar puncture opening pressure (LP OP) was measured. OP 25 cm HAmong 116 patients (61 males) included, 16 patients (14 %) had ELPOP (11 males). The average age of those patients was 32.4 years (SD = 9.8), and the mean OP was 31.7 cm HThis study fills the void of information lacking on the frequency of ELPOP in aseptic meningitis. Its association with increased BMI may be related to the pathogenesis. LP OP should be measured in all patients with aseptic meningitis. Additional research is needed to determine the threshold of tolerated intracranial pressure (ICP).

Aseptic meningitis, including culture negative and viral meningitis, contributes a significant health-care burden, including unnecessary antibiotic use and hospitalisation to treat possible bacterial meningitis. This study analysed aseptic meningitis hospitalisations in New Zealand (NZ) children over 29 years.In this population-based study, aseptic meningitis hospitalisations in NZ children15 years old were analysed from 1991 to 2020. Incident rate ratios were calculated using Poisson regression models. Variations in hospitalisations by age, year, sex, ethnicity, geographical region and socio-economic deprivation were analysed.There were 5142 paediatric aseptic meningitis hospitalisations from 1991 to 2020. Most were unspecified viral meningitis (64%), followed by enterovirus (29%). Hospitalisation rates varied annually with a median of 18.4/100 000 children including a peak in 2001 of 56.4/100 000 (51.7-61.6). From 2002 to 2019, rates increased by 8.4%/year (7.2-9.5%) in infants90 days old but decreased in all other age groups. In 2020, a reduction in hospitalisations to 9.6/100 000 (7.9-11.8) occurred, and in infants90 days old were 0.37 times expected. Hospitalisations were 1.50 times (1.49-1.68) higher in males than females; higher in children of Māori (P 0.001) and Pacific (P 0.001) versus European ethnicity; and higher for children living in the most (2.44 times, (2.16-2.75)) versus least deprived households; and in northern versus southern NZ.Aseptic meningitis hospitalisations increased in young infants during 29 years of surveillance, apart from 2020 when admissions reduced during the COVID-19 pandemic. In contrast, hospitalisations decreased in children aged1 year. Further investigation into reasons for higher admissions by ethnic group, geographical location and increased deprivation are required.

Enterovirus infections pose a serious threat for patients with humoral deficiencies and may be lethal, whilst the efficacy of proposed treatment options such as corticosteroids, intravenous immunoglobulins and fluoxetine remains debated.Viral clearance was investigated in a patient with rituximab-induced B-cell depletion and chronic echovirus 13 (E13) meningoencephalitis/myofasciitis in response to intravenous immunoglobulins and fluoxetine using sequential semi-quantitative E13 viral load measurements by real-time reverse transcription polymerase chain reaction. Fluoxetine concentrations in plasma and cerebrospinal fluid were determined by liquid chromatography mass spectrometry.Intravenous immunoglobulins appeared ineffective in this case of E13 infection, whereas virus clearance in cerebrospinal fluid was obtained after 167 days of oral fluoxetine. Since treatment with corticosteroids resulted in a flare of symptoms, rechallenge with viral load measurements was not attempted.In this report of a patient with rituximab-associated chronic echovirus 13 meningoencephalitis, viral clearance in response to single treatment options is assessed for the first time. Our observations further support the in vivo efficacy of fluoxetine against enteroviral infections. More research is needed to establish its efficacy in different enterovirus strains.

Amenamevir has been approved for the treatment of herpes zoster (HZ); however, its therapeutic efficacy against central nervous system (CNS) infection may be insufficient due to its low spinal fluid permeability. We herein report a case of aseptic meningitis in a 91-year-old Japanese man treated with amenamevir for HZ in the trigeminal nerve region. Several cases of CNS infection have been reported in patients receiving amenamevir treatment for HZ. Patients with CNS complications often have skin rashes near the trigeminal region. Thus, we should be alert for signs of CNS infection when administering amenamevir to patients with such rashes.

Kikuchi disease, also called histiocytic necrotizing lymphadenitis, is an idiopathic and generally self-limiting disease affecting young adults and children. Kikuchi disease does not commonly manifest neurological complications at its initial presentation. We herein report two cases of Kikuchi disease that initially presented with aseptic meningitis and encephalitis rather than the more common signs of lymphadenopathy, rash, and arthritis. A 15-year-old boy presented with aseptic meningitis with an extremely high intracranial pressure. A 28-year-old man presented with dysesthesia of the right lower extremity, coinciding with abnormal magnetic resonance imaging findings. In both cases, painful cervical lymphadenopathy was observed following the central nervous system symptoms. Both patients improved after treatment with steroids. Kikuchi disease occasionally affects the central nervous system, to which lymphadenitis may be observed subsequently. A repeated, careful physical examination of the cervical lymph nodes may be helpful for the diagnosis.

Fabry disease (FD) is an X-linked lysosomal storage disease caused by the mutation in the α-galactosidase A gene that leads to a consequently decreased α-galactosidase A enzyme activity and a series of clinical presentations. However, FD accompanied with aseptic meningitis can be relatively scarce and rarely reported, which leads to significant clinical misdiagnosis of this disease.Sixteen patients diagnosed with FD based on a decreased activity of α-galactosidase A enzyme and/or genetic screening were identified through a 6-year retrospective chart review of a tertiary hospital. Clinical presentations, brain magnetic resonance imaging, cerebrospinal fluid analysis, treatment and outcome data were analyzed in cases of aseptic meningitis associated with FD.Three out of 16 cases exhibited aseptic meningitis associated with FD. There was one female and two male patients with a mean age of 33.3 years. A family history of renal failure or hypertrophic cardiomyopathy was found in 3 cases. All cases presented with a persistent or intermittent headache and recurrent ischemic stroke. The cerebrospinal fluid analyses showed mild pleocytosis in 2 patients and an elevated level of protein in all patients. Cerebrospinal fluid cytology revealed activated lymphocytes, suggesting the existence of aseptic meningitis. In the literature review, up to 9 cases presenting with FD and aseptic meningitis were found, which bore a resemblance to our patients in demographic and clinical characteristics.Our cases suggested that aseptic meningitis in FD might be under-detected and easily misdiagnosed, and should be more thoroughly examined in further cases.

The aim of presenting this case was to show the difficulties in making the differential diagnosis of viral meningitis during the COVID pandemic situation. We report a case of a young man with clinical features of viral meningitis and with epidemiological history of COVID-19 in his family. The patient complained of fever, headache, photophobia, nausea, myalgia, and fatigue. He gave a history of diarrhea and vomiting two weeks before admission and close relatives with COVID-19. The neurological examination revealed a meningeal irritation syndrome. The diagnostic tests we performed were as follows: nasopharyngeal swab and PCR of cerebrospinal fluid (CSF) for SARS CoV-2, computed tomography scan of the head, general CSF examination, viral tests, and microbiology of CSF, enzyme-linked immunosorbent assay (ELISA) IgM and IgG. The results were consistent with viral meningitis due to HSV-1 in simultaneously found high titres of plasma SARS CoV-2 specific IgA and SARS CoV-2 specific IgG and active viral serum infection for CMV and EBV.

Background and Purpose The usual neurologic manifestations of Vogt-Koyanagi-Harada (VKH) disease include aseptic meningitis and headaches. We performed the present study to review all unusual neurologic manifestations reported in VKH disease to summarize them. Methods A literature search was performed in the English language on Scopus and Medline via PubMed from 1946 to July 31, 2021, by using the following terms: “Vogt Koyanagi Harada disease” OR “VKH disease” AND “Brain” OR “Spinal cord” OR “CNS” OR “Central nervous system” OR “Neurologic” OR “Peripheral nervous system” OR “Polyneuropathies. Our inclusion criteria were unusual neurologic manifestations of VKH disease. Results Our literature search yielded 417 total articles (PubMed = 334, Scopus = 83) from which 32 studies comprising 43 patients (22 men and 21 women, of which 62.8% were younger than 50 years) were included in this systematic literature review. Regarding the study design, all studies were case reports and published between 1981 and 2021. CNS involvement was the most reported (93%) in VKH disease. Peripheral nervous system involvement represents 7% of cases. The cerebral lesions were parenchymal inflammatory lesions in the white matter or posterior fossa with or no contrast enhancement (16.3%), leptomeningitis (9.3%), pachymeningitis (7%), meningoencephalitis (2.3%), ischemic stroke (4.6%), hemorrhagic stroke (2.3%), transient ischemic attack (2.3%), and hydrocephalus (2.3%). The optic nerve lesions were anterior ischemic optic neuropathy (20.9%) and optic neuritis (9.3%). Concerning spinal cord lesion, it was mainly myelitis (14%). Conclusion This systematic literature review provides a summary of the different unusual neurologic manifestations reported in VKH disease.

Echoviruses are among the most common worldwide causes of aseptic meningitis, which can cause long-term sequelae and death, particularly in neonates. However, the mechanisms by which these viruses induce meningeal inflammation are poorly understood, owing at least in part to the lack of in vivo models that recapitulate this aspect of echovirus pathogenesis. Here, we developed an in vivo neonatal mouse model that recapitulates key aspects of echovirus-induced meningitis. We show that expression of the human homologue of the primary echovirus receptor, the neonatal Fc receptor (FcRn), is not sufficient for infection of the brains of neonatal mice. However, ablation of type I, but not III, interferon (IFN) signaling in mice expressing human FcRn permitted high levels of echovirus replication in the brain, with corresponding clinical symptoms, including delayed motor skills and hind-limb weakness. Using this model, we defined the immunological response of the brain to echovirus infection and identified key cytokines, such as granulocyte colony-stimulating factor (G-CSF) and interleukin 6 (IL-6), that were induced by this infection. Lastly, we showed that echoviruses specifically replicate in the leptomeninges, where they induce profound inflammation and cell death. Together, this work establishes an in vivo model of aseptic meningitis associated with echovirus infections that delineates the differential roles of type I and type III IFNs in echovirus-associated neuronal disease and defines the specificity of echoviral infections within the meninges. IMPORTANCE Echoviruses are among the most common worldwide causes of aseptic meningitis, which can cause long-term sequelae or even death. The mechanisms by which echoviruses infect the brain are poorly understood, largely owing to the lack of robust in vivo models that recapitulate this aspect of echovirus pathogenesis. Here, we establish a neonatal mouse model of echovirus-induced aseptic meningitis and show that expression of the human homologue of the FcRn, the primary receptor for echoviruses, and ablation of type I IFN signaling are required to recapitulate echovirus-induced meningitis and clinical disease. These findings provide key insights into the host factors that control echovirus-induced meningitis and a model that could be used to test anti-echovirus therapeutics.

During a mouse plague in early 2021, a farmer from New South Wales, Australia, sought treatment for aseptic meningitis and was subsequently diagnosed with locally acquired lymphocytic choriomeningitis virus infection. Whole-genome sequencing identified a divergent and geographically distinct lymphocytic choriomeningitis virus strain compared with other published sequences.

Background Myelin oligodendrocyte glycoprotein (MOG) antibody-associated demyelinating disorders (MOGAD) are increasingly being recognized in the pediatric age group. Over time, unusual presentations have expanded the clinical presentation. We report 12 cases of MOGAD where prolonged fever (PF) was an important part of the symptom complex during the course of the illness. Methods After initial recognition of this atypical clinical presentation, more patients were recruited over 2 years and followed up prospectively. Results Eight of twelve patients had no clinical/imaging evidence of demyelination until much later in the course. Three clinical presentations recognized were fever of unknown origin (4 of 12), aseptic meningitis (4 of 12), and PF seen concurrently with established acute demyelination syndrome (4 of 12). Leukocytosis, raised inflammatory markers, and cerebrospinal fluid pleocytosis were almost universal. The first two presentations frequently caused diagnostic confusion, as MOGAD was not considered until several weeks after disease onset. The third group was more a therapeutic conundrum on how to manage the PF. Early seizures without encephalopathy were not uncommon and were probably independent of the later-appearing demyelination. Conclusions This case series highlights PF as an important component of the pediatric MOGAD symptom complex. MOGAD could be considered in the differential diagnosis of these clinical presentations.

Sjögren's syndrome can be complicated by several neurological manifestations, including aseptic meningitis, which can be manifested with headache, flu-like symptoms, confusion, fever, signs of meningeal irritation, with or without focal neurological symptoms and cranial nerve palsy. Neuroimaging can reveal contrast enhancement in the lepto- or pachymeninges. Therefore, Sjögren's syndrome should be considered in the differential diagnosis of lepto- or pachymeningeal enhancement.

BackgroundDrug-induced aseptic meningitis is a rare, but challenging diagnosis, most commonly reported with nonsteoroidal anti-inflammatory drugs (NSAIDs) and antibiotics. Trimethoprim/sulfamethoxazole (TMP/SMX) is a sulfonamide that is widely used in clinical practice for the treatment and prophylaxis of various infections. The most common side effects associated with TMP/SMX are generally mild and self-limited, but serious side effects have been reported, including liver injury and aseptic meningitis.Case presentationWe report a 2,5 year old Dutch girl with both drug-induced aseptic meningitis and drug-induced liver injury while using TMP/SMX prophylaxis. Ursodeoxycholic acid was started because of cholestatic injury. After cessation of TMP/SMX, full convalescence was reached within weeks.ConclusionsThis is the first report of a young patient with both aseptic meningitis and drug-induced liver injury caused by TMP/SMX. Drug-induced aseptic meningitis and cholestatic hepatitis constitute a considerable diagnostic challenge to clinicians. In addition to a thorough evaluation for infectious causes, clinicians should be aware of drug-induced aseptic meningitis and cholestatic hepatitis.

Background Severe illness can occur in young children infected with certain types of enteroviruses including echovirus 11 (Echo11) and coxsackievirus B5 (CoxB5). The manifestations and outcomes of Echo11 and CoxB5 diseases across all ages of children remained not comprehensively characterized in Taiwan. Methods Culture-confirmed Echo11 (60 patients) or CoxB5 (65 patients) infections were identified in a hospital from 2010 to 2018. The demographics, clinical presentations, laboratory data and outcomes were abstracted and compared between the two viruses infections. Results Echo11 and CoxB5 was respectively identified in 7 (77.8%) and 2 (22.2%) of 9 calendar years. The median age of all patients was 15 months (range, 1 day–14.5 years). For infants ≤3 months old, Echo11 (23 cases) was associated with higher incidence of aseptic meningitis (35% versus 0%, P = 0.003), and a lower rate of upper respiratory tract infections (URI) (22% versus 65%, P = 0.004) compared to CoxB5 (20 cases) infections. For patients >3 months old, URI was the cardinal diagnosis (60%) for both viruses. Aseptic meningitis was also more commonly identified in elder children with Echo11 infections (27% versus 11%), though with marginal significance (P = 0.07). Acute liver failure was identified in four young infants with Echo11 infections including one neonate dying of severe sepsis and myocarditis. All patients with CoxB5 infections recovered uneventfully. Conclusion Aseptic meningitis, sepsis-like illness and acute liver failure were more commonly identified in children with Echo11 than those with CoxB5 infections, suggesting greater neurological tropism and virulence toward Echo11.

We herein report a 31-year-old man with recurrent aseptic meningitis associated with Kikuchi's disease. Although aseptic meningitis is the most common neurological complication of Kikuchi's disease, its characteristics remain unclear, especially in recurrent cases. A literature review revealed that aseptic meningitis associated with Kikuchi's disease was more likely to occur in men and was associated with a low cerebrospinal fluid (CSF)/serum glucose ratio. Lymphadenopathy tended to occur simultaneously or after the onset of meningitis. When encountering a patient with aseptic meningitis of unknown etiology, it may be worthwhile to focus on the CSF/serum glucose ratio and lymphadenopathy with a careful examination.

Aseptic meningitis sometimes occurs as a consequence of central nervous system (CNS) involvement in patients with primary Sjögren’s syndrome (SS), even in paediatric-onset cases. However, little information is available regarding the pathological role of CSF anti-Ro/SSA and anti-La/SSB antibodies in the CNS involvement in patients with primary SS. We experienced an 18-year-old adolescent female with a 7-year history of suspicion of subclinical SS who subsequently developed aseptic meningitis as an initial presentation of probable SS. Her CSF exhibited marked elevation of anti-Ro/SSA and anti-La/SSB antibodies. When compared to her CSF IgG/serum IgG ratio (0.0058), her CSF/serum ratios of anti-Ro/SSA and anti-La/SSB antibody titres were higher (0.448 and 0.068, respectively; these were 77.5 and 11.7 times higher than that of IgG, respectively), suggesting that regional production of these antibodies was attributable, at least partly, to the development of meningitis. After the initiation of prednisolone treatment, her clinical manifestations promptly subsided. Since the clinical and pathological roles of the Ro/SSA antibody system in several autoimmune conditions have been postulated, our clinical observation may add novel insight to this theory.

Virus-receptor interactions determine viral host range and tissue tropism. CD55 and human neonatal Fc receptor (FcRn) were found to be the binding and uncoating receptors for some of the echovirus-related enterovirus species B serotypes in our previous study. Echovirus 18 (E18), as a member of enterovirus species B, is a significant causative agent of aseptic meningitis and viral encephalitis in children. However, it does not use CD55 as a critical host factor. We conducted CRISPR/Cas9 knockout screening to determine the receptors and entry mechanisms and identified FcRn working as a dual-function receptor for E18. Knockout of

Background As the coronavirus disease 2019 infections are still ongoing, there is an increasing number of case reports and case series with various manifestations of life-threatening multisystem inflammatory syndrome in children . Our case aims to remind all providers to scrutinize for clinical manifestations, including neurological symptoms, which may mimic aseptic meningitis. Case presentation A 5-year-old Albanian male child with obesity was admitted to the pediatric intensive care unit due to persistent fever, headache, vomiting, abdominal pain, mucocutaneous manifestations, and fatigue. Initial laboratory results revealed high level of inflammatory markers, including C-reactive protein of 156.8 mg/l, erythrocyte sedimentation rate of 100 mm/hour, procalcitonin of 13.84, leukocytosis with neutrophilia, and lymphopenia. Liver and renal functions, and capillary blood electrolytes (Na, K, Ca), were also altered. Cerebrospinal fluid was slightly turbid, with a white blood cell count of 128/mm3 (80% mononuclear cells and 20% polymorphonuclear), consistent with aseptic meningitis. The clinical presentation with prolonged fever, multiorgan dysfunction, and elevated inflammatory markers, with no plausible alternative diagnosis, matches the case definition of multisystem inflammatory syndrome in children. Combining corticosteroid methylprednisolone with intravenous immunoglobulin was effective. Conclusions Apart from the most common presentation of multisystem organ dysfunction, neurological manifestations of multisystem inflammatory syndrome in children such as aseptic meningitis, may be present as an immune response post-viral to coronavirus disease 2019. Given the rapid deterioration of children with multisystem inflammatory syndrome, early treatment with immunoglobulins and corticosteroids should be considered.

Viral infection is the most common cause of aseptic meningitis. The purpose of this study was to identify the viruses responsible for aseptic meningitis to better understand the clinical presentations of this disease.Between March 2009 and February 2010, we collected 297 cerebrospinal fluid specimens from children with aseptic meningitis admitted to a pediatric hospital in Yunnan (China). Viruses were detected by using "in house" real-time quantitative polymerase chain reaction or reverse-transcription real-time quantitative polymerase chain reaction from these samples. Phylogenetic analyses were conducted using the Molecular Evolutionary Genetic Analysis version 7.0 software, with the neighbor-joining method.Viral infection was diagnosed in 35 of the 297 children (11.8%). The causative viruses were identified to be enteroviruses in 25 cases (71.4%), varicella-zoster virus in 5 cases (14.3%), herpes simplex virus 1 in 2 cases (5.7%), and herpes simplex virus 2, Epstein-Barr virus, and human herpesvirus 6 in 1 case each (2.9% each). Of the enteroviruses, coxsackievirus B5 was the most frequently detected serotype (10/25 cases; 40.0%) and all coxsackievirus B5 strains belonged to C group.In the study, a causative virus was only found in the minority of cases, of them, enteroviruses were the most frequently detected viruses in patients with viral meningitis, followed by varicella-zoster virus and herpes simplex virus. Our findings underscore the need for enhanced surveillance and etiological study of aseptic meningitis.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by articular and extra-articular manifestations. Among extra-articular involvement, rheumatoid meningitis (RM) is a rare condition, which may exhibit variable symptoms including headache, focal and/or generalized neurologic deficits. It may develop as the preceding manifestation of RA or occur at any time of the disease course. Some drugs used for the treatment of RA may give rise to aseptic meningitis or create a tendency to infectious meningitis due to their immunosuppressive effect. All these possibilities may lead to difficulties in the differential diagnosis. Achieving a diagnosis in a short time is crucial in terms of prognosis. Here, we would like to report a case with longstanding RA manifested by left-sided weakness and seizure shortly after initiating etanercept (ETA) therapy. ETA-induced meningitis was confirmed with appropriate diagnostic tools. Our aim with this case-based review is to attract the attention of this rare condition and discuss diagnostic challenges.

This study evaluated the diagnostic role of cerebrospinal fluid leucine-rich alpha-2 glycoprotein (CSF LRG) concentration in children with acute bacterial meningitis, and its role in differentiation from aseptic meningitis. CSF LRG concentration was measured by ELISA Kit of 50 children with bacterial meningitis, 16 aseptic meningitis, and 20 children with normal CSF; control. CSF LRG was significantly elevated (p

Mollaret’s meningitis is an aseptic recurrent benign lymphocytic meningitis lasting 2-5 days and occurs over years with spontaneous complete resolution of symptoms between episodes. An 88 years-old-male presented with acute onset headache, lethargy and altered sensorium after a recent ear infection. He had multiple similar episodes in the past, each preceded by ear or sinus infection with cerebrospinal fluid finding consistent with aseptic meningitis. However, no specific causative agent was ever identified. He was confused, disoriented and lethargic with normal vitals and systemic examination. Blood tests showed leukocytosis with neutrophilia. Cerebrospinal fluid analysis revealed increased cell count with lymphocyte predominance, elevated protein and negative polymerase chain reaction. Magnetic resonance imaging of brain showed chronic small vessel ischemic changes. He fulfilled the Bruyn’s criteria for clinical diagnosis. He was empirically administered acyclovir during hospitalization and was discharged without prophylactic antiviraldue to negative cerebrospinal fluid analysis, culture, and multiplex polymerase chain reaction.

Neuroborreliosis initially misdiagnosed as Lyme disease was discovered to be caused by the relapsing fever spirochete Borrelia turicatae., Tickborne relapsing fever spirochetes are an overlooked cause of disease around the globe. We report a case of tickborne relapsing fever in a patient in Texas, USA, who had a single febrile episode and gastrointestinal and neurologic symptoms. Immunoblot analysis using recombinant Borrelia immunogenic protein A implicated Borrelia turicatae as the causative agent.

Scrub typhus is one of the most common causes of meningo-encephalitis in endemic areas of the Indian subcontinent. Numerous studies have established the reliability of cerebrospinal fluid lactate for differentiation of bacterial meningitis from aseptic meningitis. However, there are no reported data on the predictive value of cerebrospinal fluid lactate in scrub typhus meningitis. We thus conducted a cross-sectional study to examine the diagnostic accuracy of cerebrospinal fluid lactate in the differentiation of different causes of acute meningitis. Over two years, we studied 119 patients, with almost equal gender distribution, whose mean age was 43.58 (±18) years and their overall mean duration of fever was 11.7 (±21.0) days. Commonest clinical features overall were neck stiffness; values of cerebrospinal fluid lactate were lowest in aseptic meningitis, followed by scrub typhus, TB and bacterial meningitis. We conclude that cerebrospinal fluid lactate levels may be a useful adjunct to clinical features and laboratory investigations to differentiate between bacterial, viral, tubercular and scrub meningitis.

Aseptic meningitis represents a diagnostic challenge for the clinician. Cytological and chemical parameters are key in the differential diagnosis. Hypoglycorrhachia is a strong predictor of a bacterial origin for aseptic meningitis. We report a 44-year-old male with a history of recurrent febrile headaches admitted with fever and delirium. The initial cerebrospinal fluid (CSF) analysis showed low glucose levels. Magnetic resonance imaging did not show abnormalities. The patient was discharged but was admitted again three weeks later with fever, headache and a stiff neck. The CSF was inflammatory with low glucose levels. Serology for brucellosis was positive. The patient was treated with ceftriaxone and rifampicin with a good clinical response.

BackgroundGram stain of cerebrospinal fluid (CSF) is widely used in the diagnosis of acute meningitis, however, it is often conducted in the laboratory, as only some hospitals have access to point-of-care Gram stain (PCGS). The purpose of this study was to demonstrate the clinical impact and utility of PCGS in diagnosing and treating both bacterial and aseptic meningitis in adults.MethodsThis was a hospital-based, retrospective observational study at a referral center in Okinawa, Japan. We reviewed the records of all patients aged 15 years or older who were admitted to the Division of Infectious Diseases between 1995 and 2015 and finally diagnosed with bacterial (n = 34) or aseptic meningitis (n = 97). For bacterial meningitis, we compared the treatments that were actually selected based on PCGS with simulated treatments that would have been based on the Japanese guidelines. For aseptic meningitis, we compared the rates of antibiotic use between real cases where PCGS was available and real cases where it was not.ResultsPCGS was the most precise predictor for differentiating between bacterial and aseptic meningitis (sensitivity 91.2%, specificity 98.9%), being superior in this regard to medical histories, vital signs and physical examinations, and laboratory data available in the emergency room (ER). In bacterial meningitis, PCGS reduced the frequency of meropenem use (1/34 = 3.0%) compared with simulated cases in which PCGS was not available (19/34 = 55.9%) (pp = 0.006).ConclusionsPCGS of CSF distinguishes between bacterial and aseptic meningitis more accurately than other predictors available in the ER. Patients with bacterial meningitis are more likely to receive narrower-spectrum antimicrobials when PCGS is used than when it is not. PCGS of CSF thus can potentially suppress the empiric use of antimicrobials for aseptic meningitis.

We aimed to provide a clinical case presentation of aseptic meningitis as an extrahepatic manifestation of hepatitis C. A 28-year-old lady has been admitted to the Regional Clinical Center of Neurosurgery and Neurology, Uzhhorod City, Ukraine, with mild meningeal signs and symptoms upon admission. Complex neurological, clinical, laboratory, and imaging examination was performed within 24 hours of admission. Mononuclear pleocytosis of the cerebrospinal fluid and positive express test on HCV were discovered. The patient was treated and showed full recovery. Specific neurological features of aseptic meningitis as an extrahepatic manifestation of hepatitis C in a young white adult were reported, described, and analyzed.

Echovirus 30 (E30), a member of species B enterovirus, is associated with outbreaks of aseptic meningitis and has become a global health emergency. However, the pathogenesis of E30 remains poorly understood due to the lack of appropriate animal models. In this study, we established a mouse infection model to explore the pathogenicity of E30. The 2-day-old IFNAR(−/−) mice infected with E30 strain WZ16 showed lethargy and paralysis, and some died. Obvious pathological changes were observed in the skeletal muscle, brain tissue, and other tissues, with the highest viral load in the skeletal muscles. Transcriptome analysis of brain and skeletal muscle tissues from infected mice showed that significant differentially expressed genes were enriched in complement response and neuropathy-related pathways. Using immunofluorescence assay, we found that the viral double-stranded RNA (dsRNA) was detected in the mouse brain region and could infect human glioma (U251) cells. These results indicated that E30 affects the nervous system, and they provide a theoretical basis for understanding its pathogenesis. IMPORTANCE Echovirus 30 (E30) infection causes a wide spectrum of diseases with mild symptoms, such as hand, foot, and mouth disease (HFMD), acute flaccid paralysis, and aseptic meningitis and other diseases, especially one of the most common pathogens causing aseptic meningitis outbreaks. We established a novel mouse model of E30 infection by inoculating neonatal mice with clinical isolates of E30 and observed the pathological changes induced by E30. Using the E30 infection model, we found complement responses and neuropathy-related genes in the mice tissues at the transcriptome level. Moreover, we found that the viral dsRNA localized in the mouse brain and could replicate in human glioma cell line U251 rather than in the neuroblastoma cell line, SK-N-SH.

The literature regarding the utility of cerebrospinal fluid (CSF) procalcitonin (PCT) in the diagnosis of post-craniotomy bacterial meningitis and differentiating it from aseptic meningitis is sparse.CSF total WBC count, sugar, protein, and PCT were measured in febrile patients with suspected post-craniotomy meningitis during the first 30 days following an intradural cranial procedure for non-trauma indications. Patients were diagnosed as postoperative bacterial meningitis if CSF culture was positive (PBM, n = 28) or postoperative aseptic meningitis if CSF culture was sterile and there was no evidence of systemic infection (PAM, n = 31). CSF cytochemical parameters and PCT values were compared between the groups. Normal values of CSF PCT were obtained from 14 patients with noninfectious indications with hydrocephalus.There was no significant difference in CSF total WBC count, sugar, and protein levels between PAM and PBM groups. The median PCT level in CSF in the normal group was 0.03 ng/mL (interquartile range [IQR] 0.02-0.07 ng/mL). CSF PCT in the PBM group (median 0.37 ng/mL, IQR 0.2-1.4 ng/mL) was significantly higher than normal values as well as PAM group (median 0.12 ng/mL, IQR 0.07-0.26 ng/mL (P = 0.0004). The area under the receiver operating characteristic (ROC) curve for CSF PCT was 0.767. A cutoff value of 0.12 ng/mL yielded a sensitivity of 85.7% (95% CI: 67.3% to 96%), specificity of 51.6% (95% CI: 33% to 69.9%), positive predictive value of 61.5% (95% CI: 51.9% to 70.3%), and negative predictive value of 80% (95% CI: 60.3.8% to 91.3%).CSF PCT assay in patients who are febrile during the first 30 days post-non-trauma neurosurgical procedures has a role in the early diagnosis of bacterial meningitis.

Summary Background Drug-induced aseptic meningitis (DIAM) is potentially insufficiently considered by clinician, being of rare etiology, with there being no previously published exhaustive study describing its clinical and biological features. Methods Two independent academic clinicians searched all the case reports of DIAM from 1995 until 15th April, 2017. The search was limited to studies performed in humans, published in English or French. Clinical and biological data of subjects were compared with those of patients with documented viral meningitis. Results One hundred and fifty-one case reports fulfilled our inclusion criteria. Non-steroidal anti-inflammatory drugs were the commonest drug cause of AM n = 49, followed by antibiotics n = 46, biotherapy n = 19 and finally immunomodulators n = 15. The clinical and biological presentation of DIAM varies according to the causative etiological drug, especially with respect to the interval between exposure and presentation and cerebrospinal fluid (CSF) pleiocytosis. Clinical symptoms associated with meningitis were more prevalent in viral meningitis than in DIAM, except for fever and signs of encephalitis. Cerebrospinal fluid examination in DIAM reveals an increased CSF white cell count and an increased proportion of neutrophils and protein, compared with viral meningitis. Discussion We present an extensive review of the DIAM case reports, and highlight their clinical and biological characteristics according to the drugs involved. While comparing for the first time their characteristics with those of viral meningitis, this review hopes in facilitate earlier diagnosis and management of DIAM in clinical practice.

Objectives Mumps is a highly contagious viral infection prevented by immunization with live attenuated vaccines. Mumps vaccines have proven to be safe and effective; however, rare cases of aseptic meningitis (AM) can occur after vaccination. The range of meningitis occurrence varies by different factors (strain, vaccine producer, and so on). Monovaccines or divaccines (mumps-measles vaccine), prepared from the strain Leningrad-3 (L-3), are used in Russia. Meningitis occurrence after vaccination has been established previously as very low. Nevertheless, with the number of children being vaccinated every year, vaccine-associated AM cases still occur. There is no official statistics on AM incidence after mumps vaccines, and information on AM features as an adverse event of mumps vaccination is limited and mostly devoted to vaccines, prepared from strains other than L-3. Study design The study included patients with AM who were vaccinated against mumps in the previous 30 days before the present disease onset during 2009–2019. Methods Patients admitted to Infectious Clinical Hospital No. 1, Moscow, Russia, with AM were observed by a pediatrician and were screened for etiological agents of meningitis. Results Seven patients were enrolled, and clinical features and the course of infection are presented. Conclusions Detection of only 7 cases of AM associated with mumps vaccination during the 10-year period supports very low occurrence of this adverse event after immunization with the L-3 strain–based mumps vaccines. Nevertheless, the annual number of AM cases that occur after mumps vaccination remains unknown and poorly diagnosed in practice because of the low awareness of physicians of this adverse reaction. Detection and objective coverage of such cases can lead to a weakening of ‘antivaccination’ moods in a society and to restoration of confidence in the healthcare system.

A 66-year-old male patient presented with fever, headache, mental status changes, and nuchal rigidity with a lumbar puncture revealing neutropenic pleocytosis, and a presumptive diagnosis of bacterial meningitis was made. A careful history revealed that symptoms started within hours of starting oral trimethoprim-sulfamethoxazole. Additional history uncovered a nearly identical episode 1 year earlier after 1 dose of trimethoprim-sulfamethoxazole. All microbiologic diagnostic testing for meningitis was negative and all antimicrobials were discontinued. The patient had resolution of symptoms by 96 hours after last dose of trimethoprim-sulfamethoxazole and went on to full recovery. Based on history, clinical course, and a score of 7 on the Naranjo scale, he was diagnosed with recurrent trimethoprim-sulfamethoxazole-induced aseptic meningitis (TSIAM). This case illustrates the profound importance of thorough medication history and medication reconciliation.