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Objective: The objective of the study was to study the neurological manifestations of influenza-A in children. Materials and Methods: This retrospective study was conducted in a tertiary care hospital in South India during the seasonal epidemic of flu in 2019. All children aged 1 month–12 years with evidence of neurological manifestations and positive nasopharyngeal swab for influenza A were evaluated for the clinical features, treatment, and outcome. Results: Sixteen patients had neurological manifestations and 44% of them were

BACKGROUND Data on the neurodevelopment of children who experienced central nervous system (CNS) infections with enteroviruses (EV) or parechoviruses (hPeV) is scarce and mostly limited to follow up of short-term outcomes. METHODS Parents of children who presented between 2014 and 2019, underwent a lumbar puncture and whose cerebrospinal fluid was polymerase chain reaction positive for EV or hPeV, were asked to complete a care-giver-administered neurodevelopmental assessment tool (The Ages and Stages Instrument [ASQ3]). Clinical data of the infective episode were collected from patient notes. RESULTS Of 101 children, 43 (10 hPeV+, 33 EV+) submitted ASQ3 results. Median age at assessment was 38.9 months (interquartile range, 15.4-54.8), the follow-up interval 3 years (median 37 months; interquartile range, 13.9-53.1). Age, inflammatory markers, and cerebrospinal fluid pleocytosis during the infective event were not associated with ASQ3 scores. In 23 children (17 EV+, 6 hPeV+), no neurodevelopmental concerns were reported. Two more had preexisting developmental delay and were excluded. Of the remaining, 18/41 (43.9%) reported ASQ3 scores indicating need for monitoring or professional review in at least 1 category, not differing by pathogen (EV 14/31, 45.2%; hPeV 4/10, 40%; P = 0.71). Seven children will require formal review, scoring ≥2 SD below the mean in at least 1 category (6/31 EV+, 1/10 hPeV+, P = 0.7), 3 scored ≥2 SD below the mean in more than 1 area. CONCLUSIONS Parent-administered developmental assessment of children with a history of early picornavirus infection of the CNS identified a subgroup that requires formal neurodevelopmental review. Wider application of community-based developmental screening will complement our understanding of the impact of CNS infections in early childhood.

It is common practice to perform a lumbar puncture in infants presenting with fever and a bulging fontanelle in order to rule out bacterial meningitis. However, most of these infants have benign, self-limiting diseases. The objective was to determine whether there is an association between bulging fontanelle and bacterial meningitis in febrile infants. This retrospective cohort study included febrile children with a bulging fontanelle who underwent lumbar puncture at Meir Medical Center from 2005 through 2015. A total of 764 children ages 2-18 months underwent lumbar puncture during the study period. Among them, 304 had a bulging fontanelle and fever on evaluation and cerebrospinal fluid pleocytosis was found in 115 (37.8%), including 1 case of bacterial meningitis (0.3%). None of the infants described on admission as appearing well on presentation was found to have bacterial meningitis. Of the 764 children who underwent lumbar puncture, 10 infants were diagnosed with bacterial meningitis, and only one (10%) presented with a bulging fontanelle.Conclusion: The finding of a bulging fontanelle has very low sensitivity and specificity for bacterial meningitis. Most causes of a bulging fontanelle in febrile infants are self-limiting diseases. The routine approach of performing a lumbar puncture in febrile infants with a bulging fontanelle should be reconsidered. What is Known: • It is common to perform a lumbar puncture in febrile infants with a bulging fontanelle, to rule out bacterial meningitis. • However, there are only few researches regarding the relationship between bulging fontanelle and bacterial meningitis. What is New: • The finding of a bulging fontanelle has very low sensitivity and specificity for bacterial meningitis • The need for routine lumbar puncture in these cases should be reconsidered.

Acute transverse myelitis is a rare and disabling disorder. Data on the imaging features in children are sparse. The aim of this study was to describe the clinical and magnetic resonance imaging findings characteristic of pediatric idiopathic acute transverse myelitis and to identify those with prognostic value. The database of a tertiary pediatric medical center was retrospectively reviewed for patients aged less than 18 years who were diagnosed in 2002-2017 with acute transverse myelitis that was not associated with recurrence of a demyelinating autoimmune event. Data were collected on clinical, laboratory, and imaging findings and outcome. A total of 23 children (11 male, 12 female) met the study criteria. Mean age at disease onset was 10 years, and mean duration of follow-up was 6 years 10 months. Spinal cord and brain magnetic resonance imaging scans were performed on admission or shortly thereafter. The most common finding was cross-sectional involvement, in 16 patients (70%). The mean number of involved spinal segments was 8. The most frequently involved region was the thoracic spine, in 17 patients (74%). Clinical factors predicting good prognosis were cerebrospinal fluid pleocytosis, absence of tetraparesis, and prolonged time to nadir. In conclusion, most children with acute transverse myelitis appear to have a good outcome. Prompt diagnosis and treatment are important. Further research is needed in a larger sample to evaluate the predictive value of imaging features.

BACKGROUND: The aims of this study were: investigate the frequency of HIV-1 RNA levels discordance between the cerebrospinal fluid (CSF) and plasma and of CSF viral escape (CVE) in patients HIV-1 subtype C on antiretroviral therapy; evaluate the CSF white blood cell (WBC) performance characteristics in predicting CSF discordance in HIV+ group; and the frequency of cognitive impairment in individuals with CSF HIV discordance or escape. METHODS: HIV-1 RNA levels were assessed in plasma and CSF samples from 68 HIV+ participants without opportunistic infection. RESULTS: CSF discordance was found in 7.4% and CVE in 10%, with comparable frequencies between HIV-1B and C. Twenty samples (29%) showed increased CSF WBC counts. This group had higher CSF and plasma HIV-1 RNA levels than the group with normal WBC counts (p < 0.0001 and 0.006, respectively). The odds of CSF discordance were 18 times higher for a person with CSF WBC count of >5cells/mm(3) than the group with normal CSF WBC count. CSF WBC counts (cut-off of 15 cells/mm(3)) showed high-performance characteristics as a predictive biomarker of CSF discordance (AUC the ROC curve 0.98). The frequency of cognitive impairment for CSF escape or discordance, was 83%, and 80%. The odds of cognitive impairment in these groups were 19 and 15 times higher, than those for a HIV(−) person. CONCLUSION: Viral discordance or escape in the CNS occurs at a comparable frequency for HIV-1C and HIV-1B. The CSF WBC count was effective as a predictive biomarker of CSF and plasma discordance.

Guillain-Barré syndrome (GBS) is a rare complication of chickenpox. All cases of post-varicella GBS published in the literature have been associated with the classical albuminocytological dissociation. We report the case of a 48-year-old male with flaccid areflexic quadriparesis and bilateral seventh, ninth, tenth, and twelfth cranial nerve palsies 10 days after chickenpox. Cerebrospinal fluid (CSF) analysis done in the second week showed marked lymphocytic pleocytosis. Electroneurographic studies were suggestive of acute inflammatory demyelinating polyradiculopathy. He had near-total neurological recovery with intravenous immunoglobulin. Our case demonstrates that GBS can occur after primary varicella infection, and marked CSF pleocytosis can be an additional feature.

Background:Status epilepticus (SE) has traditionally been thought to cause cerebrospinal fluid (CSF) pleocytosis. However, attributing CSF pleocytosis solely to SE without addressing the underlying etiology may lead to poor outcomes. Leukocyte recruitment to CSF has been shown to peak around 24 hours after prolonged seizures in animal studies, suggesting that CSF pleocytosis within the first 24 hours of SE onset may be due to underlying causes. The goal of this study is to assess if SE is associated with CSF pleocytosis, independent of other causes within the first 24 hours of onset.Methods:We completed a historical cohort study of adult patients with SE admitted to the intensive care unit of Vancouver General Hospital between March 2010 and May 2019.Results:Of the 441 patients admitted with SE during the study period, 107 met our inclusion criteria leading to 111 lumbar punctures (LPs), with 4 patients receiving two LPs. CSF pleocytosis was seen in 12 of 72 patients who underwent an LP within the first 24 hours of SE onset. In all 12 patients, a secondary etiology for the pleocytosis was observed aside from SE. Of the six CSF samples collected after 24 hours of onset that demonstrated pleocytosis, four had no cause for pleocytosis other than SE.Conclusions:In all 12 patients with CSF pleocytosis in the first 24 hours of onset of SE, an underlying etiology was identified. Therefore, any pleocytosis noticed within the first 24 hours of onset of refractory SE should not be attributed solely to SE.

Rapidly progressive dementia mimicking Creutzfeldt-Jakob disease (CJD) is a relatively rare presentation but a rewarding one to become familiar with, as the potential diagnoses range from the universally fatal to the completely reversible. Patients require urgent decisions about assessment and investigation and have quickly evolving needs for treatments and support, through symptom management and end-of-life care in most cases. We have based this pragmatic review on the experiences of a specialist prion referral centre in the UK, which, unsurprisingly, is strongly biased towards seeing patients with CJD. Cases eventually proven not to have prion disease might be described as 'CJD-mimics'; being referred from UK neurologists, these are the most challenging cases. CJD in its classical presentation is very rarely mimicked; however, it is highly heterogeneous, and atypical forms can mimic virtually all common neurodegenerative syndromes. Warning features of a mimic include generalised seizures, hyponatraemia, fever, a facial movement disorder, a normal neurological examination and a modestly rapid presentation. Contrast-enhancing lesions or MRI signal hyperintensity outside the striatum, thalamus or cortex and a cerebrospinal fluid pleocytosis are key investigation pointers to a CJD mimic.

Background The clinical manifestations of the transient headache and neurologic deficits with cerebrospinal fluid lymphocytosis (HaNDL) syndrome are variable, and involuntary movements have not been reported. The etiology and treatment of the syndrome are not entirely clarified. Case A 25-year-old female presented with recurrent transient headache, involuntary movements (left upper extremity chorea) and paralysis. Lumbar punctures showed intracranial hypertension and cerebrospinal fluid pleocytosis. Symptoms and intracranial hypertension were relieved after administration of steroids. Discussion/conclusion Chorea may also present in the HaNDL syndrome. Steroids might relieve the symptoms of the HaNDL syndrome, which indicates the possible treatment strategy for HaNDL and supports the infectious or postinfectious autoimmune etiology hypothesis.

Neurotuberculosis usually responds well to standard antitubercular therapy. Some; patients have prolonged course A 11 year old boy diagnosed TBM, an immunocompetent patient, had an unusual course of illness in the form of prolonged fever, persistent hyponatremia and CSF; pleocytosis despite adequate treatment. Clinical course in the management of TBM can be; protracted with complications despite adequate therapy.

Nontuberculous mycobacteria (NTM) comprise many bacterial pathogens that are divided by their growth features into two main groups: slow-growing and rapid-growing mycobacteria. The most important sites of infection include the pulmonary system, the skin and soft tissue, and disseminated disease. NTM infections involving the central nervous system infection are rarely reported but when they occur, this group of infections is associated with potentially severe complications or death. Most reported cases occur among immunocompromised hosts and predominantly among individuals with advanced HIV-associated immunosuppression. Additionally, advances in neurosurgical procedures including intracranial prosthetic devices (cerebrospinal shunts or Ommaya reservoirs) and potentially other prosthetic devices such as deep brain stimulators for neurodegenerative disorders may increase the risk of acquiring NTM by their ability to establish biofilms. Clinically, the most frequent presentation of NTM CNS infection is in the form of meningoencephalitis with important cerebrospinal fluid pleocytosis, high protein levels, and hypoglycorrachia. Treatment of NTM meningoencephalitis requires prolonged courses of a combination or oral and/or intravenous antimicrobials with the ability to penetrate the blood-brain and blood-cerebrospinal fluid barriers. Similar to tuberculous meningitis, the use of corticosteroids has proven beneficial in many of the reported cases of CNS infection caused by NTM. However, due to the paucity of cases of NTM CNS infections compared to tuberculous meningitis, the use of corticosteroids has not been systematically evaluated.

WOS: 000417628500023, PubMed ID: 29081366, Previous multicenter/multinational studies were evaluated to determine the frequency of the absence of cerebrospinal fluid pleocytosis in patients with central nervous system infections, as well as the clinical impact of this condition. It was found that 18% of neurosyphilis, 7.9% of herpetic meningoencephalitis, 3% of tuberculous meningitis, 1.7% of Brucella meningitis, and 0.2% of pneumococcal meningitis cases did not display cerebrospinal fluid pleocytosis. Most patients were not immunosuppressed. Patients without pleocytosis had a high rate of unfavorable outcomes and thus this condition should not be underestimated. (C) 2017 The Author(s). Published by Elsevier Ltd on behalf of International Society for Infectious Diseases., Grant-A-Starr Foundation, Grant-A-Starr Foundation.

Background: Sepsis-like illness is a main cause for hospital admission in young infants. Our aim was to investigate incidence, epidemiology and clinical characteristics of enterovirus (EV) and human parechovirus (HPeV) infections in young infants with sepsis-like illness. Methods: This is a prospective observational cohort study in which infants younger than 90 days of age, presenting with sepsis-like symptoms in a secondary care children's hospital, underwent a full sepsis work-up. Clinical signs and infectious indices were recorded. EV or HPeV RNA was detected by polymerase chain reaction in plasma and/or cerebrospinal fluid (CSF). Results: Infants were diagnosed with EV, HPeV, fever of unknown origin or severe infection. EV and HPeV were detected in 132 of 353 (37%) and 52 of 353 (15%) of cases, respectively. EV and HPeV have distinct seasonability. Some differences in clinical signs and symptoms occurred between children with EV and HPeV infection but were of limited clinical value. CSF pleocytosis occurred in 44% of EV positive infants, and only in 13% of those with HPeV infection. Conclusions: EV and HPeV infections are major causes of sepsis-like illness in infants < 90 days of age. Neither clinical characteristics nor laboratory indices were predictive for EV/HPeV infection. CSF pleocytosis occurs, but not in all patients. Testing for EV and HPeV in all young infants with sepsis-like illness is strongly advised.

BACKGROUND: Lumbar puncture with quantification of leukocytes and differential count of cellular subsets in the cerebrospinal fluid is a standard procedure in cases of suspected neuroinfectious conditions. However, a number of non-infectious causes may result in a low leukocyte number (0-1000 cells/ml). We wanted to assess the diagnostic diversity of unselected adult patients with pleocytosis in the cerebrospinal fluid.METHODS: The study is based on data from cerebrospinal fluid (CSF) analyses of all adult patients (15 years or older) admitted to a large university hospital in Denmark during a two-year period (2008-2009). Data from the local patient administrative system supplied with data from patient charts were combined with laboratory data.RESULTS: A total of 5390 cerebrospinal fluid samples from 3290 patients were included. Pleocytosis >5 leucocytes/μl was found in samples from 262 patients of which 106 (40.5%) were caused by infection of the central nervous system (CNS), 20 (7.6%) by infection outside CNS, 79 (30.2%) due to non-infectious neurological diseases, 23 (8.8%) by malignancy, and 34 (13.0%) caused by other conditions. Significantly higher mean CSF leukocytes was found in patients suffering from CNS infection (mean 1135 cells/μl, p-value CONCLUSIONS: CNS infection, non-infectious neurological disease, malignancy, and infection outside CNS can cause pleocytosis of the cerebrospinal fluid. Leukocyte counts above 100/μl is mainly caused by CNS infection, whereas the number of differential diagnoses is higher if the CSF leukocyte counts is below 50/μl. These conditions are most commonly caused by non-infectious neurological diseases including seizures.

Previous multicenter/multinational studies were evaluated to determine the frequency of the absence of cerebrospinal fluid pleocytosis in patients with central nervous system infections, as well as the clinical impact of this condition. It was found that 18% of neurosyphilis, 7.9% of herpetic meningoencephalitis, 3% of tuberculous meningitis, 1.7% of Brucella meningitis, and 0.2% of pneumococcal meningitis cases did not display cerebrospinal fluid pleocytosis. Most patients were not immunosuppressed. Patients without pleocytosis had a high rate of unfavorable outcomes and thus this condition should not be underestimated.

In this report we discuss a case of a patient with systemic lupus erythematosus who developed herpes simplex virus type 1(HSV-1) infection presenting with encephalitis as well as necrotic and non-necrotic retinitis. The patient presented with typical clinical symptoms and radiologic abnormalities consistent with HSV-1 encephalitis and HSV-1 retinitis in patients with HIV infection, but lacked cerebrospinal fluid pleocytosis and had bilateral retinitis with poor visual acuity. To the best of our knowledge, this is the first such case reported in the literature.

Cerebrospinal fluid pleocytosis has rarely been described as a possible transient finding following epileptic activity. We report a 68-year-old woman who presented with acute confusion and Cerebrospinal fluid pleocytosis. No evidence of an inflammatory, infectious or neoplastic cause explaining the pleocytosis was found. We presume that the pleocytosis in this patient was a result of epileptic convulsions. The mechanism for this finding is not fully understood.

The term rhombencephalitis refers to inflammatory diseases affecting the hindbrain (brainstem and cerebellum). Rhombencephalitis has a wide variety of etiologies, including infections, autoimmune diseases, and paraneoplastic syndromes. Infection with bacteria of the genus Listeria is the most common cause of rhombencephalitis. Primary rhombencephalitis caused by infection with Listeria spp. occurs in healthy young adults. It usually has a biphasic time course with a flu-like syndrome, followed by brainstem dysfunction; 75% of patients have cerebrospinal fluid pleocytosis, and nearly 100% have an abnormal brain magnetic resonance imaging scan. However, other possible causes of rhombencephalitis must be borne in mind. In addition to the clinical aspects, the patterns seen in magnetic resonance imaging can be helpful in defining the possible cause. Some of the reported causes of rhombencephalitis are potentially severe and life threatening; therefore, an accurate initial diagnostic approach is important to establishing a proper early treatment regimen. This pictorial essay reviews the various causes of rhombencephalitis and the corresponding magnetic resonance imaging findings, by describing illustrative confirmed cases.

West Nile virus (WNV) is the most frequent cause of arbovirus infection in the USA. Only 20% of infected individuals are symptomatic. Less than 1% of symptomatic individuals display West Nile neuroinvasive disease. We report a rare case of WNV-associated brachial plexopathy in a young immunocompetent individual, without cerebrospinal fluid pleocytosis or encephalitis. Additionally, there was subjective and objective improvement after high-dose corticosteroids. This case adds to the clinical spectrum of WNV neuroinvasive disease. The literature regarding immunomodulatory treatment and WNV is reviewed.

To distinguish between febrile infants with cerebrospinal fluid pleocytosis who are finally diagnosed with Kawasaki disease and those with enterovirus meningitis poses a diagnostic challenge. We compared clinical and laboratory features at admission between two groups of infants, aged 30-90 days, to identify markers of Kawasaki disease that initially presented as cerebrospinal fluid pleocytosis. During a 2-year period, 100 patients exhibiting cerebrospinal fluid pleocytosis were studied, including six (6.0%) with Kawasaki disease and 30 (30.0%) with enterovirus meningitis. A longer duration of fever before admission (P < 0.01), higher absolute neutrophil count (P < 0.01), increased C-reactive protein level (P < 0.01), pyuria (P = 0.02), and less prominent cerebrospinal fluid pleocytosis (P = 0.01) were identified as initial features of infants finally diagnosed with Kawasaki disease. No significant differences were evident in white blood cell count; platelet count; levels of hemoglobin, alanine aminotransaminase, aspartate aminotransferase, albumin, and sodium; cerebrospinal fluid chemistry; or presence of a rash. Our observations may offer early indicators of Kawasaki disease for timely diagnoses in febrile infants with cerebrospinal fluid pleocytosis.

Aim: Haemophagocytic lymphohistiocytosis (HLH) is a life-threatening disturbance of immunoregulation. HLH comprises primary and acquired forms with different disease severity. A large proportion of deaths occur early into treatment. We investigated association with early death for laboratory and clinical parameters before the start of and 2 weeks into therapy. Methods: A total of 232 children from Scandinavia, Germany or Italy, fulfilling diagnostic criteria and/or with familial disease and/or HLH-causing mutations, receiving HLH treatment 1994–2008 were included. The relation between clinical findings and early pre-transplant death was examined using the Cox proportional hazards model, with a 4-month right-truncation of the outcome. Patients were censored at last follow-up or transplant. Statistically significant predictors were adjusted for sex, age and each other. Results: The following features were significantly associated with adverse outcome: hyperbilirubinaemia (>50 μmol/L; adjusted hazard ratio (aHR) 3.2; 95% confidence interval 1.3–8.1, p = 0.011), hyperferritinaemia (>2000 μg/L; aHR 3.2; 1.2–8.6, p = 0.019), cerebrospinal fluid pleocytosis (>100 × 106/L; aHR 5.1; 1.4–18.5, p = 0.012) at diagnosis, and thrombocytopenia ( 2000 μg/L; aHR 10.6; 1.2–96.4, p = 0.037) 2 weeks into therapy. Non-improvement of fever, anaemia and/or thrombocytopenia also had adverse impact. Conclusion: There seem to be easily available clinical predictors of early mortality in HLH patients, which may help guide treatment decisions.

OBJECTIVE. The purpose of this study was to review the experience with herpes simplex encephalitis at the Hospital for Sick Children over the past 12 years. METHODS. All patients who were admitted to our institution with acute encephalitis between January 1994 and December 2005 were enrolled prospectively in an encephalitis registry. Children from the registry with herpes simplex encephalitis were included in this study; we detailed the clinical presentations, laboratory findings, electroencephalographic findings, diagnostic imaging findings, treatments, and outcomes for all cases. RESULTS. Of 322 cases of acute encephalitis, 5% were caused by herpes simplex virus. Initially negative herpes simplex virus cerebrospinal fluid polymerase chain reaction results were found in 2 cases (13%), but results became positive in repeat cerebrospinal fluid analyses. Classic clinical presentations were seen in 75% of cases, cerebrospinal fluid pleocytosis was found in 94%, elevated cerebrospinal fluid protein levels were found in 50%, electroencephalographic changes were observed in 94%, and diagnostic imaging abnormalities were noted in 88%. All patients were treated with intravenous acyclovir. Neurologic sequelae occurred in 63% of cases, including seizures in 44% and developmental delays in 25%. There were no deaths in this study group. CONCLUSIONS. Herpes simplex encephalitis continues to be associated with poor long-term neurologic outcomes despite appropriate therapy. Cerebrospinal fluid polymerase chain reaction results may be negative early in the course of herpes simplex encephalitis; therefore, repeat cerebrospinal fluid analysis should be considered if herpes simplex encephalitis is suspected. Atypical forms of herpes simplex virus central nervous system disease may occur in children.

Sterile cerebrospinal fluid pleocytosis occurs in febrile infants with urinary tract infection. Coinfection with enterovirus is a possible cause. We evaluated 57 infants with urinary tract infection and cerebrospinal fluid pleocytosis. All had enterovirus testing by polymerase chain reaction. An explanation for pleocytosis was determined for 24 infants (42%). Enterovirus infection was detected in 4 and is an uncommon cause of cerebrospinal fluid pleocytosis in infants with urinary tract infection.

Between late May and July 2012, 105 children (62 boys) originating from 2 cities of Thrace were examined because of fever, headache and abdominal pain. Thirty-three of them were hospitalized. They had normal hemograms, and mild to moderate cerebrospinal fluid pleocytosis. Echovirus 30 was isolated from fecal and cerebrospinal fluid samples. Among confirmed cases of echoviral illness, the meningitis attack rate was 51.9%.

Research definitions of encephalitis vary widely. When surveyed on the criteria used in clinical diagnosis, 88 pediatric specialists demonstrated diverse responses, with pediatric neurologists and pediatric infectious disease specialists differing significantly in their consideration of cerebrospinal fluid pleocytosis and abnormal neuroimaging. Results emphasize the need for a uniform definition.

We report a case of a 10-year-old girl who had several episodes of severe headache, altered consciousness, and temporary neurologic signs and symptoms within a 2-month period. Cerebrospinal fluid examination showed lymphocytic pleocytosis and increased protein. Extensive microbiologic investigation and neuroimaging studies were negative. Cerebrospinal fluid findings were normalized within a 3-month period, and the patient has not had further episodes through 15 months of follow-up. This combination of symptoms represents a benign, monophasic illness without further progression. The etiology, however, remains unclear. ( J Child Neurol 2005;20:439—441).

Summary Objectives Ommaya reservoirs (OmR) are used in the treatment of cancer yet risk factors and outcome of infection are not well characterized. We therefore examined our experience with this device. Methods Using administrative databases, we identified all patients with OmR in situ between 1993 and 2008 at Memorial Sloan-Kettering Cancer Center. Charts were reviewed for laboratory, demographic, and clinical information. Results During the study period, 616 patients with OmRs received care at MSKCC comprising 462,467 Ommaya-days. 34 patients with OmR infection were identified (5.5% of patients, 0.74 infections per 10,000 Ommaya-days). 32% of infections occurred within 30 days of OmR placement. Most (74%) OmR infections occurring after 30 days post-placement were associated with OmR access in the preceding 30 days. Recovered organisms included coagulase-negative staphylococci (56%) and Propionibacterium acnes (24%). 70% of patients had fever and/or headache and 69% had cerebrospinal fluid pleocytosis. 50% of patients had the reservoir removed during treatment of the infection. Conclusions OmR infection occurs in one of every 20 persons with the device. A third of the infections appear related to OmR placement while the remainder may occur at any time and usually are associated with recent reservoir access. Treatment often includes device removal.

The aim of this paper is to reassess the significance of postmortem cerebrospinal fluid pleocytosis. Published articles of CSF changes after death were reviewed, and reanalysis, in the light of modern views on the significance of bacterial postmortem isolates, was undertaken. There is theoretical and experimental evidence that the blood brain barrier to the movement of protein and cells is preserved in the first few hours after death. The number of mononuclear cells in the cerebrospinal fluid does rise in the first 24 hours after death, and this is most probably due to detachment of leptomeningeal lining cells. But the marked increase in lymphocyte counts seen in some cases of sudden infant death syndrome (SIDS) and in other deaths in the paediatric age range could well be a marker of inflammation.

Purpose. Diagnosis of WNV (WNV) relies upon serologic testing which may take several days after the onset of clinical symptoms to turn positive. Anecdotal reports suggest the presence of plasma cells or plasmacytoid lymphocytes in the cerebrospinal fluid (CSF) may be an early indicator of WNV infection.Methods. The CSFs of 89 patients (12 with WNV, 12 with other viral illness{OVI}, and 65 with nonviral illness{NVI}) were compared for the presence of either plasma cells or plasmacytoid lymphocytes.Results. Plasma cells were rarely seen in any of the patients. Plasmacytoid lymphocytes were more commonly seen in WNV (58%) and OVI (50%) than NVI (11%). The differences were significant for WNV versus NVI, but not WNV versus OVI (P<0.001andP=0.58,resp.).Conclusions. A CSF pleocytosis with plasma cells or plasmacytoid lymphocytes was neither sensitive nor specific for the diagnosis of WNV infection.