Risk factors for cerebrospinal fluid shunt infections during an outbreak: a case-control study.

BACKGROUND: There are few published reports of cerebrospinal fluid (CSF) shunt infection outbreaks. In 2017-2018, British Columbia Children's Hospital (BCCH) experienced an increase in CSF shunt infections co-incident with a move to new operating rooms and a change in shunt catheters used. AIMS: To describe how an outbreak was detected, investigations were undertaken to determine the cause, risk factors associated with CSF shunt infection during the outbreak, and changes implemented to attempt to control the outbreak. METHODS: Retrospective case-control study. Population included patients who underwent new shunt insertion or revision. Univariate logistic regression models were fitted for each of the variables. Associations with P-values <0.2 were considered of potential interest for further investigation. FINDINGS: There were six cases of CSF shunt infection and 19 controls. The causative organism was different in each case. The only risk factors that met the criteria for further investigation were being a neonate at the time of surgery [odds ratio (OR) 9.0, 95% confidence interval (CI) 0.7-125.3, P=0.10] and the presence of gastrointestinal disease (OR 3.8, 95% CI 0.5-26.2, P=0.18). No association was found with the operating room used or the surgical staff. In response to the outbreak, human traffic through the operating rooms was limited, rigid adherence to the wearing of surgical masks was enforced, and return to the previous CSF shunt catheters used was implemented. CONCLUSION: No modifiable risk factors were associated with CSF shunt infection. After implementation of surgical protocol changes, no further cases of CSF shunt infection linked to the outbreak were identified.

CSF in acute and chronic infectious diseases.

Infections of the nervous system are an important and challenging aspect of clinical neurology. Immediate correct diagnosis enables to introduce effective therapy, in conditions that without diagnosis may leave the patient with severe neurological incapacitation and sometimes even death. The cerebrospinal fluid (CSF) is a mirror that reflects nervous system pathology and can promote early diagnosis and therapy. The present chapter focuses on the CSF findings in neuro-infections, mainly viral and bacterial. Opening pressure, protein and glucose levels, presence of cells and type of the cellular reaction should be monitored. Other tests can also shed light on the causative agent: serology, culture, staining, molecular techniques such as polymerase chain reaction. Specific examination such as panbacterial and panfungal examinations should be examined when relevant. Our chapter is a guide-text that combines clinical presentation and course with CSF findings as a usuaful tool in diagnosis of neuroinfections.

Criteria for the diagnosis of noninfectious and infectious complications after aneurysmal subarachnoid hemorrhage in DISCHARGE-1.

Patients with aneurysmal subarachnoid hemorrhage (aSAH) frequently develop secondary noninfectious and infectious complications that have an important impact on clinical course and outcome. We here report on criteria for the diagnosis of the most important complications after aSAH based on clinical status, neuroimaging, and laboratory tests, including cerebrospinal fluid parameters. These criteria will be used for a retrospective analysis of aSAH patients who were recruited at the Charité Berlin for the CoOperative Study on Brain Injury Depolarisations (COSBID) before the Depolarisations in Ischaemia after Subarachnoid Haemorrhage-1 (DISCHARGE-1) trial started. Moreover, they serve for the survey of complications in DISCHARGE-1. We also report on a customized, Web-based database that has been developed for the documentation of the clinical course after aSAH. This database is used for the COSBID outcome study on aSAH and for DISCHARGE-1.

Serum S100B levels in patients with cerebral and extracerebral infectious disease.

S100B has been shown to increase in cerebrospinal fluid (CSF) and serum after various neurological diseases and it has been postulated that S100B could serve as a serum marker for brain damage. However there is limited information concerning serum S100B levels in infectious diseases of the brain. Blood samples were collected from patients at the Department of Infectious Diseases at or soon after admission. The different diagnoses studied were bacterial meningitis, pneumonia, viral meningitis, cerebral abscess, enteritis, erysipelas, viral encephalitis and neuroborreliosis. A serum S100B level > 0.15 microg/l was defined as increased. 57 patients were included in the study. S100B was elevated in 33% of patients (19/57). 73% (8/11) of patients with bacterial meningitis showed increased levels compared to 7% (1/14) of patients with viral meningitis. Viral encephalitis showed the highest mean S100B levels (mean 0.58 microg/l). 25% (6/24) of patients with extracerebral infections showed raised S100B levels. S100B levels were generally higher in patients with cerebral infections than in extracerebral infections. However, both false negative and false positive S100B levels were observed which may limit the use of S100B as a brain specific serum marker.

[Polyspecific response in the central nervous system. Use of antibody index]. / Respuesta inmune poliespecífica en el sistema nervioso central. Empleo del índice de anticuerpo.

INTRODUCTION: The immune response, oligoclonal in cerebrospinal fluid (CSF), in comparison with the blood evidences is different and polyspecific. Together with specific antibodies against the causative agent, antibodies with many different specificities were synthesized. It is more complex in chronic neurological diseases. OBJECTIVE: Broadcast the characteristics of the polyspecific oligoclonal response and the use of antibody index as diagnostic tool in infectious and chronic diseases. DEVELOPMENT: The use of antibody index discriminates between the blood-derived antibody fraction and the brain-derived specific antibody fraction. Once the CSF/serum specific antibody and the IgG ratio are calculated, the antibody index is the quotient between both ratios. Antibody specific ratio may be obtained by titulation but it is less sensible. It is much better to employ immunoenzymatic methods. To avoid false negative results we must use the limit ratio according to reibergram instead of IgG ratio when the last one is greater than the limit ratio. Pathological antibody indexes are > or = 1.5. In chronic, autoimmune diseases, like lupus eritematosus, Sjögren syndrome or Wegener granulomatosis, could exist pathological antibody index against different viral agents like the antibody index against measles (M), rubella (R) and zoster (Z) viruses, known as MRZ reaction. CONCLUSIONS: The use of antibody index permits the diagnosis of infectious neurological diseases and the characterization of the secondary polyspecific response in chronic neurological processes.

Are elevated cerebrospinal fluid levels of IL-6 in sudden unexplained deaths, infectious deaths and deaths due to heart/lung disease in infants and children due to hypoxia?

Many SIDS cases probably die after periods of hypoxia and it has been shown that hypoxia may stimulate IL-6 production. The purpose of this paper was to examine if there were any correlations between hypoxanthine in vitreous humour and IL-6 in CSF. The concentration of IL-6, IL-1beta and TNFalpha in cerebrospinal fluid of 50 Sudden Infant Death syndrome (SIDS) cases, 9 borderline SIDS cases, 18 infectious deaths, 8 violent deaths and 22 cases with heart/lung disease were measured by ELISA. The hypoxanthine (Hx) vitreous humour concentrations in the same groups were determined by high performance liquid chromatography. The IL-6 levels in cases of infectious death, heart/lung disease and borderline cases were significantly higher than in the SIDS cases (p < 0.01). The Hx levels were in the same range in cases of SIDS, borderline SIDS and infectious death, and they were significantly higher than the levels in cases of violent death and heart/lung disease (p < 0.01). There was no correlation between hypoxanthine and IL-6 in any of the groups. In the cases studied IL-6 elevation is probably not induced by hypoxia, but is rather a result of immunological stimulation.

[Clinical observations in the enterovirus cerebrospinal meningitis outbreak in the Plotsk region in the fall of 1995]. / Zróznicowanie kliniczne epidemii enterowirusowego zapalenia opon mózgowo-rdzeniowych w województwie plockim jesienia 1995 roku.

Clinical and epidemiological observations in a small outbreak of enterovirus cerebrospinal meningitis were presented. The epidemic consisted of 154 cases who were hospitalized in the observation and infectious disease departments of the Provincial Hospital in Plock. The outbreak started on September 7, 1995 and lasted 2 months up to November 19, 1995. The initial cases were school children. There were 92 males and 62 females, 64% of patients (92 cases) were inhabitants of urban areas. 114 cases (about 80%) were children under 15 years of age and 56 of them belonged to the youngest age group, below 7 years of age. Etiology of the disease was identified in 17 patients: one case with Coxsackie B4 virus in cerebrospinal fluid, two cases with enterovirus A9 in stool, two cases with enterovirus E30 in stool and two cases with cytopathogenic factor also in stool. In 10 cases enteroviral etiology was confirmed by the positive serological findings. There were two group of patients: I--149 cases with mild cerebrospinal meningitis and II--5 cases of encephalopathy. The course of the disease in the majority of cases was mild, although 3% of cases were severe encephalopatic forms, with symptoms of brain damage. Youngest children with disfunction of the immunological system experienced the most serious course of the disease.

The compartmental IgM and IgA response within the central nervous system.

The diagnostic value of the locally synthesized IgA and IgM fractions in cerebrospinal fluid is described. The differentiation of the CSF immunoglobulins was performed with the help of a diagram that had been established on empirical grounds. Immunoglobulin G generally dominates the humoral immune response within the central nervous system, but in some diseases a comparatively strong participation of the other immunoglobulins was found: IgA in purulent meningitis and neurotuberculosis, IgM in tick-borne early summer meningoencephalitis. In meningopolyneuritis Bannwarth and mumps meningoencephalitis a broad three class response was found. The diagnostic significance of these findings is independent of the disease stage, since the compartmental immune response lacks the Nossal-Switch from IgM- to IgG- antibodies.

Free kappa light chains in multiple sclerosis spinal fluid.

Based on prior reports of free light chains of immunoglobulin G (IgG) in the cerebrospinal fluid (CSF) of patients with multiple sclerosis (MS), we quantitated free kappa and lambda chains and whole IgG concentrations using sensitive and specific radioimmunoassays (RIAs). The RIA for free kappa chains had a sensitivity of 0.25 micrograms/ml and was capable of specifically measuring free kappa chains in whole CSF or serum even in the presence of a 4-log excess of whole IgG. By RIA, free kappa chains were detected in CSF samples from 33 (84%) of 39 MS patients but in only 1 (2.4%) of 42 controls. The control patients included 10 with noninfectious inflammatory diseases and 9 with central nervous system infections. The concentration of free kappa chains in the CSF of the MS patients was 1.40 +/- 1.21 micrograms/ml. Free kappa chains were concentrated in the CSF 71- to 120-fold relative to reference proteins. In contrast, increased levels of free lambda chains or of whole IgG were nonspecific; abnormalities were seen in controls with infections or inflammatory diseases as often as in MS patients. These studies suggest that the measurement of free kappa light chains may have important diagnostic usefulness, since the specificity of the finding for MS appears to be high.