RESUMEN
Bacterial infections in the central nervous system (CNS) can be life threatening and often impair neurological function. Biofilm infection is a complication following craniotomy, a neurosurgical procedure that involves the removal and replacement of a skull fragment (bone flap) to access the brain for surgical intervention. The incidence of infection following craniotomy ranges from 1% to 3% with approximately half caused by Staphylococcus aureus (S. aureus). These infections present a significant therapeutic challenge due to the antibiotic tolerance of biofilm and unique immune properties of the CNS. Previous studies have revealed a critical role for innate immune responses during S. aureus craniotomy infection. Experiments using knockout mouse models have highlighted the importance of the pattern recognition receptor Toll-like receptor 2 (TLR2) and its adaptor protein MyD88 for preventing S. aureus outgrowth during craniotomy biofilm infection. However, neither molecule affected bacterial burden in a mouse model of S. aureus brain abscess highlighting the distinctions between immune regulation of biofilm vs. planktonic infection in the CNS. Furthermore, the immune responses elicited during S. aureus craniotomy infection are distinct from biofilm infection in the periphery, emphasizing the critical role for niche-specific factors in dictating S. aureus biofilm-leukocyte crosstalk. In this review, we discuss the current knowledge concerning innate immunity to S. aureus craniotomy biofilm infection, compare this to S. aureus biofilm infection in the periphery, and discuss the importance of anatomical location in dictating how biofilm influences inflammatory responses and its impact on bacterial clearance.
Asunto(s)
Biopelículas , Infecciones Bacterianas del Sistema Nervioso Central/microbiología , Craneotomía/efectos adversos , Inmunidad Innata , Infecciones Estafilocócicas/microbiología , Staphylococcus aureus/inmunología , Infección de la Herida Quirúrgica/microbiología , Animales , Biopelículas/crecimiento & desarrollo , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Infecciones Bacterianas del Sistema Nervioso Central/metabolismo , Infecciones Bacterianas del Sistema Nervioso Central/terapia , Interacciones Huésped-Patógeno , Humanos , Factor 88 de Diferenciación Mieloide/metabolismo , Infecciones Estafilocócicas/inmunología , Infecciones Estafilocócicas/metabolismo , Infecciones Estafilocócicas/terapia , Staphylococcus aureus/crecimiento & desarrollo , Infección de la Herida Quirúrgica/inmunología , Infección de la Herida Quirúrgica/metabolismo , Infección de la Herida Quirúrgica/terapia , Receptor Toll-Like 2/metabolismoRESUMEN
Brain abscess formation is extremely rare in patients with osteopetrosis. Herein, we report a case of viridans streptococci brain abscess in an immunocompromised child diagnosed with osteopetrosis. The patient presented with a sudden change in mental status and convulsions. Radiological evaluation revealed a temporal lobe brain abscess, and intravenous antibiotherapy was started immediately. The patient underwent abscess drainage, and laboratory investigation of pus material revealed viridans streptococci.
Asunto(s)
Agammaglobulinemia/inmunología , Absceso Encefálico/microbiología , Infecciones Bacterianas del Sistema Nervioso Central/microbiología , Huésped Inmunocomprometido , Osteopetrosis/inmunología , Infecciones Estreptocócicas/microbiología , Estreptococos Viridans/aislamiento & purificación , Adolescente , Agammaglobulinemia/diagnóstico , Agammaglobulinemia/genética , Antibacterianos/uso terapéutico , Absceso Encefálico/diagnóstico , Absceso Encefálico/inmunología , Absceso Encefálico/terapia , Infecciones Bacterianas del Sistema Nervioso Central/diagnóstico , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Infecciones Bacterianas del Sistema Nervioso Central/terapia , Drenaje , Humanos , Masculino , Osteopetrosis/diagnóstico , Osteopetrosis/genética , Factores de Riesgo , Infecciones Estreptocócicas/diagnóstico , Infecciones Estreptocócicas/inmunología , Infecciones Estreptocócicas/terapia , Resultado del Tratamiento , Estreptococos Viridans/efectos de los fármacosRESUMEN
Central nervous system infections, which are rarely seen in systemic lupus erythematosus (SLE), have considerably high mortality but they are difficult to distinguish from neuropsychiatric manifestation of lupus. This article reports the case of a patient with SLE with brain abscess which developed during immunosuppressive therapy for lupus nephritis. The patient completely recovered without neurological sequelae by open surgical drainage and 12-week antibiotic therapy. It is recommended that CNS infections must be excluded in patients with SLE, particularly who are receiving immunosuppressive therapy.
Asunto(s)
Absceso Encefálico/microbiología , Infecciones Bacterianas del Sistema Nervioso Central/microbiología , Infecciones por Bacterias Grampositivas/microbiología , Huésped Inmunocomprometido , Inmunosupresores/efectos adversos , Lupus Eritematoso Sistémico/tratamiento farmacológico , Nefritis Lúpica/tratamiento farmacológico , Micrococcus luteus/aislamiento & purificación , Infecciones Oportunistas/microbiología , Adulto , Antibacterianos/administración & dosificación , Técnicas Bacteriológicas , Absceso Encefálico/diagnóstico , Absceso Encefálico/inmunología , Absceso Encefálico/terapia , Infecciones Bacterianas del Sistema Nervioso Central/diagnóstico , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Infecciones Bacterianas del Sistema Nervioso Central/terapia , Diagnóstico Diferencial , Drenaje , Femenino , Infecciones por Bacterias Grampositivas/diagnóstico , Infecciones por Bacterias Grampositivas/inmunología , Infecciones por Bacterias Grampositivas/terapia , Humanos , Lupus Eritematoso Sistémico/diagnóstico , Lupus Eritematoso Sistémico/inmunología , Nefritis Lúpica/diagnóstico , Nefritis Lúpica/inmunología , Vasculitis por Lupus del Sistema Nervioso Central/diagnóstico , Vasculitis por Lupus del Sistema Nervioso Central/inmunología , Imagen por Resonancia Magnética , Micrococcus luteus/efectos de los fármacos , Micrococcus luteus/inmunología , Infecciones Oportunistas/diagnóstico , Infecciones Oportunistas/inmunología , Infecciones Oportunistas/terapia , Valor Predictivo de las Pruebas , Resultado del TratamientoRESUMEN
Borrelia miyamotoi is a newly recognized human pathogen in the relapsing fever group of spirochetes. We investigated a case of B. miyamotoi infection of the central nervous system resembling B. burgdorferi-induced Lyme neuroborreliosis and determined that this emergent agent of central nervous system infection can be diagnosed with existing methods.
Asunto(s)
Infecciones por Borrelia/diagnóstico , Infecciones por Borrelia/microbiología , Borrelia , Infecciones Bacterianas del Sistema Nervioso Central/diagnóstico , Infecciones Bacterianas del Sistema Nervioso Central/microbiología , Huésped Inmunocomprometido , Anciano , Anticuerpos Antibacterianos/inmunología , Protocolos de Quimioterapia Combinada Antineoplásica , Biomarcadores , Borrelia/clasificación , Borrelia/genética , Borrelia/inmunología , Infecciones por Borrelia/inmunología , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Femenino , Genes Bacterianos , Humanos , Linfoma no Hodgkin/complicaciones , Linfoma no Hodgkin/diagnóstico , Linfoma no Hodgkin/tratamiento farmacológico , Tipificación de Secuencias Multilocus , ARN Ribosómico 16S/genéticaAsunto(s)
Infecciones Bacterianas del Sistema Nervioso Central , Sistema Nervioso Central/microbiología , Modelos Animales de Enfermedad , Infecciones por Spirochaetales , Spirochaetales , Animales , Infecciones por Borrelia/inmunología , Infecciones por Borrelia/microbiología , Infecciones por Borrelia/patología , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Infecciones Bacterianas del Sistema Nervioso Central/microbiología , Infecciones Bacterianas del Sistema Nervioso Central/patología , Humanos , Leptospirosis/inmunología , Leptospirosis/microbiología , Leptospirosis/patología , Ratones , Neurosífilis/inmunología , Neurosífilis/microbiología , Neurosífilis/patología , Conejos , Ratas , Infecciones por Spirochaetales/inmunología , Infecciones por Spirochaetales/microbiología , Infecciones por Spirochaetales/patologíaRESUMEN
The prognosis of course and outcome of inflectional inflammatory diseases of central nervous system, indicators of inflammatory reaction and immune response in cerebrospinal liquor in patients has been investigated.
Asunto(s)
Infecciones Bacterianas del Sistema Nervioso Central/líquido cefalorraquídeo , Infecciones Fúngicas del Sistema Nervioso Central/líquido cefalorraquídeo , Infecciones Parasitarias del Sistema Nervioso Central/líquido cefalorraquídeo , Factores Inmunológicos/líquido cefalorraquídeo , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Infecciones Bacterianas del Sistema Nervioso Central/microbiología , Infecciones Fúngicas del Sistema Nervioso Central/inmunología , Infecciones Fúngicas del Sistema Nervioso Central/microbiología , Infecciones Parasitarias del Sistema Nervioso Central/inmunología , Infecciones Parasitarias del Sistema Nervioso Central/parasitología , Humanos , Índice de Severidad de la EnfermedadRESUMEN
BACKGROUND: Studies of the apoptosis mechanisms involved in the pathogenesis of tuberculosis have suggested that Mycobacterium tuberculosis can actively interfere with the apoptosis of infected cells. In vivo studies have been performed in adult populations but have not focused on this process in children. In the present study, we analyzed spontaneous T lymphocyte (PBT) apoptosis in the peripheral blood of children with central nervous system tuberculosis (CNS TB), before and after chemotherapy, and compared the results with healthy controls. METHODS: A case-control study was conducted from January 2002 to June 2009. It included 18 children with CNS TB and 17 healthy controls. Spontaneous apoptosis of PBTs, including CD4+, CD8+ and CD8+/CD28+ T cells, was evaluated after 24 and 72 h of culture in complete medium, using the Annexin V detection test. Analysis was conducted before and after chemotherapy, and expression of the apoptotic markers CD95 (Fas) and Fas ligand (FasL) was evaluated. RESULTS: Higher percentages of apoptotic T cells and CD4 lymphocytes were isolated from children with acute phase CNS TB than from children in the control group (p < 0.05). This difference significantly decreased after 60 days of specific treatment. In children with CNS TB, high levels of Fas ligand expression were detected in lymphocyte populations, associated with a high percentage of Fas positive cells, before and after treatment. In contrast to the CD4+ apoptosis profile, we did not find any significant difference in total CD8+ cell apoptosis between children with acute phase disease and the control group. However, the percentage of apoptotic CD8+/CD28+ T cells was significantly higher in the children with acute phase disease than in the healthy controls. CONCLUSIONS: Our findings indicate that CNS TB in pediatric patients increases the sensitivity of CD4 and CD8+/CD28+ T cells to apoptosis, suggesting a hypoergic status of this infection. This could play a key role in the immunopathogenesis of this complicated form of TB. Interestingly, specific chemotherapy is able to normalize both apoptosis sensitivity and T-cell activation.
Asunto(s)
Apoptosis/inmunología , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Sistema Nervioso Central/inmunología , Mycobacterium tuberculosis/inmunología , Linfocitos T/metabolismo , Tuberculosis del Sistema Nervioso Central/inmunología , Estudios de Casos y Controles , Niño , Preescolar , Proteína Ligando Fas/metabolismo , Femenino , Humanos , Activación de Linfocitos , Masculino , Mycobacterium tuberculosis/metabolismo , Linfocitos T/inmunología , Tuberculosis del Sistema Nervioso Central/patología , Receptor fas/metabolismoRESUMEN
Clinical reports suggest an association of distinct Mycobacterium tuberculosis strains with CNS disease. We therefore examined CNS dissemination by different laboratory strains (two M. tuberculosis H37Rv, one CDC1551) in a guinea pig aerosol infection model. Although all strains grew exponentially in lungs, with similar bacterial burdens at the time of extrapulmonary dissemination, M. tuberculosis CDC1551 disseminated to the CNS significantly more than the H37Rv strains. No CNS lesions were observed throughout the study, with only a modest cytokine response. These data suggest that M. tuberculosis may have virulence factors that promote CNS dissemination, distinct from those required for pulmonary TB.
Asunto(s)
Encéfalo/microbiología , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Citocinas/inmunología , Pulmón/microbiología , Mycobacterium tuberculosis/patogenicidad , Bazo/microbiología , Tuberculosis Pulmonar/inmunología , Aerosoles , Animales , Encéfalo/patología , Infecciones Bacterianas del Sistema Nervioso Central/microbiología , Infecciones Bacterianas del Sistema Nervioso Central/patología , Modelos Animales de Enfermedad , Cobayas , Pulmón/patología , Bazo/patología , Tuberculosis Pulmonar/microbiología , Tuberculosis Pulmonar/patología , VirulenciaRESUMEN
The exact cellular and molecular mechanisms of sepsis-induced encephalopathy remain elusive. The breakdown of the blood-brain barrier (BBB) is considered a focal point in the development of sepsis-induced brain damage. Contributing factors for the compromise of the BBB include cytokines and chemokines, activation of the complement cascade, phagocyte-derived toxic mediators, and bacterial products. To date, we are far from fully understanding the neuropathology that develops as a secondary remote organ injury as a consequence of sepsis. However, recent studies suggest that bacterial proteins may readily cross the functional BBB and trigger an inflammatory response in the subarachnoid space, in absence of a bacterial invasion. A better understanding of the pathophysiological events leading to septic encephalopathy appears crucial to advance the clinical care for this vulnerable patient population.
Asunto(s)
Barrera Hematoencefálica/microbiología , Infecciones Bacterianas del Sistema Nervioso Central/etiología , Hipoxia-Isquemia Encefálica/fisiopatología , Sepsis/complicaciones , Biomarcadores , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Infecciones Bacterianas del Sistema Nervioso Central/fisiopatología , Cuidados Críticos , Humanos , Microcirculación , Sepsis/inmunología , Sepsis/fisiopatologíaRESUMEN
PURPOSE OF REVIEW: Septic encephalopathy is a frequent complication in severe sepsis, the pathogenesis and mechanisms of which are not fully understood. Here, we review recent advances in our understanding of septic encephalopathy, from molecular mechanisms to behavioral alterations, from diagnostic tools to potential therapeutic agents. RECENT FINDINGS: Recent insights into septic encephalopathy include: microcirculatory failure precedes changes in evoked potential responses; blood-brain barrier alteration is prevented by reducing intercellular adhesion molecule expression and pericyte detachment; reducing infiltration of CD68 macrophages and inhibiting complement activation alleviates neuroinflammation in septic encephalopathy; and reducing mitochondrial dysfunction and inducible nitric oxide synthase expression can restore altered brain function. In addition, other factors such as the circulating levels of growth hormone are independent predictors for mortality and correlate with the severity of sepsis. Similar to humans, septic rats present recognition memory impairment and depressive-like symptoms but not anxiety-like behavior and will serve as efficient models to study the underlying mechanisms of septic encephalopathy. SUMMARY: Septic encephalopathy is a dynamic disease caused by a complex network of systems and pathways going awry. More insights into the pathogenesis of septic encephalopathy are expected to lead to new cellular and molecular targets, which in turn will permit design of specific septic encephalopathy-alleviating drugs and prevent its negative influence on survival.
Asunto(s)
Infecciones Bacterianas del Sistema Nervioso Central/etiología , Infecciones Bacterianas del Sistema Nervioso Central/fisiopatología , Sepsis/complicaciones , Sepsis/fisiopatología , Animales , Biomarcadores/metabolismo , Barrera Hematoencefálica/fisiología , Infecciones Bacterianas del Sistema Nervioso Central/tratamiento farmacológico , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Activación de Complemento , Modelos Animales de Enfermedad , Humanos , Hipoxia-Isquemia Encefálica/patología , Hipoxia-Isquemia Encefálica/fisiopatología , Microcirculación , Sepsis/tratamiento farmacológico , Sepsis/inmunologíaRESUMEN
While glial cells are recognized for their roles in maintaining neuronal function, there is growing appreciation that resident central nervous system (CNS) cells initiate and/or augment inflammation following trauma or infection. We have recently demonstrated that microglia and astrocytes constitutively express nucleotide-binding oligomerization domain-2 (NOD2), a member of the novel nucleotide-binding domain leucine-rich repeat region containing a family of proteins (NLR) that functions as an intracellular receptor for a minimal motif present in all bacterial peptidoglycans. In this study, we have confirmed the functional nature of NOD2 expression in astrocytes and microglia and begun to determine the relative contribution that this NLR makes in inflammatory CNS responses to clinically relevant bacterial pathogens. We demonstrate the increased association of NOD2 with its downstream effector molecule, Rip2 kinase, in primary cultures of murine microglia and astrocytes following exposure to bacterial antigens. We show that this cytosolic receptor underlies the ability of muramyl dipeptide to augment the production of inflammatory cytokines by glia following exposure to specific ligands for disparate Toll-like receptor homologues. In addition, we demonstrate that NOD2 is an important component in the in vitro inflammatory responses of resident glia to N. meningitidis and B. burgdorferi antigens. Finally, we have established that NOD2 is required, at least in part, for the astrogliosis, demyelination, behavioral changes, and elevated inflammatory cytokine levels observed following in vivo infection with these pathogens. As such, we have identified NOD2 as an important component in the generation of damaging CNS inflammation following bacterial infection.
Asunto(s)
Astrocitos/metabolismo , Infecciones Bacterianas del Sistema Nervioso Central/patología , Microglía/metabolismo , Proteína Adaptadora de Señalización NOD2/fisiología , Análisis de Varianza , Animales , Animales Recién Nacidos , Antígenos Bacterianos/aislamiento & purificación , Antígenos Bacterianos/farmacología , Astrocitos/efectos de los fármacos , Astrocitos/microbiología , Borrelia burgdorferi/patogenicidad , Encéfalo/citología , Separación Celular , Células Cultivadas , Infecciones Bacterianas del Sistema Nervioso Central/tratamiento farmacológico , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Infecciones Bacterianas del Sistema Nervioso Central/fisiopatología , Relación Dosis-Respuesta a Droga , Sinergismo Farmacológico , Inmunoprecipitación , Inyecciones Intraventriculares , Interleucina-6/metabolismo , Lipopolisacáridos/farmacología , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Microglía/efectos de los fármacos , Microglía/microbiología , Actividad Motora , Neisseria meningitidis/patogenicidad , Proteína Adaptadora de Señalización NOD2/deficiencia , Oligodesoxirribonucleótidos Antisentido/uso terapéutico , Transportador de Péptidos 1 , Fenoles , Propionatos/farmacología , Proteína Serina-Treonina Quinasas de Interacción con Receptores/metabolismo , Simportadores/metabolismo , Factor de Necrosis Tumoral alfa/metabolismoRESUMEN
This article gives a review of the most frequent infective agents reasonable for CNS infections in immunocompetent patients as well as their localisation and imaging specifications. MRI scanning is the gold standard to detect inflammatory conditions in the CNS. Imaging can be normal or nonspecifically altered although the infection is culturally or bioptically proven. There are no pathognomonic, pathogen-specific imaging criteria. The localization and dimension of the inflammation depends on the infection pathway.
Asunto(s)
Encéfalo/inmunología , Encéfalo/patología , Infecciones Bacterianas del Sistema Nervioso Central/diagnóstico , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Encefalitis Viral/diagnóstico , Encefalitis Viral/inmunología , Huésped Inmunocomprometido/inmunología , Imagen por Resonancia Magnética/métodos , HumanosRESUMEN
CNS infections caused by infective agents are rare in immunocompetent hosts, but more frequent in immunocompromised patients. In addition, the spectrum of causative agents is completely different. There are no pathognomonic alterations in radiologic imaging, even in clinically severely ill patients imaging is often non-specific or inconspicious. This article gives a review of the most frequent infective agents and image alterations. Modern radiology is not yet able to replace the gold standard of pathogen detection.
Asunto(s)
Encéfalo/inmunología , Encéfalo/patología , Infecciones Bacterianas del Sistema Nervioso Central/diagnóstico , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Encefalitis Viral/diagnóstico , Encefalitis Viral/inmunología , Huésped Inmunocomprometido/inmunología , Imagen por Resonancia Magnética/métodos , HumanosRESUMEN
La alta incidencia de infección en los drenajes ventriculares externos (0-45) representa un serio problema para los pacientes y las instituciones no sólo en el aspecto médico sino también en el económico y legal. Consideramos que la sistematización y la aplicación multidisciplinaria de guías de manejo son de gran importancia para la prevención de la infección. Por lo cual se debatieron los puntos de controversia en un grupo interdisciplinario constituido por especialistas en neurocirugía, terapia intensiva e infectología, enfermeros de terapia intensiva y el comité de infecciones, realizando por consenso las recomendaciones. Palabras clave: guía de manejo, infección, profilaxis antibiótica, ventriculitis, ventriculostomía.
The high incidence of infections fo the external ventricular drainages (0-45) represents a serious problem for patients and institutions not only in the medical aspects, but also int economic and legal ones. We believe that the systematic and multidisciplinary application of guides is of grat value for the prevention of infections. Based on the controversial points, a group comprised by neurosurgeons, intensive care phisicians, intensive care nurses, infectologists and the hospital infections comittee, discussed these issue and wrote the recomendations. Key words: antibiotics prophylaxis, infection, management guidelines, ventriculitis, vetriculostomy.
Asunto(s)
Humanos , Profilaxis Antibiótica , Enfermería Primaria , Drenaje/efectos adversos , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Ventriculostomía/efectos adversosRESUMEN
La alta incidencia de infección en los drenajes ventriculares externos (0-45) representa un serio problema para los pacientes y las instituciones no sólo en el aspecto médico sino también en el económico y legal. Consideramos que la sistematización y la aplicación multidisciplinaria de guías de manejo son de gran importancia para la prevención de la infección. Por lo cual se debatieron los puntos de controversia en un grupo interdisciplinario constituido por especialistas en neurocirugía, terapia intensiva e infectología, enfermeros de terapia intensiva y el comité de infecciones, realizando por consenso las recomendaciones. Palabras clave: guía de manejo, infección, profilaxis antibiótica, ventriculitis, ventriculostomía.(AU)
The high incidence of infections fo the external ventricular drainages (0-45) represents a serious problem for patients and institutions not only in the medical aspects, but also int economic and legal ones. We believe that the systematic and multidisciplinary application of guides is of grat value for the prevention of infections. Based on the controversial points, a group comprised by neurosurgeons, intensive care phisicians, intensive care nurses, infectologists and the hospital infections comittee, discussed these issue and wrote the recomendations. Key words: antibiotics prophylaxis, infection, management guidelines, ventriculitis, vetriculostomy.(AU)
Asunto(s)
Humanos , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Profilaxis Antibiótica , Ventriculostomía/efectos adversos , Drenaje/efectos adversos , Enfermería PrimariaRESUMEN
La alta incidencia de infección en los drenajes ventriculares externos (0-45) representa un serio problema para los pacientes y las instituciones no sólo en el aspecto médico sino también en el económico y legal. Consideramos que la sistematización y la aplicación multidisciplinaria de guías de manejo son de gran importancia para la prevención de la infección. Por lo cual se debatieron los puntos de controversia en un grupo interdisciplinario constituido por especialistas en neurocirugía, terapia intensiva e infectología, enfermeros de terapia intensiva y el comité de infecciones, realizando por consenso las recomendaciones. Palabras clave: guía de manejo, infección, profilaxis antibiótica, ventriculitis, ventriculostomía.(AU)
The high incidence of infections fo the external ventricular drainages (0-45) represents a serious problem for patients and institutions not only in the medical aspects, but also int economic and legal ones. We believe that the systematic and multidisciplinary application of guides is of grat value for the prevention of infections. Based on the controversial points, a group comprised by neurosurgeons, intensive care phisicians, intensive care nurses, infectologists and the hospital infections comittee, discussed these issue and wrote the recomendations. Key words: antibiotics prophylaxis, infection, management guidelines, ventriculitis, vetriculostomy.(AU)
Asunto(s)
Humanos , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Profilaxis Antibiótica , Ventriculostomía/efectos adversos , Drenaje/efectos adversos , Enfermería PrimariaRESUMEN
In contrast to the role of lipopolysaccharide from Gram-negative bacteria, the role of Gram-positive bacterial components in inducing inflammation in the CNS remains controversial. We studied the potency of highly purified lipoteichoic acid and muramyl dipeptide isolated from Staphylococcus aureus to activate primary cultures of rat microglia. Exposure of pure microglial cultures to lipoteichoic acid triggered a significant time- and dose-dependent production of pro-inflammatory cytokines (tumour-necrosis factor-alpha, interleukin-1beta, interleukin-6) and nitric oxide. Muramyl dipeptide strongly and selectively potentiated lipoteichoic acid-induced inducible nitric oxide synthase expression and nitric oxide production. However, it did not have any significant influence on the production of pro-inflammatory cytokines. As bacterial components are recognised by the innate immunity through Toll-like receptors (TLRs) we showed that lipoteichoic acid was recognised in microglia by the TLR2 and lipopolysaccharide by the TLR4, as cells isolated from mice lacking TLR2 or TLR4 did not produce pro-inflammatory cytokines and nitric oxide upon lipoteichoic acid or lipopolysaccharide stimulation, respectively. Lipoteichoic acid-induced glia activation was mediated by p38 and ERK1/2 MAP kinases, as pretreatment with inhibitor of p38 or ERK1/2 decreased lipoteichoic acid-induced cytokine release, iNOS mRNA expression and nitric oxide production. The observed pro-inflammatory response induced by lipoteichoic acid-activated microglia could play a major role in the inflammatory response of CNS induced by Gram-positive bacteria.
Asunto(s)
Acetilmuramil-Alanil-Isoglutamina/farmacología , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Lipopolisacáridos/farmacología , Microglía/inmunología , Óxido Nítrico/metabolismo , Ácidos Teicoicos/farmacología , Receptor Toll-Like 2/metabolismo , Acetilmuramil-Alanil-Isoglutamina/inmunología , Acetilmuramil-Alanil-Isoglutamina/metabolismo , Animales , Animales Recién Nacidos , Células Cultivadas , Infecciones Bacterianas del Sistema Nervioso Central/metabolismo , Citocinas/inmunología , Citocinas/metabolismo , Relación Dosis-Respuesta a Droga , Encefalitis/inmunología , Encefalitis/metabolismo , Encefalitis/fisiopatología , Inhibidores Enzimáticos/farmacología , Quinasas MAP Reguladas por Señal Extracelular/efectos de los fármacos , Quinasas MAP Reguladas por Señal Extracelular/metabolismo , Mediadores de Inflamación/inmunología , Mediadores de Inflamación/metabolismo , Mediadores de Inflamación/farmacología , Lipopolisacáridos/inmunología , Microglía/efectos de los fármacos , Microglía/metabolismo , Óxido Nítrico Sintasa de Tipo II/efectos de los fármacos , Óxido Nítrico Sintasa de Tipo II/genética , Óxido Nítrico Sintasa de Tipo II/inmunología , Ratas , Transducción de Señal/efectos de los fármacos , Transducción de Señal/inmunología , Ácidos Teicoicos/inmunología , Factores de Tiempo , Receptor Toll-Like 2/efectos de los fármacos , Receptor Toll-Like 4/efectos de los fármacos , Receptor Toll-Like 4/inmunología , Receptor Toll-Like 4/metabolismo , Proteínas Quinasas p38 Activadas por Mitógenos/efectos de los fármacos , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismoRESUMEN
Neurological infections due to rapidly growing mycobacteria (RGM) have rarely been reported. We recently investigated two unrelated immunocompetent patients, one with community-acquired lymphocytic meningitis and the other with cerebral thrombophlebitis. Mycobacterium mucogenicum was isolated in pure culture and detected by PCR sequencing of cerebrospinal fluid samples. Both patients eventually died. The two isolates exhibited an overlapping antimicrobial susceptibility pattern. They were susceptible in vitro to tetracyclines, macrolides, quinolones, amikacin, imipenem, cefoxitin, and trimethoprim-sulfamethoxazole and resistant to ceftriaxone. They shared 100% 16S rRNA gene sequence similarity with M. mucogenicum ATCC 49650T over 1,482 bp. Their partial rpoB sequences shared 97.8% and 98.1% similarity with M. mucogenicum ATCC 49650T, suggesting that the two isolates were representative of two sequevars of M. mucogenicum species. This case report should make clinicians aware that M. mucogenicum, an RGM frequently isolated from tap water or from respiratory specimens and mostly without clinical significance, can even be encountered in the central nervous system of immunocompetent patients.
Asunto(s)
Infecciones Bacterianas del Sistema Nervioso Central/microbiología , Infecciones por Mycobacterium no Tuberculosas/microbiología , Micobacterias no Tuberculosas/patogenicidad , Adulto , Anciano , Anciano de 80 o más Años , Infecciones Bacterianas del Sistema Nervioso Central/inmunología , ADN Bacteriano/genética , ARN Polimerasas Dirigidas por ADN/genética , Farmacorresistencia Bacteriana , Resultado Fatal , Genes Bacterianos , Humanos , Inmunocompetencia , Masculino , Datos de Secuencia Molecular , Infecciones por Mycobacterium no Tuberculosas/inmunología , Micobacterias no Tuberculosas/clasificación , Micobacterias no Tuberculosas/efectos de los fármacos , Micobacterias no Tuberculosas/genética , ARN Bacteriano/genética , ARN Ribosómico 16S/genética , Especificidad de la EspecieAsunto(s)
Infecciones Bacterianas del Sistema Nervioso Central/inmunología , Infecciones por Chlamydia/microbiología , Chlamydophila pneumoniae/aislamiento & purificación , Esclerosis Múltiple/microbiología , Infecciones Bacterianas del Sistema Nervioso Central/microbiología , Infecciones por Chlamydia/inmunología , Chlamydophila pneumoniae/inmunología , HumanosRESUMEN
Experimental allergic encephalitis (EAE) is considered by many to be a model for human multiple sclerosis. Intraperitoneal inoculation of mice with Chlamydia pneumoniae, after immunization with neural antigens, increased the severity of EAE. Accentuation of EAE required live infectious C. pneumoniae, and the severity of the disease was attenuated with antiinfective therapy. After immunization with neural antigens, systemic infection with C. pneumoniae led to the dissemination of the organism into the central nervous system (CNS) in mice with accentuated EAE. Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS. These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE. We propose that infection of the CNS by C. pneumoniae can amplify the autoreactive pool of lymphocytes and regulate the expression of an autoimmune disease.