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At least 19 recordsLinked to original sources
PubMed1998

Pharmacokinetic optimisation of the treatment of bacterial central nervous system infections.

Central nervous system (CNS) infections caused by bacteria with reduced sensitivity to antibacterials are an increasing worldwide challenge. In successfully treating these infections the following conditions should be considered: (i) Antibacterials do not distribute homogeneously in the central nervous compartments [cerebrospinal fluid (CSF), extracellular space of the nervous tissue, intracellular space of the neurons, glial cells and leucocytes]. Even within the CSF, after intravenous administration, a ventriculo-lumbar concentration gradient is often observed. (ii) Valid parameters of drug entry into the CSF are the CSF: serum concentration ratio in steady state and the CSF: serum ratio of the area under the concentration-time curves (AUCCSF/AUCS). Frequently, the elimination half-life (t1/2 beta) in CSF is longer than t1/2 beta in serum. (iii) For most antibacterials, lipophilicity, molecular weight and serum protein binding determine the drug entry into the CSF and brain tissue. With an intact blood-CSF and blood-brain barrier, the entry of hydrophilic antibacterials (beta-lactam antibacterials, glycopeptides) into the CNS compartments is poor and increases during meningeal inflammation. More lipophilic compounds [metronidazole, quinolones, rifampicin (rifampin) and chloramphenicol] are less dependent on the function of the blood-CSF and blood-brain barrier. (iv) Determination of the minimal inhibitory concentrations (MIC) of the causative organism is necessary for optimisation of treatment. (v) For rapid sterilisation of CSF, drug concentrations of at least 10 times MIC are required. The minimum CSF concentration: MIC ratio ensuring successful therapy is unknown. Strategies to achieve optimum antibacterial concentrations in the presence of minor disturbances of the blood-CSF and blood-brain barrier include, the increased use of low toxicity antibacterials (e.g., beta-lactam antibiotics), the use of moderately lipophilic compounds, and the combination of intravenous and intraventricular administration. Antibacterials which do not interfere with bacterial cell wall synthesis delay and/or decrease the liberation of proinflammatory bacterial products, delay or inhibit tumour necrosis factor release, and may reduce brain oedema in experimental meningitis. Conclusive evidence of the reduction of neuronal damage by this approach, however, is lacking.

Anti-Bacterial Agents↗
PubMed2005

Blood-brain barrier drug discovery for central nervous system infections.

Central nervous system (CNS) infections are formidable diseases with high rates of morbidity and mortality. Since the majority of antimicrobial agents discovered so far do not cross the blood-brain barrier (BBB), the treatment of CNS infections is a major challenge issue. The development of drugs to treat those diseases requires consideration of achievable brain concentrations by targeting the following question. How can the chemistry and biology of the BBB, and infectomics be exploited for the development of drugs against CNS infections? To date drug targeting approaches, such as chemistry-based, biology-based, and infectomics-based, have been implicated in the development of drugs for treatment of CNS infections. The chemistry-based strategies rely on lipid-mediated BBB drug transport as substances that readily permeate the BBB. These usually include small molecular weight of lipophilic or hydrophobic molecules. The biology-based strategies depend on endogenous BBB transport systems, including carrier-mediated transport (CMT), active efflux transport (AET), and receptor-mediated transport (RMT). These transporters play important roles in the influxes and/or effluxes of drugs including antimicrobial agents in brain capillary endothelial cells that form the BBB. Both microbial and host signatures of infectomes, which can be dissected by infectomics, provide invaluable fountains in the search for novel antimicrobial therapies. Key markers associated with the mechanisms of neuronal injury may be identified, and thus, provide important targets for the prevention and treatment of CNS infections. This review focuses on the major BBB drug targeting strategies in the development of therapeutics for CNS infections. A combination of these strategies will ultimately lead to improved treatments.

Animals↗
PubMed1999

Cerebrospinal fluid testing for the diagnosis of central nervous system infection.

The central nervous system (CNS) is susceptible to bacterial, viral, and fungal infections, and prion diseases. Examination of the cerebrospinal fluid (CSF) is crucial in diagnosing these infections. Cerebrospinal tests may directly identify an organism and its nucleic acid and surface constituents by culture, polymerase chain reaction (PCR), or antigen detection. Alternatively, antibody to an organism may be identified in CSF by enzyme-linked immunosorbent assay (ELISA), Western blot, or complement fixation assay. This article discusses how these CSF tests are performed and addresses the sensitivity and specificity of such tests for the diagnosis of selected CNS infections.

Antibody Specificity↗
PubMed1999

Central nervous system infections. Basic concepts.

Central nervous system infections have the potential to be very dangerous and life-threatening. Advances in the understanding and care of patients experiencing these infections have aided in their detection and treatment. Caring for these patients requires a thorough knowledge of the diseases as well as a holistic approach which encompasses the patient and family.

Central Nervous System Infections↗
PubMed1999

Outpatient parenteral antimicrobial therapy for central nervous system infections.

Patients with central nervous system (CNS) infections are increasingly treated with intravenous antimicrobials outside the hospital, but the safety and problems associated with this therapy have not been well defined. To examine this issue, we reviewed 68 cases in which outpatient intravenous antimicrobial therapy (OPAT) was received through our physician office-based infusion clinic. All infections were cured, and no deaths occurred during therapy. Seizures occurred in 2 patients but without significant injury and apparently were unrelated to antimicrobial therapy. Eleven patients (16%) were hospitalized after starting OPAT, 5 for procedures and 6 for medical reasons. The antimicrobial used was changed in 13 cases (19%) because of an adverse effect or clinical failure. OPAT can be safe and effective for patients with CNS infections, but patients must be carefully selected and monitored closely.

Adolescent↗
PubMed2006

Central nervous system infections in transplantation.

Central nervous system (CNS) infections are a rare but serious complication of transplantation. An appropriate diagnostic workup should be streamlined with stratification of infection risk by length and degree of immune suppression, lesion localization, and timing. Polymerase chain reaction has high sensitivity and specificity for rapid identification of viral infections and should be used when available. Early diagnosis is imperative, and biopsy should be pursued if a diagnosis is not readily obtained with noninvasive testing. Treatment is pathogen specific. Combination antifungal therapy should be considered for cerebral aspergillosis. Zygomycetes and related invasive fungi require surgical resection and high-dose antifungal therapy. Viral meningoencephalitis therapy should be continued until resolution of clinical signs and symptoms, and viral clearance is verified with repeat cerebrospinal fluid analysis. Cytomegalovirus encephalitis requires ongoing maintenance therapy until clearance of viremia or antigenemia. Bacterial meningitis is uncommon in transplantation and should be treated with 21 days of antibiotics. CNS bacterial abscesses, including nocardiosis, should be surgically drained if feasible and treated until resolution of clinical and radiographic evidence of infection.

Journal Article↗
PubMed2005

Virus signaling and apoptosis in the central nervous system infection.

Viruses target the central nervous system (CNS) incidentally, due to complications of systemic infection, or specifically, by ascending via the axons of peripheral and cranial nerves. In the CNS, viruses cause acute disease (viz. encephalitis), latent infections or neurodegenerative pathology. Causation of acute disease or immune-mediated pathology, and virus involvement in the etiology of chronic neurodegenerative diseases depends, at least in part, on the ability to commander signaling pathways. Better understanding of these virus-host cell interactions will help identify molecular targets for the development of improved therapeutic strategies.

Animals↗
PubMed1983

Cerebral perfusion pressure in central nervous system infections of infancy and childhood.

Central nervous system infections may be complicated by development of severe brain edema, which can be a significant factor in mortality and morbidity. Increased intracranial pressure can cause additional damage to the central nervous system by impairment of cerebral blood flow, which is dependent on cerebral perfusion pressure. A reduction of cerebral perfusion pressure, caused by elevation of intracranial pressure, may cause cerebral ischemia. We studied cerebral perfusion pressure in 17 patients, ages 45 days to 11 years, with severe central nervous system infections and who were in deep coma. Meningitis was diagnosed in 64.7%, and encephalitis in 29.4%. The patients who survived (64.7%) did not differ significantly from those who died (36.5%) in severity of disease and maximal intracranial pressure during the course of the illness. A striking difference in minimal cerebral perfusion pressure recorded was found between survivors and nonsurvivors: all patients with minimal cerebral perfusion pressure greater than 30 mm Hg survived, whereas those with lower pressure died. In survivors, cerebral perfusion pressure could be maintained adequately by reduction of intracranial pressure, but nonsurvivors developed noncompliance of brain tissue, and cerebral perfusion pressure could not be maintained at levels that ensure adequate cerebral blood flow, resulting in cerebral ischemia and death. Continuous monitoring of mean arterial blood pressure and intracranial pressure in children with severe central nervous system infections will enable rapid diagnosis and initiation of treatment when cerebral perfusion pressure is reduced to critical levels. Such treatment might improve the prognosis.

Blood Pressure↗
PubMed2000

Central nervous system infections in the pediatric population.

Central nervous system infections and sequelae in the pediatric population may present differently depending on the patient's stage of development. Infections contracted from conception through the neonatal period may affect central nervous system formation, whereas infections acquired later tend to cause parenchymal destruction. This article discusses congenital, focal parenchymal, extra-axial, and diffuse parenchymal infections and their effect on the developing brain.

Brain Damage, Chronic↗
PubMed2002

Central nervous system infections in injection drug users.

Central nervous system infections in injection drug users are often devastating in terms of excess morbidity and mortality. In injection drug users with infective endocarditis, embolization from infected valvular vegetations may cause cerebral infarction, intracranial hemorrhage, and the formation of brain abscess. Focal intracranial infections (i.e., brain abscess and spinal epidural abscess) may occur in the absence of infective endocarditis, resulting from bacteremia that seeds the brain or epidural space. Antimicrobial therapy, combined with surgical intervention, may be essential to improve outcome from these neurologic complications. Toxin-mediated diseases (especially tetanus and wound botulism) are also seen in injection drug users. Inoculation of Clostridium spp at injection sites may lead to toxin generation and disease. Clinicians must maintain a high level of suspicion for these diagnoses in injection drug users.

Brain Abscess↗
PubMed2005

Parasitic central nervous system infections: echinococcus and schistosoma.

Central nervous system (CNS) manifestations of Echinococcus and Schistosoma infections occur throughout the world, with incidence increasing in developed regions. A detailed literature review generated a current summary on epidemiology, parasitology, pathology, clinical manifestations, imaging studies, diagnosis, and treatment of neuroechinococcosis and neuroschistosomiasis. Recent advancements have been made in diagnosis, treatment, and prevention of these parasitic CNS infections. Ongoing advancements in neuroimaging and diagnostic studies, as well as efforts to better understand the parasite genome and host-parasite relationships, will likely continue to improve patient management.

Animals↗
PubMed1997

[Central nervous system infection caused by mumps virus].

Central nervous system infection caused by mumps virus is reviewed. Aseptic meningitis, acute encephalitis, chronic encephalitis, hydrocephalus, ataxia, transverse myelitis, Guillain-Barré syndrome and deafness are noted as central nervous system complications of mumps. Among these complications, acute and chronic encephalitis, hydrocephalus, transverse myelitis and deafness occasionally result in severe sequelae. Aseptic meningitis due to mumps vaccine strain increased significantly after the introduction of trivalent measles, mumps and rubella vaccination in Japan. Recently, a differentiation method of mumps vaccine strain from wild viruses has been established using molecular analysis. Mumps virus infection is still one of the most common communicable viral infections, although it is preventable by vaccination. We emphasize the importance of mumps vaccination to prevent such severe complications as encephalitis and deafness.

Central Nervous System Diseases↗
PubMed2006

Central nervous system infections - a potential complication of systemic immunotherapy.

PURPOSE OF REVIEW: Multiple sclerosis is a chronic inflammatory disease of the central nervous system, characterized by demyelination and axonal damage. With the emergence of more efficient immune therapies, severe sometimes even fatal central nervous system infections were observed. This review will address the role of the systemic immune system in central nervous system immune surveillance and discuss implications for the development of novel immunotherapies in multiple sclerosis. RECENT FINDINGS: In the last decade, a number of immunosuppressive and immunomodulatory agents have been approved for the treatment of multiple sclerosis, based on the results of double-blind placebo-controlled randomized clinical trials. A better understanding of the pathogenesis of the disease has prompted exploration of the therapeutic utility of new drugs that more potently disrupt the pathophysiological cascade of events that culminates in central nervous system tissue damage. One potential side-effect of these newer therapies is their interference with the control of central nervous system infections by the immune system. SUMMARY: Any increase in potency of multiple sclerosis therapies could well interfere with protective immunosurveillance of the central nervous system. One possible outcome is an increased incidence of opportunistic infections. A heightened vigilance for central nervous system infections in the setting of immunosuppression is necessary to prevent serious side-effects in the future.

Central Nervous System↗
PubMed1986

Analysis of JHM central nervous system infections in rats.

Intracerebral inoculation of murine coronavirus JHM into 2- to 3-day-old Wistar Furth rats causes an acute encephalomyelitis, while inoculations at 10 days of age usually result in hind leg paralysis. To examine the distribution of viral antigens within this infected central nervous system (CNS) tissue, we used the avidin-biotin-peroxidase method to detect monoclonal and polyclonal antibodies bound to JHM structural proteins; in addition we used the Western blot technique to detect viral proteins. Our study demonstrated the following characteristics: Infected neuronal and glial cells produced viral nucleocapsid and E2 glycoprotein. The synthesis of these viral structural proteins was not restricted to cells in any particular part of the central nervous system. While JHM E2 proteins could be detected in individual cells of JHM-infected CNS tissue, the relative level of detectable E2 protein in the total CNS tissue of infected rats was reduced by more than 13-fold compared with JHM-infected tissue culture cells. Hippocampus neuronal cells provided a sensitive indication of JHM infection. These cells invariably contained antigens in both acutely and chronically infected animals. The distribution of cells containing viral antigens differed markedly for JHM-induced acute encephalitis and chronic demyelinating disease. Acutely infected brains had large lesions containing low levels of viral antigen scattered throughout the brain. One percent to ten percent of histologically normal cells in many parts of the brain contained viral antigens; in addition, more neuronal cells than glial cells were observed to be antigen-positive. The hippocampus appeared normal with hematoxylin-eosin staining; however, a scattered infection of neuronal cells was apparent.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Prevention of central nervous system infections in patients at risk.

Infections of the central nervous system in patients at risk are relatively uncommon when compared with pneumonia, bacteremia, and soft tissue infection. However, they carry serious morbidity and are frequently fatal. Each of the diverse conditions that can place a patient at risk for central nervous system infection is associated with a fairly predictable spectrum of etiologic organisms. Various forms of trauma (including blunt and penetrating injuries and neurosurgery, especially when a cerebrospinal fluid shunt is implanted) predispose to infection with common pathogenic bacteria. Defects of cellular immunity including congenital immune deficiencies, immunosuppressive drug therapy, leukemia, lymphoma, and the acquired immune deficiency syndrome are more likely to give rise to infection with a distinctive spectrum of opportunistic viruses, fungi, and protozoa. Other underlying conditions include sinus, ear, and mastoid infections, congenital heart disease, intrathoracic suppuration, endocarditis, and bacteremia, hypogammaglobulinemia, and complement deficiencies. Some preventive measures including vaccines, antibiotics, and surgical procedures are available. However, for many of these central nervous system infections, preventive measures are lacking or less effective than those for infections in other organs. In the future, opportunistic central nervous system infections will increase in frequency as the number of patients at risk continues to grow.

Anti-Bacterial Agents↗
PubMedDate not supplied

Molecular genetic methods in diagnosis and direct characterization of acute bacterial central nervous system infections.

Acute bacterial infection of the central nervous system requires rapid and adequate management. Etiological diagnosis is hence crucial. Moreover, the epidemic threat of certain bacteria necessitates a reliable characterization of the involved bacterial strains to follow the spread of epidemic strains. Conventional identification and characterization of etiological agents are basically based on culture and identification of bacterial markers most frequently by serological assays. Molecular identification and characterization of bacteria have been employed. They provide more reliable analysis of bacterial isolates. Molecular methods for non-culture diagnosis of bacterial infections have recently been developed. In many cases, the molecular assays have decreased the identification time of positive cultures and rescued detection of pathogens in culture-negative clinical samples.

Acute Disease↗