Bacterial Infections Of Central Nervous System Research Articles

Incarceration and the acquired immunodeficiency syndrome: Autopsy results in Texas prison inmates

The Texas Department of Criminal Justice (TDCJ) houses many subjects with acquired immunodeficiency syndrome (AIDS) who receive medical care in a comprehensive AIDS treatment center. In this case-control autopsy survey, we compared pathological outcomes of TDCJ inmates treated at the center (n = 155) with nonincarcerated patients who died during the same period (n = 155). Using multiple regression analysis and a proportional hazards model, survival time in the prisoners was equivalent to that in the controls. With few exceptions, the prevalences of opportunistic viral, fungal, protozoal, and bacterial infections contributing to mortality were equivalent between groups. Mycobacterium tuberculosis was isolated more frequently in the inmates, and M avium intracellulare was isolated less frequently ( P < .0001). The inmates had a higher prevalence of bacterial infection of the central nervous system (CNS) (9.1% v 1.4%; P < .006); half of all CNS bacterial infections were caused by M tuberculosis. Inmates had significantly lower prevalences of vacuolar myelopathy ( P < .006) and severe wasting disease ( P < .0009). We conclude that survival of prison inmates with AIDS treated in a comprehensive AIDS treatment center was equivalent to that of nonincarcerated subjects with AIDS. Prevalences of certain complications of AIDS differed in the inmates, showing that the prison environment influenced some of the underlying causes of AIDS morbidity and mortality.

Passage of cefotaxime and ceftriaxone into cerebrospinal fluid of patients with uninflamed meninges

Cefotaxime and ceftriaxone have proven to be effective in pyogenic infections of the central nervous system. Since in some bacterial central nervous system infections the blood-cerebrospinal fluid (CSF) barrier is either minimally impaired or recovers in the course of the illness, we studied the penetration of both antibiotics in the absence of inflamed meninges. Patients who had undergone external ventriculostomies for noninflammatory occlusive hydrocephalus received either cefotaxime (2 g/30 min) or ceftriaxone (2 g/30 min) to treat extracerebral infections. Serum and CSF were drawn repeatedly after the first dose. With ceftriaxone, they were also drawn after the last dose. The concentrations of cefotaxime, its metabolite desacetylcefotaxime, and ceftriaxone were determined by high-performance liquid chromatography with UV detection. Maximum concentrations of cefotaxime in CSF were reached 0.5 to 8 h (median = 3 h; n = 6) after the end of the infusion and ranged from 0.14 to 1.81 mg/liter (median = 0.44 mg/liter; n = 6). Maximum levels of ceftriaxone in CSF ranging from 0.18 to 1.04 mg/liter (median = 0.43 mg/liter; n = 5) were seen 1 to 16 h (median = 12 h; n = 5) after the infusion. The elimination half-life of cefotaxime in CSF was 5.0 to 26.9 h (median = 9.3 h; n = 5), and that of ceftriaxone was 15.7 to 18.4 h (median = 16.8 h; n = 3). It is concluded that after a single dose of 2 g, maximal concentrations of cefotaxime and ceftriaxone in CSF do not differ substantially. The long elimination half-lives guarantee uniform concentrations in CSF. These concentrations reliably inhibit highly susceptible bacteria but cannot be relied on to inhibit staphylococci and penicillin G-resistant Streptococcus pneumoniae.

Antibiotic treatment of community acquired bacterial meningitis

Community acquired meningitis is predominantly caused by three agents: Haemophilus influenzae, Streptococcus pneumoniae and Neisseria meningitidis Four physical properties of available drugs—molecular size, protein binding, lipid solubility and ionization—affect drug entry to the central nervous system (CNS). These factors, coupled with acute changes in bloodbrain barriers and intrinsic bactericidal activity, have a bearing on the success of treatment with all agents. Third generation cephalosporins have largely supplanted older regimens due to their intrinsic qualities of greater bactericidal activity, optimal cerebrospinal fluid pharmacokinetics, and low toxicity. The pharmacological principles of treatment of CNS bacterial infections, pharmacology of available drugs, and current treatment recommendations are reviewed.

Incidence and prognosis of central nervous system infections in a birth cohort of 12,000 children.

All types of central nervous system (CNS) infections were investigated in a 1966 birth cohort of 12,000 children from Northern Finland followed up from birth to the age of 14. 174 CNS infections occurred in 167 children, 110 boys and 64 girls. The annual incidence of bacterial CNS infections was 36.3/100,000 and that of viral infections 688.0/100 000. It is concluded that bacterial CNS infections were recorded very fully but only 2/3 of the viral infections could be traced, even though the more severe cases were quite well documented. 8/55 children (14.5%) with bacterial meningitis died; the corresponding figure for viral encephalitis and meningitis (excluding mumps) was 3/67 (4.5%). 17/55 (30.9%) developed mental retardation, epilepsy, cerebral palsy or hearing defect or some combination of these after bacterial CNS infection, and 9 (8.1%) after viral infection. The difference with respect to the children who had not experienced CNS infection was statistically significant only for the bacterial infection cases. CNS infections explained 7.6% of all deaths from 28 days to 14 years, 3% of the handicapping cases of cerebral palsy, mental retardation and epilepsy or some combination of these, and 6.6% of the hearing defects.

Increased risk of experimental central nervous system listeriosis in rats with chronic serum sickness. An immunohistopathological study.

The incidence and severity of central nervous system (CNS) infection were increased following the intraperitoneal innoculation of Listeria monocytogenes in adult Wistar rats with experimental chronic serum sickness. The results were attributed to an alteration in the blood-cerebrospinal fluid barrier induced by immune complex deposits in the choroid plexus of animals hyperimmunized with bovine serum albumin. CNS inflammation occurred in 16 of 40 (40%) of the test animals studied; one of 36 (2.8%) controls had CNS inflammation. There were extensive pathological changes in the choroid plexus, subarachnoid space, and neural parenchyma of the test animals, as compared with only small inflammatory foci limited to the choroid plexus and subarachnoid space in the one affected control. This experimental model for inducing bacterial CNS infection simulates certain predisposing conditions in chronic immune disease, and may therefore be useful in studying the pathogenesis of CNS infection in such cases.