Water Res 2010,44(3):789–796 PubMedCrossRef 31 Herrera Melián JA

Water Res 2010,44(3):789–796.PubMedCrossRef 31. Herrera Melián JA, Doña Rodríguez JM, Viera Suárez A, Tello Rendón E, Valdés do Campo C, Arana J, Pérez Peña J: The photocatalytic disinfection of urban waste waters. Chemosphere 2000,41(3):323–327.PubMedCrossRef 32. Ubomba-Jaswa MG 132 E, Navntoft C, Polo-Lopez MI, Fernandez-Ibanez P, McGuigan KG: Solar disinfection of drinking water (SODIS): an investigation of the effect of UV-A dose on inactivation efficiency. Photoch Photobio Sci 2009,8(5):587–595.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions The project was designed by SK, RR and MR. All experiments were performed

by SK under supervision of

RR. The paper was co-drafted by SK and RR. All authors approved the final version of the manuscript.”
“Background Tuberculosis (TB) of the central nervous system (CNS) is a devastating and often fatal CBL-0137 mw disease, primarily affecting young children. Even when treatment is administered in a timely manner, mortality is extraordinarily high, with surviving patients often experiencing severe neurological sequelae. CNS TB comprises approximately 1% of TB disease worldwide, disproportionately affecting GSK690693 cell line children in developing nations [1]. Coinfection with human immunodeficiency virus increases the likelihood of CNS TB [2, 3], and the emergence of drug resistant strains further complicates CNS TB due to limited permeability at the blood-brain barrier (BBB) of several second-line TB drugs. Delays in treatment due to drug-susceptibility D-malate dehydrogenase testing further reduce the efficacy of available patient care [4]. The CNS is protected from the systemic circulation by the BBB, composed principally of specialized and tightly apposed brain microvascular endothelia (BMEC), supported by astrocyte processes [5, 6]. According to the widely accepted hypothesis by Rich et al (1933), lesions (Rich foci) develop around bacteria seeded in the brain parenchyma and meninges during the initial

hematogenous dissemination. Subsequent rupture of these foci results in the release of bacteria directly into the CSF, causing extensive inflammation and meningitis [7]. The onset of meningitis is most commonly observed in young children (between the ages of 0 and 4), and is also associated with HIV co-infection or recent corticosteroid use [8]. In addition to host risk factors, recent clinical reports have indicated the association of distinct Mycobacterium tuberculosis strains with CNS disease [9–12], and microbial factors which promote CNS disease have been identified in numerous other neuroinvasive pathogens [13]. While it is clear that M. tuberculosis invade the CNS and that microbial factors may be required for CNS disease, the identity of such virulence determinants remains elusive.

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