Aperture effects on the oxygen abundance determinations from Califa data

This paper aims to provide aperture corrections for emission lines in a sample of spiral galaxies from the Calar Alto Legacy Integral Field Area Survey (CALIFA) database. In particular, we explore the behavior of the log([O III] λ5007/Hβ)/([N II] λ6583/Hα) (O3N2) and log[N II] lambda 6583/Hα (N2) flux ratios since they are closely connected to different empirical calibrations of the oxygen abundances in star-forming galaxies. We compute the median growth curves of Hα, Hα/Hβ, O3N2, and N-2 up to 2.5R(50) and 1.5 disk R-eff. These distances cover most of the optical spatial extent of the CALIFA galaxies. The growth curves simulate the effect of observing galaxies through apertures of varying radii. We split these growth curves by morphological types and stellar masses to check if there is any dependence on these properties. The median growth curve of the Hα flux shows a monotonous increase with radius with no strong dependence on galaxy inclination, morphological type, and stellar mass. The median growth curve of the Hα/HβH ratio monotonically decreases from the center toward larger radii, showing for small apertures a maximum value of ≈10% larger than the integrated one. It does not show any dependence on inclination, morphological type, and stellar mass. The median growth curve of N-2 shows a similar behavior, decreasing from the center toward larger radii. No strong dependence is seen on the inclination, morphological type, and stellar mass. Finally, the median growth curve of O3N2 increases monotonically with radius, and it does not show dependence on the inclination. However, at small radii it shows systematically higher values for galaxies of earlier morphological types and for high stellar mass galaxies. Applying our aperture corrections to a sample of galaxies from the SDSS survey at 0.02 ≤ z ≤ 0.3 shows that the average difference between fiber-based and aperture-corrected oxygen abundances, for different galaxy stellar mass and redshift ranges, reaches typically to ≈11%, depending on the abundance calibration used. This average difference is found to be systematically biased, though still within the typical uncertainties of oxygen abundances derived from empirical calibrations. Caution must be exercised when using observations of galaxies for small radii (e.g., below 0.5 R_eff) given the high dispersion shown around the median growth curves. Thus, the application of these median aperture corrections to derive abundances for individual galaxies is not recommended when their fluxes come from radii much smaller than either R_50 or R_eff.

Single-nucleotide polymorphism in two representative multidrug-resistant Mycobacterium bovis isolates collected from patients in a Spanish hospital harboring a human infection outbreak

Mycobacterium bovis is the etiological agent of tuberculosis in domestic and wild animals. Its involvement as a human pathogen has been highlighted again with the recent descriptions of transmission through dairy products (18), reactivation or primary infection in human immunodeficiency virus-infected patients (5), and association with meat industry workers, animal keepers, or hunters (3). Strains resistant to antituberculous drugs (M. bovis is naturally resistant to pyrazinamide) pose an additional risk (2). Several studies have demonstrated that mutations in target genes are associated with resistance to antituberculous drugs (4, 7, 10, 11, 16). However, most of them have been developed in Mycobacterium tuberculosis strains and limited data are available regarding M. bovis isolates. The aim of this study was to characterize by sequencing the main genes involved in antibiotic resistance in two multidrug-resistant (MDR) M. bovis isolates in a human outbreak detected in a hospital in Madrid that subsequently spread to several countries (5, 6, 15). The isolates were resistant to 11 drugs, but only their rpoB and katG genes have been analyzed so far (1, 14). We studied the first (93/R1) and last (95/R4) M. bovis isolates of this nosocomial outbreak, characterized by spoligotyping as SB0426 (hexacode 63-5F-5E-7F-FF-60 in the database at www.mbovis.org) (1, 13). Several genes involved in resistance to isoniazid (katG, ahpC, inhA, and the oxyR-ahpC intergenic region), rifampin (rpoB), streptomycin (rrs, rpsL), ethambutol (embB), and quinolones (gyrA) were studied. These genes, or fragments of genes, were amplified and sequenced as previously described (12). The sequence analysis revealed polymorphisms in five (ahpC, rpoB, rpsL, embB, and gyrA) out of nine analyzed genes (Table 1). Nucleotide substitutions in four genes cause a change in the encoded amino acid. Two additional synonymous mutations in ahpC and rpsL differentiated the first and last isolates from the outbreak.