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Background Evidence supporting combination treatment with a beta-lactam plus an aminoglycoside (C-BA) for endocarditis caused by viridans and gallolyticus group streptococci (VGS-GGS) with intermediate susceptibility to penicillin (PENI-I) is lacking. We assessed the clinical characteristics and outcomes of PEN-I VGS-GGS endocarditis and compared the effectiveness and safety of C-BA with third-generation cephalosporin monotherapy. Methods Retrospective analysis of prospectively collected data of a cohort of definite endocarditis caused by penicillin-susceptible and PENI-I VGS-GGS (penicillin minimum inhibitory concentration ranging from 0.25 to 2 mg/L) between 2008 and 2018 in 40 Spanish hospitals. We compared cases treated with monotherapy or with C-BA and performed multivariable analyses of risk factors for in-hospital and 1-year mortality. Results A total of 914 consecutive cases of definite endocarditis caused by VGS-GGS with complete or intermediate susceptibility to penicillin were included. A total of 688 (75.3%) were susceptible to penicillin and 226 (24.7%) were PENI-I. Monotherapy was used in 415 (45.4%) cases (cephalosporin in 331 cases) and 499 (54.6%) cases received C-BA. In-hospital mortality was 11.9%, and 190 (20.9%) patients developed acute kidney injury. Heart failure (odds ratio [OR]: 6.06; 95% confidence interval [CI]: 1.37–26.87; P =.018), central nervous system emboli (OR: 9.83; 95% CI: 2.17–44.49; P =.003) and intracardiac abscess (OR: 13.47; 95% CI: 2.24–81.08; P =.004) were independently associated with in-hospital mortality among PEN-I VGS-GGS cases, while monotherapy was not (OR: 1.01; 95% CI:.26–3.96; P =.982). Conclusions Our findings support the use of cephalosporin monotherapy in PEN-I VGS-GGS endocarditis in order to avoid nephrotoxicity without adversely affecting patient outcomes. [ABSTRACT FROM AUTHOR]

The activity of eight aminoglycosides (amikacin, apramycin, arbekacin, gentamicin, kanamycin, neomycin, netilmicin and tobramycin) against a collection of 257 amoxicillin/clavulanic acid (AMC)-resistant Escherichia coli isolates was determined by microdilution. Aminoglycoside resistance rates, the prevalence of aminoglycoside-modifying enzyme (AME) genes, the relationship between AME gene detection and resistance phenotype to aminoglycosides, and the association of AME genes with mechanisms of AMC resistance in E. coli isolates in Spain were investigated. Aminoglycoside-resistant isolates were screened for the presence of genes encoding common AMEs [ aac(3)-Ia , aac(3)-IIa , aac(3)-IVa , aac(6 ′ )-Ib , ant(2 ″ )-Ia , ant(4 ′ )-IIa and aph(3 ′ )-Ia ] or 16S rRNA methylases ( armA , rmtB , rmtC and npmA ). In total, 105 isolates (40.9%) were resistant to at least one of the aminoglycosides tested. Amikacin, apramycin and arbekacin showed better activity, with MIC 90 values of 2 mg/L (arbekacin) and 8 mg/L (amikacin and apramycin). Kanamycin presented the highest MIC 90 (128 mg/L). The most common AME gene was aac(6 ′ )-Ib (36 strains; 34.3%), followed by aph(3 ′ )-Ia (31 strains; 29.5%), ant(2 ″ )-Ia (29 strains; 27.6%) and aac(3)-IIa (23 strains; 21.9%). aac(3)-Ia , aac(3)-IVa , ant(4 ′ )-IIa and the four methylases were not detected. The ant(2 ″ )-Ia gene was usually associated with OXA-1 [21/30; 70%], whilst 23/25 (92%) strains producing CTX-M-15 had the aac(6 ′ )-Ib gene. The most prevalent AME gene was aac(6 ′ )-Ib (18/41; 44%) in nosocomial isolates, whilst ant(2 ″ )-Ia and aph(3 ′ )-Ia genes (20/64; 31%) were more frequent in strains of community origin. In 64.6% isolates the phenotypic profile correlated with the presence of commonly encountered AMEs. [ABSTRACT FROM AUTHOR]