A novel approach in the management of right-sided endocarditis: percutaneous vegectomy using the AngioVac cannula.

The AngioVac is a vacuum-based device introduced in 2012 to percutaneously remove undesirable material from the intravascular system. In scattered reports, the AngioVac has been used for removal of device-led vegetations and right-sided thrombi. In this article, we describe three cases of right-sided endocarditis treated with AngioVac: a mobile mass extending from the vena cava into the right atrium, large native tricuspid vegetations, and bioprosthetic tricuspid vegetations. This device shows benefit in reducing vegetation load, decreasing septic lung embolization, and reducing reinfection in active intravenous drug users. These cases exhibit the AngioVac's arrival as a new and exciting tool in endocarditis treatment, providing an alternative to open surgery and accessorizing antimicrobial treatment.

Intravenous Tigecycline Facilitates Cure of Severe Clostridium difficile Infection (CDI) After Failure of Standard Therapy: A Case Report and Literature Review of Tigecycline Use in CDI.

Standard treatment for severe Clostridium difficile infection (CDI) is oral vancomycin with metronidazole. After failure of this standard regimen, treatment becomes challenging. A young woman treated for septic shock developed CDI. Standard treatment failed and she was ineligible for fecal transplant. Addition of tigecycline to her regimen resulted in cure.

Improvements in antimicrobial prescribing for treatment of upper respiratory tract infections through provider education.

BACKGROUND: Inappropriate use of antimicrobials to treat acute upper respiratory tract infections (URIs), which usually have a viral etiology, contributes to emergence and spread of antimicrobial resistance in Streptococcus pneumoniae and other human bacterial pathogens. OBJECTIVE: To reduce antimicrobial use for management of acute URIs in adult and pediatric patients. DESIGN: Prospective, nonrandomized, controlled trial. SETTING: Four primary care clinics within a staff model HMO in Detroit, Mich. PARTICIPANTS: Twenty-one primary care physicians at clinics where the educational intervention was implemented, and 9 primary care physicians at control clinics where no educational programs were implemented. MEASUREMENTS: Antibiotic prescribing for acute URIs during the baseline and study years among the intervention and control groups. RESULTS: A generalized linear mixed-effects model was used and showed that antimicrobial prescribing among the intervention group physicians decreased 24.6% from the baseline to the postintervention period (P<.0001) for both pediatric and adult medicine physicians. From the baseline to the study period, there was no significant decline in rates of antimicrobial prescribing by the control group of physicians (pediatricians, P=.35; internists, P=.42). The rates of decline in antimicrobial prescribing differed significantly between the intervention and control groups (P<.0003 for pediatricians and P<.01 for Internists). CONCLUSIONS: An interactive, case-based educational program for physicians and their staff proved effective for reducing unwarranted prescribing of antibiotics in the treatment of URIs by primary care physicians in a Medicaid HMO setting.

Tackling antibiotic resistance.

The development and spread of antibiotic resistance in bacteria is a universal threat to both humans and animals that is generally not preventable but can nevertheless be controlled, and it must be tackled in the most effective ways possible. To explore how the problem of antibiotic resistance might best be addressed, a group of 30 scientists from academia and industry gathered at the Banbury Conference Centre in Cold Spring Harbor, New York, USA, from 16 to 18 May 2011. From these discussions there emerged a priority list of steps that need to be taken to resolve this global crisis.

Accuracies of beta-lactam susceptibility test results for Pseudomonas aeruginosa with four automated systems (BD Phoenix, MicroScan WalkAway, Vitek, and Vitek 2).

Contemporary clinical isolates and challenge strains of Pseudomonas aeruginosa were tested by four automated susceptibility testing systems (BD Phoenix, MicroScan WalkAway, Vitek, and Vitek 2; two laboratories with each) against six broad-spectrum beta-lactams, and the results were compared to reference broth microdilution (BMD) and to consensus results from three validated methods (BMD, Etest [AB Biodisk, Solna, Sweden], and disk diffusion). Unacceptable levels of error (minor, major, and very major) were detected, some with systematic biases toward false susceptibility (piperacillin-tazobactam and imipenem) and others toward false resistance (aztreonam, cefepime, and ceftazidime). We encourage corrective action by the system manufacturers to address test biases, and we suggest that clinical laboratories using automated systems should consider accurate alternative methods for routine use.

Mutational replacement of Leu-293 in the class C Enterobacter cloacae P99 beta-lactamase confers increased MIC of cefepime.

The class C beta-lactamase from Enterobacter cloacae P99 confers resistance to a wide range of broad-spectrum beta-lactams but not to the newer cephalosporin cefepime. Using PCR mutagenesis of the E. cloacae P99 ampC gene, we obtained a Leu-293-Pro mutant of the P99 beta-lactamase conferring a higher MIC of cefepime (MIC, 8 microg/ml, compared with 0.5 microg/ml conferred by the wild-type enzyme). In addition, the mutant enzyme produced higher resistance to ceftazidime but not to the other beta-lactams tested. Mutants with 15 other replacements of Leu-293 were prepared by site-directed random mutagenesis. None of these mutant enzymes conferred MICs of cefepime higher than that conferred by Leu-293-Pro. We determined the kinetic parameters of the purified E. cloacae P99 beta-lactamase and the Leu-293-Pro mutant enzyme. The catalytic efficiencies (k(cat)/K(m)) of the Leu-293-Pro mutant beta-lactamase for cefepime and ceftazidime were increased relative to the respective catalytic efficiencies of the wild-type P99 beta-lactamase. These differences likely contribute to the higher MICs of cefepime and ceftazidime conferred by this mutant beta-lactamase.

Mutations in the aph(2")-Ic gene are responsible for increased levels of aminoglycoside resistance.

Random PCR mutagenesis of the enterococcal aph(2")-Ic gene followed by selection for mutant enzymes that confer enhanced levels of aminoglycoside resistance resulted in mutants of APH(2")-Ic with His-258-Leu and Phe-108-Leu substitutions, all of which conferred rises in the MICs of several aminoglycosides. The mutated residues are located outside conserved regions of aminoglycoside phosphotransferases.

Multiplex PCR for detection of aminoglycoside resistance genes in enterococci.

A multiplex PCR procedure for detecting the aminoglycoside resistance genes aac(6')-Ie-aph(2")-Ia, aph(2")-Ib, aph(2")-Ic, aph(2")-Id, aph(3')-IIIa, and ant(4')-Ia was evaluated and found to determine accurately the presence of these genes in enterococci.