Urinary tract infection in a human male patient with Staphylococcus pseudintermedius transmission from the family dog.

Staphylococcus pseudintermedius is increasingly recognized as a human pathogen. We report the first case of an urinary tract infection in a male patient with this organism.

Persistent infection with Staphylococcus pseudintermedius in an adult oncology patient with transmission from a family dog.

Staphylococcus pseudintermedius is a well known commensal organism of dogs but also a canine opportunistic pathogen. Reports of this organism being recovered from specimens from humans might suggest an increase prevalence in human infections and/or improved diagnostic leading to more accurate identification. Here we report a case of persistent S. pseudintermedius infection in an adult female oncology patient including colonization of the tip of an indwelling catheter. Diligence by laboratories in correctly isolating and identifying this pathogen (including susceptibility testing) is essential for optimal patient care.

Comparative minimum inhibitory and mutant prevention drug concentrations of enrofloxacin, ceftiofur, florfenicol, tilmicosin and tulathromycin against bovine clinical isolates of Mannheimia haemolytica.

Mannheimia haemolytica is the most prevalent cause of bovine respiratory disease (BRD) and this disease accounts for 75% of morbidity, 50-70% of feedlot deaths and is estimated to cost up to $1 billion dollars annually in the USA. Antimicrobial therapy is essential for reducing morbidity, mortality and impacting on the financial burden of this disease. Due to the concern of increasing antimicrobial resistance, investigation of antibacterial agents for their potential for selecting for resistance is of paramount importance. A novel in vitro measurement called the mutant prevention concentration (MPC) defines the antimicrobial drug concentration necessary to block the growth of the least susceptible cells present in high density (≥10(7) colony forming units/ml) bacterial populations such as those seen in acute infection. We compared the minimum inhibitory concentration (MIC) and MPC values for 5 antimicrobial agents (ceftiofur, enrofloxacin, florfenicol, tilmicosin, tulathromycin) against 285 M. haemolytica clinical isolates. The MIC(90)/MPC(90) values for each agent respectively were as follows: 0.016/2, 0.125/1, 2/≥16, 8/≥32, 2/8. Dosing to achieve MPC concentrations (where possible) may serve to reduce the selection of bacterial subpopulations with reduced antimicrobial susceptibility. The rank order of potency based on MIC(90) values was ceftiofur > enrofloxacin > florfenicol = tulathromycin > tilmicosin. The rank order of potency based on MPC(90) values was enrofloxacin > ceftiofur > tulathromycin > florfenicol ≥ tilmicosin.

In vitro killing of Escherichia coli, Staphylococcus pseudintermedius and Pseudomonas aeruginosa by enrofloxacin in combination with its active metabolite ciprofloxacin using clinically relevant drug concentrations in the dog and cat.

Enrofloxacin is a fluoroquinolone antibacterial agent used to treat infections in companion animals. Enrofloxacin's antimicrobial spectrum includes Gram positive and Gram-negative bacteria and demonstrates concentration-dependent bacteriocidal activity. In dogs and cats, enrofloxacin is partially metabolized to ciprofloxacin and both active agents circulate simultaneously in treated animals at ratios of approximately 60-70% enrofloxacin to 30-40% ciprofloxacin. We were interested in determining the killing of companion animal isolates of Escherichia coli, Staphylococcus pseudintermedius and Pseudomonas aeruginosa by enrofloxacin and ciprofloxacin combined using clinically relevant drug concentrations and ratios. For E. coli isolates exposed to 2.1 and 4.1µg/ml of enrofloxacin/ciprofloxacin at 50:50, 60:40 and 70:30 ratios, a 1.7-2.5log(10) reduction (94-99% kill) was seen following 20min of drug exposure; 0.89-1.7log(10) (92-99% kill) of S. pseudintermedius following 180min of drug exposure; 0.85-3.4log(10) (98-99% kill) of P. aeruginosa following 15min of drug exposure. Killing of S. pseudintermedius was enhanced in the presence of enrofloxacin whereas killing of P. aeruginosa was enhanced in the presence of ciprofloxacin. Antagonism was not seen when enrofloxacin and ciprofloxacin were used in kill assays. The unique feature of partial metabolism of enrofloxacin to ciprofloxacin expands the spectrum of enhanced killing of common companion animal pathogens.

Application of two methods to determine killing of Streptococcus pneumoniae by various fluoroquinolones.

Minimum inhibitory concentration (MIC) testing measures the lowest drug concentration that prevents microbial growth using an inoculum of 10(5) colony forming units/ml (cfu/ml) whereas the mutant prevention concentration (MPC) (inoculum approximately 10(10) cells) defines the antimicrobial drug concentration threshold that would require an organism to possess two simultaneous mutations for continued growth in the presence of the drug. The rates at which multidrug-resistant Streptococcus pneumoniae [MDRSP] were killed by the respiratory fluoroquinolones, gatifloxacin, gemfloxacin, levofloxacin and moxifloxacin, were compared based on the MIC and MPC drug concentrations and at inocula ranging from 10(6)-10(9) cfu/ml. The MIC drug concentration failed to eradicate all viable cells whereas the MPC drug concentration resulted in 99.9% to 100% cellular reduction following 12-24 hours of drug exposure. MPC values against S. pneumoniae were different for each fluoroquinolone. The MPC drug concentration prevents the selection of multidrug-resistant or fluoroquinolone-resistant S. pneumoniae. The value of dosing of antimicrobial agents based on MPC thresholds results in a rapid reduction in viable cells--even at higher inocula which are more reflective of organism burden in pneumonia. The rapid reduction in viable cells observed at MPC drug concentrations may not only have an impact on preventing the selection of resistant mutants but may also help explain the rapid symptom resolution seen with new fluoroquinolones since these agents lead to little or low release of cell contents which are known to drive the inflammatory response.