Resistance challenges in veterinary medicine: Who's to blame for "superbugs" and how do we deal with them (Proceedings)


Resistance challenges in veterinary medicine: Who's to blame for "superbugs" and how do we deal with them (Proceedings)

Aug 01, 2010

This presentation attempts to summarize some of the major concerns in resistance development along with key articles explaining relevance, epidemiology, and prevalence. It is not intended to be an exhaustive review of the literature and the interested practitioner should use the cited literature herein as a basis for continued, extended reading.

I. So where do these things come from? Here is the basic questions.

     • Do resistant organisms develop from spontaneous mutations in your patient (or a population of patients, such as in some food animal applications) during antimicrobial use and then proliferate within the favorable climate of antimicrobial selection pressure?
     • Or, are they already present at a low prevalence level and then proliferate in the new environmental "rules" imposed by the presence of antimicrobials (clonal dissemination and selection)?

My impression from the literature and sitting through and participating in meetings, debates, and outright arguments is that dissemination of resistant bacterial clones is a primary driver in what we are seeing in human and veterinary medicine. Spontaneous mutations can and do occur, but the rapid changes in resistance over broad areas, and also the similarities between isolates suggests that the spread of clones is a primary driver.

Another very basic concept is that selection for a resistant pathogen or bacteria may be due to an entirely different selection pressure than the antimicrobial in which we happen to be interested. Multiple-drug resistance mechanisms allow co-selection for resistance traits; and, it doesn't even have to be an antimicrobial in the way we typically think of them. Co-selection by environmental disinfectants can co-select for antimicrobial resistance, as demonstrated for pine oil for E. coli, and triclosan for Pseudomonas aeruginosa. The presence of pathogens such as Vancomycin-Resistant Enterococci (VRE), Pseudomonas, and Methicillin-Resistant Staphylococcus aureus (MRSA) on surfaces, pagers, and stethoscopes has been well documented in human studies.

We don't cause the original spontaneous mutations. But, once these mutations take hold in an environment, we are responsible for aiding in selection and spread. As Pogo said, "We have met the enemy and he is us".

II. What are the challenges on the human side of medicine?

Hospital acquired infections. One publication gives us a quick look into the challenges in human hospitals. These data are from a Centers for Disease Control and Prevention (CDC) summary. The objective was to describe the frequency of selected antimicrobial resistance patterns among pathogens causing device-associated and procedure-associated healthcare-associated infections (HAIs) reported by hospitals in the National Healthcare Safety Network (NHSN). Data were collected on HAIs reported to the Patient Safety Component of the NHSN between January, 2006 and October, 2007. These HAIs included central line-associated bloodstream infections, catheter-associated urinary tract infections, ventilator-associated pneumonia, and surgical site infections. Overall, 463 hospitals reported 1 or more HAIs: 412 (89%) were general acute care hospitals, and 309 (67%) had 200-1,000 beds. There were 28,502 HAIs reported among 25,384 patients. The 10 most common pathogens accounting for 84% of reported HAIs were...

As many as 16% of all HAIs in this report were associated with the following multidrug-resistant pathogens.
     • Methicillin-resistant Staph. aureus (8% of HAIs),
     • Vancomycin-resistant Enterococcus faecium (4%),
     • Carbapenem-resistant Pseudomonas aeruginosa (2%),
     • Extended-spectrum cephalosporin-resistant Klebsiella pneumoniae (1%),
     • Extended-spectrum cephalosporin-resistant E. coli (0.5%),
     • Carbapenem-resistant A. baumannii, K. pneumoniae, K. oxytoca, and E. coli (0.5%).