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.
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".