Ellie J. C. Goldstein, MD, discusses the interplay and interchange between long-term and short-term acute care hospitals and explains how transitions in care can result in the spread of antibiotic resistance.
Segment Description: Ellie J. C. Goldstein, MD, director of the R.M. Alden Research Laboratory. and clinical professor at the UCLA School of Medicine, discusses the interplay and interchange between long-term and short-term acute care hospitals and explains how transitions in care can result in the spread of antibiotic resistance.
Interview Transcript (modified slightly for readability):
“I go to both an acute care hospital and a long-term care hospital. Depending on the nature of your acute-care hospital, often the length of stay is short, there isn’t that much resistance that occurs, but there are a number of patients who don’t get better—they are too sick to go to a nursing home, but not sick enough to stay in the acute-care hospital.
Across America, there are a lot of long-term acute care hospitals. These patients have heavy prior antibiotic exposure, often have multiple co-morbidities, maybe 40% will have respiratory failure, many of them will be on a ventilator, [and] 20% will have renal insufficiency. And these patients are at high risk of having a resistant gram-negative isolate when they come. They’ll get it at the acute-care hospital or they could, less likely, pick it up at the long-term care. But, it’s thought that the long-term cares are reservoirs for resistant isolates, and that is, in part, true.
The interplay and interchange between the long-term acute care and the short-term acute care hospitals is significant. Many patients are in and out of different hospitals. These are sick patients who come and in transitions of care go back and forth, leading to the potential spread of resistance, or at least, having both short-term acute care as well as long-term acute care hospitals encounter these resistant gram-negative rods.
Up to now, there mostly have been studies published as part of the randomized trials for licensure and some areas where they have a high rate. But there aren’t that many real-life experiences that go on where we see what’s going on at the moment. At our long-term acute care [hospital], our regional microbiology laboratory services 12 Southern California hospitals and we looked at our resistant-Pseudomonas especially ceftazidime-resistant Pseudomonas aeruginosa isolates — I think about 111 of them. And we looked at our resistant Enterobacteriaceae and we wanted to know what the activity was against these 2 new agents: ceftolozane/tazobactam vs ceftazidime/avibactam. The ceftazidime/avibactam did very well against the carbapenem-resistant Enterobacteriaceae (CRE).
We also looked at the ceftazidime resistant-Pseudomonas which is an isolate we encounter often. What we found was that 88% of our Pseudomonas—of our ceftazidime resistant-Pseudomonas—was susceptible to ceftolozane/tazobactam; 72% were susceptible to ceftazidime/avibactam, and there were no isolates that were susceptible to ceftazidime/avibactam but were resistant to ceftolozane. And so, ceftolozane/tazobactam really has a niche for Pseudomonas while the ceftazidime/avibactam is a good CRE drug.”