From collateral damage to collateral sensitivity

“Every disadvantage has an advantage” is one of the many brilliant quotes from the late Dutch philosopher Johan Cruijff. This now also seems to hold for antibiotic resistance. The conventional belief is that resistance development is unidirectional: pathogens cumulatively acquire resistance traits, until being a multidrug resistant superbug. This now seems not always true; resistance development to antibiotic A, may – at the same time – increase susceptibility to antibiotic B, a phenomenon called “collateral sensitivity” that may help us in treating chronic infections. Continue reading

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What’s up for 2018?

I hope you enjoyed Christmas time and wish you all the best for this year. From my side, I will continue to reflect what I meet professionally, what surprises me, confirms what I thought to know or what confirms my ignorance. In 2017 I did that 41 times (a surprise to me!) and here are some trending topics that will most likely return in 2018. Continue reading

The prevention paradox: E. coli versus Klebsiella

The prevention paradox, as described in 1981, is the “seemingly contradictory situation where the majority of cases of a disease come from a population at low or moderate risk of that disease, and only a minority of cases come from the high risk population (of the same disease). This is because the number of people at high risk is small”, see. In our world this reflects the question how to prevent transmission of ESBL-producing E. coli (ESBL-EC) or K. pneumoniae (ESBL-KP), or both. A new study may help to decide. Continue reading

What about E. coli ST131?

One of the faces of the global antibiotic resistance crisis is Escherichia coli ST131, frequently portrayed as a pandemic clone, combining hypervirulence, ciprofloxacin resistance and ESBL production. A recent study in Genome Research, a journal you may not read every month, though, sheds a whole new light on this “superbug”. Continue reading

The antibiotic resistance crisis resolved by bacteriophages (part 2)

Earlier this week I blogged on the potential (yet poorly proven) effects of bacteriophages as salvage therapy for infections caused by AMR, and stated: “Phages and their active enzymes are proteins that evoke an immunological host response when injected, and up till now all attempts to circumvene those unwanted effects have failed.” Two recent case reports challenge part of that statement. Continue reading

The antibiotic resistance crisis resolved by bacteriophages

I am regularly asked why we don’t treat infections caused by multidrug resistant bacteria with bacteriophages. Last Friday, the same question made it to the best viewed talkshow on Dutch television (The World Turns On), and in about 10 minutes the global threat of antibiotic resistance was resolved. Here is how….  Continue reading

How to predict ESBL (part 4)

Two months ago I provided an update on the ESBL-predict study that Tim Deelen from our group coordinates. In short: Every hospital in the world can participate, through a user-friendly electronic CRF (in a secured environment), in the validation of 2 scoring systems to predict that sepsis is caused by ESBL-producing bacteria. Only relevant for those of us that are not yet ready to start meropenem/amikacine for every patient that starts with antibiotics! This tool may help, …. if reliable. We passed the 3,000 episodes! Here is a short update and info for those that want to join. Continue reading