Epidemiology of antimicrobial resistance in bloodstream infections

Figures & data

Figure 1. Data shown on the graph are obtained from the following sources: Australia: Australian Group on Antimicrobial Resistance (AGAR). Available at http://www.agargroup.org, France, Germany, Greece, UK: European Antimicrobial Resistance Surveillance Network (EARS Net). Available at http://www.ersnet.org, Turkey: The data for the period of 2003–2008 are derived from EARSS European Antimicrobial Resistance Surveillance System (EARSS) available at http://www.rivm.nl. For 2009–2010; personal communication with Dolunay Gulmez, M.D. For 2011–2013; from National Antimicrobial Resistance Surveillance System Yearly Reports 2011–2013. Turkish Public Health Insititution. Available at http://uamdss.thsk.gov.tr, USA: Resistance Map-The Center for Disease Dynamics Economics & Policy (CDDEP) 2015. Available at: http://resistancemap.cddep.org.

Table 1 Frequent resistance mechanisms for selected antibacterial antibiotics in clinically important gram-negative bacteria (47,48,50,55,58,59,61,63,70,76,84,91) Main resistance determinants.

Bacteria	Cephalosporins	Carbapenems	Aminoglycosides	Quinolones	Polymyxins
Enterobacteriacea (E. coli, Klebsiellae)	ESBLs, mainly CTX-M type are major concern. E. coli ST131 with CTX-M-15 has epidemic potential woldwide. Isolates retain sensitivity to carbapenems if not co-produced with carbapenemsases. Many are also resistant to non-beta-lactams for which resistance genes are encoded on the same plasmid.	KPC, OXA-48 and NDM are most important carbapenemases. Isolates only susceptible to colistin, tigecycline and fosfomycin, although not all strains are susceptible. Less frequently, porin loss coupled with ESBL and AmpC beta-lactamase production can lead resistance to carbapenems.	Mainly due to aminoglycoside modifying enzymes or ribosomal (r)RNA methylases that may block aminoglycosides to bind modified bacterial ribosomes. These enzymes are frequently encoded on the same plasmid with ESBLs.	Mutations affecting chromosomal topoisomerase genes gyrA and parC are main reistance mechanisms.	Chromosomally mediated modificiation of Lipid A component of lipopolysccharide (LPS) leading reduced affinity for polymyxins. Recently described plasmid-mediated colistin resistance through mcr-1 gene in China, East and South-East Asia and Europe is a big concern.
Other enterobacteriaceae (e.g. Enterobacter spp. Citrobacter spp. and Serratia spp.)	In addition to ESBL, hyperproduced chromosomally mediated beta-lactamases (e.g. AmpC).	Same as above	Same as above	Same as above	Same as above, but less frequent. mcr-1 has shown only in Salmonella, so far.
Non-fermenters
P. aeruginosa	ESBLs (e.g. PER-1 and VEB-1), hyperproduction of AmpC beta-lactamases, upregulated efflux are major resistance mechanisms.	Porin mutations blocking carbapenem entry through outher membrane is the most frequent cause. Various carbapenemases including IMP, VIM, SMP, GIM and NDM are less frequently reported.	In addition to above mechanisms, decreased outer membrane permeability and upregulated influx are invloved.	In addition to topoisomerase mutations, upregulated efflux is a major resistance determinant.	Same as above. Plasmid-mediated resistance is yet to be identified.
A. baumannii	ESBL production is the main resistance mechanism. PER, VEB and GES-type ESBLs are prevalent worldwide. CTX-M type enzymes are rare.	Several carbapenemases are involved and main causes of resistance (see text).	Arm-A meythylase confers high-level resistance. rRNA methylases are also described. Efflux-mediated multidrugresistance is also important.	Upregulated efflux is main mechanism of resistance usually leading co-resistance to aminoglycosides, trimetoprim, tetracyclines and chloramphenicol.	In addition to above, complete loss of LPS production has been described.

Abbreviations: ESBL: Extended-spectrum β-lactamase.

ST131: sequence type 131.

Center for Disease Dynamics, Economics & Policy. State of the World's Antibiotics, 2015. CDDEP: Washington, D.C., 2015

 Google Scholar