| Group 1 |
Non‐typhoidal Salmonella enterica serovars resistant to 3rd‐GCs, carbapenems or fluoroquinolones. |
Invasive infections (invasive non‐typhoidal Salmonella; INTS) caused by this food‐borne pathogen require treatment with antimicrobials targeting intracellular sites of infection, e.g. within the reticuloendothelial system or gallbladder. Due to the common resistance to aminopenicillins, the 3rd‐GCs, fluoroquinolones and carbapenems are the preferred options for those infections, which occur with an incidence of ~ 1.1 per 100,000 population in Europe (Non‐Typhoidal Salmonella Invasive Disease Collaborators, 2019).
Salmonella Enteritidis, the monophasic variant of S. Typhimurium, S. Typhimurium are common in INTS, although Salmonella Dublin, Choleraesuis, Heidelberg, Napoli and Virchow are also among those most likely to cause bacteraemia (Jones et al., 2008; Mastrorilli et al., 2020). A large proportion of S. Enteritidis lineages, and those of serovars commonly found associated with INTS, show resistance to fluoroquinolones or to 3rd‐GCs. Resistance to carbapenems has also been occasionally observed in S. Infantis and S. Kentucky, serotypes that can also sporadically cause INTS (de Curraize et al., 2017).
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Campylobacter spp. resistant to macrolides, fluoroquinolones, aminoglycosides or carbapenems. |
Antibiotic treatment is required for invasive Campylobacter infections, a rarely reported condition (Kaakoush et al., 2015). Although mostly caused by C. jejuni, C. coli, C. fetus and C. lari have also been associated with this zoonosis. Resistance to macrolides and fluoroquinolones, the common therapeutic options, is frequently observed.
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| Enterobacterales other than Salmonella spp. resistant to 3rd‐, 4th‐ and 5th‐GCs, carbapenems, colistin, plazomicin, fluoroquinolones or glycylcyclines. |
E. coli, K. pneumoniae and Enterobacter spp., common causes of serious infections, are increasingly presenting multidrug resistance profiles including to last resort antibiotics. Those resistant human infections have been often caused by particular E. coli (e.g. ST131 H30, ST10, ST38, ST69, ST393, ST405, ST410, ST648) or K. pneumoniae (e.g. ST258, ST307, ST11, ST15, ST101, ST147) lineages/sub-lineages. Among the Enterobacter spp., certain carbapenem‐resistant E. hormaechei lineages have been increasingly identified in human infections (e.g. ST171, ST78) (Guzmán et al., 2019; Gou et al., 2020; Tavovoschi et al., 2020). There is evidence of resistant ExPEC of food origin causing human infections, although the burden of disease associated with this origin is still controversial (Mughini‐Gras et al., 2019). Recent studies have focused on K. pneumoniae, but there remains little information regarding the role of food‐producing animals and food products on the transmission of this pathogen to humans. Even less information is available for E. hormaechei.
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S. aureus resistant to methicillin, 5th‐generation cephalosporins, glycopeptides, oxazolidinones, lipopeptides or glycylcyclines. |
The mean percentage of methicillin‐resistant S. aureus (MRSA) causing human invasive infections in the EU was 15.5% in 2019, ranging from 1.1% to 46.7% among member states (ECDC, 2020). MRSA with additional resistance to other antimicrobial groups is common and occurs in a diversity of types of MRSA, including MRSA associated with healthcare or community settings or livestock. Vancomycin, ceftaroline, ceftobiprole, linezolid, daptomycin or tigecycline are used as alternative antimicrobials in human settings and contamination of food system environments with MRSA presenting resistance to these antimicrobials may occur.
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Enterococcus faecium and E. faecalis resistant to glycopeptides or oxazolidinones, lipopetides or glycylcyclines. |
Hospital‐associated infections by E. faecium (HA‐E. faecium) and E. faecalis often require treatment with glycopeptides and oxazolidinones due to the intrinsic and acquired resistance presented by those species. HA‐E. faecium comprises a specialised subpopulation of E. faecium (clade A; nowadays mainly dominated by ST78‐related strains such as ST80, ST117 and ST203) enriched in virulence and resistance genes (Freitas et al., 2018). These multidrug‐resistant clones frequently carry vancomycin resistance genes on plasmids and, with increasing frequency, also point mutations or transferable genes encoding linezolid resistance (Egan et al., 2020). Resistant E. faecalis lineages causing infections are diverse and reflect the generalist lifestyle of this organism. However, they have mainly been associated with particular subpopulations (e.g. ST6, ST9, ST28, ST40, ST87, ST103) that are enriched in antimicrobial resistance and virulence genes (Guzmán Prieto et al., 2016; Raven et al., 2016).
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Acinetobacter baumannii and Pseudomonas aeruginosa resistant to carbapenems and colistin. |
A. baumannii multi‐drug resistant strains causing hospital infections predominantly belong to particular lineages (e.g. CC231, CC208, CC447, ST944 and ST950) with evidence of enhanced virulence and resistance (Silva et al., 2021). Particular clones (e.g. ST111, ST175, ST244 and ST253) of P. aeruginosa presenting MDR and plasmid‐encoded carbapenemases with enhanced virulence also often cause human infections (Gaiarsa et al., 2019). These human clinical lineages have not been as far as we know reported in food products.
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| Group 2 |
Enterobacterales, Pseudomonas spp., Acinetobacter spp., Aeromonas spp. and Vibrio spp. with mobile resistance genes to last resort antibiotics |
Environmental or commensal bacteria could act as donor of resistance genes to Gram negative pathogenic bacteria. Mobile genes encoding carbapenemases, ESBL/AmpC cephalosporinases, 16S rRNA methylases or resistance to glycylcycline, polymixines and fluoroquinolones are of highest relevance. The human disease burden resulting from antimicrobial resistant indigenous aquatic or fish bacteria has been insufficiently studied. Moreover, insufficient information on the lineages or serotypes able to cause infection and on the AMR profiles of aquatic and fish indigenous bacteria belonging to Vibrio parahaemolyticus, V. vulnificus, Aeromonas or non‐aeruginosa Pseudomonas species precludes their current inclusion in Group 1.
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Enterococcus spp. with mobile resistance genes to last resort antibiotics |
These commensal bacteria could act as donor of genes conferring resistance to last resort antimicrobials to other Gram‐positive pathogenic bacteria. Mobile resistance genes for isoxazolidinones and vancomycin are of highest relevance.
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Staphylococcus spp. with mobile resistance genes to last resort antibiotics |
These commensal bacteria could act as donor of genes conferring resistance to last resort antimicrobials to other Gram‐positive pathogenic bacteria. Mobile genes encoding resistance to methicillin (e.g. mecB, mecC and mecA) isoxazolidinones are of highest relevance.
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