Docsity
Docsity

Prepare for your exams
Prepare for your exams

Study with the several resources on Docsity


Earn points to download
Earn points to download

Earn points by helping other students or get them with a premium plan


Guidelines and tips
Guidelines and tips

Review of Sources on Intrinsic Resistance in Antimicrobial Susceptibility Testing, Study notes of Microbiology

An analysis of intrinsic resistance to various antibiotics as reported by primary sources such as Magiorakos et al. and CLSI, and supplementary sources like Sanford et al. and Gilbert et al. The document also distinguishes between intrinsic and acquired resistance, and acknowledges instances of disagreement among sources. It covers resistance to amoxicillin, penicillin, Enterobacteriaceae, Pseudomonas aeruginosa, Acinetobacter spp, Coagulase-negative Staphylococci (CoNS), and Enterococcus. The document also discusses the potential impact of new drugs such as ceftazidime-avibactam and ceftolozane-tazobactam on Gram-negative bacteria.

What you will learn

  • What is intrinsic resistance and how does it differ from acquired resistance?
  • Which antibiotics are intrinsically resistant to certain bacteria?

Typology: Study notes

2021/2022

Uploaded on 09/27/2022

ralphie
ralphie 🇬🇧

4.8

(8)

214 documents

1 / 5

Toggle sidebar

This page cannot be seen from the preview

Don't miss anything!

bg1
Appendix A Intrinsic, implied and default resistance
Magiorakos et al. [1] and CLSI [2] are our primary sources of information on intrinsic resistance.
Sanford et al. [3] and Gilbert et al. [4] have been used to fill in missing susceptibilities,
but do not distinguish between acquired and instrinsic resistance. In cases where Sanford
et al. [3] and Gilbert et al. [4] indicate resistance we therefore rely on other sources to
distinguish between intrinsic and acquired resistance. These sources are explicitly acknowledged
in the following notes, as are instances of disagreement among our primary sources:
Amoxicillin and penicillin: Amoxicillin is similar to ampicillin [5], and penicillin does
not cover Gram-negative bacilli [6].
Enterobacteriacea: We assume that all Enterobacteriaceae resistant to ceftriaxone,
cefazolin or cefotaxime produce ESBLs, AmpC beta-lactamases, or KPCs, and are
therefore resistant to flouroquinolones, trimethaprim-sulfamethoxazole, penicillins,
cephalosporins, cephamycins, and β-lactam/lactamase inhibitor combinations [4, 7,
8]. We assume that all Enterobacteriaceae resistant to carbapenems produce KPCs,
and are therefore also resistant to chloramphenicol [4, 8]. CLSI [2] provides breakpoints
for Polymyxin B, and FDA drug labels indicate susceptibility among E. coli, Enterobacter
aerogenes, and Klebsiella pneumoniae strains. We assume that resistance to cephalexin
among Enterobacter spp. and Serratia marcescens strains [3, 4] is intrinsic, and that
all strains are intrinsically resistant to oxacillin and cloxacillin [5].
Pseudomonas aeruginosa: CLSI [2] suggests that P. aeruginosa is intrinsically resistant
to fosfomycin, but Magiorakos et al. [1] does not. We follow Magiorakos et al. [1].
FDA labels and Sanford et al. [3] suggest that some strains were once susceptible to
ceftriaxone, but we follow CLSI [2] and assume intrinsic resistance. We also assume
that resistance to the following drugs [3, 4] is intrinsic: nitrofurantoin, tigecycline,
ampicillin, cefotaxime, cephalexin, oxacillin, cloxacillin and ceftaroline.
pf3
pf4
pf5

Partial preview of the text

Download Review of Sources on Intrinsic Resistance in Antimicrobial Susceptibility Testing and more Study notes Microbiology in PDF only on Docsity!

Appendix A Intrinsic, implied and default resistance

Magiorakos et al. [1] and CLSI [2] are our primary sources of information on intrinsic resistance. Sanford et al. [3] and Gilbert et al. [4] have been used to fill in missing susceptibilities, but do not distinguish between acquired and instrinsic resistance. In cases where Sanford et al. [3] and Gilbert et al. [4] indicate resistance we therefore rely on other sources to distinguish between intrinsic and acquired resistance. These sources are explicitly acknowledged in the following notes, as are instances of disagreement among our primary sources:

  • Amoxicillin and penicillin: Amoxicillin is similar to ampicillin [5], and penicillin does not cover Gram-negative bacilli [6].
  • Enterobacteriacea: We assume that all Enterobacteriaceae resistant to ceftriaxone, cefazolin or cefotaxime produce ESBLs, AmpC beta-lactamases, or KPCs, and are therefore resistant to flouroquinolones, trimethaprim-sulfamethoxazole, penicillins, cephalosporins, cephamycins, and β-lactam/lactamase inhibitor combinations [4, 7, 8]. We assume that all Enterobacteriaceae resistant to carbapenems produce KPCs, and are therefore also resistant to chloramphenicol [4, 8]. CLSI [2] provides breakpoints for Polymyxin B, and FDA drug labels indicate susceptibility among E. coli, Enterobacter aerogenes, and Klebsiella pneumoniae strains. We assume that resistance to cephalexin among Enterobacter spp. and Serratia marcescens strains [3, 4] is intrinsic, and that all strains are intrinsically resistant to oxacillin and cloxacillin [5].
  • Pseudomonas aeruginosa: CLSI [2] suggests that P. aeruginosa is intrinsically resistant to fosfomycin, but Magiorakos et al. [1] does not. We follow Magiorakos et al. [1]. FDA labels and Sanford et al. [3] suggest that some strains were once susceptible to ceftriaxone, but we follow CLSI [2] and assume intrinsic resistance. We also assume that resistance to the following drugs [3, 4] is intrinsic: nitrofurantoin, tigecycline, ampicillin, cefotaxime, cephalexin, oxacillin, cloxacillin and ceftaroline.
  • Acinetobacter spp: Given potential susceptibility to extended-spectrum cephalosporins, we assume susceptibility to ceftaroline.
  • Coagulase-negative Staphylococci (CoNS): According to FDA labels nitrofurantoin, clindamycin and ampicillin have in vitro activity against at least some strains of CoNS, so we assume susceptibility. CLSI [2] give breakpoints for doxycycline and minocycline, and our data show some susceptibility to doxycycline, so we assume former susceptibility.
  • Enterococcus: CLSI [2] claims intrinsic resistance to all cephalosporins, but Gilbert et al. [4] claims that E. faecalis is susceptible to ceftaroline. We assume susceptibility. Sanford et al. [3] and Gilbert et al. [4] also claim resistance to erythromycin and tetracycline but CLSI [2] provides breakpoints so we assume that at least some strains are susceptible. Gilbert et al. [4] claims partial susceptibility of E. faecium to imipenem, but Magiorakos et al. [1] suggests intrinsic resistance, so we assume resistance. We assume that resistance to the following drugs [3, 4] is intrinsic: rifampin (E. faecium), ciprofloxacin (E. faecium), levofloxacin (E. faecium), cefotetan, cefoxitin, cloxacillin and oxacillin. We used understanding of common multi-drug resistant strains (table 3) to fill gaps in our example antibiogram. We also used the following general knowledge of resistance patterns, assuming 100% susceptibility or resistance in cases where testing was not done:
  • Enterobacteriaceae are generally susceptible to carbapenems [2] and generally resistant to ampicillin [4].
  • A. baumanii strains are generally susceptible to polymixins [2].
  • Staphylococci are generally susceptible to daptomycin, linezolid, quinupristin-dalfopristin, and vancomycin [2], and generally resistant to ampicillin [4].

References

  1. Magiorakos AP, Srinivasan A, Carey RB et al. Multidrug-resistant, extensively drug-resistant and pandrug-resistant bacteria: an international expert proposal for interim standard definitions for acquired resistance. Clin Microbiol Infec 2012;18:268–281.
  2. CLSI: Clinical and Laboratory Standards Institute. Performance standards for antimicrobial susceptibility testing: 23rd informational supplement M100-S19. CLSI, Wayne, PA, USA, 2013.
  3. Sanford JP, Gilbert DN, Moellering RCJ et al., eds. The Sanford guide to antimicrobial therapy. 27th ed. Vienna, VA: Antimicrobial Therapy Inc., 1997.
  4. Gilbert DN, Chambers HF, Eliopoulous GM et al., eds. The Sanford guide to antimicrobial therapy. 44th ed. Sperryville, VA: Antimicrobial Therapy Inc., 2014.
  5. Zaffiri L, Gardner J, Toledo-Pereyra LH. History of antibiotics: From salvarsan to cephalosporins. J Invest Surg 2012;25:67–77.
  6. Medeiros AA. Evolution and dissemination of beta-lactamases accelerated by generations of beta-lactam antibiotics. Clin Infect Dis 1997;24 Suppl 1:19–45.
  7. MSH: Mount Sinai Hospital. Antimicrobial susceptibility testing manual. 2013. http://www.mountsinai.on.ca/education/staff-professionals/microbiology.
  8. Vasoo S, Barreto JN, Tosh PK. Emerging issues in gram-negative bacterial resistance: an update for the practicing clinician. Mayo Clin Proc 2015;90:395–403.
  9. Sader HS, Castanheira M, Flamm RK et al. Ceftazidime/avibactam tested against Gram-negative bacteria from intensive care unit (ICU) and non-ICU patients, including those with ventilator-associated pneumonia. Int J Antimicrob Agents 2015;46:53–59.
  10. Farrell DJ, Sader HS, Flamm RK et al. Ceftolozane/tazobactam activity tested against Gram-negative bacterial isolates from hospitalised patients with pneumonia in US and European medical centres (2012). Int J Antimicrob Agents 2014;43:533–539.
  1. Sader HS, Farrell DJ, Flamm RK et al. Ceftolozane/tazobactam activity tested against aerobic Gram-negative organisms isolated from intra-abdominal and urinary tract infections in European and United States hospitals (2012). J Infect 2014;69:266–277.
  2. Sader HS, Farrell DJ, Castanheira M et al. Antimicrobial activity of ceftolozane/tazobactam tested against Pseudomonas aeruginosa and Enterobacteriaceae with various resistance patterns isolated in European hospitals (2011-12). J Antimicrob Chemother 2014;69:2713–2722.