Microbiology · Short notes

Antimicrobial Resistance: Short Notes & Cheat Sheet

Resistance mechanisms, how resistance genes spread, key resistant organisms, susceptibility testing, WHO AWaRe groups and the situation in Pakistan.

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Short notes

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How bacteria resist antibiotics

Most resistant organisms combine several mechanisms, which is why multidrug resistance is common.

Mechanisms

Enzymatic inactivation: β-lactamases (including ESBLs and carbapenemases such as NDM-1, KPC and OXA-48), aminoglycoside-modifying enzymes and chloramphenicol acetyltransferase.
Target change: altered penicillin-binding protein PBP2a (mecA gene) in MRSA, D-Ala-D-Lac cell wall precursors in VRE, gyrase mutations for quinolones, rpoB mutations for rifampicin, and ribosomal methylation (erm) for macrolides.
Reduced entry: loss of outer-membrane porins, especially in Pseudomonas and Enterobacterales.
Efflux pumps push out tetracyclines, fluoroquinolones and macrolides.
Bypass pathways: altered enzymes that the drug no longer blocks (e.g. sulfonamide-resistant dihydropteroate synthase).

How resistance spreads

Intrinsic resistance is natural to a species (e.g. Gram-negatives resist vancomycin). Acquired resistance arises by mutation or gene transfer.
Horizontal gene transfer: transformation (uptake of free DNA), transduction (via bacteriophage) and conjugation (plasmid transfer through a pilus).
Conjugation is the most important route for spreading multidrug resistance; transposons and integrons collect several resistance genes together.
Drivers: overuse and misuse of antibiotics (including sale without prescription), incomplete courses, poor infection control, and antibiotic use in animals.

Testing and control

Kirby–Bauer disc diffusion uses Mueller–Hinton agar and an inoculum matched to 0.5 McFarland. Zone sizes are read against CLSI or EUCAST breakpoints.
MIC is the lowest concentration that stops visible growth (broth microdilution, E-test). MBC is the lowest concentration that kills 99.9%.
WHO AWaRe groups antibiotics as Access (e.g. amoxicillin), Watch (e.g. ciprofloxacin, ceftriaxone, azithromycin) and Reserve (e.g. colistin, linezolid) to guide stewardship.
Pakistan faces XDR typhoid, widespread ESBL and NDM-producing organisms, and MDR-TB. It adopted a National Action Plan on AMR in 2017.
ESKAPE pathogens: Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter species.

Cheat sheet

High-yield facts in one place. Cover the right-hand column and test yourself.

Resistant organism → mechanism → options

Organism	Mechanism · treatment options
MRSA	PBP2a (mecA) · vancomycin, linezolid, daptomycin
VRE	D-Ala-D-Lac (vanA) · linezolid, daptomycin
ESBL producers	β-lactamase · carbapenems
Carbapenem-resistant Enterobacterales	Carbapenemase · colistin, newer β-lactam combinations
XDR typhoid	Multiple genes · azithromycin, meropenem
MDR-TB	rpoB + katG/inhA mutations · bedaquiline regimens

Gene transfer

Process	Vehicle
Transformation	Free (naked) DNA
Transduction	Bacteriophage
Conjugation	Plasmid through a sex pilus
Transposition	Jumping genes (transposons)

Memory aids

ESKAPE: Enterococcus faecium, Staphylococcus aureus, Klebsiella, Acinetobacter, Pseudomonas, Enterobacter: the organisms that 'escape' antibiotics.

Exam traps

MRSA's resistance comes from an altered PBP (PBP2a), not from β-lactamase.
Conjugation, not transformation, spreads most plasmid-mediated multidrug resistance.
MIC stops growth; MBC kills. A drug is bactericidal when MBC is close to MIC.
Disc diffusion uses Mueller–Hinton agar, not nutrient agar.

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