Bacterial Efflux Pump: Antibiotic Extrusion Simulator

Drug & Environment

External antibiotic level 1.00×

Membrane permeability (k_in) 0.12 /s

Efflux Pump (AcrAB-TolC-style)

Active pump count 16

Pump turnover rate 0.30 /s

Live Readouts

Cell status: —

Intracellular conc.

0.0 µM

Extracellular conc.

0.0 µM

Net flux (in − out)

0.0 /s

Efflux capacity V_max

0.0 /s

How it works

Gram-negative bacteria like E. coli and Pseudomonas resist many antibiotics without any enzyme or target mutation at all — they simply pump the drug back out faster than it leaks in. The RND-family transporter AcrB sits in the inner membrane, AcrA bridges the periplasm, and TolC forms a channel through the outer membrane; together the AcrAB-TolC complex uses the proton-motive force (H⁺ flowing back into the cell) to actively extrude a broad range of antibiotics, dyes and detergents.

The intracellular concentration obeys a balance between passive diffusive influx and saturable, enzyme-like efflux:

dC_in/dt = k_in · C_out − (V_max · C_in) / (K_m + C_in)

k_in  = membrane permeability (passive diffusion in)
V_max = pump_count × turnover_rate  (total extrusion capacity)
K_m   = pump half-saturation constant (≈ 20 µM here)

External antibiotic level — raises C_out, driving more passive influx.
Membrane permeability — how leaky the outer membrane/porins are to the drug.
Active pump count — how many AcrAB-TolC complexes are expressed (over-expression is the classic MDR phenotype).
Pump turnover rate — how fast each pump cycles, set by proton-motive force strength.

When V_max comfortably outruns k_in·C_out, C_in settles far below the minimum inhibitory concentration (MIC, dashed line) and the cell survives — the same mechanism that lets efflux-overexpressing clinical isolates tolerate drug levels that would kill a wild-type cell.

Antibiotic molecule Efflux pump (active) Efflux pump (inactive)

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