Infectious disease · Test 05
Across 48 parameter combinations, faster killing never produced a larger resistant fraction at clearance.
Antibiotic regimens that kill quickly trade against resistance emergence, because rapid killing leaves a larger window in which surviving cells face strong selection.Source: Incoprea Theory XX, entry 4
Faster killing should select resistance more strongly at equal clearance.
Deterministic two-strain competition model: susceptible and resistant strains, logistic growth, fitness cost 0–0.25, cross-resistance 2–50%, kill rates 1–32 per hour. Treatment runs until total load falls below 10⁴; resistant fraction is measured at that point.
Among regimens that cleared, the resistant fraction fell as killing accelerated. With zero fitness cost and 2% cross-resistance, it was 11.4% at k = 8, 5.9% at k = 16 and 4.5% at k = 32. The same direction held at every fitness cost and cross-resistance level tested; no combination produced a rising trend. Faster regimens that fail to clear at all are excluded, because they do not satisfy the claim's 'at equal clearance' condition.
Not supported, and in this model the sign is opposite: faster killing ends the selection window before resistance can amplify. This refutes the simple competition version of the claim, not every version — the posted mechanism invokes persisters, which this model does not contain.
What would change this answer. Adding a persister compartment, or mutation to resistance during treatment, would test the mechanism the claim actually names. The code and inputs are included so the check can be repeated.