Proposed mechanisms: *Reduced expression of penicillin binding proteins during stationary growth phase *Induction of microbial resistance mechanisms (such as beta lactamases with short half-lives) by high drug concentrations *Precipitation of antimicrobial drug in vitro, possibly also leading to the crystallized drug being mis-detected as colonies of the microbe. *Self-antagonising the receptor with which it binds (penicillin binding proteins, for example, in the case of a penicillin). Penicillin is a bactericidal antibiotic that works by inhibiting cell wall synthesis but this synthesis only occurs when bacteria are actively replicating (or in the log phase of growth). In cases of extremely high bacterial burden (such as with Group A Strep), bacteria may be in the stationary phase of growth. In this instance since no bacteria are actively replicating (presumably due to nutrient restriction) penicillin has no activity. This is why adding an antibiotic like clindamycin, which acts ribosomally, kills some of the bacteria and returns them to the log phase of growth.
Eagle effect
Baskerville effect
Hook effect
Flynn effect
Mandelbaum effect
Martha Mitchell effect
Bowditch effect
Bouba/kiki effect