An analytical system comprising a bacterium and a protozoan was used t
o pinpoint the metabolic lesion whereby chlorhexidine (CLX) produced c
ell death. Nicotinic acid but not nicotinamide annulled the biocidal a
ction of CLX. The results suggest that CLX may not permit bioconversio
n of nicotinamide to nicotinic acid to annul the growth inhibition ind
uced by CLX.