Aromatic and aliphatic aldehydes were tested for their effectiveness a
gainst Clostridium botulinum spores and cells. Six-tenths millimolar b
enzaldehyde, piperonal, phenylacetaldehyde, alpha-amylcinnamaldehyde,
vanillin, or phenylglyoxal delayed germination in botulinal assay medi
um (BAM) broth after 6 h exposure at 32-degrees-C. Sporicidal activity
was observed with 1.25 mM vanillin, 39 mM isobutyraldehyde, 156 mM py
ruvaldehyde or valeraldehyde, 625 mM benzaldehyde, and 2,500 mM alpha-
amylcinnamaldehyde. Twenty-five millimolars of cinnamaldehyde, phenyla
cetaldehyde, pyruvaldehyde, and vanillin were most active against vege
tative cells at pH 7.0 in BAM broth, while 125 mM was required for ben
zaldehyde, acetaldehyde, piperonal, or phenylglyoxal. Three millimolar
s benzaldehyde, 5.0 mM phenylglyoxal, 150 mM cinnamaldehyde, 200 mM py
ruvaldehyde and vanillin, and 300 mM piperonal inhibited 9 h dipicolin
ic acid release in BAM broth at 32-degrees-C. Spore resistance to a 20
-min 80-degrees-C thermal treatment was reduced when challenged with p
rior exposure to 100 mM cinnamaldehyde, piperonal, pyruvaldehyde, vani
llin, or phenylglyoxal. Inhibition by cinnamaldehyde, piperonal, and p
henylglyoxal was retained in commercial canned chicken and in beef bro
ths. Five millimolars of benzaldehyde, cinnamaldehyde, piperonal, pyru
valdehyde, or phenylglyoxal delayed neurotoxin production for 48 h at
32-degrees-C, while 25 mM was required for vanillin. These results ind
icate that certain aldehydes inhibit C. botulinum, and aromaticity imp
roves efficacy.