Tinidazole inhibitory and cidal activity against anaerobic periodontal pathogens.
The in vitro activity of tinidazole against anaerobic periodontal pathogens (25 Prevotella buccae, 18 Prevotella denticola, 10 Prevotella intermedia, 6 Prevotella melaninogenica, 5 Prevotella oralis, 10 Fusobacterium nucleatum and 8 Veillonella spp.) was determined by agar dilution. MIC(90) values (minimum inhibitory concentration for 90% of the organisms) were 8 microg/mL for Veillonella spp., 4 microg/mL for P. intermedia, 2 microg/mL for P. buccae, 1 microg/mL for Fusobacterium spp. and 0.5 microg/mL for other Prevotella spp. Cidal activity was studied by killing curves with tinidazole and amoxicillin (alone and in combination) at concentrations similar to those achieved in crevicular fluid (41.2 microg/mL tinidazole and 14.05 microg/mL amoxicillin) against an inoculum of ca. 10(7)colony-forming units/mL of four bacterial groups, each one composed of four different strains of the following periodontal isolates: Prevotella spp., Fusobacterium spp. and Veillonella spp. (anaerobes) and one amoxicillin-susceptible Streptococcus spp. (facultative) in a proportion of 1:1:1:1. When only beta-lactamase-negative Prevotella or Fusobacterium strains were tested, significantly higher reductions were found with amoxicillin (>4 log reduction at 48 h) versus controls. The presence of beta-lactamase-positive Prevotella spp. or F. nucleatum strains rendered amoxicillin inactive (no reductions at 48 h), with no differences from controls. Amoxicillin+tinidazole produced >3 log reduction at 24h and >4 log reduction at 48 h regardless of the presence or not of beta-lactamase-positive strains. The presence in crevicular fluid of beta-lactamases produced by beta-lactamase-positive periodontal pathogens may have ecological and therapeutic consequences since it may protect beta-lactamase-negative periodontal pathogens from amoxicillin treatment. In vitro, tinidazole offered high antianaerobic activity against beta-lactamase-positive and -negative periodontal pathogens, avoiding amoxicillin inactivation.
Alou
L
L
Microbiology Department, School of Medicine, Universidad Complutense, Avenida Complutense s/n, 28040 Madrid, Spain.
Giménez
M J
MJ
Manso
F
F
Sevillano
D
D
Torrico
M
M
González
N
N
Granizo
J J
JJ
Bascones
A
A
Prieto
J
J
Maestre
J R
JR
Aguilar
L
L
D000658:Amoxicillin / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001421:Bacteria, Anaerobic / Q000187:drug effects; D001426:Bacterial Proteins / Q000096:biosynthesis; D005673:Fusobacterium / Q000187:drug effects*; D006801:Humans; D008826:Microbial Sensitivity Tests; D050296:Microbial Viability; D010510:Periodontal Diseases / Q000382:microbiology*; D018720:Prevotella / Q000187:drug effects*; D013291:Streptococcus / Q000187:drug effects*; D014011:Tinidazole / Q000494:pharmacology*; D014678:Veillonella / Q000187:drug effects*; D018440:beta-Lactam Resistance; D001618:beta-Lactamases / Q000096:biosynthesis
D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D014011:Tinidazole; D000658:Amoxicillin; D001618:beta-Lactamases