D.B. Drucker

Clinical significance of dental root canal microflora

OBJECTIVES Previous work by this group has shown that a significant association exists between pain and the presence of either Prevotella or Peptostreptococcus spp. in dental root canals. The aim of this study was to examine a more extensive series of canals microbiologically, to determine whether any other particular endodontic symptoms or clinical signs showed specific associations with individual bacterial species. METHODS Seventy root canals were examined microbiologically and clinical data collected to investigate in detail such associations. RESULTS Of the canals studied, 37 were associated with pain, 49 with tenderness to percussion, 23 with swelling, six with purulent exudate and 57 presented with wet root canals. Anaerobes were isolated from 70.3% of painful canals and from 29.7% of pain-free canals. Significant associations were found between (a) pain and either Prevotella spp. or peptostreptococci, both with P < 0.01; (b) tenderness to percussion and Prevotella spp. (P < 0.01) or anaerobes (P < 0.05); (c) swelling and Eubacterium spp. (P < 0.01), or with Prevotella spp. or Pstr. micros, both with P < 0.05; (d) purulent exudate and any one of F. necrophorum (P < 0.01), Prev. loescheii, Streptoccoccus constellatus or Bacteroides spp. (each P < 0.05); (e) wet canal and facultative anaerobes (P < 0.01), and any one of the genera of Eubacterium, Peptostreptococcus, Prevotella or Propionibacterium (each P < 0.05). CONCLUSION It was concluded that several different endodontic clinical signs and symptoms are significantly associated with specific bacterial species.

The nasopharyngeal bacterial flora in the sudden infant death syndrome

The nasopharyngeal bacterial flora in babies who had died of the sudden infant death syndrome (SIDS) (n = 46) and in healthy infants aged 2 weeks to 6 months (n = 46) is described. Of those who had died, 41.3% carried Staphylococcus aureus (95% confidence limits: 27.3-55.3%) compared with 28.3% of healthy infants (95% confidence limits: 15.3-41.3%). The isolation rate of streptococci was 78.3% in cases (95% confidence limits: 66.4-90.2%) and 32.6% in healthy infants (95% confidence limits: 19.1-46.1%) (significant difference P less than 0.0001). Enterobacteria were isolated from 45.6% of cases (95% confidence limits: 31.2-60%) but only 2.2% of healthy infants (95% confidence limits 0-6.4%) (significant difference, P less than 0.0001). These results indicate a disordered nasopharyngeal flora in SIDS. They also provide baseline data for investigating the hypothesis that common bacterial toxins are involved in the pathogenesis of SIDS.

Association of IL-10 genotype with sudden infant death syndrome.

Sudden infant death syndrome (SIDS) is a major cause of infant death of unknown etiology. We propose that SIDS results from a genetically determined imbalance in the production of inflammatory and anti-inflammatory cytokines in response to the infants microbial flora. We were especially interested to know the relationship between SIDS and genetically determined higher or lower production of IL-10, an anti-inflammatory cytokine. Biallelic polymorphisms in the promoter region of the IL-10 gene associated with higher or lower production of IL-10 were determined in a SIDS and in a control group using a sequence-specific oligonucleotide approach. One particular allele of the IL-10 gene, the IL-10-592*A allele, was significantly associated with SIDS. Indeed, 70% of the SIDS babies carried the IL-10-592*A allele (p = 0.007 compared with control). In addition, there was a significant reduction in the frequency of homozygosity for the allele IL-10-592*C (p = 0.001 compared with control). Carrying the A allele (either A/A or A/C) had an odds ratio of 3.3 (95% confidence interval 1.4-8.0). In the same patients there was no association with other IL-10 gene polymorphisms nor with other cytokine (TNF-alpha, TGF-beta 1) genotypes, emphasizing the particular relationship between SIDS and the IL-10-592*A allele.

Lethal challenge of gnotobiotic weanling rats with bacterial isolates from cases of sudden infant death syndrome (SIDS).

An attempt was made to produce an animal model of sudden infant death syndrome (SIDS). The experimental animals (germ free weanling rats) were exposed to nasopharyngeal isolates from cases of SIDS to test the hypothesis that common bacteria may have an aetiological role in the disease. Negative results were obtained when the strains were tested in isolation, but certain combinations of organisms (specifically some Staphylococcus aureus and Escherichia coli) killed the animals rapidly (less than 18 hours) without prolonged terminal illness. Post mortem histological findings were consistent with those of SIDS. The lethal toxigenic potential of nasopharyngeal bacteria, which are regarded as harmless in adults, should be reconsidered in respect of the aetiology of SIDS.

Lethal synergy between toxins of staphylococci and enterobacteria: implications for sudden infant death syndrome.

AIM--To test the hypothesis that lethal synergy occurs between toxin preparations of nasopharyngeal staphylococci and enterobacteria from sudden infant death syndrome (SIDS) victims and matched healthy infants. METHODS--SIDS and matched healthy babies were studied if both staphylococcal and enterobacterial strains were isolated from the nasopharynx. The lethality of toxin preparations from each bacterial isolate (separately and combined) was assessed over a range of dilutions using the chick embryo assay system. RESULTS--Staphylococci and enterobacteria were isolated together from the nasopharynx of seven SIDS babies but from only one normal healthy infant. Enterobacterial toxins were lethal at high dilutions. Staphylococcal toxins were less toxic. Simultaneous testing in the chick assay of staphylococcal and enterobacterial toxins, from each baby, at non-lethal concentrations enhanced lethality levels by 177 to 1011% compared with lethality expected by an additive effect alone. CONCLUSIONS--Synergy occurs between the toxins of nasopharyngeal staphylococci and enterobacteria. This combination of strains is more likely to occur in the nasopharynx of SIDS victims than that of healthy infants.

The relative cariogenicities of Streptococcus milleri and other viridans group streptococci in gnotobiotic hooded rats.

Abstract Isolates of Streptococcus milleri were tested for cariogenicity in gnotobiotic Liverpool hooded rats. Representative strains of Streptococcus mitis , Streptococcus mutons , Streptococcus salivarius and Streptococcus sanguis were included for comparative purposes. Some strains of Strep, milleri appeared to be considerably more cariogenic than the strains of Strep. mitis , strep. salivarius or Strep. sanguis examined, although not as cariogenic as the strains of Strep. mutans .

Sensitivity of Candida albicans to negative air ion streams

J.M. SHARGAWI, E.D. THEAKER, D.B. DRUCKER, T. MACFARLANE and A.J. DUXBURY.1999.Negative air ions (NAIs) are known to kill C. albicans; however, their precise mechanism of action is uncertain. Elucidation of this has been hampered by a lack of reproducibility between results obtained by different investigators. The aim of this study was to determine the influence of variation in experimental parameters on the sensitivity of C. albicans to negative air ions and the role of ozone in this process. Ten strains of C. albicans were exposed to NAIs generated at different emitter distances, exposure times, relative humidities and under aerobic and oxygen‐free conditions. In further experiments, ozone levels were measured under the same conditions. The effect of NAIs on C. albicans growth was assessed by measuring the area of the zone of inhibition generated around the electrode of the ionizer. There was a significant reduction in area of zone of inhibition with increasing emitter distance (P < 0·05), relative humidity(P < 0·05) or under oxygen‐free conditions(P < 0·05). Increases in exposure time resulted in a significant increase in growth inhibition (P < 0·05). Ozone levels increased with increasing exposure times (P < 0·01) but were significantly reduced as emitter distance increased (P < 0·01). When utilized in a nonventilated room, levels of ozone produced did not exceed recognized safety limits. These results (a) demonstrate the importance of careful control of experimental parameters if reproducibility of studies involving NAIs is to be achieved, and (b) highlight the possible role of ozone in the microbicidal effects of NAIs.

Amoxycillin with clavulanic acid and tetracycline in periodontal therapy

The effects of tetracycline and amoxycillin with clavulanic acid on the clinical parameters and subgingival flora of eight patients with rapidly progressive periodontitis was assessed. Subjects received either tetracycline 250 mg four times daily or amoxycillin 250 mg with clavulanic acid 125 mg three times daily for a period of 2 weeks together with subgingival scaling and root planning. Both treatment regimens produced significant reductions in bleeding on probing and probing pocket depths which were still present 16 weeks after the antibiotic therapy. A significant reduction in the mean percentage of black-pigmented Bacteroides spp., Fusobacterium nucleatum and anaerobic corroding bacilli was also obtained. Both treatment regimens were equally effective in reducing the clinical parameter and altering the subgingival flora. The MIC values for Bacteroides gingivalis (Porphyromonas gingivalis). Bacteroides intermedius (Prevotella intermedia) and F. nucleatum to amoxycillin with clavulanic acid remained constant throughout the period of investigation. The MIC values of these organisms to tetracycline increased.

Lethal synergistic action of toxins of bacteria isolated from sudden infant death syndrome.

AIM: To test the hypothesis that lethal toxins of bacteria associated with sudden infant death syndrome (SIDS) can act synergistically. METHODS: Bacteria occurring together in the nasopharynx of cases of cot death were studied. The lethal toxicity of crude toxin preparations was determined over a range of dilutions by injections into the chorioallantoic vein of the chick embryo. Toxin preparations of low lethality for the chick embryo SIDS model were then tested in combination. RESULTS: Staphylococcus aureus toxin preparations showed low lethality when tested alone, even at low dilution. At 1 in 100 dilution S aureus toxin was lethal to one out of 15 chick embryos. Escherichia coli toxin preparations showed high lethality except on high dilution (1 in 80) when lethality fell to two out of 15 of chick embryos. When the same toxin preparations were tested simultaneously in combination, lethality rose to 14 out of 15. Similar findings were observed over a range of toxin dilutions. This finding was highly significant (p = 0.0012). CONCLUSIONS: That synergy between toxins can enhance the lethality of toxins elaborated by bacteria associated with SIDS.

Possible lethal enhancement of toxins from putative periodontopathogens by nicotine: implications for periodontal disease.

AIM: To test the hypothesis that lethal synergy in the chick embryo model may occur between nicotine and bacterial products (cell-free extracellular toxins and cell lysates) of five putative periodontopathogens. METHODS: The lethality of cell-free extracellular toxins and cell lysates of five periodontal species was assessed with or without nicotine in the chick embryo assay system. Ten putative periodontopathogens (five species) were studied: Prevotella intermedia (n = 5), Porphyromonas gingivalis (n = 1), Porphyromonas asaccharolytica (n = 1), Fusobacterium nucleatum (n = 2), and Fusobacterium necrophorum (n = 1). RESULTS: Simultaneous testing of cell-free extracellular toxins from isolates W50, PS2, PS3, PS4, and PS5 and nicotine resulted in a percentage kill significantly greater than expected (Fishers Exact test). Simultaneous testing of cell lysates from isolates W50, PS2, and PS5 and nicotine resulted in a percentage kill significantly greater than expected (Fishers Exact test). CONCLUSIONS: Lethal synergy in the chick embryo model may occur between nicotine and toxins from putative periodontopathogens (both cell-free extracellular toxins and cell lysates). This may be an important mechanism by which smoking increases the severity of periodontal disease.