The katE gene, which encodes the catalase HPII of Mycobacterium avium.

Disseminated Mycobacterium avium-Mycobacterium intracellulare disease is a prevalent opportunistic infection in patients with acquired immune deficiency syndrome (AIDS). These pathogens are generally resistant to isoniazid (INH), a powerful antituberculosis drug. It is now generally accepted that the INH susceptibility of Mycobacterium tuberculosis results from the transformation of the drug into a toxic derivative, as a result of the action of the enzyme catalase-peroxidase (HPI), encoded by the katG gene. It has been speculated that the presence of a second catalase (HPII) in some mycobacterial species, but lacking in M. tuberculosis, may impair the action of INH. In this report, the nucleotide sequence of the M. avium katE gene, encoding catalase HPII, is described. This enzyme shows strong similarity to Escherichia coli catalase HPII and eukaryotic catalases. All amino acids previously postulated as participating directly in catalysis by liver catalase and most of the amino acids binding the prosthetic group are conserved in M. avium catalase HPII. The enzyme is expressed in E. coli and is inhibited by 3-amino-1,2,4-triazole (AT). Furthermore, Southern blot hybridizations and polymerase chain reaction experiments demonstrate the distribution of katE gene in several mycobacterial species. To evaluate the potentially antagonistic effect of HPII catalase on INH susceptibility, the katE gene was transformed into M. tuberculosis H37Rv and the minimum inhibitory concentration (MIC) for INH was determined. Despite strong expression of the katE gene, no change in MIC was observed, thus ruling out a possible contribution of this enzyme to the natural resistance of M. avium to the drug. The availability of the gene probe, encoding the second mycobacterial catalase HPII, should open the way for the development of new drugs and diagnostic tests to combat drug-resistant pathogen strains

Periodontal conditions in adolescents with cleft lip, alveolus and palate following treatment in a co-ordinated team approach

The aim of the present investigation was to evaluate the oral hygiene habits and the periodontal conditions of a group of cleft lip, alveolus and palate patients at the end of a longitudinal multidisciplinary treatment. From a total of 120 patients who had been supervised at the University of Berne, Clinic for Pediatric Surgery for at least 18 years in a co-ordinated team approach, 80 were selected on the basis of availability. Plaque control record (PCR), calculus index (CI), gingival bleeding index (GBI), pocket probing depth (PD), loss of attachment (LA) and furcation involvement were recorded. Using the technique and the ruler described by Schei et al., the radiographic height of the alveolar crest from the cemento-enamel junction was determined. Between the different groups of deformities, no statistically significant differences were found for all the clinical parameters with the exception of the mean PD orally and the mean PD bucally which were shallower in the isolated cleft lip group. These differences were attributed to the long-term orthodontic therapy with fixed appliances. When the PD and the LA at the sites adjacent to the cleft region were compared to two 'unaffected' control sites, no statistically significant differences were found, whereas the comparison with the radiographic bone loss showed a statistically significant bone height. These results may indicate the presence of a long connective tissue attachment without bony support in the cleft region. As a result of inadequate oral hygiene, the patients with cleft lip, alveolus and palate showed beginning periodontitis with loss of attachment and beginning furcation involvement in most of the cases. Since these patients need long-term orthodontic therapy with fixed appliances, they should be incorporated in intensive prophylaxis programs as early in age as possible.link_to_subscribed_fulltex

Oral microbiota in subjects with a weak or strong response in experimental gingivitis

The purpose of the present study was to examine the composition of the oral microbiota in subjects who had previously demonstrated to develop either a weak or strong response to experimental gingivitis. For this study, subjects were selected from a pool of 25 individuals who had participated twice in an experimental gingivitis trial. Out of these 25 panellists, 6 subjects were selected who had developed 2× a weak gingival inflammatory response and 7 subjects who had developed 2× a strong gingival inflammatory response. Approximately 9 months after the 2nd experimental gingivitis trial, we evaluated the clinical condition and the prevalence of a panel of selected oral micro-organisms in these subjects. The subjects were clinically examined for the presence of plaque, bleeding, pocket depth and loss of attachment. For the microbiological evaluation, samples were taken from the mucous membranes, subgingival sites and saliva. Samples were analyzed for the presence of Actiilobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Peptostreptococcus micros. Actinomyces spp., Fusohacterium mucleatum, Campylobacter rectus, spirochaetes and motile rods. Clinical evaluation showed that most subjects had a relatively healthy periodontal condition. No clinically significant differences could be detected between the weak and strong responding groups. The microbial evaluation showed absence of A. actinomycetemcomitans, P. gingivalis and P. micros in all subjects in either group. Analysis of the microbial data for the weak and strong responding group showed no differences between the groups. This indicates that differences in response to experimental gingivitis are probably not caused by major differences in the compositon of the oral microbiota. The strong or weak inflammatory response may be related to differences in the microflora at the time of the experiments and/or differences in host response