PubMed Health⌕ Search

PubMed · 9642935

[Epidemiological study on penicillin-resistant Streptococcus pneumoniae].

Abstract

We studied the differences among clinical isolates of Penicillin-resistant Streptococcus pneumoniae by polymerase chain reaction (PCR) of pbp2b gene, followed by serotyping and pulsed field gel electrophoresis (PFGE) analysis. Clinical isolates were recovered from sputum samples from patients with respiratory infection in Tottori University Hospital between June 1986 and May 1996. By PCR, altered pbp2b genes of the resistant isolates were detected in 76.5%. The percentages of the isolates that had altered pbp2b genes increased concomitantly with the minimum inhibitory concentration (MIC). By serotyping the percentage of 19F, 23F, 6B and 14 was 54.5%, 18.2%, 9.1% and 9.1% respectively. The frequency of isolates resistant to penicillin increased rapidly from 1991 in this hospital and most isolates belonged to serotype 19F. The resistant isolates in this hospital and 4 clinical resistant isolates of S. pneumoniae 19F in a second hospital were studied by PFGE. 14 of 18 resistant 19F isolates in this hospital and all 19F isolates from the second hospital presented an identical pattern. The remaining 4 samples were similar though not completely identical. These results indicate that the penicillin resistant 19F isolates have a common clonal origin and have spread rapidly from 1991 in this hospital.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S Yamasaki, Y Sugimoto, Y Matsumoto. 1998. [Epidemiological study on penicillin-resistant Streptococcus pneumoniae].. https://doi.org/10.11150/kansenshogakuzasshi1970.72.475

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Mutation in the edd gene encoding the 6-phosphogluconate dehydratase of Pseudomonas chlororaphis O6 impairs root colonization and is correlated with reduced induction of systemic resistance.

AIMS: The primary objective of this study was to determine the role of 6-phosphogluconate dehydratase in root colonization and the induction of systemic resistance by the rhizobacterium, Pseudomonas chlororaphis O6. METHODS AND RESULTS: The edd gene encoding for 6-phosphogluconate dehydratase, which is one of the key enzymes in glucose utilization, was cloned. Transcription of the gene was higher in medium containing sugars than with organic acids. An edd mutant failed to grow on glucose but grew on organic acids. The edd mutant colonized tobacco roots at wild-type levels early after inoculation, but levels were lower by 12 days. The edd mutant failed to induce the systemic resistance in tobacco to a soft-rot pathogen at wild-type level. CONCLUSIONS: 6-Phosphogluconate dehydratase in P. chlororaphis O6 contributes to root colonization and induction of systemic resistance presumably as the consequence of its essential role in the Entner-Doudoroff (ED) pathway. SIGNIFICANCE AND IMPACT OF THE STUDY: Metabolism of sugars through the ED pathway in P. chlororaphis O6 may be important because it facilitates the production of inducers of systemic resistance including butanediol.

Genes, Bacterial↗

Mutations in penicillin-binding protein (PBP) genes and in non-PBP genes during selection of penicillin-resistant Streptococcus gordonii.

Penicillin resistance in Streptococcus spp. involves multiple mutations in both penicillin-binding proteins (PBPs) and non-PBP genes. Here, we studied the development of penicillin resistance in the oral commensal Streptococcus gordonii. Cyclic exposure of bacteria to twofold-increasing penicillin concentrations selected for a progressive 250- to 500-fold MIC increase (from 0.008 to between 2 and 4 microg/ml). The major MIC increase (> or = 35-fold) was related to non-PBP mutations, whereas PBP mutations accounted only for a 4- to 8-fold additional increase. PBP mutations occurred in class B PBPs 2X and 2B, which carry a transpeptidase domain, but not in class A PBP 1A, 1B, or 2A, which carry an additional transglycosylase domain. Therefore, we tested whether inactivation of class A PBPs affected resistance development in spite of the absence of mutations. Deletion of PBP 1A or 2A profoundly slowed down resistance development but only moderately affected resistance in already highly resistant mutants (MIC = 2 to 4 microg/ml). Thus, class A PBPs might facilitate early development of resistance by stabilizing penicillin-altered peptidoglycan via transglycosylation, whereas they might be less indispensable in highly resistant mutants which have reestablished a penicillin-insensitive cell wall-building machinery. The contribution of PBP and non-PBP mutations alone could be individualized in DNA transformation. Both PBP and non-PBP mutations conferred some level of intrinsic resistance, but combining the mutations synergized them to ensure high-level resistance (> or = 2 microg/ml). The results underline the complexity of penicillin resistance development and suggest that inhibition of transglycosylase might be an as yet underestimated way to interfere with early resistance development.

Genes, Bacterial↗

The majority of genes in the pathogenic Neisseria species are present in non-pathogenic Neisseria lactamica, including those designated as 'virulence genes'.

BACKGROUND: Neisseria meningitidis causes the life-threatening diseases meningococcal meningitis and meningococcal septicemia. Neisseria gonorrhoeae is closely related to the meningococcus, but is the cause of the very different infection, gonorrhea. A number of genes have been implicated in the virulence of these related yet distinct pathogens, but the genes that define and differentiate the species and their behaviours have not been established. Further, a related species, Neisseria lactamica is not associated with either type of infection in normally healthy people, and lives as a harmless commensal. We have determined which of the genes so far identified in the genome sequences of the pathogens are also present in this non-pathogenic related species. RESULTS: Thirteen unrelated strains of N. lactamica were investigated using comparative genome hybridization to the pan-Neisseria microarray-v2, which contains 2845 unique gene probes. The presence of 127 'virulence genes' was specifically addressed; of these 85 are present in N. lactamica. Of the remaining 42 'virulence genes' only 11 are present in all four of the sequenced pathogenic Neisseria. CONCLUSION: Assessment of the complete dataset revealed that the vast majority of genes present in the pathogens are also present in N. lactamica. Of the 1,473 probes to genes shared by all four pathogenic genome sequences, 1,373 hybridize to N. lactamica. These shared genes cannot include genes that are necessary and sufficient for the virulence of the pathogens, since N. lactamica does not share this behaviour. This provides an essential context for the interpretation of gene complement studies of the pathogens.

Genes, Bacterial↗