Selected Abstracts

Genetic and Biochemical Characterization of Citrobacter rodentium sp. nov.

David B. Schauer, Brian A. Zabel, Isabel F. Pedraza, Caroline M. O'Hara, Arnold G. Steigerwalt, and Don J. Brenner

An unusual bacterial pathogen of laboratory mice has been previously classified as an atypical biotype of Citrobacter freundii. Designated C. freundii biotype 4280, this bacterium is the etiological agent of transmissible murine colonic hyperplasia. An eaeA gene has been shown to be present in this organism and to be necessary for virulence in laboratory mice. However, other biotypes of C. freundii lack DNA homology with the eaeA gene. Because of the recent reclassification in which five named species and three unnamed species, all previously considered C. freundii, were described, we determined the toxonomic status of C. freundii biotype 4280. With a battery of biochemical tests and DNA relatedness studies, three isolates of C. freundii biotype 4280 were shown to be members of an unnamed Citrobacter species, designated species 9. In total, six isolates of Citrobacter species 9, but none of the other type strains of the other eight named species or of the two remaining unnamed species of Citrobacter, were shown to possess DNA homology with both the eaeA and the eaeB genes. Species 9 was named Citrobacter rodentium sp. nov.

Journal of Clinical Microbiology , Vol. 33, No. 8, August 1995, pp. 2064-2068.

Detection of Helicobacter pylori in Drinking Water Using Polymerase Chain Reaction Amplification

Jason Handwerker, James G. Fox, and David B. Schauer

Direct person-to-person spread is the primary mode of transmission of H. pylori infection in humans. The existence of environmental reservoirs has been suggested, and epidemiological studies indicate that water can be a source of H. pylori infection. Demonstration of H. pylori organisms in environmental samples is complicated by the fact that viable, coccoid forms of the bacterium may not be culturable. We have used polymerase chain reaction (PCR) amplification of 16S ribosomal gene sequences to permit the sensitive and specific detection of H. pylori in environmental water samples. This method has been used to demonstrate that H. pylori is present in some environmental water samples collected from a region of Columbia, South America in which there is a high prevalence of H. pylori infection. We have also developed a method to rapidly concentrate microorganisms in large samples of environmental water using rotating membrane ultrafiltration (RMU). The concentration of environmental samples by RMU followed by PCR amplification should permit the identification of water sources contributing to the to the risk of human H. pylori infection.

95th General Meeting American Society for Microbiology Washington, DC 21-25 May 1995 p. 435

DNA Homology Between an Attaching and Affacing Citrobacter Species and the eaeB Locus of Enteropathogenic Escherichia coli

Brian A. Zabel, Isabel F. Pedraza, and David B. Schauer

The causative agent of transmissible murine colonic hyperplasia, previously known as Citrobacter freundii biotype 4280, is a member of Citrobacter genomospeceis 9. This organism produces attaching and effacing histopathology in the descending colon of laboratory mice. It has been reported that in enteropathogenic E. coli (EPEC) the genes involved in attaching and effacing lesion formation, including eaeB, map to an ca. 35-kb fragment of chromosomal DNA. We have hybridized an internal fragment of DNA from EPEC eaeB to Citrobacter genomospecies 9 DNA. Under conditions of high stringency, Southern blot analysis reveals the presence of eaeB homology in this genomospecies. Under conditions of low stringency, eaeB homology was not detected in 10 other Citrobacter genomospecies. In genomospecies 9, the eaeB homology was mapped to a 15-kb fragment of chromosomal DNA that has previously been shown to contain the entire Citrobacter eaeA gene, as well as an unusual series of direct DNA repeats . These data suggest that, like EPEC, Citrobacter genomospecies 9 may contain a cluster of genes involved in attaching and effacing lesion formation.

95th General Meeting American Society for Microbiology Washington, DC 21-25 May 1995 p. 194

Back to Schauer Lab home page . o Schauer Lab home page .