We obtained a catalase-deficient (Kat-) strain of Neisseria gonorrhoeae isolated from a patient who had been unsuccessfully treated with penicillin. Quantitative enzyme assays and electrophoresis of cell extracts on native polyacrylamide gels subsequently stained for catalase and peroxidase activities failed to detect both enzymes. The strain exhibited no growth anomalies or unusual requirements when grown under ordinary laboratory conditions. However, the Kat- strain proved extremely sensitive to exogenous hydrogen peroxide, and analysis of the bacterial DNA after such exposure showed extensive single-strand breakage in both chromosomal and plasmid DNAs. Partial characterization of the gonococcal catalase from a Kat+ laboratory strain revealed that the enzyme had the physical and chemical properties of both catalase and peroxidase.

Thirty isolates of Haemophilus ducreyi collected in Thailand in 1984 were characterized by plasmid content. Three novel plasmids with estimated molecular masses of 1.8, 2.6, and 2.8 MDa were observed in 29 isolates, in addition to the 3.2-, 5.7-, and 7.0-MDa beta-lactamase and 4.4-MDa sulfonamide resistance plasmids. At least three of the seven plasmids were observed in each of the 29 isolates. The number and diversity of plasmids observed in these isolates of H. ducreyi distinguish them from strains previously described.

Similar to Neisseria gonorrhoeae, tetracycline-resistant isolates of N. meningitidis, Kingella denitrificans, and Eikenella corrodens contained 25.2-megadalton plasmids carrying the TetM determinant. In contrast, tetracycline-resistant N. subflava biovar perflava-N. sicca and N. mucosa isolates carried the TetM determinant in the chromosome.

Journal Article Frequency and Distribution in the United States of Strains of Neisseria gonorrhoeae with Plasmid-Mediated, High-Level Resistance to Tetracycline Get access Joan S. Knapp, Joan S. Knapp Sexually Transmitted Diseases Laboratory Program, Center for Infectious Diseases, and the Epidemiology Research Branch, Center for Prevention Services, Centers for Disease Control, Atlanta, Georgia Please address requests for reprints to Dr. Joan S. Knapp, Center for Infectious Diseases, Neisseria Research Laboratory, Sexually Transmitted Diseases Laboratory Program, Building 1, Room 3254, Centers for Disease Control, Atlanta, Georgia 30333. Search for other works by this author on: Oxford Academic PubMed Google Scholar Jonathan M. Zenilman, Jonathan M. Zenilman Sexually Transmitted Diseases Laboratory Program, Center for Infectious Diseases, and the Epidemiology Research Branch, Center for Prevention Services, Centers for Disease Control, Atlanta, Georgia Search for other works by this author on: Oxford Academic PubMed Google Scholar James W. Biddle, James W. Biddle Sexually Transmitted Diseases Laboratory Program, Center for Infectious Diseases, and the Epidemiology Research Branch, Center for Prevention Services, Centers for Disease Control, Atlanta, Georgia Search for other works by this author on: Oxford Academic PubMed Google Scholar Goldie H. Perkins, Goldie H. Perkins Sexually Transmitted Diseases Laboratory Program, Center for Infectious Diseases, and the Epidemiology Research Branch, Center for Prevention Services, Centers for Disease Control, Atlanta, Georgia Search for other works by this author on: Oxford Academic PubMed Google Scholar Wallis E. DeWitt, Wallis E. DeWitt Sexually Transmitted Diseases Laboratory Program, Center for Infectious Diseases, and the Epidemiology Research Branch, Center for Prevention Services, Centers for Disease Control, Atlanta, Georgia Search for other works by this author on: Oxford Academic PubMed Google Scholar Myrtle L. Thomas, Myrtle L. Thomas Sexually Transmitted Diseases Laboratory Program, Center for Infectious Diseases, and the Epidemiology Research Branch, Center for Prevention Services, Centers for Disease Control, Atlanta, Georgia Search for other works by this author on: Oxford Academic PubMed Google Scholar Steve R. Johnson, Steve R. Johnson Sexually Transmitted Diseases Laboratory Program, Center for Infectious Diseases, and the Epidemiology Research Branch, Center for Prevention Services, Centers for Disease Control, Atlanta, Georgia Search for other works by this author on: Oxford Academic PubMed Google Scholar Stephen A. Morse Stephen A. Morse Sexually Transmitted Diseases Laboratory Program, Center for Infectious Diseases, and the Epidemiology Research Branch, Center for Prevention Services, Centers for Disease Control, Atlanta, Georgia Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Infectious Diseases, Volume 155, Issue 4, April 1987, Pages 819–822, https://doi.org/10.1093/infdis/155.4.819 Published: 01 April 1987 Article history Received: 09 June 1986 Revision received: 05 September 1986 Published: 01 April 1987

Eighty-nine strains of Haemophilus ducreyi from a chancroid epidemic in Orange County, California, were examined for plasmid content. Seventy-eight (88%) of these isolates were found to contain a plasmid of 3.2 megadaltons which conferred beta-lactamase production. Restriction endonuclease digests indicated that this was the same plasmid that was found in some strains of beta-lactamase-producing Neisseria gonorrhoeae.

Plasmid profiles, the location of cholera toxin subunit A genes, and the presence of the defective VcA1 prophage genome in classical Vibrio cholerae isolated from patients in Bangladesh in 1982 were compared with those in older classical strains isolated during the sixth pandemic and with those in selected eltor and nontoxigenic O1 isolates. Classical strains typically had two plasmids (21 and 3 megadaltons), eltor strains typically had no plasmids, and nontoxigenic O1 strains had zero to three plasmids. The old and new isolates of classical V. cholerae had two HindIII chromosomal digest fragments containing cholera toxin subunit A genes, whereas the eltor strains from Eastern countries had one fragment. The eltor strains from areas surrounding the Gulf of Mexico also had two subunit A gene fragments, which were smaller and easily distinguished from the classical pattern. All classical strains had 8 to 10 HindIII fragments containing the defective VcA1 prophage genome; none of the Eastern eltor strains had these genes, and the Gulf Coast eltor strains contained a different array of weakly hybridizing genes. These data suggest that the recent isolates of classical cholera in Bangladesh are closely related to the bacterial strain(s) which caused classical cholera during the sixth pandemic. These data do not support hypotheses that either the eltor or the nontoxigenic O1 strains are precursors of the new classical strains.

Three strains of Neisseria gonorrhoeae carried novel plasmids of 7.8 megadaltons (mdal) molecular mass in addition to plasmids previously observed in this organism. The presence of the 7.8-mdal plasmids was not accompanied by any distinguishable phenotype in the strain possessing them. Analysis of plasmid DNA with restriction endonucleases showed that these plasmids were composed of three directly repeated copies of a 2.6-mdal cryptic plasmid frequently found in N. gonorrhoeae. In addition, the 7.8-mdal plasmids exhibited characteristics common to the 2.6-mdal plasmid, structural lability and sites resistant to cleavage with HpaII. The concatemeric forms of the cryptic plasmid appear to be stable in these strains and do not undergo internal recombination to produce the 2.6-mdal monomer, nor were higher concatemers detected.

Evidence is presented that defective prophage dVcA1 in Vibrio cholerae strain 162 was transposed to the hybrid P::Tn1 plasmid pSJ5. Properties of the resulting conjugative plasmid, pSJ15, indicated that bacteriophage VcA1, like coliphage Mu, can insert at many sites. By analogy with other Hfr-like donors, the high-frequency, polarized chromosomal transfer mediated by plasmid pSJ15 in strain 162 appeared to depend on plasmid integration through the homologous dVcA1 sequences in both replicons. When strain 162(pSJ15) donors were mated to the nonlysogenic El Tor strain RJ1, many potential ampicillin-resistant transconjugants were zygotically induced. However, surviving transconjugants (i) were immune to phage VcA1, (ii) cotransferred immunity and ampicillin resistance to nonlysogenic recipients, and (iii) did not preferentially transfer any chromosomal markers. Recombinant plasmids that transferred wild-type VcA1 prophages were readily isolated from strain RJ1 (VcA1+) lysogens that contained plasmid pSJ15. Physical measurements revealed that plasmid pSJ15 and the recombinant plasmids were about one VcA1 genome (22 to 24 megadaltons) larger than the 51-megadalton pSJ5 plasmid. Similar Hfr-like donors were constructed by introducing plasmid pSJ15 into different strain RJ1 (VcA1+) lysogens. Transfer properties of these donors indicated that the VcA1 prophage was integrated at several sites in the strain RJ1 chromosome.

A man who acquired gonococcal urethritis in the Philippines was not cured by repeated treatment with spectinomycin. Culture of a post-treatment urethral specimen grew penicillinase-producing Neisseria gonorrhoeae (PPNG) which was resistant to concentrations of spectinomycin of more than 2048 μg/ml. The bacterial resistance to spectinomycin was probably due to ribosomal changes that are a result of a chromosomal mutation. This is the first known infection caused by PPNG resistant to spectinomycin, an antibiotic widely used to treat PPNG infections.

The ampicillin resistance transposon Tn1 was translocated from the R plasmid RP4 to the Vibrio cholerae conjugative plasmid, P. The hybrid sex factor P::Tn1 was highly transmissible and expressed the biological activities of the P factor. In addition, P::Tn1 facilitated transfer of RP4 to V. cholerae recipients. Physical studies of P::Tn1 indicated that the Tn1 transposon was added to the otherwise unaltered P plasmid.