Several iron-regulated proteins of Neisseria gonorrhoeae have been reported. One of these, a 37,000molecular-weight protein (37K protein), appears to be common to all gonococcal isolates. Recently, the occurrence of a similar protein has also been noted in N. meningitidis. The gonococcal 37K protein has been purified and used to produce both rabbit monospecific antiserum and murine monoclonal antibodies. Using these antibody reagents, we analyzed 57 strains from nine species of Neisseria and the closely related organism Branhamella catarrhalis for the presence of proteins antigenically related to the gonococcal 37K protein. Strains grown on medium with low iron content were probed for antigenic reactivity by Western blot techniques and an enzyme-linked immunosorbent assay. Proteins which cross-reacted with the rabbit monospecific antiserum were designated as AgR-37K proteins. The data indicated that the AgR-37K proteins were conserved among the 40 strains of N. gonorrhoeae, N. meningitidis, N. lactamica, and N. cinerea tested. Seventeen strains from other species of Neisseria and Branhamella did not express AgR-37K proteins with the exception of one N. subflava isolate. All AgR-37K proteins appeared to be regulated by the amount of available iron in the growth medium. Murine monoclonal antibodies were used to probe the antigenic heterogeneity of the AgR-37K proteins from different Neisseria spp. Two of seven monoclonal antibodies were broadly cross-reactive, recognizing the AgR-37K proteins from all species examined. The remaining five monoclonal antibodies were more discriminating, recognizing the AgR-37K proteins from certain species. The antigenic conservation of these AgR-37K proteins, particularly among the pathogenic members of the genus Neisseria, may imply that these proteins serve a common function in pathogenicity.
Between January 1983 and October 1984, 446 cases of infection due to chromosomally mediated resistance in Neisseria gonorrhoeae (CMRNG) were reported in 23 states. Eighty percent were detected as primary penicillin or ampicillin treatment failures. Gonococcal isolates were submitted from 175 (40%) for confirmation of resistance, susceptibility testing, gonococcal strain typing using monoclonal antibodies specific for outer membrane Protein I, and auxotyping. All were typed as Protein I serogroup IB (WII/WIII), and the majority were proline or prototrophic auxotypes. All were resistant in vitro to less than 1 microgram/ml of either penicillin or tetracycline. Comparing CMRNG with penicillinase-producing Neisseria gonorrhoeae (PPNG), we found that CMRNG were significantly more resistant to tetracycline and erythromycin, but PPNG were more resistant to penicillin (P less than .01). Because of increasing reports of gonococcal resistance in the United States, improved surveillance of clinical and laboratory resistance is needed in support of control and treatment recommendations for gonorrhea.
A total of 40 Neisseria gonorrhoeae isolates, representing 19 penicillin-resistant isolates (from 8 heterosexual patients and 11 homosexual patients) and 21 penicillin-susceptible isolates (from 15 heterosexual patients and 6 homosexual patients) and obtained from the same geographic area, were examined. Lectin agglutination patterns were based on the reactivity of the isolates with the following 14 lectins: concanavalin A, Lens culinaris, Trichosanthes kinlowii, Griffonia simplicifolia I, Arachis hypogeae (peanut agglutinin), Glycine max (soybean agglutinin), Dolichos bifloris, Griffonia simplicifolia II, Solanum tuberosum (potato starch agglutinin), Triticum vulgaris (wheat germ agglutinin), Limax flavus, Phaseolus vulgaris, Ukx europaeus I, and Lotus tetragonolobus. All isolates were serotyped with monoclonal antibodies specific for gonococcal outer membrane protein I and auxotyped, and the plasmid content was determined. Resistant patient isolates were selected for their decreased penicillin susceptibility, and control isolates were selected for their penicillin susceptibility. Even though the patient isolates demonstrated resistance to penicillin, no phenotypic differences in lectin
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