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Analysis of antibioticograms of 390 O1 and O139 serogroup Vibrio cholerae strains isolated from humans within 1927-2005 in various regions of the world showed that the strains of V. cholerae isolated within 1927-1966 were susceptible to 22 antibacterials, the strains isolated within 1938-1993 possessed 1-3 resistance markers and the strains isolated within 1994-2005 had 3-8 resistance markers including resistance to fluoroquinolones. All the strains of O139 serogroup V. cholerae isolated in 1993 and 1994 possessed 3 resistance markers. Studies on albino mice with generalized experimental cholera due to the V. cholerae eltor 1 strain (P-18826, 2005) isolated from a cholera patient, which was highly resistant to nalidixic acid, streptomycin, ampicillin and trimethoprim/sulfamethoxazole and showed cross resistance to fluoroquinolones (ciprofloxacin, ofloxacin, pefloxacin and norfloxacin) and moderate resistance to ceftriaxone and cefotaxime, revealed that the only efficient antibiotics were tetracyclines and aminoglycosides (except streptomycin). The investigation demonstrated an extension of the antibiotic resistance spectra of the epidemically significant strains of the cholera pathogen and the necessity of using antibacterial drugs in strict accordance with the antibioticograms in emergent prophylaxis and therapy of cholera and immediate replacement of the drug by a more active one.

Activity of 16 antibacterial agents against human isolates of Vibrio cholerae O1 and O139 serogroups (P-5879, 4990, 143/23, and MO-45, P- 16065 respectively) was studied in vitro. The efficacy of the agents was studied in a model of generalized cholera in albino mice. Susceptibility of Vibrio cholerae P-5879 (used as the control) in the in vitro experiments with respect to the antibacterial agents correlated with their in vivo efficacy. The strains of Vibrio cholerae O1 and O139 serogroups isolated within the recent years had transmissive markers of resistance to streptomycin, trimethoprime/sulfamethoxazole, tetracycline, chloramphenicol and not transmitted by conjugation markers of resistance to rifampicin, furazolidone, nalidixic acid. The specific feature of the experimental infection due to such strains was the failure not only of the antibacterials of the resistance spectrum of the pathogen but also of the antibiotics showing in vitro susceptibility (betalactams, fluoroquinolones) that required additional bacteriological control on the 2nd or 3rd day of the etiotropic therapy for early replacement of the antibacterial agent.