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The susceptibility of S. flexneri 1b and 3b strains to killing action of serum was investigated. Differences in sensitivity to bactericidal action of complement appeared to result from different structure of their LPS-es. The protective effect of LPS-es depends both on their origin and concentration.
Bacillus thuringiensis subsp. israelensis strain 1884 and B. thuringiensis subsp. morrisoni strain PG14 have the same toxicity toward mosquito larvae. Their protein crystal contents were compared either on native electrophoretic systems or on gel filtration. Analysis of electroeluted native proteins in SDS-PAGE showed that the 28-Kd protein alone, without the 68- or 130-Kd protein, was not larvicidal; however, toxicity was recorded as soon as 28- and 68-Kd proteins were associated. After gel filtration of 1884 soluble crystal, the 68-Kd protein alone, without 28 or 130 Kd, was not toxic; toxicity was also recorded when 28- and 68-Kd proteins and higher molecular weight proteins were associated. A comparable pattern was observed with PG14 soluble crystals.
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Two major changes in the epidemiology of salmonellosis occurred in the second half of the 20th century: the emergence of food-borne human infections caused by S. Enteritidis and by multiple-antibiotic resistant strains of Salmonella. This review updates information on the S. Enteritidis pandemic and focuses on the emergence of Salmonella, carrying the SGI1 antibiotic resistance gene cluster, resistant to extended-spectrum cephalosporins, or resistant to fluoroquinolones. The factors responsible for the emergence of these Salmonella strains could be either of human origin or related to bacterial genome evolution. However, our increasing understanding of the molecular fluidity of the genome shows that any attempt to counteract bacteria results in further bacterial evolution or adaptation of other bacteria to take place in the new free ecological niche. In these conditions, we can ask who is faster: humans who want to eliminate bacterial pathogens or bacteria that continuously evolve to gain new niches.
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Monoclonal antibodies against the surface antigens of Shigella flexneri 1b and S. dysenteriae 1 were prepared. The specificities of the antibodies were evaluated by enzyme-linked immunosorbent assay (ELISA), and quantitative agglutination using microtiter plate. Monoclonal antibodies against S. flexneri 1b, designated Sf2B2 and Sf2G4, belonged to IgG2a and IgG1 subclass, respectively. The former was specific for S. flexneri 1b, whereas the latter was reactive not only to S. flexneri 1b, but also weakly to 3a and 4b. Monoclonal antibody against S. dysenteriae 1, Sd5E1 (IgM), reacted with S. dysenteriae 1, 3, 6, 7, and S. boydii 2.
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Outbreaks of epizootic hemorrhagic disease of deer and of bluetongue began in British Columbia in August and October 1987 respectively and recrudescence of infection by both viruses was detected the following year in August. Weather records for up to 18 days before the initial outbreaks of disease, isolation of virus or seroconversion were examined to determine if the viruses could have been introduced by infected Culicoides carried on the wind. Data on temperature, rainfall, wind speed and direction and pressure together with backward trajectory analysis showed that there were suitable winds which could have introduced Culicoides infected with epizootic hemorrhagic disease of deer virus on 13 August 1987 (14 days before disease was observed), Culicoides infected with bluetongue virus on 1 October 1987 (7 days before virus was isolated and 13 days before disease in sheep) and Culicoides infected with bluetongue or epizootic hemorrhagic disease of deer viruses on 20 July 1988 (15 days before seroconversion was detected). The arrival on 13 August 1987 coincided with the passage of a cold front and rain and that on 1 October 1987 with a fall in temperature and calm winds. The source of the Culicoides before arrival could have been the Okanogan Valley as far south as the junction of the Okanogan and Columbia rivers in Washington, USA. Flight would have been at temperatures of 12.6 degrees C or higher and at heights up to 1.5 km.
Specific-pathogen-free chickens inoculated with isolate VA (variant A) or isolate IM of infectious bursal disease virus (IBDV) were examined for mitogenic response to T-cell mitogens, primary and secondary antibody response to sheep erythrocytes and Brucella abortus, and gross and histologic lesions in thymus and bursa. Both isolates induced comparable depression in the mitogenic and antibody response, and both caused extensive gross and histologic lesions in the bursa of Fabricius. However, bursal necrosis induced by the IM isolate was accompanied by an inflammatory response, whereas the inflammatory component was lacking in the lesion induced by the VA isolate. Furthermore, the IM isolate induced extensive lesions in the thymus, but the VA isolate did not.
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