The effect on the virulence and infectivity of Salmonella typhimurium and Salmonella gallinarum of acquiring antibiotic resistance plasmids from organisms that had caused serious outbreaks of disease.
Antibiotic resistance plasmids from organisms that had caused serious epidemics, including those responsible for epidemics of chloramphenicol-resistant typhoid fever and dysentery in Central America, were transferred to a strain of Salmonella typhimurium and of Salmonella gallinarum. The virulence and infectivity of these R(+) forms were then compared with the R(-) parent forms in orally inoculated chickens.None of the R(+) forms were more virulent than their R(-) parent forms. The mortality rates they produced were either the same as or less than that of their R(-) parent forms. The mortality rates were not increased by feeding the chickens on diets containing antibiotics against which the plasmids provided resistance.The removal of the plasmids from some R(+) forms of decreased virulence was not accompanied by any alteration in virulence, indicating that they were less virulent mutants of the parent strain that had conjugated preferentially. In other cases their virulence was increased, indicating that the very possession of the plasmid was involved in their decreased virulence. Of four forms of the S. gallinarum strain harbouring the plasmid that had been incriminated in the Central American dysentery outbreak, one was as virulent as the parent R(-) form and the other three were less virulent. Preferential conjugation by an avirulent mutant was responsible for the lack of virulence of one of them but the very possession of the plasmid appeared responsible for the decreased virulence of the other two. The decreased virulence of de-repressed F(+) and I(+) forms of the S. typhimurium strain was increased to that of repressed F(+) form and of the parent form by plasmid removal.Organisms of the R(+) forms of the S. typhimurium strain were not excreted in larger amounts or for longer periods of time by infected chickens than organisms of the R(-) parent form were. Neither did organisms of the R(+) forms of this strain or the S. gallinarum strain spread more rapidly or more extensively from infected chickens to in-contact chickens than organisms of the R(-) parent forms did. When antibiotics against which the infecting R(+) organisms provided resistance were included in the diet of these chickens the R(+) organisms were usually excreted in greater amounts, for longer periods of time and spread more rapidly and more extensively from the infected chickens to the in-contact chickens.
D000667:Ampicillin / Q000494:pharmacology; D000818:Animals; D002645:Chickens; D003227:Conjugation, Genetic; D005144:F Factor / Q000187:drug effects; D005243:Feces / Q000382:microbiology; D010403:Penicillin Resistance; D010957:Plasmids; D011200:Poultry; D011201:Poultry Diseases / Q000382:microbiology; D011815:R Factors / Q000187:drug effects; D012475:Salmonella / Q000472:pathogenicity*; D012481:Salmonella Infections, Animal / Q000382:microbiology; D012486:Salmonella typhimurium / Q000472:pathogenicity*; D014774:Virulence
D000667:Ampicillin