Location of increased serum survival gene and selected virulence traits on a conjugative R plasmid in an avian Escherichia coli isolate.
Avian colibacillosis is a costly disease for the poultry industry. The mechanisms of virulence employed by the etiologic agent of this disease remain ill defined. However, accumulated evidence suggests that complement resistance and the presence of the increased serum survival gene (iss) in an avian Escherichia coli isolate may be indicative of its ability to cause disease. This association of iss with the E. coli implicated in avian disease may mean that iss and/or, perhaps, the genes associated with it are important contributors to avian E. coli virulence. For this reason, we have begun a search for iss's location in the bacterial genome. Thus far, iss in an avian E coli isolate has been localized to a conjugative R plasmid and estimated to be about 100 kilobase (kb) in size, encoding resistance to tetracycline and ampicillin. Hybridization studies have revealed that this plasmid contains sequences with homology to tsh, a gene associated with virulence of avian E coli; intI 1, a gene encoding the integrase of Class 1 integrons; and certain genes of the aerobactin- and CoIV-encoding operons. Sequences homologous to merA, a gene of the mercury resistance operon, were not identified on this R plasmid. This plasmid, when transferred into an avirulent, recipient strain by conjugation, enhanced the transconjugant's resistance to complement but not its virulence, in spite of the plasmid's possession of several putative virulence genes and traits. Such results may reflect the multifactorial nature of virulence, the degree of the recipient's impairment for virulence, or an inability of the embryo assay used here to detect this plasmid's contribution to virulence. Additionally, this plasmid contains genes encoding antimicrobial resistances, which may provide a selective advantage to virulent E. coli in the production environment. Further study will be needed to determine whether this plasmid is widespread among virulent E. coli and to ascertain the implications that this link between virulence and antimicrobial resistance genes may have for poultry management.
Johnson
Timothy J
TJ
Department of Veterinary and Microbiological Sciences, North Dakota State University, Fargo 58105, USA.
Giddings
Catherine W
CW
Horne
Shelley M
SM
Gibbs
Penelope S
PS
Wooley
Richard E
RE
Skyberg
Jerod
J
Olah
Pam
P
Kercher
Ronda
R
Sherwood
Julie S
JS
Foley
Steven L
SL
Nolan
Lisa K
LK
D000818:Animals; D002645:Chickens; D003165:Complement System Proteins; D003227:Conjugation, Genetic; D024881:Drug Resistance, Bacterial / Q000235:genetics; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics* / Q000472:pathogenicity; D004927:Escherichia coli Infections / Q000188:drug therapy / Q000382:microbiology / Q000662:veterinary; D029968:Escherichia coli Proteins / Q000235:genetics* / Q000276:immunology; D006824:Hybridization, Genetic; D009876:Operon; D011201:Poultry Diseases / Q000188:drug therapy / Q000382:microbiology; D011506:Proteins / Q000235:genetics* / Q000276:immunology; D011815:R Factors / Q000235:genetics*; D017385:Sequence Homology; D014774:Virulence / Q000235:genetics; D037521:Virulence Factors / Q000235:genetics*
D029968:Escherichia coli Proteins; C409210:Iss protein, E coli; D011506:Proteins; D037521:Virulence Factors; D003165:Complement System Proteins