Resistance to serum complement, iss, and virulence of avian Escherichia coli

• Published in: Veterinary research communications 2003-02, Vol.27 (2), p.101-110
• Main Authors: Nolan, L K, Horne, S M, Giddings, C W, Foley, S L, Johnson, T J, Lynne, A M, Skyberg, J
• Format: Article
• Language: English
• Subjects: Animals; Complement System Proteins - immunology; Escherichia coli - genetics; Escherichia coli - immunology; Escherichia coli - pathogenicity; Escherichia coli Infections - immunology; Escherichia coli Infections - veterinary; Escherichia coli Proteins - genetics; Escherichia coli Proteins - immunology; Poultry - microbiology; Poultry Diseases - immunology; Poultry Diseases - microbiology; Proteins - genetics; Proteins - immunology; Virulence - genetics; Virulence - physiology
• ISSN: 0165-7380; 1573-7446
• DOI: 10.1023/A:1022854902700

Control of avian colibacillosis is hampered by lack of easily identifiable markers for virulent Escherichia coli. Resistance to serum complement appears to be a widespread trait of virulent avian E. coil, suggesting that bacterial factors promoting survival in serum may be useful in discriminating between virulent and avirulent isolates. Such distinguishing factors may prove useful in diagnostic protocols or as targets in future colibacillosis control protocols. Interestingly, the factors responsible for resistance to complement differ in the E. coli isolated from mammalian and avian hosts, which may reflect differences in the nature of avian and mammalian colibacillosis. In some cases, genetic determinants for serum complement resistance in avian E. coli are found on aerobactin- or Colicin V-encoding plasmids. One such gene, iss, first described for its role in the serum resistance associated with a ColV plasmid from a human E. coli isolate, occurs much more frequently in isolates from birds with colibacillosis than in faecal isolates from healthy birds. Efforts to identify the genomic location of iss in a single, virulent avian E. coli isolate have revealed that it occurs in association with several purported virulence genes, all linked to a large conjugative R plasmid. At this time, it is not known whether iss merely marks the presence of a larger pathogenicity unit or is itself a contributor to virulence. Nevertheless, the presence of the complement-resistance determinant, iss, may be a marker of virulent avian E. coli exploitable in controlling avian colibacillosis.