Detection of virulence-associated genes in pathogenic and commensal avian Escherichia coli isolates

Abstract

Poultry colibacillosis due to Avian Pathogenic Escherichia coli (APEC) is responsible for several extra-intestinal pathological conditions, leading to serious economic damage in poultry production. The most commonly associated pathologies are airsacculitis, colisepticemia, and cellulitis in broiler chickens, and salpingitis and peritonitis in broiler breeders. In this work a total of 66 strains isolated from dead broiler breeders affected with colibacillosis and 61 strains from healthy broilers were studied. Strains from broiler breeders were typified with serogroups O2, O18, and O78, which are mainly associated with disease. The serogroup O78 was the most prevalent (58%). All the strains were checked for the presence of 11 virulence genes: 1) arginine succinyltransferase A (astA); ii) E.coli hemeutilization protein A (chuA); iii) colicin V A/B (cvaA/B); iv) fimbriae mannose-binding type 1 (fimC); v) ferric yersiniabactin uptake A (fyuA); vi) iron-repressible high-molecular-weight proteins 2 (irp2); vii) increased serum survival (iss); viii) iron-uptake systems of E.coli D (iucD); ix) pielonefritis associated to pili C (papC); x) temperature sensitive haemaglutinin (tsh), and xi) vacuolating autotransporter toxin (vat), by Multiplex-PCR. The results showed that all genes are present in both commensal and pathogenic E. coli strains. The iron uptake-related genes and the serum survival gene were more prevalent among APEC. The adhesin genes, except tsh, and the toxin genes, except astA, were also more prevalent among APEC isolates. Except for astA and tsh, APEC strains harbored the majority of the virulence-associated genes studied and fimC was the most prevalent gene, detected in 96.97 and 88.52% of APEC and AFEC strains, respectively. Possession of more than one iron transport system seems to play an important role on APEC survival.

Environmental adaptation and vertical dissemination of ESBL‐/pAmpC‐producing Escherichia coli in an integrated broiler production chain in the absence of an antibiotic treatment

“…Investigations on the phenotypic characteristics and virulence patterns of ESBL‐/pAmpC‐producing E. coli indicate that certain traits usually associated with virulence factors correlate with the ability to adhere, persist and adapt to certain environmental circumstances (Guenther et al ., 2012; Rodiger et al ., 2015; Mo et al ., 2016; Paixao et al ., 2016; Schaufler et al ., 2016a). In our study, high prevalence strains of ST‐354 could be assigned as ExPEC and overall showed the highest number of ExVAGs, especially genes referring to adhesion factors, compared to low prevalent strains of ST‐117 and ST‐2307.…”

“…Intestinal pathogenic E. coli (IPEC) are causing diarrhoea syndromes and seldom colonize healthy humans whereas extraintestinal pathogenic E. coli (ExPEC) often innocuously colonize the gut but have the ability to cause severe infections such as meningitis or blood stream infections (Vila et al ., 2016). Recent studies compared the occurrence of certain virulence‐associated genes (VAGs) in avian pathogenic E. coli (APEC), uropathogenic E. coli (UPEC) and commensal E. coli from humans and broiler chickens (Kemmett et al ., 2013; de Carli et al ., 2015; van Hoek et al ., 2016; Paixao et al ., 2016; Silveira et al ., 2016). It turned out that certain VAGs (e.g.…”

Studies on avian pathogenic Escherichia coli in commercial broiler chicken in South East Queensland

“…However, no single or specific set of VGs have been systematically linked with APEC pathogenicity. It is very rare to find the same set of VGs in all APEC, in the same study and/or different studies (Kawamura-Sato et al, 2010;Kemmett et al, 2013;Paixao et al, 2016;Rodriguez-Siek et al, 2005a;Zhao et al, 2005). Nevertheless, APEC harbour several VGs that enable the bacteria to invade, colonise, evade the immune system and cause avian colibacillosis (Guastalli et al, 2013;Horn et al, 2012;Kemmett et al, 2014;Pires-dos-Santos et al, 2013).…”

“…The clinical signs associated with avian colibacillosis are nonspecific and vary with age, species, type of infection and whether it is localised or systemic (Kabir, 2010;Nolan et al, 2013). Affected birds demonstrate signs of respiratory distress, reduced appetite, poor growth, depression and fever, which may also be accompanied by a high mortality rate (Kabir, 2010;Paixao et al, 2016). Characteristic fibrinous lesions, such as, airsacculitis, pericarditis, perihepatitis, peritonitis and salpingitis are commonly found during post-mortem examination of the internal organs Vandekerchove et al, 2004b) (see Figure 1-1).…”

“…The disease is a complex syndrome that can occur as a localised (subacute form) or systemic infection (acute form) Paixao et al, 2016). The disease can manifest itself in different forms, such as, yolk sac infections (omphalitis), respiratory tract infections (air sacculitis), swollen-head syndrome, septicaemia, polyserositis, coligranuloma, enteritis, coliform cellulitis, salpingitis, pericarditis and perihepatitis in chickens, turkeys and other commercial avian species (Dho-Moulin and Fairbrother, 1999;Moulin-Schouleur et al, 2006;Paixao et al, 2016). …”