Infection of humans by Shiga toxin-producing Escherichia coli (STEC) results in various clinical manifestations such as diarrhea, hemorrhagic colitis and (occasionally fatal) hemolytic uremic syndrome (HUS) [1]. This bacterial zoonotic agent is a pathogen of a public health concern due to its potential to cause large food- and waterborne outbreaks, as well as its association with the hemorrhagic uremic syndrome (HUS) [2, 3], a leading cause of acute renal failure among children [4]. Although most STEC strains associated with human illness belong to serogroup O157, there are more than a hundred of non-O157 serotypes [5], some of which have been associated with large outbreaks of severe illness.
STEC has various virulence factors that are important in pathogenicity. Shiga toxin is the major factor in virulence and there are two toxin forms, stx1, and stx2 encoded by stx1 and stx2 genes [6]. There are three subtypes of the stx1 gene, namely, stx1a, stx1c and stx1d. On the other hand, the stx2 group is divided into seven subtypes, namely, stx2a, stx2b, stx2c, stx2d, stx2e, stx2f and stx2g. The stx2 subtype is associated with more severe HUS syndrome [7].
Shiga toxins bind to the surface of eukaryotic cells, inhibit protein synthesis, thereby causing the death of their hosts [8]. A virulence factor coded by the eae gene is intimin. Intimin is reported to facilitate bacteria's attachment to intestinal epithelia during colonization leading to lesions and diarrhea [9, 10]. Enteropathogenic E. coli (EPEC) also possess the intimin virulence factor [11]. Enterohaemolysin is another Shiga toxin associated with E. coli, this protein toxin damages erythrocyte cell membranes and is used in the detection of Shiga toxin E. coli as a surrogate tool [12, 13]. While enterohaemolysin activity can be easily visualized in blood agar cultures, PCR amplification of the ehxA gene usually results in confirmation [14, 15]. Other E. coli strains including O26, O103, O111, O118, O128, O121, O45 and O145 also have the potential to produce disease syndromes and are reported to be enterohaemolysin-positive Shiga toxins producers [16].
Animals are a major potential source of human STEC infection due to their ability to maintain STEC carriage even in the absence of continuous exposure to STEC (i.e. reservoirs or amplifying hosts), including farm and abattoir (slaughter) animals that are frequently exposed to STEC from the environment [17].
Although ruminants, and particularly cattle, are regarded as the main reservoir for STEC [18, 19], there is evidence for non-ruminants, particularly poultry being significant spill-over hosts for STEC. These are animals that are susceptible to colonization by STEC but do not maintain such colonization in the absence of continuous exposure [17, 20, 21, 22].
The role of meat products as vehicles of STEC have been widely reported [23, 24], moreover, STEC strains isolated from animal and food were identified carrying resistance genes against multiple antimicrobial classes, such as aminoglycosides, tetracycline and b-lactams [25]. Thus, more information about the prevalence and spread of STEC among animals and food is needed.
The present study aims to investigate the spatial prevalence and virulence characteristics of STEC present in abattoirs, fresh and retail (frozen) chicken carcasses in Osogbo, Osun State, Nigeria. Reports from a recent study [26], showed the presence of non-O157 STEC strains in selected beef abattoirs at most of the study sites sampled within the Osogbo metropolis. In Southwestern Nigeria, poultry and bovine abattoirs are typically spatially separated, the present study provides some basis for comparing the prevalence and virulence characteristics of E. coli strains isolated from beef and chicken abattoirs. This is with a view to providing baseline information necessary to develop best practices needed to limit the spread of STEC and to improve on practices in the local abattoirs, thereby improving public health practice within the study area.