Purpose: This study evaluated the Shiga toxins, plasmid profiles and incompatibility groups in STECs.
Methods: 72 STECs (13 O157:H7 and 59 non-O157:H7) from humans and foods were analyzed. Non-O157:H7 STEC variants included O8:H8, O103, O121, O123, O174, O45, O69, O5, O8, O80, O165, O111 and O26. A PCR-based replicon typing scheme was used to detect the presence of IncA/C, B/O, Frep, FIA, FIB, FIC, FIIA, HI1, HI2, I1, K/B, L/M, N, P, T, W, X, and Y. Additionally, Shiga toxin genes (stx1 and stx2) were detected in these isolates using PCR and ELISA.
Results: Data indicated that ~60% of the isolates harbored either the stx1 or stx2 gene and 40% harbored both genes. Both genes remained undetected in only one isolate (EC O26). Nearly 30% of O157:H7 isolates carried 1 to 3 plasmids (~0.2 to 100 kb), while 93% of the non-O157:H7 isolates carried 1 to 11 plasmids (~0.25 to 165 kb). Replicon typing data indicated that IncFIB plasmids were detected in 92% of O157:H7 and 76% of non-O157:H7 STEC isolates, while 40% of non-O157:H7 STEC isolates carried IncB/O plasmids. Plasmids for IncB/O, IncFIC, IncP and IncFIA were detected in 8 to 16% of O157:H7 STEC isolates, while IncP, IncK/B, IncI1 and HI2 plasmids were identified in 3 to 7% in non-O157:H7 STEC isolates. Interestingly, only one clinical isolate, EC O111, carried IncX, IncN and IncL/M plasmids.
Significance: STECs harboring plasmids have a greater propensity to cause infections and spread diseases in humans because of the ability these plasmids to encode for multiple virulence, antimicrobial resistance and transfer-associated genes.