Prevalence and Characteristics of Plasmid-Encoded Serine Protease EspP in Clinical Shiga Toxin-Producing Escherichia coli Strains from Patients in Sweden

Author:

Wang Lei12,Hua Ying1,Bai Xiangning34,Zhang Ji5,Mernelius Sara6ORCID,Chromek Milan7ORCID,Frykman Anne89,Hansson Sverker89ORCID,Matussek Andreas1346

Affiliation:

1. Department of Microbiology, Division of Laboratory Medicine, Institute of Clinical Medicine, University of Oslo, 0372 Oslo, Norway

2. Jinan Center for Disease Control and Prevention, Jinan 250021, China

3. Department of Microbiology, Division of Laboratory Medicine, Oslo University Hospital, 0372 Oslo, Norway

4. Department of Clinical Microbiology, Division of Laboratory Medicine, Karolinska Institutet, 141 52 Stockholm, Sweden

5. Fonterra Research and Development Centre, Dairy Farm Road, Palmerston North 4442, New Zealand

6. Laboratory Medicine, Department of Clinical and Experimental Medicine, Linköping University, Jönköping Region County, SE-581 83 Linköping, Sweden

7. Division of Pediatrics, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Karolinska University Hospital, 141 52 Stockholm, Sweden

8. Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, 40530 Gothenburg, Sweden

9. Queen Silvia Children’s Hospital, Sahlgrenska University Hospital, 416 50 Gothenburg, Sweden

Abstract

Shiga toxin-producing Escherichia coli (STEC) infection can cause a broad spectrum of symptoms spanning from asymptomatic shedding to mild and bloody diarrhea (BD) and even life-threatening hemolytic-uremic syndrome (HUS). As a member of the serine protease autotransporters of Enterobacteriaceae (SPATE) family, EspP has the ability to degrade human coagulation factor V, leading to mucosal bleeding, and also plays a role in bacteria adhesion to the surface of host cells. Here, we investigated the prevalence and genetic diversity of espP among clinical STEC isolates from patients with mild diarrhea, BD, and HUS, as well as from asymptomatic individuals, and assessed the presence of espP and its subtypes in correlation to disease severity. We found that 130 out of 239 (54.4%) clinical STEC strains were espP positive, and the presence of espP was significantly associated with BD, HUS, and O157:H7 serotype. Eighteen unique espP genotypes (GTs) were identified and categorized into four espP subtypes, i.e., espPα (119, 91.5%), espPγ (5, 3.8%), espPδ (4, 3.1%), and espPε (2, 1.5%). espPα was widely distributed, especially in strains from patients with BD and HUS, and correlated with serotype O157:H7. Serogroup O26, O145, O121, and O103 strains carried espPα only. Ten GTs were identified in espPα, and espPα/GT2 was significantly associated with severe disease, i.e., BD and HUS. Additionally, espP was strongly linked to the presence of eae gene, and the coexistence of espPα and stx2/stx2a + stx2c was closely related to HUS status. To sum up, our data demonstrated a high prevalence and genetic diversity of the espP gene in clinical STEC strains in Sweden and revealed an association between the presence of espP, espP subtypes, and disease severity. espP, particularly the espPα subtype, was prone to be present in more virulent STEC strains, e.g., “top-six” serotypes strains.

Publisher

MDPI AG

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