Spectrum of bacterial pathogens in inflammatory and noninflammatory cutaneous ulcers of American tegumentary leishmaniasis

Author:

Kariyawasam Ruwandi12,Gascon Bryan3,Challa Priyanka4,Mah Jordan5,Lau Rachel6,Valencia Braulio M.78,Llanos-Cuentas Alejandro7,Boggild Andrea K.91011ORCID

Affiliation:

1. Public Health Laboratory, Alberta Precision Laboratories, Edmonton, AB, Canada

2. Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada

3. Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada

4. Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, ON, Canada

5. School of Medicine, Duke University, Durham, NC, USA

6. Public Health Ontario Laboratories, Public Health Ontario, Toronto, ON, Canada

7. Instituto de Medicina Tropical “Alexander von Humboldt”, Universidad Peruana Cayetano Heredia, Unidad de Leishmaniasis y Malaria, Lima, Peru

8. Kirby Institute, University of New South Wales, Sydney, NSW, Australia

9. Temerty Faculty of Medicine, University of Toronto, ON, Canada

10. Tropical Disease Unit, Toronto General Hospital, 200 Elizabeth Street, 13EN-218, Toronto, ON M5G 2C4, Canada

11. Department of Medicine, University of Toronto, Toronto, ON, Canada

Abstract

Background: Cutaneous leishmaniasis (CL) ulcers exhibiting an inflammatory phenotype, characterized by purulent exudate, erythema, pain, and/or lymphatic involvement, are empirically treated with antibiotics. Objective: The spectrum of bacteria present in localized versus inflammatory phenotypes of CL is elucidated herein. Methods: Filter paper lesion impressions (FPLIs) from 39 patients with CL (19 inflammatory and 20 noninflammatory ulcers) were evaluated via real-time polymerase chain reaction (qPCR) and end-point PCR targeting: Staphylococcus aureus, Enterobacter cloacae, Streptococcus pyogenes, Enterococcus spp., Citrobacter freundii, Escherichia coli, Pseudomonas aeruginosa, Klebsiella pneumoniae, and 16S rDNA. Whole genome sequencing (WGS) was performed on six specimens. Results: In total, 30/39 (77%) patients’ ulcers had ⩾1 bacterium detected, which included the following species: S. aureus ( n = 16, 41%), C. freundii ( n = 13, 33%), P. aeruginosa ( n = 12, 31%), E. cloacae ( n = 12, 31%), K. pneumoniae ( n = 11, 28%), Enterococcus spp. ( n = 7, 18%), E. coli ( n = 6, 15%), and S. pyogenes ( n = 4, 10). Prevalence of bacterial species did not differ by CL phenotype ( p = 0.63). However, patients with inflammatory phenotypes were, on average, over a decade older than patients with noninflammatory phenotypes (42 years vs 27 years) ( p = 0.01). The inflammatory phenotype was more prevalent among ulcers of Leishmania Viannia braziliensis (58%) and L. V. panamensis (83%) compared to those of L. V. guyanensis (20%) ( p = 0.0369). Conclusion: The distribution of flora did not differ between inflammatory and noninflammatory CL phenotypes. Further prospective analysis, including additional WGS studies of all CL ulcers for nonbacterial organisms, is necessary to determine the role of empiric antibiotic therapy in inflammatory and purulent CL.

Funder

University Health Network

Public Health Ontario

Temerty Faculty of Medicine, University of Toronto

Publisher

SAGE Publications

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