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Background: Buruli ulcer, caused by Mycobacterium ulcerans, is a debilitating skin disease prevalent in tropical regions. Secondary bacterial infections may complicate this condition, necessitating comprehensive bacteriological investigations to inform effective treatment. This study aimed to determine the presence and prevalence of Pseudomonas spp., Klebsiella spp., and Escherichia spp. in wound samples from Buruli ulcer patients and evaluate their impact on clinical outcomes.
Methods: A total of 177 samples were collected from patients with Buruli ulcer lesions. Bacterial identification and antimicrobial susceptibility testing were performed using the bioMérieux® VITEK-2 Compact system, while Extended-Spectrum Beta-Lactamase (ESBL) genes were detected with an optimized real-time PCR assay.
Results: Out of 177 isolates, 48 (27%) were Gram-positive and 128 (73%) were Gram-negative. Among the Gram-negative isolates identified, Pseudomonas spp. constituted the largest proportion (24, 19%), followed by Klebsiella spp. (16, 13%) and Escherichia spp. (11, 9%). The predominant bacterial species identified were Escherichia coli (9, 81%), Klebsiella pneumoniae ssp. pneumoniae (9,56%) and Pseudomonas aeruginosa (19,79%) were found among Escherichia spp., Klebsiella spp., and Pseudomonas spp., respectively. Lesions with higher bacterial diversity and load were linked to delayed healing (p=0.001) and both K. pneumoniae ssp. pneumoniae and P.aeruginosa persisted in lesions during treatment.
A significant antimicrobial resistance profile was seen in E. coli against commonly used antibiotics such as Tetracycline (6/8, 75%), Ampicillin/Sulbactam (4/8, 50%), Ciprofloxacin (3/8, 38%), Cefotaxime (3/8, 38%), and Cefpodoxime (3/8, 38%). For K. pneumoniae ssp. pneumoniae, resistance to Tetracycline (3/8, 38%) and Ampicillin (9/9, 100%) was observed. Additionally, ESBL genes (bla_CTX-M and bla_TEM) were found in both E. coli and K. pneumoniae ssp., emphasizing the clinical importance of these multidrug-resistant pathogens in Buruli ulcer infections. Low resistance was observed in Pseudomonas aeruginosa to Piperacillin/Tazobactam (2/13, 15%), Ceftazidime (2/17, 12%), and Ciprofloxacin (3/17, 18%).
Conclusion: This study reveals the presence and resistance patterns of Pseudomonas spp., Klebsiella spp., and Escherichia spp. in Buruli ulcer patients. These findings emphasize the need to integrate effective strategies for managing secondary bacterial infections into Buruli ulcer treatment protocols to improve patient outcomes.