Background/Objectives: Colistin has re-emerged as a critical last-resort antimicrobial for treating infections caused by multidrug-resistant Gram-negative bacteria. The discovery of plasmid-mediated mobile colistin resistance (mcr) genes in 2015 fundamentally changed the understanding of colistin resistance by demonstrating its capacity for horizontal transfer across bacterial species, hosts, and environments. Since then, increasing evidence has documented the widespread occurrence of mcr genes across Africa, threatening the long-term effectiveness of colistin. Earlier reviews have largely addressed single sectors or regions; here, we integrate all sectors, distinguish direct detection from inferred transmission, and propose prioritised actions. Methods: This narrative review synthesises current evidence on mobile colistin resistance in Africa through a One Health lens, integrating findings from human, animal, food, wildlife, and environmental sectors. Results: We provide a comprehensive overview of the molecular mechanisms, epidemiology, transmission pathways, and drivers of mcr dissemination across the continent. Available evidence indicates that mcr genes, particularly mcr-1, are distributed among clinical isolates, livestock, retail food products, wastewater, surface waters, agricultural soils, and wild birds, which is consistent with connected transmission across sectors. Key drivers include inappropriate antimicrobial use, livestock intensification, inadequate wastewater treatment, environmental contamination, climate change, and human and animal mobility. Conclusions: The frequent association of mcr genes with mobile genetic elements and other antimicrobial resistance determinants facilitates their persistence through horizontal gene transfer and co-selection. Despite increasing recognition of this threat, major gaps remain in surveillance, genomic characterisation, environmental monitoring, and understanding of transmission dynamics. Addressing these challenges will require stronger One Health surveillance, antimicrobial stewardship, genomic monitoring, improved environmental management, and coordinated policy interventions to mitigate the spread of mobile colistin resistance and preserve the clinical utility of colistin across Africa.
Staphylococcus aureus infections, including methicillin-resistant S. aureus (MRSA), inflict considerable economic burdens upon the dairy industry through bovine subclinical mastitis. Here, S. aureus isolates were recovered from milk, cow dung, and teat swabs of dairy cows (n = 68) on three commercial farms in the Free State Province, South Africa, and screened for antibiotic resistance determinants and virulence-associated genes. Out of 204 samples collected (68 milk samples, 68 teat swabs, and 68 cow dung samples), S. aureus isolates were recovered from 50/68 (73.5%) milk samples, 42/68 (61.7%) teat swab samples, and 15/68 (22.0%) cow dung samples. The mecA-targeted PCR screening identified genotypic MRSA in 14.0% (7/50) milk, 11.9% (5/42) teat swabs, and 40.0% (6/15) cow dung isolates. Screening for aminoglycoside resistance genes identified a high prevalence of strB among all isolates, often concomitant with strA, aadA, and aac(6′)-Ib. Successful amplification of virulence determinants (spa, coa, hla, hlb) identified the highest allelic diversity among milk isolates. Phenotypic–genotypic discrepancy was observed with regard to cefoxitin, where, despite all isolates carrying mecA, only 14.3% (1/7) milk, 50.0% (3/6) cow dung, and 0.0% (0/5) teat swab isolates were phenotypically resistant, while the remaining isolates were either intermediate or susceptible. Low resistance was detected toward streptomycin, tobramycin, gentamicin, and amoxicillin/ac. clavulanique. The co-occurrence of these antimicrobial resistance and virulence determinants represents possible risk trajectories that are important for both human health and dairy herd health. These findings indicate the need for farm-specific hygiene practices, enhanced mastitis prevention, and continued molecular epidemiologic surveillance to elucidate staphylococcal ecology within the “One Health” paradigm.
Syphilis is a systemic sexually transmitted infection caused by Treponema pallidum subsp. pallidum. Despite effective penicillin-based therapy, it remains a major public health challenge due to ongoing transmission, latent infection, congenital disease, and the lack of a licensed vaccine. While the resurgence of bacteriophage research has stimulated interest in alternative antimicrobials for sexually transmitted infections, direct extrapolation of classical lytic phage therapy to T. pallidum is premature. This pathogen is experimentally demanding, grows slowly, lacks validated lytic phages, and possesses an unusual outer membrane with sparse surface-exposed targets. However, comparative genomics has identified prophage-like elements in several Treponema species, while the T. pallidum-lineage genomes examined by Ridgway et al. did not contain detectable prophage regions. This shifts the rationale from endogenous T. pallidum prophage exploitation toward cautious evaluation of heterologous treponemal phage-derived modules, with cross-species target compatibility as a central requirement. This review critically evaluates phage-derived strategies against T. pallidum, discussing biological barriers, prophage genomics, candidate modalities, biosafety filters, and regulatory considerations. We propose a staged translational roadmap progressing from evidence appraisal and candidate prioritization to biochemical validation, direct T. pallidum testing, ex vivo assessment, in vivo validation, and product-class-specific development. Currently, the most credible outputs of this field are research tools, diagnostic binding modules, and early antimicrobial prototypes rather than clinical phage therapy for syphilis.
Background/Objectives: Clinical trials have shown that piperacillin–tazobactam prophylaxis is beneficial in pancreatoduodenectomy, especially after preoperative biliary drainage, yet patient-level microbiological data are scarce. We compared the observed coverage of intraoperative bile isolates by our institutional standard for stented patients, ampicillin–sulbactam, with the coverage that the guideline-endorsed piperacillin–tazobactam would have provided, as estimated by simulation. Methods: Retrospective study of consecutive elective PD patients from 2015 to 2023. Microbiological complete coverage denoted susceptibility of all bile isolates. For stented patients receiving ampicillin–sulbactam, we simulated piperacillin–tazobactam susceptibility sequentially until complete coverage was achieved. Non-stented patients were studied separately. Pathogen persistence, postoperative outcome parameters and antibiotic escalation were evaluated. Results: Of 363 patients, 177 underwent preoperative biliary stenting, of whom 160 received ampicillin–sulbactam. Coverage was complete in 63 (39.4%), incomplete coverage in 97 (60.6%). Among the latter, simulated piperacillin–tazobactam coverage was complete in 65 (67.0%). Assuming a translation of initial ampicillin–sulbactam coverage to piperacillin–tazobactam, an upper limit for coverage of 128/160 (80.0%) was reached. In exploratory clinical outcome analyses, incomplete ampicillin–sulbactam coverage was associated with more abdominal wound infections (25.8% versus 11.1%, p = 0.027). CR-POPF (17.5% vs. 13.4%, p = 0.325) or the rate of intra-abdominal abscesses (20.6% vs. 16.5%, p = 0.534) were not statistically different. With simulated piperacillin–tazobactam coverage wound infection rates did not any more differ significantly (23.1% vs. 31.3%, p = 0.461). CR-POPF and intraabdominal abscesses remained statistically indifferent. Ampicillin–sulbactam was escalated for infectious complications in 44/97 patients (45.4%), mainly to piperacillin–tazobactam or ciprofloxacin. Conclusions: Simulated piperacillin–tazobactam offered broader microbiological coverage than ampicillin–sulbactam. Although this benefit was limited to wound infections, these patient-level findings support both our long-standing practice of escalated prophylaxis in stented patients and adherence to the updated guideline recommendations.
Background/Objectives: Evidence on the association between antibiotic appropriateness and clinical outcomes in urinary tract infection (UTI) remains inconsistent. We comprehensively evaluated the appropriateness of antibiotic therapy throughout the treatment course in patients with UTI and examined its association with clinical outcomes. Methods: Hospitalized patients with UTI at a Korean university-affiliated hospital were retrospectively reviewed. Appropriateness was assessed for antibiotic selection, dosage, route, and duration; patients in whom any component could not be assessed, including those who died within 3 days of antibiotic initiation, were excluded. Outcomes in complicated UTI were compared using inverse probability of treatment weighting (IPTW). Results: Of 629 patients, 94 had uncomplicated and 535 had complicated UTI. Overall appropriate therapy was more frequent in complicated UTI (77.2% vs. 27.7%). In-hospital mortality was 3.6% with appropriate and 4.1% with inappropriate therapy, and appropriate therapy was not associated with mortality after IPTW adjustment (adjusted odds ratio 1.31, 95% CI 0.43–4.01); length of stay, parenteral therapy duration, and antibiotic days of therapy did not differ. Conclusions: Comprehensively assessed appropriateness was not significantly associated with mortality or resource utilization in complicated UTI; however, the estimates were imprecise and compatible with both benefit and harm, and this finding should be regarded as exploratory. The administration route in uncomplicated UTI and treatment duration in both groups are stewardship targets, and the handling of unassessable cases can alter observed associations.
