Antimicrobial resistance (AMR) is one of the most important global public health problems. The imprudent use of antibiotics in humans and animals has resulted in the emergence of antibiotic-resistant bacteria. The dissemination of these strains and their resistant determinants could endanger antibiotic efficacy. Therefore, there is an urgent need to identify and develop novel strategies to combat antibiotic resistance. This review provides insights into the evolution and the mechanisms of AMR. Additionally, it discusses alternative approaches that might be used to control AMR, including probiotics, prebiotics, antimicrobial peptides, small molecules, organic acids, essential oils, bacteriophage, fecal transplants, and nanoparticles.

Avian hosts constitute a natural reservoir for thermophilic Campylobacter species, primarily Campylobacter jejuni and Campylobacter coli, and poultry flocks are frequently colonized in the intestinal tract with high numbers of the organisms. Prevalence rates in poultry, especially in slaughter-age broiler flocks, could reach as high as 100% on some farms. Despite the extensive colonization, Campylobacter is essentially a commensal in birds, although limited evidence has implicated the organism as a poultry pathogen. Although Campylobacter is insignificant for poultry health, it is a leading cause of food-borne gastroenteritis in humans worldwide, and contaminated poultry meat is recognized as the main source for human exposure. Therefore, considerable research efforts have been devoted to the development of interventions to diminish Campylobacter contamination in poultry, with the intention to reduce the burden of food-borne illnesses. During the past decade, significant advance has been made in understanding Campylobacter in poultry. This review summarizes the current knowledge with an emphasis on ecology, antibiotic resistance, and potential pre- and postharvest interventions.

Campylobacter species are commonly transmitted to humans through consumption of contaminated foods such as milk and meat. The aim of this study was to investigate the prevalence, antimicrobial resistance, and genetic determinants of resistance of Campylobacter isolated from raw milk and beef carcasses in Tanzania. The antimicrobial resistance genes tested included bla_OXA-61 (ampicillin), aph-3-1 (aminoglycoside), tet(O) (tetracycline), and cmeB (multi-drug efflux pump). The prevalence of Campylobacter was 9.5% in beef carcasses and 13.4% in raw milk, respectively. Using multiplex-polymerase chain reaction (PCR), we identified 58.1% of the isolates as Campylobacter jejuni, 30.7% as Campylobacter coli, and 9.7% as other Campylobacter spp. One isolate (1.6%) was positive for both C. jejuni and C. coli specific PCR. Antimicrobial susceptibility testing using the disk diffusion assay and the broth microdilution method showed resistance to: ampicillin (63% and 94.1%), ciprofloxacin (9.3% and 11.8%), erythromycin (53.7% and 70.6%), gentamicin (0% and 15.7%), streptomycin (35.2% and 84.3%), and tetracycline (18.5% and 17.7%), respectively. Resistance to azithromycin (42.6%), nalidixic acid (64.8%), and chloramphenicol (13%) was determined using the disk diffusion assay only, while resistance to tylosin (90.2%) was quantified using the broth microdilution method. The bla_OXA-61 (52.6% and 28.1%), cmeB (26.3% and 31.3%), tet(O) (26.3% and 31.3%), and aph-3-1 (5.3% and 3.0%) were detected in C. coli and C. jejuni. These findings highlight the extent of antimicrobial resistance in Campylobacter occurring in important foods in Tanzania. The potential risks to consumers emphasize the need for adequate control approaches, including the prudent use of antimicrobials to minimize the spread of antimicrobial-resistant Campylobacter.

The use of contaminated water has been associated with severe disease outbreaks. Due to widespread pollution with untreated sewage, concerns have been raised over water quality in Lebanon, a country with well-documented challenges in infrastructure. Here, we evaluated the water quality of major rivers in Lebanon by quantifying the densities of fecal indicator bacteria (fecal coliforms and Escherichia coli). Additionally, we assessed the dissemination of antibiotic-resistant E. coli in river water. Composite water samples (n = 132) were collected from fourteen rivers, and 378 E. coli were isolated and analyzed. Fecal coliforms and E. coli were detected in 96.29% and 95.5% of the samples, respectively. Additionally, 73.48–61.3% and 31.81% of the samples exceeded the microbiological acceptability standards for irrigation and the fecal coliform limit for recreational activities, respectively. The E. coli exhibited resistance to ampicillin (40% of isolates), amoxicillin + clavulanic acid (42%), cefepime (4%), cefotaxime (14%), cefalexin (46%), cefixime (17%), doripenem (0.3%), imipenem (0.5%), gentamicin (6%), kanamycin (9%), streptomycin (35%), tetracycline (35%), ciprofloxacin (10%), norfloxacin (7%), trimethoprim-sulfamethoxazole (32%), and chloramphenicol (13%). Notably, 45.8% of the isolates were classified as multidrug resistant (MDR). Our results highlight the need to urgently address fecal pollution and the dissemination of antibiotic resistance in Lebanese rivers.

Campylobacter jejuni , a gram-negative, microaerophilic bacterium, is a predominant cause of bacterial gastroenteritis in humans. Although considered fragile and fastidious and lacking many classical stress response mechanisms, C . jejuni exhibits a remarkable capacity for survival and adaptation, successfully infecting humans and persisting in the environment. Consequently, understanding the physiological and genetic properties that allow C . jejuni to survive and adapt to various stress conditions is crucial for therapeutic interventions. Of importance is polyphosphate (poly-P) kinase 1 (PPK1), which is a key enzyme mediating the synthesis of poly-P, an essential molecule for survival, mediating stress responses, host colonization, and virulence in many bacteria. Therefore, we investigated the role of PPK1 in C . jejuni pathogenesis, stress survival, and adaptation. Our findings demonstrate that a C . jejuni Δ ppk1 mutant was deficient in poly-P accumulation, which was associated with a decreased ability to form viable-but-nonculturable cells under acid stress. The Δ ppk1 mutant also showed a decreased frequency of natural transformation and an increased susceptibility to various antimicrobials. Furthermore, the Δ ppk1 mutant was characterized by a dose-dependent deficiency in chicken colonization. Complementation of the Δ ppk 1 mutant with the wild-type copy of ppk1 restored the deficient phenotypes to levels similar to those of the wild type. Our results suggest that poly-P plays an important role in stress survival and adaptation and might contribute to genome plasticity and the spread and development of antimicrobial resistance in C . jejuni . These findings highlight the potential of PPK1 as a novel target for therapeutic interventions.