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Predicting the post-storage quality of cherry fruits is crucial for determining their suitability for long-distance shipping or domestic distribution. This study aimed to forecast key quality attributes of Staccato sweet cherries after storage, simulating shipping conditions, by analyzing spring soil, leaf, fruitlet, and at-harvest data from thirty orchards in the Okanagan Valley, British Columbia, Canada, over two years. A support vector machine (SVM) was used to predict post-storage variables, with pre-harvest and at-harvest data selected by a genetic algorithm. The SVM accurately predicted soluble solids (R2 = 0.88), firmness (R2 = 0.83), and acidity (R2 = 0.79) after four weeks of storage, as well as visual disorders like slip skin and stem browning. Spring soil properties (Ca, Mg), leaf (N, Ca, Mg, Fe, Zn, B), and fruitlet data (N, Ca, Mg, B) were key predictors. Leaf Ca was vital for firmness and total soluble solids (TSS) prediction, while N in leaves and fruitlets influenced firmness, acidity, and disorders. Leaf Zn helped predict weight and acidity/TSS ratio, and Mg impacted fruit color. Pre-harvest leaf nutrition measured 3–4 weeks before harvest, proved most effective in predicting post-storage quality. [ABSTRACT FROM AUTHOR]

Antibiotic resistance (AR) phenotypes and acquired resistance determinants (ARDs) detected by in silico analysis of genome sequences were examined in 55 Shiga toxin-producing Escherichia coli (STEC) isolates representing diverse serotypes recovered from surfaces waters and sediments in a mixed use urban/agricultural landscape in British Columbia, Canada. The isolates displayed decreased susceptibility to florfenicol (65.5%), chloramphenicol (7.3%), tetracycline (52.7%), ampicillin (49.1%), streptomycin (34.5%), kanamycin (20.0%), gentamycin (10.9%), amikacin (1.8%), amoxicillin/clavulanic acid (21.8%), ceftiofur (18.2%), ceftriaxone (3.6%), trimethoprim-sulfamethoxazole (12.7%), and cefoxitin (3.6%). All surface water and sediment isolates were susceptible to ciprofloxacin, nalidixic acid, ertapenem, imipenem and meropenem. Eight isolates (14.6%) were multidrug resistant. ARDs conferring resistance to phenicols (floR), trimethoprim (dfrA), sulfonamides (sul1/2), tetracyclines (tetA/B), and aminoglycosides (aadA and aph) were detected. Additionally, narrow-spectrum β-lactamase blaTEM-1b and extended-spectrum AmpC β-lactamase (cephalosporinase) blaCMY-2 were detected in the genomes, as were replicons from plasmid incompatibility groups IncFII, IncB/O/K/Z, IncQ1, IncX1, IncY and Col156. A comparison with surveillance data revealed that AR phenotypes and ARDs were comparable to those reported in generic E. coli from food animals. Aquatic environments in the region are potential reservoirs for the maintenance and transmission of antibiotic resistant STEC, associated ARDs and their plasmids. [ABSTRACT FROM AUTHOR]

Bacteriophages have shown promise as therapeutic alternatives to antibiotics for the control of infectious bacteria, including the human pathogen Salmonella. However, the development of effective phage-based applications requires the elucidation of key interactions between phages and target hosts, particularly since host resistance to phage is inevitable. Little is known about the alteration of host phenotypes following the development of resistance to phage. The aim of this study is to evaluate the antibiotic susceptibility and virulence of a Salmonella isolate following the development of resistance to bacteriophage SI1. We observed enhanced susceptibility to tetracycline and decreased invasion capacity in a differentiated Caco-2 intestinal cell line. Whole genome sequence analysis revealed an array of mutations, most notably, truncations in vgrG1_2, a core gene involved in Type VI secretion and mutations in the lipopolysaccharide, thereby indicating the plausible attachment site of phage SI1. These findings shed light on understanding the underlying mechanism for phage immunity within the host. Importantly, we reveal an associated genetic cost to the bacterial host with developing resistance to phages. Taken together, these results will aid in advancing strategies to delay or eliminate the development of host resistance when designing informed phage-based antimicrobials. [ABSTRACT FROM AUTHOR]