, a highly infectious and rapidly spreading new pneumonia of unknown cause was reported to the Chinese WHO Country Office. A cluster of these cases had appeared in Wuhan, a city in the Hubei Province of China. These infections were found to be caused by a new coronavirus which was given the name "2019 novel coronavirus" (2019-nCoV). It was later renamed "severe acute respiratory syndrome coronavirus 2," or SARS-CoV-2 by the International Committee on Taxonomy of Viruses on February 11, 2020. It was named SARS-CoV-2 due to its close genetic similarity to the coronavirus which caused the SARS outbreak in 2002 (SARS-CoV-1). The aim of this review is to provide information, primarily to the food industry, regarding a range of biocides effective in eliminating or reducing the presence of coronaviruses from fomites, skin, oral/nasal mucosa, air, and food contact surfaces. As several EPA approved sanitizers against SARS-CoV-2 are commonly used by food processors, these compounds are primarily discussed as much of the industry already has them on site and is familiar with their application and use. Specifically, we focused on the effects of alcohols, povidone iodine, quaternary ammonium compounds, hydrogen peroxide, sodium hypochlorite (NaOCl), peroxyacetic acid (PAA), chlorine dioxide, ozone, ultraviolet light, metals, and plant-based antimicrobials. This review highlights the differences in the resistance or susceptibility of different strains of coronaviruses, or similar viruses, to these antimicrobial agents.

Salmonella enterica subsp. enterica can colonize tomato fruit as it interacts with fruit surface compounds. The exometabolome of tomato fruit contains a mixture of compounds, including fatty acids, which could affect Salmonella fitness. Fatty acids detected in fruit exudates were investigated for Salmonella inhibition. Pelargonic, lauric, myristic, palmitic, margaric, stearic, and oleic acids were suspended in water dissolved in dimethyl sulfoxide (DMSO) or emulsified in water and quillaja saponin to assess how bioavailability impacted Salmonella growth. The minimum inhibitory concentrations of fatty acids were determined using a resazurin assay. Quillaja saponin emulsion and DMSO solution of pelargonic acid were inhibitory to Salmonella at 31.25 mM. Lauric and myristic acid emulsions inhibited growth at 1 M concentrations in quillaja emulsions and 62.5 mM in DMSO. Lauric and myristic acids significantly affected growth of Salmonella Newport, Javiana, and Typhimurium (p ≤ 0.05). Growth curve analysis using the Baranyi model revealed reduced maxima populations for all treatments (p ≤ 0.001) and shorter lag phase durations for Salmonella Newport with lauric acid (p < 0.01) and Salmonella Javiana with lauric (p < 0.001) and myristic (p < 0.001) acids. Salmonella Newport and Javiana exhibited an accelerated growth rate with lauric acid (p < 0.001) as a result of early stationary phase transition (shorter log phase). In myristic acid-amended media, Salmonella Javiana also displayed a faster growth rate (p < 0.001). Pelargonic acid (31.25 mM) treatment of Salmonella cells resulted in a drop in culturable cells to below detection in an hour. Microscopic analysis with Cyto-dye and propidium iodide of bacterial cells treated with pelargonic acid indicated a mixture of live and dead cells, with cell lysis of some cells. A subset of cells exhibited elongation-possibly indicating filament formation, a known antibiotic stress response. The results suggest that fatty acids present in tomato fruit surface exudates may exert a restrictive effect on Salmonella growth on fruit.

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Under stressful conditions,Salmonella entericaforms multinucleated elongated filaments. The triggers and outcomes of filamentation are not well characterized.S. entericaserotypes Newport, Javiana, and Typhimurium were evaluated for their ability to form filaments upon exposure to 20 mM pelargonic acid.S.Newport was used as a model to investigate the progression and fate of filamentation via culturable population size, cell length, and viability assays. All serotypes displayed filament formation after 16 h of incubation. Pelargonic acid amendment of tryptic soy broth (TSBpel) produced a 5-log CFU reduction compared to TSB after 24 h (P < 0.05), and the growth rate decreased (P < 0.02). Cell elongation started within 12 h, peaked at 16 h, and was followed by filament disintegration at 20 to 24 h. The ratio of filaments to regular-sized cells (F/R) in TSBpel was 3.87 ± 0.59 at 16 h, decreasing to 0.23 ± 0.04 and 0.03 ± 0.01 (P < 0.05) at 20 and 24 h, respectively. Mg2+supplementation repressed filamentation (F/R = 0.25 ± 0.11) and enhanced culturable cell counts (P < 0.05). Continued exposure to pelargonic acid inhibited growth in TSB and M9 compared to that in unamended media (P < 0.05). However, in M9 medium without Mg2+amended with 20 mM pelargonic acid (M9pel), filament fragmentation progressed independently of pelargonic acid or Mg2+. When cells were pretreated with pelargonic acid to induce filamentation and then transferred to fresh medium, a positive effect of Mg2+was noted under nutrient-deficient conditions, with higher live/dead cell ratios in M9 supplemented with 5 mM Mg2+(M9Mg) than in M9 (P < 0.05). No change was observed when pelargonic acid was also added. Filamentation was ubiquitous in all serotypes tested, transient, and sensitive to Mg2+. Fragmentation, but not recovery, progressed irrespective of antimicrobial or Mg2+presence.IMPORTANCESome bacteria form elongated multinucleated structures, or filaments, when exposed to stress. The filamentous form of foodborne bacterial pathogens can interfere with food protection practices and diagnostic testing. Filamentation inSalmonella entericaNewport was investigated in response to pelargonic acid, a compound naturally found in several fruit and vegetables, and also used commercially as an herbicide.Salmonellareadily formed filaments when exposed to pelargonic acid. Filaments were not stable, however, and fragmented to individual cells even when the fatty acid was still present, recovering fully when the stress was alleviated. A deeper exploration of the molecular mechanisms regulating filamentation and the conditions that induce it in agriculture and the food supply chain is needed to devise strategies that curb this response.

The efficacy of ozone and ultraviolet light (UV) treatment as hurdles against Listeria monocytogenes suspended in fresh (9% NaCl, 91.86% transmittance) and spent brines (20.5% NaCl, 0.01% transmittance) was evaluated. Brines were inoculated with a cocktail of L. monocytogenes-strains N1-227, N3-031, and R2-499. Ozonation was performed by sparging gaseous ozone into brine. This was followed by UV irradiation (253.7 nm) of the brine in sterile quartz cuvettes. Enumeration was performed by spread plating on modified Oxford medium and Trypticase Soy agar supplemented with yeast extract. In fresh brines containing L. monocytogenes, ten minutes of ozonation lead to a 7.44±0.13 log CFU/ml mean reduction and 10 minutes of UV radiation caused a 1.95±0.41 log CFU/ml mean reduction. Ten minutes of ozonation and UV exposure in combination resulted in > 9 log CFU/ml reduction in L. monocytogenes populations in fresh brine. Sixty minutes of ozonation of spent brines resulted in a 4.85±0.61 log CFU/ml mean reduction of L. monocytogenes populations. Ten minutes of UV exposure in spent brines resulted in 0.49±0.14 log CFU/ml mean reduction in L. monocytogenes. A combination of 60 minutes ozonation and 10 minute UV exposure resulted in an excess of 5 log CFU/ml reduction in L. monocytogenes cells in spent brine. Ozonation did not cause a significant increase in the transmittance of the spent brine to aid UV penetration but resulted in color change. Ozonation in combination with UV treatment may serve as an effective treatment in reducing L. monocytogenes in chill brines.

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The presence of dust is ubiquitous in the produce growing environment and its deposition on edible crops could occur. The potential of wind-distributed soil particulate to serve as a vehicle for S. Newport transfer to tomato blossoms and consequently, to fruits, was explored. Blossoms were challenged with previously autoclaved soil containing S. Newport (9.39log CFU/g) by brushing and airborne transfer. One hundred percent of blossoms brushed with S. Newport-contaminated soil tested positive for presence of the pathogen one week after contact (P<0.0001). Compressed air was used to simulate wind currents and direct soil particulates towards blossoms. Airborne soil particulates resulted in contamination of 29% of the blossoms with S. Newport one week after contact. Biophotonic imaging of blossoms post-contact with bioluminescent S. Newport-contaminated airborne soil particulates revealed transfer of the pathogen on petal, stamen and pedicel structures. Both fruits and calyxes that developed from blossoms contaminated with airborne soil particulates were positive for presence of S. Newport in both fruit (66.6%) and calyx (77.7%). Presence of S. Newport in surface-sterilized fruit and calyx tissue tested indicated internalization of the pathogen. These results show that airborne soil particulates could serve as a vehicle for Salmonella. Hence, Salmonella contaminated dust and soil particulate dispersion could contribute to pathogen contamination of fruit, indicating an omnipresent yet relatively unexplored contamination route.