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Pulsed light (PL) treatment can effectively inactivate a large proportion of contaminating bacteria on surfaces and in clear solutions. An important issue that needs to be investigated is whether repeated exposure to PL treatment causes any changes to the growth and resistance behavior of the bacteria surviving the treatment. To test this, three challenge microorganisms were used: Listeria monocytogenes, Listeria innocua, and Escherichia coli. Cells of the challenge bacteria were treated with either low or high PL doses. Survivors of the PL treatment were enumerated, isolated, regrown, and exposed again to PL treatment. PL inactivation curves were generated for the survivors of each exposure cycle (as well as controls) to examine possible differences induced by repeated treatments. Growth curves of L. monocytogenes, L. innocua, and E. coliisolates recovered from exposure to either 1.1 or 10.1 J/cm2were not significantly different from the growth curves of untreated cells. Reduction levels of up to 4 and up to 6 log CFU were obtained after exposure to 1.1 and 10.1 J/cm2, respectively, both for the controls and the repeatedly treated and recovered isolates. These results show that PL did not significantly change the growth kinetics or resistance to PL of the target microorganisms after up to 10 exposures. These findings have significance for the practical application of PL treatment, as they indicate that this technology does not select for microorganisms with increased resistance.

The main objective of this work was to evaluate the effectiveness of pulsed light (PL) treatment for the inactivation of Escherichia coliin liquids with different levels of clarity. Nonpathogenic E. coliATCC 25922 and pathogenic E. coliO157: H7 were used as challenge organisms. Butterfield's phosphate buffer (BPB), tryptic soy broth (TSB), apple juice, and apple cider were used as substrates. The inoculated liquids were placed in a thin layer (1.3 mm) into glass chambers (23 by 53 by 11 mm) and exposed to PL doses of up to 13.1 J/cm2. PL treatments were performed in a Xenon RS-3000C PL unit, both in static mode and under turbulence. Survivors were determined by standard plate counting or the most-probable-number technique. For static treatments, reduction levels exceeding 8.5 log were obtained in BPB for all strains and reduction levels of about 3.5 log were obtained in TSB. For apple juice, inactivation levels of 2.66±0.10 log were obtained for E. coliATCC 25922 and 2.52±0.19 log for E. coliO157:H7. In cider, inactivation levels of 2.32±0.16 log and 3.22±0.29 log were obtained for the nonpathogenic and pathogenic strains, respectively. Inactivation kinetics was characterized using the Weibull model. Turbulent treatments resulted in 5.76±0.06 log reduction in cider and 7.15±0.22 log reduction in juice, which satisfies the U.S. Food and Drug Administration requirement of 5-log reduction of E. coli. These results show promise for the use of PL for the effective reduction of E. coliin apple juice and cider.

The risk of listeriosis associated with ready-to-eat foods is a major concern in the United States. Pulsed light (PL) treatment has been effective for killing Listeria. The possibility of enhancing the antilisterial capability of PL treatment by combining PL with an additional hurdle, the natural antimicrobial nisin, was explored in this study. First, the ability of Listeria innocuato mimic the response of Listeria monocytogenesto PL treatment was demonstrated. Subsequently, a series of inoculation studies was performed in which canned sausages were surface inoculated with L. innocuaas a surrogate for L. monocytogenesand then treated with a commercial preparation of nisin (Nisaplin), PL, or a combination of the two treatments. The application of a Nisaplin dip alone resulted in an immediate reduction of L. innocuaby 2.35±0.09 log CFU. PL reduced L. innocuaby 1.37±0.30 log CFU after exposure to 9.4 J/cm2. A total reduction of 4.03±0.15 log CFU was recorded after the combined treatment of Nisaplin and PL for 48 h at 4°C. The long-term survival of L. innocuawas evaluated on sausages stored at 4°C. Treatment with Nisaplin and PL resulted in a 4- to 5-log reduction for two replicate studies. The combination treatment resulted in no significant microbial growth during 28 and 48 days of refrigerated storage in the first and second replicates, respectively. These results suggest that this combination treatment can be used as an effective antilisterial step in the production of ready-to-eat foods.

Pulsed light (PL) treatment is an alternative to traditional thermal treatment that has the potential to achieve several log-cycle reductions in the concentration of microorganisms. One issue that is still debated is related to what specifically causes cell death after PL treatments. The main objective of this work was to elucidate which portions of the PL range are responsible for bacterial inactivation. Stainless steel coupons with controlled surface properties were inoculated with a known concentration of Listeria innocuain the stationary growth phase and treated with 1 to 12 pulses of light at a pulse rate of 3 pulses per s and a pulse width of 360 μs. The effects of the full spectrum (λ= 180 to 1,100 nm) were compared with the effects obtained when only certain regions of UV, visible, and near-infrared light were used. The effectiveness of the treatments was determined in parallel by the standard plate count and most-probable-number techniques. At a fluence of about 6 J/cm2, the full-spectrum PL treatment resulted in a 4.08-log reduction of L. innocuaon a Mill finish surface, the removal of λ< 200nm diminished the reduction to only 1.64 log, and total elimination of UV light resulted in no lethal effects on L. innocua. Overwhelmingly, the portions of the PL spectrum responsible for bacterial death are the UV-B and UV-C spectral ranges (λ< 300 nm), with some death taking place during exposure to UV-A radiation (300 <λ< 400 nm) and no observable death upon exposure to visible and near-infrared light (λ> 400 nm). This work provides additional supporting evidence that cell death in PL treatment is due to exposure to UV light. Additionally, it was shown that even a minor modification of the light path or the UV light spectrum in PL treatments can have a significant negative impact on the treatment intensity and effectiveness.