Ultraviolet C irradiation: an alternative antimicrobial approach to localized infections?

Abstract

This review discusses the potential of ultraviolet C (UVC) irradiation as an alternative approach to current methods used to treat localized infections. It has been reported that multidrug-resistant microorganisms are equally sensitive to UVC irradiation as their wild-type counterparts. With appropriate doses, UVC may selectively inactivate microorganisms while preserving viability of mammalian cells and, moreover, is reported to promote wound healing. UVC is also found in animal studies to be less damaging to tissue than UVB. Even though UVC may produce DNA damage in mammalian cells, it can be rapidly repaired by DNA repair enzymes. If UVC irradiation is repeated excessively, resistance of microorganisms to UVC inactivation may develop. In summary, UVC should be investigated as an alternative approach to current methods used to treat localized infections, especially those caused by multidrug-resistant microorganisms. UVC should be used in a manner such that the side effects would be minimized and resistance of microorganisms to UVC would be avoided.

Figure 1. Spectrum of ultraviolet light

UV: Ultraviolet.

Figure 2. Dose–responses of mean fungal luminescence of the mouse burns infected with Candida albicans and treated by use of a single ultraviolet C exposure on day 0 (30 min; n = 11) and day 1 (24 h; n = 12) postinfection, respectively

The data are displayed as mean plus SD. UVC: Ultraviolet; D0: Day 0; D1: Day 1. Reprinted with permission from [15].

Figure 3. Ultraviolet C treatment of toenail onychomycosis

(A) Before ultraviolet C treatment. (B) 28 weeks after ultraviolet C treatment.

Figure 4. Comparison of averaged fluence-dependent survival fractions in response to ultraviolet C irradiation of bacteria with that of keratinocytes using identical irradiation conditions and colony-forming assays

The error bars represent the SD. Reprinted with permission from [37].

Figure 5. Effect of ultraviolet C at the effective antifungal dose on mouse skin

(A–C) Morphologies of a representative mouse skin before, immediately after, and 24 h after being exposed to ultraviolet C at a dose of 6.48 J/cm², respectively. (D–F) Representative immunofluorescence micrographs of cyclobutane pyrimidine dimers in skin cell nuclei. (G–I) Micrographs of diamidino-2-phenylindole counterstaining of cell nuclei. (J–L) Micrographs of Masson’s trichrome-stained sections. Biopsies were taken before (D, G, J), immediately after (E, H, K) and 24 h after (F, I, L) being exposed to UVC at a dose of 6.48 J/cm², respectively, from the same mouse. Arrow in (C): UVC-induced lesion on mouse skin. Arrows in (D–F): mouse skin surface. Arrow in (L) shows epidermal shrinkage. Scale bars shown in panels (D–L) are 20 μm. Reprinted with permission from [15].

Figure 6. Dose responses of Trichophyton rubrum in vitro to five consecutive sublethal ultraviolet C inactivation cycles

The data are representative experiments performed in triplicate and are displayed as mean plus standard deviation. Reprinted with permission from [14].