Fish exposed to UV-B may experience a depressed immune system and subsequent vulnerability to infection by pathogens [29,30]. Epidermal lesions from sunburn allow invasion by pathogens, especially fungi [2,31]. During laboratory studies, fungal hyphae were frequently observed at the margins of the sunburned fish skin within one or two days of the initial sunburn . These fungal infections progressed over the dorsal surface of the fish and the fish died soon after. Extensive fungal infection was also noted among tiger salamander larvae that had developed skin lesions during UV exposure [Carey personal communication]. In mammals, UV-B-induced immunosuppression may occur through isomerization of urocanic acid from the trans to the cis form [32-34], The cis form of urocanic acid may modulate cell-mediated immunity by binding to receptors [35,36], Urocanic acid occurs in mammalian skin predominantly as the trans isomer. Upon UV-B irradiation of the skin, urocanic acid isomerizes to the cis isomer along with concurrent suppression of the immune response. In mammals this is thought to be a protective mechanism by preventing uncontrolled autoimmune destruction of sun-damaged skin cells . Exposure to high levels of UV-B could cause hyperstimulation of this mechanism with subsequent increased susceptibility to pathogens. In a preliminary study, a substance that appeared to be traws-urocanic acid was found in the skin of UV-B-exposed and unexposed rainbow trout , Thus, a similar mechanism of immunosuppression may be induced by UV-B in fish. Although it remains to be established that urocanic acid functions similarly in fish epidermis as it does in mammals, the detection of this chemical raises the possibility that localized immunosuppression may also be responsible for epidermal infections observed in fish and other aquatic organisms .
Peptides on the skin surface have been shown to play an immunological role by binding to pathogens in amphibians [38-40]. The amino acid composition of these peptides may be vulnerable to photo-decomposition or photo-transformation by UV causing the peptide to be less effective as bactericidal or fungicidal agents. In such cases, UV could directly lead to increased vulnerability to epidermal infection. Sustained exposure to solar radiation may play an important role in the initiation of disease outbreaks in freshwater fish. Suppression of the immune system may occur in UV-B-exposed fish, making the fish more susceptible to disease organisms. Conversely, low-level infection by pathogens may increase the vulnerability of the skin of fish to ambient levels of solar UV-B. For example, Bullock  observed increased radiation damage in the skin of plaice (Pleuronectes platessa), a marine fish infested with an ectoparasite that also occurs on the skin of cultured salmonids reared in freshwater. Apparently, very low doses of UV-B were sufficient to enhance the rate of breakdown in skin structure initiated by the ectoparasite. Thus, conditions that affect the integrity of the epidermis prior to, and during, exposure to solar UVR can lead to increased susceptibility of the fish to UV-B.
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