Abstract

Skin infections have been associated with Acanthamoeba, nevertheless the events during skin invasion and UV-B light effects on it are unknown. The early morphological events of Acanthamoeba castellanii skin invasion are shown in SKH-1 mice that were chronically UV-B light irradiated. Mice that developed skin lesions (group 1) were topical and intradermally inoculated with A. castellanii trophozoites and sacrificed 48 h or 18 days later. Mice that showed no skin lesions (group 2) were intradermally inoculated and sacrificed 24, 48 or 72 h later. Mice ventral areas were considered controls with and without trophozoites intradermally inoculated. Skin samples were processed by histological and immunohistochemistry techniques. In group 1, trophozoites were immunolocalized in dermal areas, hair cysts, sebaceous glands, and blood vessels, and collagen degradation was observed. One of these mice shown trophozoites in the spleen, liver, and brain. In group 2, few trophozoites nearby collagenolytic activity zones were observed. In control samples, nor histological damage and no trophozoites were observed. Adherence and collagenolytic activity by A. castellanii were corroborated in vitro. We can infer that UV-B light irradiated skin could favor A. castellanii invasiveness causing damage in sites as far away as the brain, confirming the invasive capacity and pathogenic potential of these amphizoic amoebae.

Highlights

  • The general amoebae biological characteristics include ubiquitous distribution, use of soil and water habitats, air use as dispersal media, and ecologically they participate in bacterial population control [1,2]

  • Out of the five SKH-1 mice chronically irradiated with UV-B light, in two of them it was confirmed evident damage caused by UV-B light chronic irradiation (Figure 1A,B)

  • During the implementation of the murine model of skin irradiated with UV-B light, UV-B radiation was found to cause skin lesions in SKH-1 mice; an erythematous lesion and a lesion related to the development of neoplasic lesion which coincides with Mäkinen and Stenbäck [31] and Cano et al [32], who reported that excessive exposure to UV-B is carcinogenic and that epidermal and dermal lesions are easier to be induced by UV-B radiation in SKH-1 mice

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Summary

Introduction

The general amoebae biological characteristics include ubiquitous distribution, use of soil and water habitats, air use as dispersal media, and ecologically they participate in bacterial population control [1,2]. Acanthamoeba spp. are etiology agents of human pathologies, such as amoebic keratitis (AK), granulomatous amoebic encephalitis (GAE) and skin infections [2]. These protozoans have been more appropriately designated as amphizoic microorganisms, due to their ability to exist in the environment as free-living organisms or as opportunistic parasites. The GAE is a subacute or chronic infection causing necrosis and inflammatory lesions, whose entry route can be hematogenous or through the respiratory tract, affecting mainly immunocompromised people [5], with multiple sclerosis or diabetes [2,6,7]. Acanthamoeba skin infections may be the manifestation of an infection that initiated in another organ and spread hematogenously or are the primary focus of infection through skin wounds or burns and that posteriorly spread to other organs [21,24,25]

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