Potential Delayed Healing in Wounds with Scabies Comorbidity: A Review about Immunological State and Oxidative Stress in Scabies Infestation
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Abstract
Scabies is a highly contagious skin disease caused by the human itch mite Sarcoptes scabiei var. hominid. Having scabies infestation coexisting in the same human body with a wound potentially lead to delayed wound healing. We constituted this literature review discussing wound healing in relation woth immunological state and oxidative stress in scabies infestation using information from literatures obtained from Google Scholar and PubMed.
The immune response to scabies infection involves multiple layers of defense mechanisms, including the skin's defense mechanisms, T-cells, keratinocytes, and cytokines. Scabies mites can trigger upregulation of pro-inflammatory cytokines interleukins-1α (IL-1α) and interleukins-1β (IL-1β), which play a critical role in the early phases of wound healing by promoting the recruitment of immune cells and stimulating the production of growth factors and extracellular matrix proteins. Scabies mite infestation also triggers a sustained release of reactive oxygen species (ROS) from neutrophils which later becomes an oxidative stress leading to delayed healing and chronic inflammation. Topical treatment for scabies usually involves pesticide substances which, despite its therapeutic effect, have side effect of triggering ROS production. Comprehending the immunological state and oxidative stress in scabies infestation is essential in planning proper management for every wound with scabies comorbidity.
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