Staphylococcus Infection: Relapsing Atopic Dermatitis and Microbial Restoration

Atopic Dermatitis (AD) skin is susceptible to Staphylococcus aureus (SA) infection, potentially exposing it to a plethora of toxins and virulent determinants, including Panton-Valentine leukocidin (PVL) (alpha-hemolysin (Hla) and phenol-soluble modulins (PSMs)), and superantigens. Depending on the degree of infection (superficial or invasive), clinical treatments may encompass permanganate (aq) and bleach solutions coupled with intravenous/oral antibiotics such as amoxicillin, vancomycin, doxycycline, clindamycin, daptomycin, telavancin, linezolid, or tigecycline. However, when the skin is significantly traumatized (sheathing of epidermal sections), an SA infection can rapidly ensue, impairing the immune system, and inducing local and systemic AD presentations in susceptible areas. Furthermore, when AD presents systemically, desensitization can be long (years) and intertwined with periods of relapse. In such circumstances, the identification of triggers (stress or infection) and severity of the flare need careful monitoring (preferably in real-time) so that tailored treatments targeting the underlying pathological mechanisms (SA toxins, elevated immunoglobulins, impaired healing) can be modified, permitting rapid resolution of symptoms.

Automated summary

Atopic dermatitis skin is prone to Staphylococcus aureus infection, exposing it to various toxins and virulent determinants. Treatment options depend on the degree of infection and may include topical solutions and oral/IV antibiotics. Severe skin trauma can lead to rapid SA infection, impairing the immune system and causing local and systemic AD presentations. The desensitization of systemic AD is a lengthy process with potential relapses, necessitating careful monitoring of triggers and flare severity to modify targeted treatments for rapid resolution of symptoms.