<unk><unk><unk>  is one of the tertiary presentations of European lyme borreliosis. Borrelia afzelii is known as the most predominant responsible microorganism. Nevertheless, other borrelia species such as borrelia garinii and borrelia burgdorferi (B. burgdorferi sensu lato) have been also detected in<unk><unk><unk>  patients. Transmission of this infection probably occur via ixodes tick (such as Ixodes ricinus), mosquito and horsefly bite. These vectors themselves get infected by feeding on an infected animal reservoir. Development of various symptoms in this disease is a result of<unk> T cell mediated reaction of immune system against borrelia. This immune reaction leads to infiltration of CD3+ and CD4+ cells in the dermis. Borrelia is capable of attaching to the extracellular matrix proteins (such as glycosaminoglycan, fibronectin and decorin proteoglycan) which eventually leads to metalloproteases activation and extracellular matrix degradation. Pro-inflammatory cytokines, such as tumor necrosis factor alpha and interleukin-4, have been detected in skin biopsies. There is no known gene responsible in<unk>  of<unk><unk><unk>  disease. Some conditions such as lymphocytic meningoradiculitis, lichen sclerosus et atrophicus, morphea and other tick borne diseases have been associated with<unk><unk><unk> . Thinning of skin, visible veins, swelling and wrinkles are some of the features that can be noticed on gross pathology. Light and electron microscopic study of the skin biopsy shows degeneration of the elastica and collagen fibers. Thinning of dermis and epidermis, pigmented stratum germinativum, dermal blood vessels dilation and perivascular plasma cell infiltration are some of the findings on microscopic pathology.
Acrodermatitis chronica atrophicans pathophysiology
Atopic dermatitis pathophysiology
Eczema pathophysiology
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Herpes simplex pathophysiology
Molluscum contagiosum pathophysiology