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a purulent skin disease caused by pyogenic cocci. One of the commonest skin diseases, pyoderma may occur primarily on healthy skin or secondarily as a complication of a variety of mainly pruritic diseases. Factors leading to its development include cuts, pricks, scratches, and other minor traumata, contamination or excessive heating or chilling of the skin, impairment of the functioning of the internal organs or central nervous system, metabolic disorders, or increased sensitivity to pyogenic infection.
A distinction is made between acute and chronic staphylococcal and streptococcal pyodermas, which may be circumscribed or disseminated, superficial or deep. When the skin is infected by both types of cocci at the same time, the infection is called streptostaphyloderma. Localization of the process in the region of the sebaceous hair follicles and apocrine glands is characteristic of staphyloderma. This form of the disease includes ostial folliculitis, in which a pustule the size of a lentil is located in the orifice of a hair follicle and pierced in the center by a hair. Another type of staphyloderma is folliculitis, in which infection penetrates deep into the hair follicle. When this type is chronic and multiple ostial folliculitis is present, the result is the development of sycosis, furuncles, carbuncles, and hidradenitis.
Streptococcal pyoderma is marked by surface lesions on the skin, with the formation of a phlyctena, a thin-walled soft vesicle containing a cloudy substance and surrounded by an inflamed ring. The phlyctena dries, forming a small seropurulent crust, which falls off without leaving a mark. Among the acute streptococcal pyodermas are impetigo, diffuse superficial streptococcal pyoderma, and ecthyma, an ulcer that forms beneath a dried phlyctena. Chronic streptococcal pyodermas include lichen simplex of the face, perlèche, and chronic paronychia.
The treatment of pyodermas consists of the administering of such drugs as staphylococcal and streptococcal vaccines, antiphagin, bacteriophage, antibiotics, and sulfanilamides. Nonspecific methods are autohemotherapy, lactotherapy, and vitamin therapy. Local methods include the use of drugs and other methods to accelerate the healing of the inflammation, for example, aniline dyes, salicylic alcohol, pure ichthyol, and ultraviolet radiation. The disease is prevented by observing rules of personal hygiene.
I. IA. SHAKHTMEISTER