Folliculitis is an inflammation of the hair follicle caused by staphylococci, which is facilitated by a decrease in the protective functions of the skin under the influence of endogenous (focal infection, diabetes mellitus, hypovitaminosis, etc.) or exogenous factors ( trauma , non-compliance with hygiene standards, etc.). The inflammation of the hair follicle can be superficial ( folliculitis supetficialis ) or deep ( folliculitis profunda ).
Etiology of pyoderma
Most often, microorganisms such as Streptococcus haemolyticus , Staphylococcus aureus , S. albus are detected in the affected areas of the skin . These cocci secrete various exotoxins and enzymes that determine the clinical difference between different pyoderma.
Pathogenesis of pyoderma
Pyoderma develops under the influence of various exogenous and endogenous factors.
– Skin trauma .
– Skin contamination, non-compliance with hygiene standards, excessive degreasing of the skin.
– Violation of the secretory function of the skin.
– Focal infection.
– Diseases of the gastrointestinal tract.
– metabolic disorders.
– Diseases of the endocrine system.
– Neurosis, mental trauma.
– Chronic intoxication.
– Immune deficiency, HIV infection.
A small (1-3 mm diameter) erythematous infiltrate forms on the skin , in the center of which a follicular pustule forms within a few days. When it is opened, the pus dries up with the formation of a crust, which then disappears. Inflammatory infiltrate resolves gradually. In the case of deep folliculitis, the hair root is damaged, a spot scar forms on the site of the pustule . Folliculitis regresses within 5-10 days.
Differential diagnosis of folliculitis
Papulonecrotic skin tuberculosis. A characteristic long chronic course. Persons suffering from tuberculosis of the lymph nodes, lungs on the extensor surfaces of the limbs, face, buttocks appear flat, dense, superficial or deep pale pink nodules with necrosis in the center. After permission, “stamped” scars remain. Tuberculin tests are positive. Acne iodide and bromide. Large pustules suddenly appear on the face, neck, shoulders, buttocks with an island-inflammatory corolla on the periphery. In addition to pustules, erythematous , bullous, nodular and urticarial elements are often detected . There is a rapid regression of clinical manifestations after discontinuation of iodine or bromine preparations. The history of data (taking medications containing iodine, bromine) helps in the correct diagnosis.
1. Disinfecting solutions for skin treatment (alcohol solution of salicylic or boric acid with glycerol 5-10%).
2. Disinfecting liquid powders, creams, liniment, ointments ( Lotio Zinci with 10% sulfur or 5% dermatol , Linola sept , Triple antibiotic ointment , Bactroban , Betadine , Baneocin ointment , etc.). 3. Sour soap, washing oils are used to wash the skin. 4. After recovery, the skin should be lubricated with Bepanthen Plus cream or lotions containing urea. General therapy For patients with deep folliculitis: Antibiotics ( Erythromycinum 0.5 four times a day, one week or longer, Dicloxacilinum 0.5 four times a day for 7-10 days, Ciprofloxacinum 0.5 twice a day, etc.).
Deep trichophytosis is an infection caused by anthropozoophilic fungi. It begins acutely, children and adults get sick.
Epidemiology of deep trichophytosis
Deep trichophytosis is contracted by infection with the anthropozophilic fungi Trichophyton gj’pseum and Trchophytonfaviforme , which parasitize both animals (mice, rats, cows) and humans.
Clinic of deep trichophytosis
Deep trichophytosis is acute. Fungi enter the hair follicles and cause their suppuration, involving the surrounding tissue in the process. The disease begins with the formation of a limited deep hemispherical inflammatory infiltrate, on the surface of which the expanded openings of the hair follicles are visible, from where pus is secreted, and resembles a carbuncle. Regional lymph nodes increase. The untreated lesion expands, covering more and more hair follicles. On the scalp there is a hemispherical infiltrate, covered with a tan crust; a large amount of yellowish-green pus is secreted; hair is separated along with pus. The isolation of pus from damaged hair follicles was first described by the Roman doctor Celsus , so the disease and the resulting lesion of the scalp, compared with the expiration of honey from honeycombs, is called kerion Celsi . Hair bags atrophy, and when the inflammatory process is eliminated, an atrophic scar forms, the hair does not grow back. Deep trichophytosis in the area of the beard and mustache forms a thinner infiltrate and resembles sycosis ( sycosis parasitemia ). The course of the disease is chronic, after its regression, scars remain in the lesion sites. Livestock breeders suffer from deep trichophytosis, which, when infected from sick animals, often infect their children.
Mostly the stratum corneum (or hair cuticle) is affected.
It should be noted that relatively recently in the dermatological literature of the CIS (and somewhat earlier in the foreign one) the term “ skin malassesiosis ” appeared. In fact, this is a collective historical concept that combines a number of dermatoses that affect the skin and its appendages and is caused by the yeast-like lipophilic fungi of the genus Malasserria (named Malasse , who described these microorganisms in patients with seborrhea of the scalp; Eichstedt (1884) highlighted them in patients with multi-colored deprive). Currently, the term “ skin malaysiosis ” (ICD-10 code: B36.1) is considered collective; according to some authors, it includes (in addition to multi-colored lichen) A / a / omega-folliculitis, seborrheic dermatitis and dandruff (A.Yu. Sergeev, Yu.V. Sergeev, 2003). Several researchers associated with malasseriyami other pathological processes ( pustulosis neonates, rosacea , atopic dermatitis, etc.), But the specific etiopathogenic mechanism of interconnection of these states with malasseriyami not installed.