Добавил:
Upload Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:
Les 7.doc
Скачиваний:
0
Добавлен:
01.07.2025
Размер:
163.33 Кб
Скачать

Thematic module 3. Сontagious Dermatoses lesson 7 Pyodermia. Etiology, pathogenesis. Clinical features. Diagnostics. Treatment. Prevention

1. Theme urgency

Pyodermas (Gk. pyon pus) are skin lesions characterized by the presence of pus. They account for most skin diseases and take first place among all dermatoses. Pyodermas are responsible for about half of all cases of disability caused by skin diseases. They are quite common among all population groups but are registered rather more often among persons engaged in certain branches of industry, namely, construction, metallurgical and mining industries, in transport, etc., where they have become occupational diseases. From this standpoint, pyoderma control is of state importance and is a social problem of medicine.

Pyodermas are also the most prevalent of all dermatoses encountered in pediatric dermatological practice. Diverse manifestations of pyoderma occur primarily (as various independent nosological forms) or as a complication of other dermatoses, especially in patients with pruritic dermatoses (neurodermatoses, scabies, pediculosis).

2. Concrete Objectives:

Students must know:

  1. The etiology and pathogenesis of pyodermas.

  2. Classification of pyodermas.

  3. Clinical forms of staphylodermas, streptodermas and mixed strepto-staphylococcal pyodermas.

  4. Differential diagnosis of pyodermas.

  5. Treatment and prevention of pyodermas.

Students should be able to:

  1. To collect the medical history of patient with pyodermas.

  2. To diagnose pyodermas in patient in typical case.

  3. To prescribe treatment for patient with pyodermas.

  4. To recommend preventive measures for patient with pyodermas.

3. Tasks for self-study during preparation for lesson.

3.1. Theoretical questions for the lesson:

  1. The etiology and pathogenesis of pyodermas.

  2. Classification of pyodermas.

  3. Clinical forms of staphylodermas (ostial folliculitis, sycosis, deep folliculitis, furuncle, carbuncle, hidradenitis).

  4. Clinical forms of staphylodermas encountered only among children (vesiculopustulosis, multiple skin abscesses (pseudofurunculosis), pemphigus epidemicus neonatorum, and Ritter's disease).

  5. Clinical forms of streptodermas (clinical varieties of streptococcal impetigo, ecthyma vulgaris).

  6. Clinical forms of mixed strepto-staphylococcal pyodermas (a superficial form - impetigo vulgaris and atypical varieties of deep pyodermas: chronic ulcero-vegetative pyoderma, pyoderma chancriforme).

  7. Investigations of pyodermas.

  8. Differential diagnosis of pyodermas.

  9. Treatment and prevention of pyodermas.

The subject-matter:

Etiology. Various species of staphylococcus and streptococcus are the most common causative agents of pyoderma. The disease may also be caused by the blue-pus bacillus, Proteus vulgaris, Escherichia coli, fungi, pneumococcus, gonococcus, and many other microorganisms. The extensive spread of staphylococci and streptococci in nature (on the clothes, in the house, at places of work, in street dust, etc.), on the skin of sick persons, and on the mucous membranes and skin of individuals who have no noticeable pathological changes (20 to 75 per cent of persons examined prove to be bacilli-carriers), the possibility of the transformation of non-pathogenic forms to pathogenic forms on the skin surface under definite conditions—all this makes the extensive prevalence of pyoderma understandable.

It is an established fact that staphylococci are almost always present on the skin of healthy persons (usually in the orifices of the hair sacs and in the ducts of the sebaceous glands), but the identified strains are pathogenic in only 10 per cent of them, whereas among patients with pyoderma and those with a history of the disease the percentage of pathogenic strains increases sharply (to 90). Streptococci are found much less frequently on the skin of healthy persons (in up to 6 to 10 per cent) and are mainly localized in the skin folds.

Pathogenesis. The development of any form of pyoderma is determined not only by the pathogenicity and virulence of the cocci strain (though these are factors of no small importance) but also by diverse exogenic and endogenic predisposing factors which alter the protective functions of the skin and reduce, in particular, its capacity to resist the development of pyoderma.

Among the most common exogenic factors conducive to the occurrence of pyoderma the following are important: (1) superficial skin injuries (microtraumas) such as cuts, excoriations, scratches, superficial burns, etc.; (2) soiling of the skin (occupational soiling with coal, lime, cement, lubricating oils. etc. and soiling of the skin because of a faulty hygienic care of children, especially infants, should be emphasized in particular); (3) overcooling or overheating of the body in everyday life or at work; in children this occurs because their thermoregulation is imperfect.

The endogenic factors are just as diverse; note should be made of endocrine disorders (hyperglycemia), functional disorders of the nervous system (vegetative neuroses), fault in nutrition, hypovitaminosis (especially A, C and B), acute and chronic emaciating diseases, diseases of the gastro-intestinal tract and hereditary factors. An important role is played by weakening of immune defence mechanisms.

The conducive factors for the development of pyodermas in children are an imperfect physiological barrier, particularly increased moistness, looseness, and fragility of the epidermal horny layer, labile colloido-osmotic state, and high absorption capacity of the skin.

Factors present in the cocci themselves are very important in the pathogenesis of pyodermas. The pathogenicity of staphylococci and streptococci is determined to a great measure by some toxins and enzymes (coagulase, hyaluronidase, hemolysins, streptolysins, streptokinase, proteinase).

Classification. All pyodermas are subdivided into staphylococcal, streptococcal, and mixed according to the etiological factor, superficial and deep according to the depth of the localization of the process, and acute and chronic pyodermas according to the character of their course.

In staphylococcal pyodermas the process develops predominantly in the region of the hair follicles and in the sweat and sebaceous glands. The pustules are conic or semispherical, their walls are thick and tensed, and the pus is thick and yellowish-green; downy hair is often found in the centre of the pustule. Only in children staphylococci cause the development of superficial bullae which are not connected with the sebaceous-hair follicles or the sweat glands.

In streptococcal pyodermas, neither the sebaceous-hair follicles nor the sweat glands are involved in the process. The lesions are predominantly superficial in character, the vesicles are flat with thin and flabby walls (phlyctenas) and a seropurulent exudate. These pustules are marked by a tendency to peripheral growth.

Superficial pyodermas (phlyctenas) occur only within the epidermis and leave a temporary pigmentation. Deep pyodermas penetrate the dermis and sometimes the subcutaneous fat and leave scars or cicatricial atrophy.

Secondary pyoderma is a condition developing in attendance to various skin diseases.

STAPHYLOCOCCAL PYODERMAS (STAPHYLODERMAS)

The following staphylococcal pyodermas are distinguished: ostial folliculitis, sycosis, deep folliculitis, furuncle, carbuncle, hidradenitis. In these cases, the pathogenic staphylococci are mainly localized in the orifices of the hair follicles and the sweat and sebaceous glands, which determines the clinical features of staphylococcal pustules. In newborns and infants the skin structure is insufficiently formed morphologically. Moreover, the contact between the epidermis and dermis is not tight because the basement membrane is weak and the papillae are smoothed out, as a result of which non-follicular lesions of the type of bullae form when pathogenic staphylococci penetrate the skin. At the same time, the ability of children's skin to develop an intensive inflammatory reaction with generalization of the eruption leads to extensive and severe staphylococcal lesions in the newborn. In view of this, a group of staphylococcal pyodermas in the newborn is distinguished: vesiculopustulosis, multiple skin abscesses (pseudofurunculosis), pemphigus epidemicus neonatorum, and Ritter's disease (dermatitis exfoliativa neonatorum).

Ostial Folliculitis, or Staphylococcal Impetigo (Impetigo Staphylogenes)

The lesion in this disease is a follicular pustule the size of a millet grain or pin head, found in the centre of the hair follicle and surrounded by a narrow hyperemic band of acute inflammation. The lesions are either circumscribed and restricted to a small skin area or are scattered, in which case there are many of them. Ostial folliculitis, or staphylococcal impetigo (L. impetus assault) sets in with redness and some pain around the orifice of a follicle or sebaceous gland. A semispherical or conic swelling forms soon with a pustule in the centre; the top of the pustule is yellow because of the pus that accumulates under it. A few days later the contents of the pustule dry up and a crust forms, the surrounding inflammation subsides and the process terminates without a trace or only a light pigmentation remains. The lesions in ostial folliculitis show no tendency to spread along the periphery; when there are many of them they are arranged in groups close to one another and never coalesce.

Occasional lesions sometimes grow to the size of a large pea and are usually pierced by a fine hair in the centre. This condition is called Bockhart's staphylococcal impetigo which is often encountered on the dorsal surface of the hand as a complication of scabies.

Ostial folliculitis develops most commonly on the skin of the face, neck, forearms, crura, and thighs. Factors conducive to it are mechanical irritation of the skin (shaving, rubbing, maceration of the skin under a compress) and continuous exposure of the skin to harmful agents (kerosene, benzine, lubricating oils, tar, etc.). In the last case the folliculitis is occupational in character and is marked by very many lesions, which often transform into deep folliculitis.

In children, ostial folliculitis may occur from the age of 2 or 3 years, but is encountered most frequently among older children; maceration, increased sweating, cooling or overheating, and faulty skin hygiene are the conducive factors.

Treatment. The causes conducive to the origin of ostial folliculitis are removed. Some of the pustules are opened and the pus removed, after which the foci of affection are painted twice a day with 1-2 per cent alcohol solution of aniline dyes (l% Sol. Gentianvioleti, seu Methyleni coerulei, seu Virides nitens) in 70 per cent ethyl alcohol. The hair in the area of the lesions is cut, but not shaved, and for preventive purposes the surrounding skin is wiped with 2 per cent salicylic or boric acid or with a solution of camphor and alcohol (2.5 ml of camphor alcohol and 45 ml of 40 per cent rectified spirit). Total-body ultraviolet irradiation with suberythema doses (daily or every other day, a total of 6 to 10 sessions) is recommended in recurrences of the disease or in copious eruption of the impetiginous lesions. Hydrotherapy is forbidden during the disease.

Deep Folliculitis (Folliculitis Profunda)

In deep folliculitis the pathogenic staphylococci penetrate the follicle deeper than they do in ostial folliculitis and cause inflammation of the greater part or of the whole follicle. Painful red nodules appear at first, which later transform into pustules pierced with a fine hair. In a few days the secretions of the pustule dry into a crust or suppuration advances and necrosis of the connective tissue occurs. If the disease follows the ordinary course, small punctate scars form in five to six days at the site of deep folliculitis. Isolated lesions of deep folliculitis are usually found on the scalp and back of the neck, though a versatile localization is possible.

Treatment. The lesions are painted with Castellani's paint, 1-2 per cent alcohol solution of methylene blue or brilliant green. The healthy skin areas close to the pustules are wiped with 2 per cent salicylic or camphor spirit to prevent dissemination. A 'flat cake' of pure ichthammol may be applied to some of the areas of deep folliculitis. Baths and showers are forbidden for some time.

Sycosis (Vulgaris, Simplex, Staphylogenes)

Staphylogenic sycosis (vulgaris) is a chronic recurrent pyoderma encountered predominantly among males. Areas of ostial folliculitis and folliculitis form usually on the scalp, in the region of the moustache and beard, and less frequently on the inner surface of the wings of the nose, on the eyebrows, in the axillae, on the eyelid margins, and on the pubis.

At the onset of the disease, a few lesions of ostial folliculitis appear on a relatively circumscribed skin area, which tend to spread to larger and larger areas. An inflammatory infiltrate forms around the lesions, as a result of which the affected area thickens and turns bluish-red and is sometimes painful. Involvement of new follicles in the process leads to slow growth of the focus of affection in which there may be a large number of inflamed follicular orifices forming a conglomerate of pustules. After the top of the pustules opens, the pus dries up into dirty-yellow crusts which stick to the hairs. Sycosis vulgaris is usually a persistent condition (remaining for years) which exacerbates now and again and has a depressing effect on the patient's mental condition, especially if it is localized on the face. In some cases there are no subjective disorders, in others the lesions are attended with a sensation of burning, mild itching or pricking.

Differential diagnosis is made with infiltrative-suppurative trichophytosis (parasitic sycosis), which is characterized by a more acute course, the formation of thick and deeper-seated nodules, a tendency to disappear without any treatment; laboratory examination reveals elements of a fungus (of the ectothrix group) in the hairs on the periphery of the foci.

Pathogenesis. Importance is attached today to diminished immunobiological resistance of the body and to the presence in the hair follicles of other foci of localized infection. Moreover, endocrine disorders are also held responsible to a great measure. Among the exogenic factors conducive to the development of sycosis are cutting of the skin in shaving, damage inflicted to it and maceration of the skin on the upper lip in persistent rhinitis.

Treatment. All identified exogenic irritating factors should be removed. Broad spectrum antibiotics (dicloxacillin, clarithromycin, erythromycin) are prescribed. External therapy includes daily painting with 2 per cent solutions of aniline dyes, 2 per cent boric acid solution, as well as bactroban, ointments and creams containing antibiotics (gentamicin or lincomicin) and steroid hormones (Celestoderm with garamicin); 2-3 per cent salicylic ointment is used in removing the crusts. Ultraviolet irradiation (erythema doses) is prescribed in marked infiltration in the foci of affection.

Furuncle (Furunculus), or Boil. Furunculosis

Furuncle is one of the common forms of pyoderma. It is acute staphylococcal pyonecrotic inflammation of the hair follicle and the surrounding connective tissue.

Etiology. The causative agent of furuncle is Staphylococcus aureus and, less frequently, Staphylococcus albus.

Pathogenesis. A furuncle may form on previously healthy skin or may be a complication of an already existing superficial or deep staphyloderma. Besides the virulence and pathogenicity of the strain of the causative agent, predisposing exogenic and endogenic factors play an important role in the development of furuncle and furunculosis. Among the exogenic factors are mild mechanical injury inflicted to the skin by particles of dust, coal or metal; scratches made with the nails (in eczema, neurodermatosis, scabies), and meteorological conditions. The important endogenic factors are emaciation of the organism, metabolic diseases (diabetes, obesity), gastro-intestinal diseases, anemia, hypovitaminosis, diseases of the nervous and endocrine systems, etc., which lead to a decrease in the body's general immunobiological reactivity. Furuncles occur more frequently in the spring and autumn. The incidence is lower among children than among adults and higher among males than among females.

A solitary furuncle (a single furuncle or one that reappears but after several months or more), recurrent solitary furuncles (the recurrences occur at very short intervals of days or weeks), and furunculosis (furuncles appear one after another) are distinguished. In formulating the diagnosis, the physician adds details characterizing the clinical features (e.g. furuncle developing into an abscess or furuncle complicated by lymphadenitis) or the localization of the process (e.g. furuncle of the upper lip, furuncle of the external acoustic meatus).

Clinical picture and course. The following three stages in the development of a furuncle are distinguished:

(1) the stage of the development of the infiltrate;

(2) the stage of suppuration and necrosis;

(3) the stage of healing.

A hard, elevated, bright-red infiltrate first forms around the hair follicle. The infiltrate acquires gradually the form of a firm tumor which grows along the periphery and becomes more painful; there is swelling of the surrounding tissues (the swelling in the region of the cheeks, eyelids, and lips may be sharply pronounced). The second stage sets in on the third or fourth day: the furuncle grows to 1-3 cm in diameter and a pyonecrotic core with a pustule on its surface forms in the centre. The furuncle takes the shape of a conic tumor with smooth, lustry blue skin. The pain is very severe in this period, body temperature may rise to 37-38° C, and symptoms of toxicosis may develop (general indisposition, malaise, headache, etc.). The top of the pustule opens spontaneously or is opened artificially and pus, sometimes with an admixture of blood, is discharged from the furuncle after which a yellowish-green necrotic 'plug' (necrotic core) comes out. After removal or rejection of the core, swelling, infiltration, and pain subside, and the remaining crater of the furuncle is filled with granulations which are replaced by a scar in two to three days. The scar is bluish-red at first, then gradually turns white and is sometimes hardly visible. The developmental cycle of a furuncle commonly lasts eight to ten days.

Furuncles may form on any area of the skin, with the exception of the skin on the soles and palms devoid of hair follicles. Solitary furuncles occur most frequently on the back of the head, the forearm, small of the back, abdomen, buttocks, and lower limbs. A furuncle of the external acoustic meatus is marked by severe pain, while a furuncle of the upper lip is a dangerous disease because thrombosis of the lymphatics and veins with the formation of septic phlebitis of the cerebral vessels and general sepsis may occur. Acute inflammation of lymphatic vessels and lymphadenitis may develop when furuncles of the neck, chest, and thighs form close to the lymph nodes. All these complications make furuncles a very grave disease in some cases. Complications may be promoted by attempts to squeeze out the furuncle, cuts from shaving, inadequate local treatment; localization of a furuncle on the face, in the nasolabial triangle, and on the skin and mucous membranes of the nose is also conducive to the development of complications.

The diagnosis of characteristic cases is easy. The condition has to be differentiated from anthrax, hidradenitis, and deep trichophytosis.

Treatment. In a case with a solitary furuncle and no complications, for instance, only external therapy is prescribed. In recurrent and complicated furuncles, in furuncles of hazardous localization, and in furunculosis, especially in the chronic and disseminated forms, external therapy is supplemented by general measures which act on the microbial flora, stimulate the defence reactive forces of the body, and contribute to the removal of intercurrent diseases revealed during examination of the patient.

Antibiotics are used extensively: erythromycin and oleandomycin, and their combinations with tetracycline—oletetrin, sigmamycin, and tetraolean. Antibioticograms and express methods which yield a result in 12 to 24 hours are used to determine the antibiotic of choice for the given patient. Following culture, the patient should be treated with oral dicloxacillin, oral cephalexin, azithromycin or clarithromycin.

Combination of antibiotics with oral antihistaminic agents is advisable.

For increasing the organism's reactive forces in the control of the infection in solitary recurrent furuncles and in chronic furunculosis it is advisable to prescribe non-specific stimulation therapy (autohemotherapy) and specific immunotherapy with the staphylococcal vaccine (polyvalent or autovaccine), staphylococcus anatoxin, and antiphagin. Gamma globulin is used in persistent furunculosis. Treatment of obesity, diabetes, intestinal atony, diseases of the internal organs, anemia, etc. is a very important component in the complex management of patients suffering from chronic furunculosis. The diet of such patients should contain food that is easily assimilated and no piquant and spicy dishes are given. Alcoholic beverages are not allowed. Vitamins A, C and the B complex as well as preparations of iron and phosphorus are recommended.

The skin around the furuncle is disinfected with a solution of salicylic alcohol, camphor spirit, ether or vodka. The hair is cut (but not shaved!) in the area of the furuncle and in the area immediately surrounding it (to prevent the development of folliculitis and new furuncles); this is done from the centre to the periphery. Pure ichthammol (possessing bactericidal, keratoplastic, local anaesthetic, and anti-inflammatory effects) is applied and covered with a thin layer of sterile cotton. An 'ichthammol cake' is applied once or twice a day. The ichthammol that was previously applied is removed with warm water; no bandage is needed. Such treatment of a solitary furuncle that has not opened sometimes prevents the further development of the pathological process. After the furuncle is opened, a dressing with a hypertonic saline solution may be applied and the periphery of the ulcer painted with pure ichthammol. After the furuncle opens the ulcer is treated with ointment dressings: 10 per cent ichthammol, 5 per cent chlortetracycline or erythromycin ointment. Dry heat or exposure to the effect of UHF electromagnetic field is advisable. Moist heat (wet compress) and water procedures are not allowed during the disease. Surgery is recommended when the furuncle develops into an abscess, as well as intensive antibiotic therapy combined with immunotherapy (hyperimmune gamma globulin, hyperimmune antistaphylococcal plasma, staphylococcus toxoid).

Prognosis. In cases with solitary furuncles (except for those with furuncle on the face) the prognosis is always favourable. The prognosis is grave in chronic furunculosis (particularly in elderly individuals, in emaciated patients, and in those with diabetes), in complicated furuncles, and in sepsis.

Carbuncle

A carbuncle is diffuse pyonecrotic inflammation of the deep layers of the dermis and hypoderm with involvement of several neighbouring hair follicles into the process. Unlike a furuncle, the pyonecrotic infiltrate in a carbuncle spreads over a larger area and penetrates into the deeper layers of the dermis and hypoderm.

The lesion is called a carbuncle (L. carbo charcoal) because the large necrotic areas formed during the pyonecrotic inflammation are dark and resemble charcoal.

The back of the head, the back, and the loins are the favoured localization.

The causative agent is Staphylococcus aureus and less frequently other staphylococcal species.

Emaciation (resulting from chronic malnutrition or a severe systemic disease) and metabolic disorders, impaired carbohydrate metabolism in particular (in diabetes mellitus), contribute to the pathogenesis.

Clinical picture and course. Infiltrate grows, sometimes to the size of a child's palm. Its surface becomes semispherical, the skin is tense and cyanotic in the centre. There is local tenderness. This is the first stage of the development of the infiltrate, which takes 8 to 12 days. After that a few pustules form in the area of the infiltrate the tops of which open and several openings form giving the carbuncle the appearance of a sieve. Pus and green necrotic masses with an admixture of blood are discharged from these openings. Larger and larger areas in the centre of the carbuncle gradually undergo necrosis. With the rejection of the masses an extensive defect in the tissues, an ulcer, forms sometimes down to the muscles. The second stage, the stage of suppuration and necrosis, lasts 14 to 20 days. After that, the ulcer is filled with granulation tissue and a course deep scar fused with the underlying tissues forms as a rule. Large scars are also left after surgery performed for a carbuncle.

Carbuncle development is attended with high fever, excruciating pain of a tearing, pulling character, a chill, and indisposition. Severe meningeal complications may develop when the carbuncle is localized in the area of the nose or upper lip.

The diagnosis is not difficult. The anthrax carbuncle should be borne in mind, in which tissue edema is more pronounced; a black scab resembling anthracite (hence the name) forms in the pustule and the specific causative agent, the aerobic Gram-positive anthrax bacillus, is identified.

Treatment. The treatment of carbuncles always includes general measures and does not differ in principle from the treatment of furuncles. Antibiotics are given. In rapid development of the carbuncle, a wide and deep cross-like incision is indicated with excision of the necrotic areas; this is carried out by a surgeon as a rule; antibiotic therapy is applied at the same time. The skin around the carbuncle is disinfected with 2 per cent camphor spirit or salicylic acid twice a day without fail and all scratches and excoriations are painted with Castellani's paint or alcohol solution of iodine.

Prognosis. The prognosis depends on the patient's general condition.

Hidradenitis

Hidradenitis (Gk. hidros sweat, aden gland) is purulent inflammation of the apocrine sweat glands in the axillae (usually unilateral) or inguinal folds, less frequently around the nipples and in the region of the large pudendal lips, scrotum, and anus.

Etiology. The most common causative agent is Staphylococcus aureus, which enters the efferent duct of the apocrine gland through the orifice of the hair follicle.

Pathogenesis. General weakening of the organism, increased sweating and sweat of alkaline reaction in the axillae, inguinal folds and anus (especially in individuals with faulty hygienic habits), macerations, microtraumas, cuts during shaving, scratches on the skin consequent upon pruritic dermatoses in individuals with nervous and endocrine (diabetes, gonadal dysfunction) disorders, and diminished local resistance are predisposing factors. The sweat apocrine glands develop only in the period of puberty. There are more of them in females than in males. By old age the activity of these glands is extinguished and hidradenitis therefore does not develop in the old.

Clinical picture and course. At the onset of the disease, solitary small hard nodes are palpated in the thickness of the dermis or hypoderm. The patient experiences mild itching or pain at this time. The nodes grow rapidly in size, adhere to the skin, become pear-shaped and protrude like nipples and resemble 'bitch's udder'; the skin turns bluish-red, swelling of the tissues develops and the painfulness increases considerably. The isolated nodes often coalesce, soften, and fluctuation appears after which they open spontaneously and thick pus with an admixture of blood is discharged. No necrotic core forms. Maturation of the lesion is attended as a rule with indisposition, moderately elevated temperature, and marked painfulness. After the nodes open, the sensation of stretching and pain subside and the ulcers heal in a few days. Recurrences are frequent, however, and lend the process a protracted course. Axillary hidradenitis is usually unilateral, though bilateral lesions are also encountered. The average duration of hidradenitis is 10 to 15 days, but a protracted recurrent course is observed quite often (particularly in obese individuals, in patients with hyperhidrosis, diabetes, and in persons who pay little attention to skin hygiene).

Diagnosis. The diagnosis is made easily from the peculiar localization of the process and the typical clinical picture. The absence of a necrotic core distinguishes hidradenitis from furuncles.

Treatment. To prevent the further development of the lesions in the early stages, it is recommended to apply ultrasonics, UHF current, ultraviolet irradiation, pure ichthammol ('cakes'). Surgery is resorted to when agminated abscesses form. Vaccine therapy is a rational measure in persistent and recurrent hidradenitis. In other respects hidradenitis is treated along the same principles as furuncles. Prevention consists in proper hygienic habits (frequent washing of the body with soap and sponge) and disinfection of the axillae with salicylic alcohol or boro-camphor spirit.

Соседние файлы в предмете [НЕСОРТИРОВАННОЕ]