Staphylodermas encountered only among children, predominantly among newborns and infants.

Vesiculopustules

Vesiculopustules are lesions commonly encountered in the newborn in the first days of life.

Etiology. The disease is caused by various staphylococcal strains.

Pathogenesis. Maceration caused by excessive sweating, prematurity, asthenia, and artificial feeding are contributing factors.

Clinical picture and course. The affection begins at the orifice of the sweat glands where small non-confluent pustules surrounded by a bright hyperemia border form. The axillary and inguinal folds, the scalp, and the skin on the trunk are the favoured localization. In weak children, extensive areas are involved in the process, which have a tendency to merge and form deep lesions.

Diagnosis. There are usually no difficulties in making the diagnosis. In scabies complicated by pyoderma the vesiculopustules are found in pairs on the palms, soles, buttocks, abdomen, around the navel, and on the extensor surface of the upper limbs. The presence of burrows between the paired vesiculopustules and the detection of the itch mite help in making the proper diagnosis.

Treatment and prevention. Washing and baths are not recommended for the baby during the disease. The healthy skin areas are rubbed with mild disinfectant solutions. Measures are taken to reduce sweating. The affected areas are painted with aqueous and alcohol solutions of aniline dyes.

Multiple Abscesses in Infants (Abscessus Multiplex Infanturn), or Finger's Pseudofurunculosis

Multiple abscesses of newborns and very young children develop when infection gains entrance into the efferent ducts and tufts of the eccrine sweat glands.

Etiology. Staphylococcus aureus is considered to be the causative agent although growth of other micro-organisms is sometimes produced (Streptococcus hemolyticus, Escherichia coli, Proteus vulgaris, etc.).

Pathogenesis. Lack of cleanliness in the care of children, overheating (underclothes and bed clothes that are too warm), rarely changed swaddling clothes, increased sweating which causes skin maceration, dystrophy, undernutrition, faulty diet, enteritis, and general infections are factors which facilitate the development of the morbid condition. The disease is mostly encountered in immature infants and in children with diminished general body resistance.

Clinical picture and course. When only the orifice of the efferent duct of the sweat gland is involved in the infection, small (the size of a millet) superficial pustules (periporitis) form which dry to crusts within a short time and heal without a trace. Most commonly, however, the whole duct and the rufts of the sweat gland are affected. In such cases multiple hard, red-blue nodes develop, they are sharply demarcated and are first the size of a pea but grow rapidly to the size of a hazel-nut. The nodes soften in the centre quite rapidly; the skin here becomes thin and fluctuation is palpated. After that the nodes open and a semi-fluid purulent content with an admixture of blood is discharged. The process terminates by cicatrization. The infants' general condition is usually satisfactory, the body temperature rises rarely.

Diagnosis. Furunculosis is a rare occurrence in children of this age. Periporitis has to be differentiated from folliculitis in which the lesion is always connected with the hair follicle and a hair shaft is often found in the centre of the pustule.

Treatment and prevention. Prevention is particularly important: cleanliness in the care of the child, frequent baths and change of linen and clothing, hygienic powdering, rational diet, and avoidance of overheating are necessary components of prevention.

Pure ichthammol in the form of a 'cake' is applied topically to the abscesses. If necessary, the abscesses are opened surgically. The healthy skin areas are wiped with camphor spirit. Baths are not allowed for some time. Antibiotics, general invigorating measures, injections of gamma globulin are prescribed.

The prognosis should be considered with caution. It is particularly grave in emaciated infants, in complications and in concomitant pneumonia and enterocolitis.

Pemphigus Epidemicus Neonatorum

Pemphigus epidemicus neonatorum is an acute contagious disease of the newborn which is characterized clinically by very rapid formation of pustules and their spreading on the skin surface.

Etiology. Staphylococcus aureus is the causative agent. Some authors, however, claim that the organism responsible for the disease is a special species of staphylococcus and even streptococcus or a filtrable virus.

Pathogenesis. An important role in the development of the disease belongs to the peculiar reactivity of the newborn's skin manifested by the development of vesicles in response to the effect of the bacterial factor, as well as immaturity, birth injury, and toxicosis of pregnancy.

Epidemiology. The disease is very contagious. The main sources of infection are the medical personnel (nurses and their assistants) and mothers who are suffering or had recently suffered from pyoderma, and also purulent foci in the infants (e.g. infection from the umbilical cord). Epidemic of the disease may occur at maternity homes when the infection is transmitted from a sick newborn to a healthy one through the hands of the personnel or the linen. If an epidemic occurs, the department where the infants are kept is immediately closed and the rooms and linen are disinfected. If there are only a few cases the sick children are isolated.

Clinical picture and course. The disease sets in the first days or on the seventh to tenth day of the newborn's life. Small bullae the size of a pea or cherry form on the previously clean or slightly erythematous skin within a few hours. The bullae have a thin tensed top and clear serous-yellowish contents. The contents of the bulla then turn cloudy and purulent. Later the bullae grow in size, spread over the whole body; their top ruptures and bright-red moist itching eroded surfaces are exposed with remnants of the epidermis on the periphery. The discharge from the erosions dries to seropurulent crusts. The favoured localization are the region of the navel, the abdomen, chest, back, buttocks and limbs. The process may also extend to the mucous membranes of the mouth, nose, eyes, and genitalia. In weak and immature infants the lesions spread rapidly, the infant becomes restless, sleeps badly and there are elevated body temperature of 38-39° C, anorexia, leucocytosis, eosinophilia, and increased ESR. Various complications may develop in such cases: otitis, pneumonia, phlegmon, and even sepsis.

If there are no complications the disease may last three to five weeks.

Diagnosis. The diagnosis is based on the bouts of bullous eruptions in the first two weeks of life, rapid evolution of the bullae and the absence of an infiltrate in their base. Differential diagnosis is first of all made with pemphigus syphiliticus neonatorum and congenital epidermolysis, which appear by the time of birth. In pemphigus syphiliticus neonatorum, bullae on an infiltrated base are usually localized on the palms, soles, and buttocks and identification of Treponema pallidum in the secretions of the bullae, positive results of Wassermann's test, precipitin reaction, T. pallidum immobilization test, etc.). In congenital epidermolysis the bullae are localized on skin areas subjected to trauma, in newborns these are the head, shoulders, and lower limbs.

Treatment. The bullae are opened and the epidermal remnants removed carefully. The erosions are treated with 5 per cent boric acid and ointment containing 2-3 per cent antibiotics or with 1 per cent solutions of aniline dyes. Warm baths with potassium permanganate may be prescribed. In severe and extensive lesions, general treatment with antibiotics (kefsol, ceporin) and vitamins of the B complex and C are applied. It is advisable to prescribe the staphylococcal gamma globulin, albumins hemodes, polyglukin. Thorough cleanliness in the treatment and care of the child is absolutely necessary.

Prognosis. In the benign form it is favourable, in the malignant form it is graver. Before the introduction of antibiotic therapy into practice, the mortality from pemphigus epidemicus ranged from 50 to 60 per cent.

Ritter's Disease (Dermatitis Exfoliativa Neonatorum)

Many authors consider this malady to be a severe form of pemphigus epidemicus neonatorum.

Etiology. Most authors believe dermatitis exfoliativa to be a staphylococcal infection (the pathogenic Staphylococcus aureus is mostly identified.

The pathogenic mechanisms are similar to those in pemphigus epidemicus neonatorum.

Clinical picture and course. The disease, like pemphigus epidemicus neonatorum, develops in the first weeks of the infant's life. A bright oedematous inflammatory erythema appears first in the mouth and then descends rapidly to the folds on the neck, to the region around the navel, the genitals, and the anus. Large spherical tensed bullae form against this background which burst soor and leave weeping eroded surfaces. With the mildest injury, the swollen and loose epidermis is detached in places. When the shreds of the epidermis around the erosions are pulled with forceps they separate from the underlying layers far beyond the seemingly healthy skin (positive Nikolsky's sign). Three stages of the disease are distinguished: erythematous, exfoliative, and regenerative. In the first stage there are diffuse redness of the skin, oedema, and bullae. The exudate forming in the epidermis and under it promotes scaling and separation of the epidermis in places (Nikolsky's sign). The second stage is characterized by the appearance of erosions which tend to grow along the periphery and coalesce. This is the gravest period (the infant resembles a patient with II degree burn) marked by high fever, dyspepsia, anaemia, leucocytosis, eosinophilia, high ESR, loss of body weight, and asthenia. In the third, regenerative stage, hyperemia and oedema of the skin diminish and the erosions undergo epithelization.

In the mild forms of the disease, the stage character is not as clear. The acute inflammation abates in 10 to 14 days and copious multilayer scaling of the epidermis in plates occurs. In severe cases the process takes a septic form and is often attended with complications (pneumonia, otitis, meningeal phenomena, acute enterocolitis, phlegmons) which may prove fatal. In older newborns the disease takes a more benign course.

As in pemphigus epidemicus neonatorum, the process may occur on the mucous membranes of the mouth, lips, nose, and genitals, with the formation of erosions and cracks (in the angles of the mouth, on the lips).

Diagnosis. The development of extensive inflammatory changes in the skin in the first two or three weeks of the infant's life with the formation of bullae, which disappear leaving scaling in plates, the sudden onset and rapid course of the disease, which is sometimes characterized by a severe general condition, the typical localization of the lesions, positive Nikolsky's sign, and the morphological changes in the blood form the basis for making the diagnosis.

The differential diagnosis is made with burns, epidermolysis bullosa, pemphigus of early congenital syphilis. The medical history makes it possible to exclude burns.

Treatment. The management of such patients is rather difficult and calls for the joint efforts of the dermatologist and pediatrician. A rational diet must be set up, thorough hygiene followed. External treatment consists in the prescription of aqueous solutions of aniline dyes, neomycin, geliomycin, 0.5-1.0-3.0 per cent erythromycin ointments as stage therapy for producing an anti-inflammatory effect and removing the purulent crusts. General treatment with antibiotics, vitamins of the B complex and vitamin C. Steroid hormones are given in severe cases. In a septic state, antibiotic therapy is complemented by low-molecular dextranes, native plasma, freshly citrated blood; contrykal are given in the respective doses.

Prevention. Measures of prevention are similar to those applied in pemphigus epidemicus neonatorum.

The prognosis is serious and is determined to a great measure by the body's resistance and the spread and intensity of the process. With the use of antibiotics and steroid hormones the fatality rate from this disease has dropped significantly.

Bullous Impetigo of the Newborn (Impetigo Bullosa Neonatorum)

The disease is regarded as a mild, abortive form of pemphigus epidemicus neonatorum to which it may transform if treatment is inadequate or the infant's health deteriorates. It is a benign form of staphyloderma characterized by the appearance of a few separately localized unilocular bullae the size of a pea to that of a cherry. The top of the bulla is thin and tensed and ruptures rapidly with the exposure of moist erosions. The contents of the bullae are serous or seropurulent. The secretions dry with the formation of thin superficial crusts. The bullae form on the skin of the trunk and limbs and have a slight tendency to disseminate and grow on the periphery. The infant's general condition is hardly disturbed.

The diagnosis presents no difficulties.

Treatment. The bullae are opened and the erosions painted with solutions of aniline dyes. The infant must be protected against intercurrent diseases which may aggravate the course of the process.

The prognosis is favourable.

STREPTOCOCCAL PYODERMAS (STREPTODERMAS)

Streptococci mainly attack the smooth skin and not the sebaceous-hair apparatus and the sweat gland as is the case with staphylococci. Streptodermas are of a superficial character as a rule. The primary lesion is a flabby bulla (phlyctena) with clear secretions and a tendency to peripheral growth. The disease is encountered more often in children and women with finer skin.

Streptococcal Impetigo (Impetigo Streptogenes)

This is an eruption of non-follicular locular lesions with a flabby top and serous contents (phlyctenae) and hyperemic oedematous base.

Etiology and pathogenesis. Most authors believe streptococcus to be the only causative agent although staphylococcus is also sometimes found in the contents of the vesicles but in lesser amounts. The contagiosity of streptococcal impetigo or impetigo vulgaris has been proved by numerous research.

Very important factors contributing to the development of the disease are impaired intactness of the skin and mucous membranes due to scratching in pruritic dermatoses and maceration of the epidermis by secretions, for instance from the nose in rhinitis. The state of the organism's resistance is also significant. Seborrhoeal phenomena, changes in skin pH and water-lipid mantle are predisposing factors. Impetigo is particularly common in infants with improper hygienic care.

Clinical picture and course. The disease begins with the appearance of a small red spot on whose surface a vesicle the size of a pin head to that of a lentile (phlyctena) forms in a few hours. In some cases the phlyctena forms on visibly normal skin. The tensed vesicles turn flabby within a very short time and their clear secretions become purulent (cloudy) and then dry into a thin grey crust which gradually falls off. The phlyctenae are usually separated one from another by healthy skin, but they also may spread by peripheral growth and coalesce to form annular lesions (impetigo circinata). The average duration of the disease is three to four weeks. A transient bluish-pink spot is left after the crust falls off. Neither scars nor atrophy of the skin are encountered. The favoured localization of the process are the face and the sides of the trunk and limbs. The disease may spread rapidly to all child contacts (hence the name impetigo contagiosa).

Impetigo bullosa, perleche, streptococcal cheilitis, pityriasis simplex, superficial panaris, intertriginous streptoderma (intertrigo streptogenes), and posterosive syphiloid (papular syphiloid impetigo) are clinical varieties of streptococcal impetigo.