Some of the bacterial, viral and fungal infections that affect the skin are considered in this section. Many skin infections are considered under the individual causative organisms.
An important role of the intact skin is to prevent the entry of infective organisms. This is achieved by the following:
THE CORNIFIED SURFACE on many body sites is difficult to breach and has a desiccating effect on some microorganisms.
SURFACE LONG-CHAIN FATTY ACIDS inhibit the growth of staphylococci.
THE RESIDENT FLORA on the skin surface can limit the growth of potential pathogens by the production of antimicrobial substances. This is especially useful on continually moist surfaces such as the flexures, where the opportunity for invasion is increased.
TRAUMA OR ABRASION of the skin removes the stratum corneum and allows infection to occur much more readily; Staph. aureus or Streptococcus pyogenes are the usual invaders. A cleft in the skin can often be seen at the site of entry of streptococci, e.g. below the ear-lobe when erysipelas ensues, causing cellulitis affecting the face.
VIRAL DISEASE OR PRIMARY DERMATOSES may allow secondary bacterial infection, e.g. impetigo can follow a ‘cold sore’ or eczema.
OTHER ORGANISMS that breach the skin include fleas and lice, and with subsequent itching and excoriation bacterial infection may spread. In patients with continuing bacterial infection (particularly children) an underlying disease such as infestation should always be sought.
STAPHYLOCOCCAL INFECTION. Staph. au reus may form part of the flora of the nose in 20% of individuals. It can also be carried on perianal skin, especially in males. In the majority of infections, invasion of the skin remains localized to, for example, a hair follicle as a furuncle or boil. Toxins produced by staphylococci, e.g. exfoliatin, are released by certain phage types and will cause separation of epidermal cells to produce toxic epidermal necrolysis. Toxic shock syndrome is associated with staphylococcal infection, serious systemic disease, widespread erythema and subsequent peeling of the
skin. Erythrogenic staphylococcal toxins may prod uce a disease that resembles scarlet fever, which is induced by streptococci.
Boils or furuncles are painful, erythematous, tender, papular lesions that are related to infection of the hair follicle and can occur on any part of the hair-bearing skin. They are most commonly seen on the neck, axillae, buttocks and thighs. Spread to involve several follicles will produce a carbuncle. Superficial infection of the follicle causes pin-point pustules over the face or legs, especially in children. With recurrent boils, patients should be screened for diabetes mellitus.
FOLLICULAR IMPETIGO. Papular lesions may occur when the whole follicle is inflamed to produce sycosis. Sycosis barbae occurs when the beard area is involved. Less commonly, crusted, necrotic or scarred lesions occur on the scalp or face. Staphylococci can sometimes be isolated from these but the pathogenesis of such lesions is not clear.
Acute lesions should only be treated with systemic antibiotics if there is marked surrounding erythema or there are associated constitutional symptoms. When the lesion is beginning to ‘point’ then the overlying skin may be broken with a sterile needle and the area gently swabbed with an antiseptic, such as chlorhexidine or povidoneiodine. Recurrent boils will require the long-term use of an antiseptic regimen over several months, including bathing with povidone-iodine. Affected sites and areas of carriage such as the nose or perianal skin will require the application of an antiseptic cream (containing chlorhexidine or neomycin) or dusting powder. With multiple-resistantStaph. au reus (MRSA, see p. 21) mupirocin in ointment form is applied to the nose or topically. Family members may also require treatment if chronic sepsis continues.
Similar treatment may be required for staphylococcal infection associated with sycosis barbae.
This crusted eruption commonly seen on the face of children may be caused by staphylococci, streptococci or a combination of the two organisms. Staphylococcal infection induces superficial bullae, which are seldom evident because they quickly rupture to leave a moist yellow crusted surface with surrounding inflammation. Typically the facial skin is involved and children are frequently affected. Bullous lesions are less commonly seen and are associated with the same phage type of staphylococcus that produces toxic epidermal necrolysis. The reason why the disease remains limited in some children whereas it becomes disseminated in others is not clear.
Care should be taken to prevent or limit spread of the disease in families or institutions. Areas should be gently bathed with an antiseptic solution such as hexachlorophane or povidone-iodine. Similar preparations in a paint or powder form should be applied to the skin after cleansing. Systemic antibiotics are prescribed if infection is widespread. Rarely, nephrotoxic strains of streptococci are associated with impetigo; the sensitivity of staphylococci should be determined. Erythromycin or cephalosporins both give adequate levels in the skin when given by mouth.