In addition to acting as a solid wall with its various keratin layers, the skin defence also comprises various cytokines and defence cells (like Langerhans cells) guarding us from intruders. However, before meeting the keratin blocks, the organisms must compete against the normal flora of the skin that provides an ecological competition for pathogenic microorganisms.
The normal flora composed of aerobic cocci, aerobic and anaerobic coryneform bacteria, gram-negative bacteria and yeasts, also hydrolyse lipids of sebum to produce free fatty acids, which are toxic to many bacteria.
A skin infection occurs when there is a breach in the skin barrier due to causes like injury, diseases, inoculation, warmth, humidity, and poor hygiene. Once the organism enters the skin, it can cause infections at various levels, even gaining entry to our circulatory system in severe cases, leading to a septicaemia. Most primary pyodermas are secondary to infections with Staphylococcus aureus or group A streptococci. Staphylococci are not part of the normal skin flora but may colonise the skin either transiently or more permanently in certain sites such as the nose, axillae, groin, and perineum.
They are common invaders of eczematous, traumatised, or immune-compromised skin and are responsible for impetigo, folliculitis, and surgical wound infections and may produce toxins. These include toxic shock syndrome, enterotoxins, Panton-Valentine Leucocidin, and exfoliative toxins (staphylococcal scalded skin syndrome).
Impetigo is a common, highly contagious, superficial skin infection that primarily affects children. Most lesions occur on the face; however, other body surfaces can also be affected. Impetigo tends to start as small blisters, which becomes filled with pus. These lesions rupture and the purulent exudate dries to form golden-coloured crusts. These lesions can be very infectious. Secondary skin infections of existing skin lesions (e.g., cuts, abrasions, insect bites, chickenpox, eczema) can also occur, leading to an acute, disseminated impetigo.
It is commonly caused by S. aureus bacteria, Streptococcus pyogenes or mixed infections. Methicillin-resistant S. aureus (MRSA) and gentamicin-resistant S. aureus strains have also been reported to cause impetigo. Impetigo is classified as either non-bullous (impetigo contagiosa – about 70% of cases) or bullous types.
Children with non-bullous impetigo commonly have multiple coalescing lesions on their face (perioral, perinasal) and extremities or in areas with a break in the natural skin defence barrier. The initial lesions are small vesicles or pustules (<2cm) that rupture and become a honey-coloured crust with a moist erythematous base. Pharyngitis is absent, but mild regional lymphadenopathy is commonly present. Non-bullous impetigo is usually a self-limiting process that may resolve within two weeks.
Bullous impetigo is considered to be less contagious than the non-bullous form. It tends to affect the face, extremities, axillae, trunk, and perianal region of neonates, but older children and adults can also be affected. The initial lesions are fragile thin-roofed, flaccid, and transparent bullae (<3cm) with a clear, yellow fluid that turns cloudy and dark yellow. Once the bullae rupture, they leave behind a rim of scale around an erythematous moist base but no crust, followed by a brown-lacquered or scalded-skin appearance, with a collarette of scale or a peripheral tube-like rim.
Bullous impetigo also differs from non-bullous impetigo in that bullous impetigo may involve the buccal mucous membranes, however regional adenopathy rarely occurs. At times, extensive lesions in infants may be associated with systemic symptoms such as fever, malaise, generalised weakness, and diarrhoea. Rarely, infants may present with signs of pneumonia, septic arthritis, or osteomyelitis.
The diagnosis of impetigo is usually made based on the history and physical examination. However, bacterial culture and sensitivity can be used to confirm the diagnosis and are recommended in the following scenarios:
- When MRSA is suspected
- In the presence of an impetigo outbreak
- In the presence of post-streptococcal glomerulonephritis (PSGN); in such cases, urinalysis is also necessary
Due to the contagious nature of this disease, utmost care must be taken to limit the spread to other children. Mild, uncomplicated cases can be easily treated with topical antibiotics and proper cleaning of the lesions with antiseptics. Several agents can be used, however, topical retapamulin is the first pleuromutilin antibacterial approved for the treatment of uncomplicated superficial skin infections caused by S. aureus and Step. Pyogenes.
It can be safely used in small children as well. While more widespread cases do require oral treatment and at times antipyretics to deal with systemic symptoms. Oral penicillin or erythromycin are easy to administer and cure most cases. Of course, the addition of a topical antibacterial, as above, does speed up the response time and decrease the infectivity of the lesions. For resistant cases, culture and sensitivity will guide the therapy.
BACTERIAL SKIN LESIONS
Bacterial infections can also cause folliculitis. This is an infection or inflammation of the hair follicles most commonly caused by S. aureus. Other organisms, like fungi and viruses are rarely implicated. This condition appears as small papules or pustules mainly on the limbs, that is pruritic and heals with post-inflammatory scars. It can last for a few years, before the patient seeks help. Fortunately, the use of oral antibiotics, like penicillin, are very effective in most cases and tend to cure the conditions.
A furuncle, or boil, is an acute, round, tender, circumscribed, perifollicular staphylococcal abscess that generally ends in central suppuration.
A carbuncle is merely two of more confluent furuncles, with separate head. These lesions begin in hair follicles and often continue for some time, before rupturing through the skin, discharging purulent, necrotic debris. Sites of predilection are the nape, axillae groin, and buttocks, but boils can occur anywhere. Most cases can be treated with oral antibiotics, topical antibiotics for open areas and anti-inflammatories for pain.
Ecthyma is an ulcerative staphylococcal or streptococcal pyoderma, nearly always of the shin or dorsal feet. The disease begins with a vesicle or pustule, which enlarges in a few days and becomes thickly crusted. When the crust is removed, there is a superficial ulcer with a raw base. Treatment entails the use of antiseptic soaps, followed by the application of fusidic acid, mupirocin, retapamulin, or bacitracin ointments twice daily. Oral dicloxacillin or cephalosporins is also indicated with adjustments made according to the cultured organisms.
Erysipelas is a superficial infection of the skin with the involvement of the dermal lymphatics. It is commonly caused by the Beta-haemolytic group A streptococcal infection, though other types of strep may be involved. It is characterised by local redness, heat, swelling, and a highly characteristic raised indurated border. The onset is often preceded by malaise, followed by fever, headaches, vomiting, and joint pains.
The skin lesions may vary from transient hyperaemia, followed by slight desquamation, to intense inflammation with vesicles and bullae. Common areas of involvement are the face and legs, with operative wounds, fissures, abrasions, or scratches being some of the predisposing factors. Erysipelas can become serious condition, leading to septicaemia, deep cellulitis, or even necrotising fasciitis. Prompt treatment with oral penicillin and even hospitalisation may be required.
Another deeper infection of the skin is called cellulitis. This is a suppurative inflammation, involving the subcutaneous tissues, caused most frequently by S. pyogenes or S. aureus. Usually, mild local erythema and tenderness, malaise and chills may be present at the onset. The erythema becomes more intense and the area becomes more infiltrated and pits on pressure. Streaks of lymphangitis may spread from the area to neighbouring lymph glands and in some cases, gangrene, metastatic abscesses and severe sepsis may follow, especially in immunocompromised patients. Keeping these in mind, one must be very aggressive in treating the patients, with oral or intravenous antibiotics for long enough periods of time. Anti-inflammatories, antipyretics, and good supportive management should also be put in place.
Our skin also keeps fungi from entering our body. Candidiasis, pityriasis versicolor, and the dermatophyte infections are traditionally known as superficial infections in that they do not penetrate the superficial layers of the skin, except sometimes in the immunocompromised. These infections are very common and can affect the skin, nails and hairs in patients of any age.
Dermatophytes are composed of three genera of fungi: Trichophyton, Epidermophyton, and Microsporum. Dermatophytes are keratinophilic fungi, living only on superficial dead keratin. They cause inflammation due to permeation of the metabolic products of the fungus into the skin or due to induction of delayed hypersensitivity. The dermatophytes are responsible for tinea infections affecting all the skin surface of the body, manifesting differently on different sites.
Candidal skin infections are commonly caused by candida albicans, which is a normal skin commensal. This fungus becomes pathogenic in the presence of predisposing factors, like diabetes, obesity, immunosuppression, intake of antibiotics, and sometimes due to oral contraceptives. Candida infection can manifest in various forms like intertrigo, paronychia, oral and genital infections. Others are more sinister, like chronic mucocutaneous and systemic candidiasis infections. Treatment with topical and oral antifungals tends to be very effective.
Tinea capitis (also known as ringworm) is common in children of lower socioeconomic areas. It occurs almost exclusively before puberty as the secretion of sebum has a protective effect in adults. The clinical picture tends to vary in severity, depending on the source of the fungus. Basically, human infections produce quite minor degree of erythema and scaling. However, zoophilic dermatophytes can induce considerable inflammation because the host resistance is usually high.
This may result in a boggy mass of inflamed and purulent skin, known as a kerion. If left untreated, it may result in permanent patches of hair loss and therefore early diagnosis is very important. The treatment consists of a sulphur-containing shampoo together with oral antifungals (griseofulvin) for at least 6-12 weeks.
Tinea lesions on other skin areas tend to be annular or arcuate plaques that spread centrifugally. The edge shows papulovesiculation, pustulation, and scaling, while the centre is usually relatively clear, though in chronic lesions, there may be nodules, hyperpigmentation and even lichenification in the centre. Tinea pedis (athlete’s foot) appears as scaling and emaciation of the interdigital spaces of the feet or a scaling plaque on the sole. Athlete’s foot tends to recur if not treated properly.
Fortunately, most of the infections respond to topical imidazoles or allylamines. Allylamine anti-fungal, is widely available as terbinafine and tends to be very effective with dermatophytes resulting in less frequent recurrences. In severe cases, oral antifungals can supplement the treatment.
Pityriasis versicolor is caused by Malassezia furfur, which is a normal flora on the skin. It represents a shift in the relationship between the host and resident yeast flora. The yeast overgrows in hot and humid conditions and releases carboxylic acid, which causes hypopigmentation due to reduced tanning of the skin. The lesions are common on the chest and back, and sweaty areas and can even look erythematous or hyperpigmented. They can coalesce into large macules and tend to have a fine scale, accentuated by scratching. Treatment is easy with topical antifungals or sulphur-containing shampoos. In severe cases, the use of oral antifungals like ketoconazole can help decrease the relapse rates.