Impetigo

Impetigo is a highly infectious superficial bacterial skin infection which is most frequently seen in children (Figure 12.1). It is more common in the summer (Loffeld et al., 2005). Both Staphylococcus aureus (S. aureus) and Streptococcus pyogenes (group A – haemolytic streptococcus, GABHS) can cause this type of superficial pyoderma or purulent skin disease. In British general practice, 2.8% of children aged 0–4 years and 1.6% of children 5–15 years consult their GP about impetigo each year (McCormick et al., 1995). It is the most common form of bacterial infection in individuals with human immunodeficiency virus (HIV).

Primary impetigo is direct bacterial invasion of skin which was previously normal whereas secondary impetigo occurs in skin where there is some underlying skin disease, for example atopic eczema or scabies, disrupting the skin barrier. Impetigo is characterised by inflammation and infection localised in the epidermis. Impetigo is also classified as non-bullous or bullous. Non-bullous impetigo is sometimes also termed impetigo contagiosa, although this terminology may be used at times synonymously as any impetigo.

Non-bullous impetigo is the most common type and accounts for more than 70% of cases (Burr, 2003). It is more common in children over the age of 2 years. Initial lesions are thin walled vesicles on skin which has previously been normal. Subsequently any areas where the skin barrier has been disrupted, for example minor abrasions, insect bites or atopic eczema, may be infected. The initial lesions rupture leaving erosions which are covered by the yellowish brown or honey-coloured crusts which are very characteristic of the condition. Individual lesions enlarge to 1–2 cm and satellite lesions appear. These can coalesce resulting in larger areas of crusted involvement. The infection can occur on any part of the body but the face, especially around the mouth and nostrils, extremities and buttocks are common. The problem usually remains localised. Widespread impetigo is most common in secondarily infected or impetiginised eczema. Diagnosis is not usually difficult. The most important point to remember is that any underlying skin disease, for example shingles, cold sores, fungal skin infections and eczema, needs recognition and must also be treated (Resnick, 2000). Although not painful, impetigo can be itchy and sore. Bullous impetigo is less common and characterised by vesicles and bullae which rupture less easily and can persist for several days (Koning et al., 2003). There are usually fewer lesions and it can affect the trunk more commonly than in non-bullous impetigo. It is more common in infants and children under 2 years of age. Neonatal bullous impetigo tends to occur in the inguinal area and on the buttocks. The lesions appear to develop on intact skin as a result of localised toxin production by S. aureus. It can be confused with thermal burns, blistering disorders (e.g. bullous pemphigoid), herpes infections and Stevens–Johnson syndrome (Koning et al., 2003). Causes

Bullous impetigo is always caused by S. aureus. Non-bullous impetigo can be caused by staphylococci or streptococci; it is possible to culture both organisms from lesions in many cases (Resnick, 2000). Historically in Britain S. aureus was the main cause of impetigo in the 1940s and 1950s after which S. pyogenes was the main causative agent for about 30 years. Currently S. aureus is the dominant cause again (Koning et al., 2003) with 10% of impetigo cases in Britain due to S. pyogenes.

Prognosis
The prognosis is generally good. Impetigo can be self-limiting but will usually persist and spread if untreated and be a source of infection for others. Local and systemic spread can rarely result in cellulitis, lymphangitis or septicaemia (Koning et al., 2003). Severe progression such as septic arthritis, pneumonia and osteomyelitis are very rare and usually limited to those with acquired in inherited immune deficiencies (Resnick, 2000). Post-streptococcal glomerular nephritis is a serious but rare complication while guttate psoriasis can also occur but probably only in those already genetically predisposed.

Management
Koning et al.’s (2003) review of 36 treatments for impetigo highlight that there is no standard therapy for impetigo. Trials show that Penicillin is not effective for impetigo and there is little evidence supporting the value of disinfecting measures. Knowledge of local resistance patterns on the basis of surveillance of specimens should be incorporated into any regional guidelines.

1. Consider taking a swab for microscopy, culture and sensitivity of in non-bullous impetigo of purulent material or bullae fluid in bullous impetigo especially if MRSA is a possibility (Box 12.1). If the child or adult is systemically unwell, consider taking blood for blood cultures.
2. Hygiene measures to reduce the spread to others: Careful hand washing, use of individual towels and bedding, avoidance of skin-to-skin contact with the child or adult until lesions have been treated.
3. Children should stay away from nursery or school until the lesions have stopped blistering or crusting or they have had 48 hours of antibiotics.
4. In limited disease topical antibiotics, for example fusidic acid, may be sufficient (other topical antibiotics seem less effective) (Koning et al., 2003).
5. Oral Flucloxacillin or Erythromycin, although there is insufficient evidence that they are better than topical (Koning et al., 2003).
6. If culture reveals both staphylococcus and streptococcus, both pathogens must be treated with appropriate antibiotics.
7. Most importantly any underlying skin condition must also be treated, e.g. impetiginised atopic eczema should be treated concurrently with appropriate topical corticosteroids and emollients (Charman and Lawton, 2006).

Box 12.1 Bacterial swab Moisten the tip of the swab; Apply to the affected skin; Rotate the swab between the fingers to pick up debris; Put into transport medium.     Source: RCN/BDNG (2008).