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Recognising the signs of impetigo

Jean Robinson
RGN RSCN BSc MA
Clinical Nurse Specialist Paediatric Dermatology
Barts and The London NHS Trust

Impetigo is a highly infectious bacterial skin condition which is a common problem in children.(1-3) It can involve any part of the body, but mainly affects the face, nostrils and extremities. It is a superficial pyoderma or superficial infection of the skin and soft tissues, and is characterised by inflammation and infection localised in the epidermis. There are two classic forms:

  • Nonbullous impetigo (impetigo contagiosa or crusted impetigo) is the more common type and accounts for more than 70% of cases. More common in children over the age of two years. The lesions usually form on skin that has been injured, eg, after minor abrasions, insect bites or atopic eczema.
  • Bullous impetigo is characterised by fragile vesicles and bullae. This type is more common in infants and children under two years. It favours humid, warm environments and so is often found on moist intertriginous areas, which were previously intact, although it can occur on the face or extremities.

Both types are caused by infection with Staphylococcus aureus and/or Streptococcus pyogenes (group A ß-haemolytic streptococcus [GABHS]). Around 70% of cases of nonbullous impetigo are due to a pure growth of Staph aureus, 15% to a mixed growth of staphylococci and streptococci, and less than 2% to streptococci alone. Impetigo is more common in the warm summer months and among children living in crowded conditions.(2)

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Photos courtesy of D@nderm

Pathophysiology
Impetigo is very contagious and spreads easily by direct physical contact. Impetiginous lesions are usually itchy, and when scratched the infection spreads to surrounding areas, other sites on the body and other family members or children. Household outbreaks are therefore common.
The aetiology and pathogenesis of localised inflammation and infection as well as many of the systemic manifestations depend upon the interaction of the host's immune system with bacterial exoproducts. Staphylococci produce virulence factors, which lead to the development of localised skin lesions. Bacterial enzymes are also secreted which interfere with phagocytosis and promote the destruction of host connective tissue.(2) In streptococci several enzymes are secreted. Additional toxins are also produced by both staphylococci and streptococci causing generalised disease in the host. Host immunity is an important determinant of the overall clinical outcome. Exposure of hosts to these toxins sometimes results in full-blown disease, but more commonly leads to an immune response, probably because there is only a small amount of toxin:

  • In nonbullous impetigo bacteria colonise the skin surface and then superficially invade any areas of broken skin. In bullous impetigo the lesions develop on intact skin due to the localised action of toxin production of Staph aureus.
  • The reservoir for staphylococci is the upper respiratory tract and asymptomatic carriers pass the bacteria to themselves or others. Between 20 and 40% of healthy people may have staphylococcal colonisation in their noses. The reservoir for streptococci is thought to be the skin.
  • Regional lymphadenopathy and leukocytosis are common in nonbullous impetigo, but not usually seen in bullous impetigo. Systemic symptoms are rare in both types of impetigo, and so if a child is systemically unwell other investigations are indicated.
  • Altered host immunity in addition to underlying skin disease, eg, atopic eczema and psoriasis, which compromises the skin barrier function, predispose the child to the subsequent development of impetigo.
  • Epidemic impetigo is particularly notable in the postdelivery ward or neonatal unit, where health workers can infect many infants in a short period of time.

Clinical features
Nonbullous impetigo
Begins as a small red macule rapidly followed by a microvesicle or pustule. These thin-roofed lesions rupture easily leaving weeping spots. Serous and purulent drainage forms a "stuck-on" crust which has the absolutely characteristic honey colour. Individual lesions enlarge to 1-2 cm and satellite lesions appear. These lesions can coalesce resulting in wider areas of crusted involvement. The face is the usual site, especially around the mouth and nostrils, but lesions on extremities and the buttocks are also common. The problem usually remains localised. Widespread impetigo is most common in secondarily infected or impetiginised eczema.

Bullous impetigo
Similar distribution to nonbullous impetigo with perioral blisters and lesions near the nostrils. Neonatal bullous impetigo tends to occur in the inguinal area and on the buttocks. The first lesion is a faint red macule that is quickly followed by a vesicle which may get bigger and stay intact to form a bullae. These bullae are fragile and tend to form annular rims of scale with central erythema that is initially glistening but then dries. Sometimes the lesions continue to get bigger.
 
Prognosis
Generally good. The problem can be self-limiting, but will usually spread and persist on the skin if left untreated, which will represent a source of infection for others. Deep ulcerations, abscesses, cellulitis, lymphadenitis, staphylococcal osteomyelitis, septic arthritis and pneumonia can occur, but such severe progression is usually limited to children with acquired or inherited immune deficiencies. Streptococcal impetigo is most commonly limited to the skin. Poststreptococcal glomerulonephritis is a rare but serious complication, possibly as a result of an abnormal immune response or hypersensitivity to streptococcal antigens. Guttate psoriasis is an additional poststreptococcal phenomenon, but probably occurs in children who have a genetic predisposition for psoriasis. 

Differential diagnosis
Clinical diagnosis is not usually difficult. However, other skin diseases can become secondarily impetiginised which may hide the primary diagnosis. The most common of these other diseases are atopic eczema, herpes simplex infections, varicella zoster and tinea capitis. These must be treated in addition to the impetigo.

Management

  • Consider taking a swab for microscopy, culture and sensitivity of either purulent material in nonbullous impetigo or bullae fluid in bullous impetigo. If the child is systemically unwell consider a full blood count and blood cultures.
  • Impetigo is usually treated systemically with flucloxacillin or erythromycin.
  • If culture reveals both staphylococci and streptococci, there is no way to determine which is causing the infection and both pathogens must be treated with appropriate antibiotics.
  • The decision to treat topically or systemically will depend on the age of the child, and the number, extent and location of lesions. All babies under six months of age should be treated systemically.
  • If the lesions are very wet and weepy the use of potassium permanganate soaks twice daily to the lesions may be indicated.
  • Topical antibiotics (eg, Fucidin®; Leo) can be used for milder cases with no facial involvement for a minimum of five days.
  • Treat any underlying skin disease, eg, atopic eczema, herpes simplex and tinea capitis.

Infection control measures are very important to prevent the spread of impetigo to others. These include:

  • Careful handwashing.
  • Using antibacterial soap.   
  • Using individual towels and bedding.
  • Cleaning individual flannels for washing.
  • Keeping fingernails short.
  • Washing clothes in hot water.
  • Avoiding skin-to-skin contact with the child until the lesions have been treated.
  • Children should stay away from nurseries or school until the lesions have stopped blistering or crusting or they have had 48 hours of antibiotics.

Recurrent episodes of impetigo
In children where recurrent episodes of impetigo occur consider nasal or other carriage. The whole family should have nose, groin and axillae swabs to detect the carriage of Staph aureus. Any carriers should be treated with topical antibiotics and nasal ointment (mupirocin).

Medical consultation/specialist referral

  • Any baby under one month of age as intravenous antibiotics are likely to be required.
  • Children who develop complications, such as cellulitis and/or abscess.
  • Any child who is not managed by firstline treatment.
  • Children with immune deficiency.
  • Children who are systemically unwell.

Follow-up
Not usually required. Uncomplicated impetigo does not scar but may result in postinflammatory pigment changes.

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References

  1. Burr S. Impetigo. In: Barnes K, editor. Paediatrics: a clinical guide for nurse practitioners. London: Elsevier Science; 2003.
  2. Resnick SD. Staphylococcal and streptococcal skin infections: pyodermas and toxin-mediated syndromes. In: Harper J, Oranje A, Prose N, editors. Textbook of pediatric dermatology. Oxford: Blackwell Science Ltd; 2000.
  3. Van Onselen J. Age-specific issues in dermatology nursing. In: Hughes E, Van Onselen J, editors. Dermatology nursing: a practical guide. London; Churchill Livingstone; 2001.

Resources
British Association of Dermatologists
W: www.bad.org.uk
Prodigy Guidance
W: www.prodigy.nhs