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Figure 12.1 Impetigo. (Source: Graham-Brown
and
Burns, 2006.) |
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.
- 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.
- 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.
- Children should stay away from nursery
or school until the lesions have stopped blistering or crusting or they have had
48 hours of antibiotics.
- In limited disease topical antibiotics, for
example fusidic acid, may be sufficient
(other topical antibiotics seem less effective)
(Koning et al., 2003).
- Oral Flucloxacillin or Erythromycin, although
there is insufficient evidence that they are better
than topical (Koning et al., 2003).
- If culture reveals both staphylococcus and
streptococcus, both pathogens must be treated
with appropriate antibiotics.
- 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).
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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. |
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Source: RCN/BDNG (2008). |
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