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I M P E T I G O

Introduction
Impetigo is a superficial pyoderma first
described by Dunn & Fox in the 1860s.
Impetigo is highly contagious gram (+)
bacterial infection of the superficial layers
of the epidermis.
The 2 forms of the disease are bullous
impetigo and nonbullous impetigo.
Epidemiology
Peak incidence during summer and fall.
The male to female ratio is equal.
Impetigo occurs in individual of all ages
more commonly in children.
The majority 90% of bullous impetigo
cases occur in children < 2 years.
Nonbullous impetigo is most common in
children age 2-5 years.
Etiology
Impetigo is caused by Staphylococcus
aureus and group A hemolytic
streptococci (GABHS)
Nonbullous impetigo most lesions are
caused by S. aureus & GABHS
Bullous impetigo Coagulase (+) group II
S. aureus, most often phaga type 71
Pathogenesis
Intact skin is usually resistant to
colonization or infection by S. aureus or
GABHS. These bacteria can be introduce
from the environment and only transiently
colonize the cutaneous surface.
High temperature and humidity, underlying
dermatologic diseases, and young age are
associated with colonization.
Pathogenesis
Skin disruption reveal fibronectin
receptors and allow for colonization or
invasion
S. aureus produce exotoxins loss of cell
adhesions in the superficial dermis
causes blisters and skin sloughing by
cleaving of the granular cell layer of the
epidermis
Pathology
In bullous impetigo, the superficial blisters
contain neutrophils and cocci, although very
early lesions will sometimes fail to
demonstrate organisms. The blisters are
typically subcorneal with epidermolysis within
the granular layer.
Pathology
Nonbullous impetigo is characterized by
oedema, hyperaemia, and an intense
inflammatory infiltrate predominated by
neutrophils
Clinical Manifestation
Nonbullous Impetigo

Begin with a single erythematous macule or
papule 2-5 mm in size
The characteristic lesion is a fragile vesicle or
pustul that readily ruptures and becomes a
honeyyellow, adherent, crusted papule or
plaque smaller than 2 cm and with minimal or
no surrounding redness
Lesion are located around the nose, mouth,
and exposed parts of the body (arms, legs)
Nonbullous Impetigo
Figure 1. Crusted erythematous
erosions becoming confluent on the
nose, cheek, lips, and chin in a child.
Figure 2. Nonbullous impetigo
on the face.
Clinical Manifestation
Bullous Impetigo

The characteristic lesion is the vesicle that
develops into a superficial flaccid bulla < 1
cm in diameter on intact skin, with minimal or
no surrounding redness.
The roof of the bulla ruptures, often leaving a
peripheral collaretteof scale and tubelike rim
at the periphery
Lesions are often found on the face but may
appear anywhere on the body
Bullous Impetigo
Figure 3. A large, single bulla with
surrounding erhytema and edema
on the thumb of a child
Figure 4. Superficial flaccid bullae of
bullous impetigo caused by
Staphylococcus aureus
Lab Studies
Impetigo is usually diagnosed clinically
Leukocytosis is present 50% of cases
Gram stain and culture of the blister
many PMN WBCs and gram (+) cocci
A KOH wet mount to exclude bullous
dermatophyte infection
A Tzanck preparation or viral culture to
exclude herpes simplex infection
Diagnosis
Usually the diagnosis of impetigo can be
made clinically without the need for
biopsies or laboratory tests.
However if the diagnosis is in question,
microbiological testing can be very helpful.

Differential Diagnosis
Nonbullous Impetigo
Figure 5. Contact dermatitis
Figure 7. Varicella
Figure 6. Echtyma
Differential Diagnosis
Bullous Impetigo
Figure 8. Bullous pemphigoid Figure 9. Insect bites
Therapy
Both topical and systemic antibiotics have
been advocated for treating impetigo.
Mild cases gentle cleansing, removing
crusts , and applying the prescription-
strength antibiotic ointment mupirocin
More severe or widespread cases
especially of bullous impetigo, may
required oral antibiotic medication
Therapy
Topical antibiotic the treatment of
choice for individuals with uncomplicated
localized impetigo
Mupirocin 2% ointment (Bactroban),
apply to lesion 3 times daily for 3-5
days
Therapy
Systemic antibiotic :
Amoxicillin/clavulanate (Augmentin),
Cefuroxime, Cephalexin, Dicloxacillin, or
Erythromysin
Adults 250-500 mg 2 times daily for 10
days
Children 90 mg per kg per day, divided,
twice daily for 10 days
Prognosis
Beyond the neonatal period, patients who
receive early and appropriate therapy
have an excellent chance of recovery
without scarring or complications
Lesions usually resolve completely in 7-10
days with treatment
Culture lesion to find resistant organisms if
the lesion have not resolved within 7-10
days
Complications
Acute post streptococcal
glomerulonephritis is a serious
complication between 1-5% of patients
with nonbullous impetigo
Other rare potential complication
sepsis, osteomyelitis, arthritis,
endocarditis, pneumonia, cellulitis,
limfangitis or limfadenitis, TSS, and SSSS
Prevention
Avoid contact with infected persons
Keep wounds clean
Wash hands after contacting lesions or
infected patients
Conclusion
Impetigo is highly contagious gram (+)
bacterial infection of the superficial layers
of the epidermis.
The 2 forms bullous and nonbullous
impetigo.
Impetigo is caused by Staphylococcus
aureus and group A hemolytic
streptococci (GABHS)
Impetigo is usually diagnosed clinically.
Therapy topical and systemis antibiotic.




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