IMPETIGO ETIOLOGY, EPIDERMELOGY, PATHOPHYSIOLOGY, TREATMENT AND DRUGS OF IMPETIGO

1. IMPETIGO
Presented by:-VIKAS
AAGRAHARI
PHARM-D 4TH YR

2. IMPETIGO
• Impetigo is a superficial skin infection that
is seen most commonly in children.
• The infection is generally classified as
bullous or non-bullous based on clinical
presentation.
• Impetigo is most common during hot,
humid weather, which facilitates microbial
colonization of the skin
• Minor trauma, such as scratches or insect
bites, allows entry of organisms into the
superficial layers of skin, and infection
ensues.
• Impetigo is highly communicable and
readily spreads through close contact,
especially among siblings and children in

3. ETIOLOGY
Most cases of impetigo were caused by
Streptococcus pyogenes, but recently
Staphylococcus aureus, either alone or
in combination with S. pyogenes, has
emerged as the principal cause of
impetigo.

4. Epidemiology:
• The bullous form most frequently affects neonates and accounts
for approximately 10% of all cases of impetigo
• Based on data from studies published since 2000 from low and
low-middle income countries, we estimate the global population of
children suffering from impetigo at any one time to be in excess of
162 million, predominantly in tropical, resource-poor contexts.
Impetigo is an under-recognised disease and in conjunction with
scabies, comprises a major childhood dermatological condition with
potential lifelong consequences if untreated.

5. Occurrence
• On exposed skin mainly on face.
• Most common during hot, humid weather, which facilitates
microbial colonization of the skin.
• Minor trauma, such as scratches or insect bites, then allows entry
of organisms into the superficial layers of skin, and infection
ensues.

7. STAGES OF IMPETIGO BY TYPE
• There are three types of impetigo based on the bacteria that
cause them and the sores they form. Each type goes through a
series of stages.
1. Non Bullous impetigo
2. Bullous impetigo
3. Ecthyma

8. NON -BULLOUS
• Non-bullous impetigo is mainly
caused by Staphylococcus aureus.
It’s the most common form of
impetigo.
• It goes through the following stages:
• It usually starts with reddish, itchy
sores around the mouth and nose.
• The sores break open, leaving
red and irritated skin around
them.
• A brownish-yellow crust

9. BULLOUS IMPETIGO
• Bullous impetigo is almost always
caused by Staphylococcus aureus
bacteria.
• It usually forms larger blisters or bullae
filled with a clear fluid that may become
darker and cloudy. The blisters start on
unbroken skin and aren’t surrounded by
reddish areas.
• The blisters become limp and clear, and
then burst open.
• A yellowish, crusty sore forms over the
area where the blisters broke open

10. ECTHYMA
• This more serious infection is much less
common. It occasionally happens when
impetigo isn’t treated. Ecthyma goes
deeper into the skin than the other forms
of impetigo, and it’s more severe.
• The infection forms painful blisters on the
skin of the buttocks, thighs, legs, ankles,
and feet.
• The blisters turn into pus- filled sores with
a thicker crust.
• Often, the skin around the sores turns red.

11. CLINICAL MANIFESTATION
General
• Exposed skin, especially the face, is the most common site for
impetigo.
Symptoms
• Pruritus is common, and scratching of the lesions may further
spread infection through excoriation of the skin.
• Other systemic signs of infection are minimal.
• Weakness, fever, and diarrhea sometimes are seen with
bullous impetigo.

12. Signs
• Non-bullous impetigo manifests initially as small, fluid-
filled vesicles.
• These lesions rapidly develop into pus-filled blisters that
rupture readily.
• Purulent discharge from the lesions dries to form golden
yellow crusts that are characteristic of impetigo.
• In the bullous form of impetigo, the lesions begin as vesicles
and turn into bullae containing clear yellow fluid.
• Bullae soon rupture, forming thin, light brown crusts.

13. PATHOPHYSIOLOGY-IMPETIGO
• Bullous impetigo is caused by staphylococci producing exfoliative
toxin that contains serine proteases acting on desmoglein, a
structurally critical peptide bond in a molecule that holds epidermal
cells together. This process allows Staphylococcus aureus to
spread under the stratum corneum in the space formed by the
toxin, causing the epidermis to split just below the stratum
granulosum. Large blisters then form in the epidermis with
neutrophil . In bullous impetigo, the bullae rupture quickly, causing
superficial erosion and a yellow crust.
•while in non-bullous impetigo, Streptococcus typically produces a
thick-walled pustule with an erythematous base. Histology of non-
bullous established lesions shows a thick surface crust composed
of serum and neutrophils in various stages of breakdown with

14. Non-bullous impetigo
Non bullous impetigo
starts as a
pink macule that
evolves into
a vesicle or pustule and
then into crusted
erosions. Untreated
impetigo usually
resolves within 2 to 4
weeks without scarring.

15. DIAGNOSIS
•Cultures should be collected.
•Crusted tops of lesions should be raised so that purulent material at the base of the
lesion can be cultured.
•Cultures should not be collected from open, draining skin pustules because they may be
colonized with staphylococci and other normal skin flora.
Laboratory Tests
Other Diagnostic Tests :-A complete blood count is often performed

16. TREATMENT
ORAL ADULT DOSE
• Dicloxacillin 250–500 mg every 6
h
• Cephalexin 250–500 mg every 6
h
• Cefadroxil 500 mg every 12 h
• Clindamycin 150–300 mg every
6–8
• Mupirocin ointment every 8 ha
ORAL
PEDIATRIC DOSE
• Dicloxacillin 25–50 mg/kg
in four divided doses
• Cephalexin 25–50 mg/kg in two
to four divided doses
• Cefadroxil 30 mg/kg in
two divided doses
• Clindamycin 10–30 mg/kg/day
in three to four divided doses
• Mupirocin ointment every 8 ha

18. MONITORING
PARAMETERS
• Clinical response should be seen within 7
days of initiating antimicrobial therapy for
impetigo. Treatment failures could be a
result of noncompliance or antimicrobial
resistance.
• A follow-up culture of exudates should be
collected for culture and sensitivity, with
treatment modified accordingly
• Fingernails should be kept short, and
patients should be advised not to scratch
any lesions to avoid spread of infection.

19. EDUCATION
• Patients should be instructed on use
of antibacterial soaps.
• Avoidance of sharing of towels and
washcloths, because impetigo is
extremely contagious.
• Children attending day care should be
removed until 48 to 72 hr after
initiation of antibiotic treatment.

20. References
• Craft, N, Lee PK, et al. “Superficial cutaneous infections and
pyodermas.” In: Wolff K, Goldsmith LA, et al. Fitzpatrick’s
Dermatology in General Medicine (seventh edition). McGraw Hill
Medical, New York, 2008: 1695-8.
• Habif TP, Campbell, JL, et al. “Impetigo.” In: Dermatology
DDxDeck. Mosby Elsevier, China, 2006: Card#46.
• Halpern AV and Heymann WR. “Bacterial diseases.” In: Bolognia
JL, et al. Dermatology. (second edition). Mosby Elsevier, Spain,
2008:1075-6.