5. Etiology
● Caused either by staphylococcus aureus/streptococcus
pyogenes
● Recurrent impetigo accounts for
Scabies
Pediculosis
Dermatophytic infection
Atopic dermatitis, malaria
6. Clinical features
● Primarily affects school children
MORPHOLOGY
● Thin walled blister on an erythematous base, ruptures
rapidly to form an area of exudation and honey
coloured crusts.
● Lesion spreads peripherally without central healing and
many lesions may coalesce to form polycyclic lesions.
● Removal of crust reveals erosion.
7. ● Fate:Crust falls leaving erythema, which fades out without
scarring.
● Lesions are usually multiple.
● Regional lymphadenopathy and occasionally constitutional
symptoms.
8.
9. Site
Face, especially around mouth and nose
Complications
● Post streptococcal glomerulonephritis
● Eczematisation
10. Investigations
● Gram stain of exudate shows polymorphs with intracellular and
extracellular gram positive cocciin chains/clusters.
● Culture of pus helps to establish the etiological agent.
Differential Diagnosis
● Bullous impetigo
● Herpes simplex
13. Etiology
● Caused by certain strains of staphylococcus aureus
Clinical features
● Seen in infants
14. MORPHOLOGY
● Bullae with turbid collection of fluid without an
erythematous halo.
● Rupture after a few days to form thin, varnish like
crusts.
● Lesions may heal in the centre to form annular
plaques.
● Mucous membranes may be involved.
15.
16.
17. Complications
● Staphylococcal scalded skin syndrome
Investigations
● Gram stain:: polymorphs with intracellular and extracellular
gram positive coccii in clusters.
● Culture:: Staphylococcus aureus
Differential Diagnosis
● Impetigo contagiosa
20. Etiology
● Staphylococcus aureus infection present at different
sites
Ear::otitis media
Lungs:: pneumonitis
Skin:: trivial wounds
● It produces an exotoxin (exfoliative toxin) which
spreads haematogenously and causes a slit in upper
layers of epidermis.
21. Clinical features
● Infants
● Acute in onset with fever and skin tenderness.
● Followed by peeling of skin in thin sheets.
● Clinically skin appears scalded.
● Mucous membranes spared.
26. Etiology
● Deeper infection caused by either streptococcus
pyogenes/Staphylococcus aureus or both.
● Predisposing factors::poor hygiene
Malnutrition
Minor injuries
Insect bites
Scabies
27. Clinical features
● Small bulla/pustule appears on an erythematous base
and soon forms a crusted, indurated, tender plaque,
with an erythematous, edematous areola.
● Removal of adherent crust reveals an irregular ulcer.
● Lesions heals without scarring.
28.
29. Sites
● Buttocks
● Thighs
● Legs
Treatment
● Local hygiene
● Systemic antibiotics -- penicillin
Erythromycin
39. Etiology
● Deep seated follicular and perifollicular infection.
● Caused by staphylococcus aureus; culminating in to
necrosis.
40. Clinical features
● Adolescent boys
● Usually 1-2 tender, firm, red, follicular nodules which
become necrotic and discharge their central core.
● Lesions heal with barely perceptible scarring.
● Occasionally lymphadenopathy and fever.
41.
42. Sites
● Hair bearing sites -- face
Axillae
Buttocks
Perineal region
Investigations
● Pus culture from lesions.
43. Treatment
Acute episodes
● Hot fomentation
● Appropriate antibiotics
● Surgical incision and
drainage of pus
Chronic, recurrent
furunculosis
● Appropriate antibiotics
● Treat carrier state with
topical mupirocin or
systemic rifampicin.
45. Etiology
● Staphylococcus aureus induced.
● Deep infection of contiguous hair follicles.
● Freequent in diabetics and patients on steroid therapy.
46. Clinical features
● Adult males
● Constitutional symptoms like fever always present.
● Tender, indurated, lobulated, intensely erythematous
plaque discharging pus from many openings.
● Back is the commonest site of involvement.
47.
48. Investigations
● Pus culture sensitivity.
● Rule oot diabetes.
Treatment
● Drainage of deep seated pockets of pus..
● Aggressive treatment with flucloxacillin or other
penicillinase -- resistant antibiotics.
50. Etiology
● Streptococcus pyogenes
● Enters through a superficial break in the skin.
● Superficial infection.
● Reccur, if there is pre-existing lymphedema or venous
stasis.
51. Clinical features
MORPHOLOGY
● Acute erythematous, warm, indurated rapidly
spreading plaques.
● Margin is sharply defined and superficial vesiculation
may occur 9n the plaque.
● Constitutional symptoms are invariable and start
before the onset of skin lesions.
52.
53. Site
● Lower limbs; less frequently.upper limb and face.
● Lymphangitis and lymphedema predispose to development
of recurrent lesions.
Complications
● Facial erysipelas, if left untreated, may prove fatal.
● Recurrences may occur in the same area and result in
lymphedema.
54. Treatment
Symptomatic treatment
● Rest
● Limb elevation
● Non steroidal
anti-inflammatory drugs
to relieve pain and
reduce inflammation.
Specific treatment
● Acute episodes::
parenteral penicillin
● Penicillin sensitive
patients:: erythromycin
● Recurrent episodes::
chemoprophylaxis with
long acting penicillin.
56. Etiology
● Streptococcus pyogenes
● Enters through superficial break the skin.
● Deeper infection.
● Recurrent cellulitis occur, if there is pre-existing
lymphedema or venous stasis.
57. Clinical features
● Erythematous, warm, indurated, rapidly spreading
plaques.
● Lesion is ill-defined and deeper.
● Constitutional symptoms are invariable and start
before the onset of skin lesions.
58.
59. Site
● Lower limbs; less frequently.upper limb and face.
● Lymphangitis and lymphedema predispose to
development of recurrent lesions.
Complications
● Recurrences may occur in the same area and result in
lymphedema.
60. Treatment
Symptomatic treatment
● Rest
● Limb elevation
● Non steroidal
anti-inflammatory drugs
to relieve pain and
reduce inflammation.
Specific treatment
● Acute episodes::
parenteral penicillin
● Penicillin sensitive
patients:: erythromycin
● Recurrent episodes::
chemoprophylaxis with
long acting penicillin.
