Dermatology course for Public Health

students

CHSM-WSU
May 2025
Superficial cutaneous infections/pyoderma
 The majority is caused by Staphylococcus aureus or Group A
streptococcus
S. aureus is an aggressive pathogen and the most common
cause of primary pyoderma and STIs.
Approximately 60% of healthy individuals have
occasional carriage of S. aureus at some site.
(This represents a common source of many
infections)
S. aureus permanently colonizes the anterior
nares in 20% of the population.
 Other sites of colonization include the axillae and toe webs(5-
10%), perineum (20%), and hands.

 Conditions predisposing to S. aureus colonization include

atopic dermatitis, diabetes mellitus, dialysis, IV drug use, liver
dysfunction, injury, and human immunodeficiency virus (HIV)
infection.

 These bacteria cause a broad clinical spectrum of infection,

ranging from superficial pyoderma to invasive soft-tissue
infections.
S. aureus in pyodermas or STIs can
invade the bloodstream, causing
metastatic infection such as
osteomyelitis, and acute infective
endocarditis.
Some strains of S. aureus also produce
exotoxins, which can cause constellations
of cutaneous and systemic symptoms such
as staphylococcal scalded-skin syndrome
(SSSS) and staphylococcal toxic shock
syndrome (TSS).
Four major categories:
Primary skin infection

Secondary infection of a primary skin disease

(e.g., infected AD)

The skin lesions as manifestations of primary

infection in some other organ system(kidney
disease, blood Ca)

Reactive skin conditions resulting from bacterial

infection (e.g., EN )
pathogenesis
Extracellular products produced by S.
aureus may contribute to its pathogenicity.

Host factors: immunosuppression,

glucocorticoid therapy, and eczema, pre-
existing tissue injury (burn, trauma, wound)
may play a major role in the pathogenesis of
staphylococcal infections.
Some strains produce one or more
exoproteins(toxins) that have potential
effects on immune cells and ultimately
inhibit the host immune response.
Innate immune factor: provided by
neutrophil: The major immune response
component is antimicrobial peptides
 Antimicrobial defense – direct kill of
pathogens
 Immune modulation- regulate and enhance
immune responses
 Maintain the balance of normal flora
 Barrier protection
Superficial pyodermas
Skin Hair follicles
Impetigo Folliculitis
Ecthyma Furuncles
Erysipelas Carbuncles
Cellulitis
Erythrasma
Pitted keratolysis
Impetigo

• Impetigo is a common, highly contagious,

bacterial inf. of superficial skin

Bullous & non bullous

Non

bullous Impetigo
Greater than 70% of cases of pyoderma
Often, both Staph and Streptococcus are involved
IP ~ 3wks, S. aureus spreads from the nose to normal skin
(~ 11 days later) and then develops into skin lesions (after
another 11 days).
Lesions commonly arise on the face or extremities
Pruritus or soreness of the area is a common complaint
Conditions that provide a portal of entry for bacteria
include insect bites, dermatophytoses, herpes simplex,
varicella, abrasions, lacerations, and thermal burns
Cutaneous lesion
The initial lesion is a transient vesicle or pustule
that quickly evolves into a honey-colored crusted
plaque lesion
Surrounding erythema may be present.
Constitutional symptoms are absent.
Regional lymphadenopathy may be present in up
to 90% of patients with prolonged, untreated
infection.
In some individuals, lesions resolve
spontaneously without scarring.
In others, the lesions extend into the dermis,
forming Ecthyma.
Impetigo Sub-corneal blister full of staph
•superficial blisters
•rapidly break to
give “honey-
coloured crusts”
Diagnosis
Typical clinical appearance in a child
Gram stain shows Gram positive cocci
Culture shows Staph aureus
Gram positive Gram negative
organisms stain black organisms stain red
Bullous impetigo
Bullous impetigo – deeper, persistent bullae
Caused by Staph phage type 71
Produce epidermolytic toxins ET-A and ET-B
which affect desmoglein 1 ( a desmosomal
cadherin)
DSG 1:
 Cell- cell adhesion (forms strong intercellular
connections e.g., keratinocyte cells)
 Epidermal barrier maintenance (protects against
pathogens, allergens, and water loss)
 Keratinocyte differentiation(skin cells mature and
move up)
Bullous impetigo in the newborn - blisters remain intact
The Nikolsky sign (sheet-like removal of
epidermis by shearing pressure) is not
present
The bullae are superficial, and within a day
or two, they rupture and collapse
Treatments of Impetigo
 Removal of crusts and good hygiene
First line
 Fusidic acid or mupirocin (topical)
 Dicloxacillin 250/500 mg TID for 5 to 7 days
 Augmentin/Cephalexin 25mg/kg or 250 -500mg QID
Second line (penicillin Allergy)
 Azithromycin 500 mg × 1, then 250 mg daily for 4 days
 Clindamycin 15 mg/kg/day tid
 Erythromycin 250-500 mg PO qid for 5-7 days
Ecthyma
characterized by thickly crusted erosions
or ulcerations
 Usually a consequence of neglected
impetigo
Caused by Gp A Strep and/or Staph
Can complicate trauma or arthropod
infestations
Commonest in children or debilitated
adults
Untreated impetigo can extend more deeply,
penetrating the epidermis, producing a
shallow crusted ulcer.
Occurs most commonly on the lower
extremities.
Poor hygiene and neglect are key elements in
pathogenesis
Adult with ecthyma before Immediately crust removed
crust removed
When the crust is removed,
the ulcer is seen to be
perfectly round.
Usually secondary to an
insect bite, scabies or atopic
eczema.
One month later Two months later
Treatment
Oral flucloxacillin
Once the infection is better, it will take at
least 4 weeks for the ulcer to heal
 Erysipelas
A distinct type of superficial cutaneous cellulitis with marked
dermal lymphatic vessel involvement
Etiology: Commonly Group A Streptococcus
Uncommonly group B, C, and G streptococcus, and rarely caused
by S. aureus.
Lymphedema, venous stasis, web intertrigo, and obesity are risk
factors in the adult patient, but can occur in the absence of an
underlying cause
Rapidly evolving inflammatory plaque with raised border,
spreading peripherally.
Sites – commonest on the face and limbs
Heat, pain, redness, swelling
Recurrent Erysipelas can cause lymphatic obstruction, leading to
lymphoedema
Erysipelas
Patient is unwell with
fever, rigors and general
malaise.
Well defined red hot
swollen skin
Blisters in centre
No obvious portal of
entry
Can be anywhere on the body
Cellulitis
Infection of deep dermis & subcutaneous tissue.

 The most common etiologic agents are St. aureus and

GAS.

Lesions are similar to erysipelas but lack distinct

margins, a deeper, firmer form of tender induration.

Regional LAP is common

Cellulitis
Patient complaining of red,
hot, swollen skin
Erythema less well defined
No blisters
Low grade fever
The affected area displays all
of the cardinal signs of
inflammation such as
rubor (erythema)
calor (warmth)
dolor (pain)
tumor(swelling)
Tender
The lesion usually has ill-
defined, non-palpable
borders.
 Treatment
Cellulitis without draining or abscess
In mild cases of cellulitis treated on an outpatient
basis,
 Dicloxacillin 500 mg PO q6h for 10-14d or

 Amoxicillin-clavulanate 875 mg/125 mg PO BID

for 10-14d or
 cephalexin 500 mg PO q6h for 10-14d

If allergic to penicillin

 Clindamycin 300-600 mg PO q8h for 10-14d
 Moxifloxacin 400 mg PO daily for 10-14d
 clarithromycin 250-500 mg q12h or

 azithromycin 500 mg single dose then, 250

mg qid x 2-5 days
Diagnosis
Red, hot, swollen area of skin - looks like erysipelas or
cellulitis
Pitted Keratolysis
This is a superficial infection of the Horny layer of the
skin.

Commonly seen on the soles and occasionally on the

palms

Hyperhidrosis, prolonged occlusion, and increased skin

surface pH are predisposing factors
 Etiology
Most infections are caused by Kytococcus
sedentarius (formerly Micrococcus
sedentarius),

but other bacteria, such as

- Dermatophilus congolensis
- Corynebacterium species and
- Actinomyces have been implicated
in rare cases.
 C /F

Its frequently involves the sole of the

forefoot & appears as numerous small
punched out circular lesions of a
macerated skin.

There may be associated hyperhidrosis of

the feet & a prominent odour.
 CLINICAL (cont’d…
Lesions consist of small crater-like
depressions in the stratum corneum; they
are present on the weight-bearing regions
of the soles and rarely involve the palms.

These small pits may coalesce into large

craters, rings of craters, or erosions.

Symmetric or asymmetric involvement of

both feet.
Clinical feature (Cont’d…

 There is usually no evidence of erythema or

inflammation, and the disease often goes
unnoticed by the patient.

 Hyperhidrosis and malodor are common

associated findings.
Pitted keratolysis: toe Deeply
pitted epidermis of an intertriginous toe, associated
with hyperhidrosis.
Pitted keratolysis. Pitted keratolysis
Pitted keratolysis
Differential Diagnosis

 Interdigital tinea pedis,

 Candida intertrigo,
 Erythrasma,
 Pseudo plantar warts
 palmoplantar keratoderma,
 Laboratory Examinations
DIAGNOSIS: Clinical diagnosis ruling out other

causes Direct Microscopy : KOH negative

for hyphae.
Wood Lamp Examination ; Negative for

bright coral-red fluorescence (erythrasma).

Culture : In some cases, rule out S. aureus,

group A streptococcus (GAS).

 Rx
The elimination of predisposing factors is
important.
Drying powders.
Aluminum chloride 10-20%
Benzoyl peroxide 5%
Topical antibiotics like clindamycin 2%,
Erythromycin 2%, mupirocin, or fusidic acid.
 Erythrasma

It is a common superficial bacterial infection of

the skin x-sed by;
- well-defined but irregular reddish-brown
patches, fissuring, and white maceration in the
toe clefts or intertriginous areas
 ETIOLOGY
• The primary causative agent is
Corynebacterium minutissimum, a Gram-
positive, non-spore-forming bacillus
which is a member of the normal skin
flora.
Predisposing factors for erythrasma

• Excessive sweating/hyperhidrosis
• Delicate cutaneous barrier
• Obesity
• Diabetes mellitus
• Warm climate
• Poor hygiene
• Advanced age
• Immunosuppression
Clinical Manifestation
 Usually asymptomatic.
 Duration: weeks to months to years.
 Erythrasma is usually a benign condition
characterised by well-demarcated, brown-
red macular patches.
 It’s commonly found in the inner thighs of
obese diabetics, but it’s mostly located in
the axilla, groin ( in men)& toe web
spaces.
 Skin Lesions Patches, sharply
marginated.

 Scaling at sites not continuously occluded. In

webspaces of feet, may be macerated,
eroded, or fissured.

 If pruritic, secondary changes of excoriation,

lichenification.

 Dermatophytosis, candidiasis, and

pseudomonal web space infection may also be
present.
Common Sites Affected:
• Intertriginous areas (where skin touches or
rubs together), such as:
• Axillae (armpits)
• Groin
• Inframammary areas
• Interdigital spaces (between toes)
Erythrasma: Axilia and webspace
 Erythrasma.
B – Hyperpigmented plaques in the inguinal
and periumblical areas
areas (intertriginous zones).
C - Well-demarcated, scaly, hyperpigmented
plaque of disciform erythrasma.
Key Diagnostic Feature:
 Wood’s lamp examination(UV light at ~365nm):
Lesions fluoresce coral red or pinkish red under
ultraviolet light due to the presence of porphyrins
produced by the bacteria. (Coproporphyrin III,
metabolic role for bacteria, no direct pathogen role)

 May not be present if the patient has bathed recently

 KOH examination: to exclude fungal infections

 In the webspaces of the feet, concomitant interdigital
tinea pedis may also be present.

 Gram or Giemsa stains may show fine bacterial

filaments.
Under Wood lamp examination, the porphyrins produced by the
bacteria fluoresce with a coral red color .A small focus is visible on
this photo.
Wood’s lamp
 Prognosis
 The prognosis is excellent; if the
predisposing factors are eliminated.

 Patient Education

 Patients with erythrasma should be

instructed to keep the area dry
Rx
 Clindamycin 2% twice daily for 4 weeks
 Erythromycin 2% lotion twice daily for 4
weeks.
 Antifungal cream twice daily for 4 weeks(If
not effective or recurrent infection)
 Erythromycin 250 mg 4 times daily for 2
weeks or
SSSS
 Folliculitis
Folliculitis is a pyoderma that begins within the hair follicle
Etiology: commonly Staphylococcus aureus
Superficial(Bockhart impetigo): a small, fragile pustules at hair
follicles(infundibulum)
 Deep folliculitis : perifollicular inflammation is common
D/t from Dermatophytic folliculitis(hair usually broken/loosened,
nodule rather than pustule, plucking of hair is painless)
Follicular pustule with erythematous halo.
Sites – scalp, scalp margins, trunk, and limbs
Furuncles
 A boil is a deep-seated inflammatory nodule around a
hair follicle, which later evolves into an abscess
Furuncles arise in hair-bearing sites, particularly in
regions subject to friction, occlusion, and perspiration,
such as the neck, face, axillae, and buttocks
 A furuncle starts as a hard, tender, red folliculocentric
nodule in hair-bearing skin that enlarges and becomes
painful and fluctuant after several days
Furuncles may occur as solitary lesions or as multiple
lesions in sites such as the buttocks
Furuncles
Deeper-seated than folliculitis
68
A carbuncle is a more extensive, deeper,
communicating, infiltrated lesion that
develops when suppuration occurs in thick
inelastic skin when multiple, closely set
furuncles coalesce.
Identify and avoid predisposing factors
Antibiotics
 Topical
 Oral
 parenteral
Eliminate aggravating agents,
 Wash with soap or benzoyl peroxide
preparation.
Keep affected areas clean
Topical antibiotics
Mupirocin (Bactroban) cream: apply a small
amount TID to the affected area x 7-10 days.
Erythromycin 2% solution BID x 7 days
Clindamycin Solution BID x 7-10 days
• Simple furunculosis -Trial of warm compresses.
• incision and drainage followed by
Dicloxacillin 250 to 500 mg (adult dose) q.i.d. for 10 days
Cephalexin 250 to 500 mg (adult dose) for 10 days; 40 to 50 mg/kg/day (children)
for 10 days

Amoxicillin Plus Clavulanic Acid (Beta-Lactamase Inhibitor) 20

mg/kg/day t.i.d. for 10 days
• Second line (penicillin allergy)
Erythromycin ethylsuccinate: 25-500 mg q.i.d./10 dys
Clarithromycin: 250 to 500 mg b.i.d. for 10 days
Azithromycin: 250 mg q.d. for 5 to 7 days
Clindamycin 150 to 300 mg (adult dose) q.i.d. for 10 dys.
Management of Recurrent Furunculosis
Identify the risk and avoid it if possible.
-Stress on personal hygiene!
-General skin care –use antiseptic solutions.
4% chlorhexidine solution, Benzoyl Peroxide
2.5%
 Apply mupirocin 2% ointment daily to the
inside of nares and other sites of S. aureus
carriage
Apply intranasally bid for 5 days.
Rifampin 600 mg PO for 7 to 10 days for
eradication of the carrier state.
Treatment

End!!