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SKIN AND SOFT TISSUE INFECTIONS o Localized clusters of vesicles:

(Overview)  Shingles
By Lester A. Deniega, MD  Herpes simplex
 Impetigo
(Pedia2 Module4/ Lecture Date: June 15, 2006)
o Painless nodules:
NORMAL SKIN  Warts
• Skin - host to variety of microorganisms  Molluscum contagiosum
• As a habitat, skin has various climatic zones:  Large lesion
Reference: Lecture notes on Infectious Diseases; Mandal
o Moist intertriginous areas - increased bacterial
population • ERYSIPELAS
o Dry, exposed skin - decreased bacterial flora
• Areas rich in sebaceous secretions - increased bacterial
flora

SKIN FLORA
• Resident flora
o regularly present on the skin; nonpathogenic
o example: S. epidermidis, micrococci, anaerobic and
aerobic diphtheroids
• Transient flora o Epidemiology
o pathogenic or nonpathogenic  Neonate and elderly
o removed easily from normal but not from diseased  Preschool or school age children – lesions in
skin lower extremities
 Surgical wounds
o Portal of entry: surgical wounds, umbilicus in NB or
STREPTOCOCCAL AND STAPHYLOCOCCAL INFECTIONS any break in skin
o Etiology – GABHS
• Usually caused by direct invasion of the organisms. They o Etiopathogenesis
may also cause disease by releasing toxins, some of  Caused by streptococcal toxin infiltrating the
which may act as superantigens skin from a small primary focus, which may be
o Whereas conventional antigens stimulate only a invisible.
small subset of T cells which have specific
receptors, superantigens bind to a part of the T cell
 In contrast to staphylococcal infection of the
receptor which is shared by many T cells and thus skin, which often generates localized pus-
stimulate massive T cell proliferation and cytokine producing lesions, S. pyogenes tends to cause
release. spreading lesions due to the production of a
variety of extracellular toxins which destroy
fibrin, cellular proteins and hyaluronic acid.
• Streptococcal infections
This facilitates the spread of infection through
MODE DISEASE MECHANISM
the tissues.
Direct • Tonsillitis By release of proteases
and attachment to host o Clinical Manifestations
• Otitis media
• Pneumonia cells  Rapidly enlarging, deeply erythematous plaque
• mpetigo with sharply demarcated, slightly elevated
• Cellulitis advancing margin
• Osteomyelitis  Involved skin: tender, indurated, peau d’
• Septicemia orange, with occasional large tension bullae
• Meningitis  Lesions advance rapidly and may involve
Toxin- • Scarlet fever Streptococcal pyrogenic entire trunk or extremities w/in 12 hrs
mediated • Erysipelas exotoxins (also called  Signs of toxicity- fever and chills
“erythrogenic toxins”). o Diagnosis
These toxins cause T cell
proliferation & cytokine  Aspirate or advancing margin of infected area
release. and C/S
 Blood culture
Post-
infectious • Glomerulo-
Immunological
response to primary o Management
nephritis infection may cause host
 Standard: Aqueous penicillin x 10 days
• Rheumatic
damage

fever  Alternative: Phenoxymethyl Penicillin x 10

• Arthritis days or Erythromycin
• Erythema
nodosum
• OTHER LOCALIZED SKIN INFECTIONS THAT MAY
BE CAUSED BY GABHS:

SKIN AND SUBCUTANEOUS INFECTION • IMPETIGO

• In many infections, the dominant clinical features are

confined to the skin, with or without deeper soft tissue
involvement. These conditions can be conveniently
grouped under two broad headings
o Infections associated with a widespread rash which
may be maculopapular, erythematous,
purpuric/hemorrhagic or papulo-vesicular e.g.
Measles, Rubella etc
o Infections associated with a localized involvement of
the skin with or without deeper tissue involvement

• CONDITIONS ASSOCIATED WITH LOCALIZED

INVOLVEMENT OF THE SKIN:

o Erythematous, tender, indurated lesions: o Epidemiology

 Erysipelas  Mainly seen in children
 Cellulitis  Most common in warm, humid climates
 Erythema nodosum  Bullous impetigo less common than classical;
may occur in nursery epidemics
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o Etiology • dental abscess – anaerobes
 Classical – GABHS, S. aureus • Local skin trauma – S.aureus
 Bullous – S.aureus (epidermolytic toxin)
o Clinical Manifestations
 Classical • CELLULITIS (NONFACIAL)
• Erythematous papules/vesicles in
traumatized areasà evolve into honey-
colored crusted plaques surrounded by
discrete erythematous margin
• Associated with regional
lymphadenopathy
• May lead to acute post-streptococcal
glomerulonephritis o Epidemiology
 May occur at any site and all ages
 Risk factors – trauma, immunocompromised
• ECTHYMA state
o Pyoderma involving both epidermis and dermis o Etiology
o Characteristic lesion deep-seated with small ulcer  Coagulase + Staphylococcus
formation  GABHS
o Painful and heal with scarring  H. influenzae
o Caused by S. aureus or GABHS
o Widespread infection treated with Penicillinase-
Resistant penicillin and Mupirocin or Fusidic acid • NECROTIZING CELLULITIS
locally

Ecthyma gangrenosum

• ERYSIPELAS AND CELLULITIS

o Necrotizing Fasciitis; Acute Streptococcal hemolytic
CELLULITIS ERYSIPELAS gangrene; synergistic necrotizing cellulitis;
gangrenous necrotizing erysipelas
o Etiology
 Aerobes – GABHS;S. aureus; Gram – enteric
organisms
 Anaerobes – anaerobic streptococcus;
bacteroides spp

CASE 1: “ SKINNY DIPPING”

Diffuse spreading infection of
deep dermis without sharp
demarcation
• CELLULITIS (BUCCAL/FACIAL)
• History
Superficial infection with
raised and sharply
demarcated edge
o Baby A is a 1 year very active boy who was brought
to the OPD because of an infected insect bite of the
left lower leg.
o The lesion was described as a red indurated
thickening of the skin which began as a small lesion
that marginally spread for 5 days. The margins had
a raised, firm, tender, palpable border.
o The lesion was associated with fever, irritability and
incessant crying upon touching the extremity.

• Diagnosis: Erysipelas

/3na

o Epidemiology
 Buccal
• Uncommon, infection occur between ages
6 mo to 5 yrs
• No identified portal of entry - ? Direct
seeding of buccal mucosa from
bloodstream or lymphatic extension from
otitis media
 Facial
• Older patient
• From direct extension from dental
infection or local trauma
o Etiology
 Buccal – almost always HiB; S. pneumoniae
(occasional)
 Facial (depends on portal of entry):