Skin Infectious diseases

Normal Skin Flora

Class Organisms Location on body

Aerobic cocci Staphylococcus aureus*, S. saprophyticus, S. All body sites, especially inter
epidermidis†, Micrococcus luteus, M. roseus, M. varians

Aerobic Corynebacterium minutissimum, C. lipophilicus, C. xerosis, C. Intertriginous areas (e.g. axilla

coryneform jeikeium, Brevibacterium epidermidis
bacteria

Anaerobic Propionibacterium acnes, P. granulosum, P. avidum Sebaceous glands and follicles

coryneform
bacteria

Gram-negative Acinetobacter spp. Axillae, perineum, antecubita

bacteria

Yeast Malassezia furfur Skin rich in sebaceous glands

Bullous and None bullous impetigo - Characteristic features

Impetigo is a common and highly contagious skin infection that mainly affects
infants and children. Impetigo usually appears as red sores on the face,
especially around a child's nose and mouth, and on hands and feet. The sores
burst and develop honey-colored crusts. Impetigo has 2 forms: Bullous and
None bullous impetigo
 Non-bullous impetigo Bullous impetigo

Epidemiology • ~70% of all cases of impetigo Less common

• Children most often affected • Often occurs in the neonatal period, bu

Clinical lesions • Early: single 2–4 mm erythem. s macule,rapidly evolves into
a short-lived vesicle or pustule
• Late: superficial erosion with a typical “honey-colored”
yellow crust and rapid direct extension of infection to
surrounding skin
• Early: small vesicles enlarge into 1
• Late: flaccid, transparent bullae measur
rupture there is a collarette of scale, but n
surrounding erythema

Distribution Face and extremities Face, trunk, buttocks, perineum, axillae e

Associated findings Mild lymphadenopathy Usually no systemic symptoms but can be

diarrhea

Clinical course • Usually a benign, self-limited process Usually resolves in 3–6 weeks without sca

• Usually resolves -2 weeks without scarring if untreated

Complications • In 5% of cases, non-bullous impetigo caused by S. In infants/young children and adults with
pyogenes (serotypes 1, 4, 12, 25 and 49) results in exfoliative toxin may disseminate and cau
acute post-streptococcal glomerulonephritis (APSG) * syndrome

•Risk of APSG is not altered by treatment with antibiotics

•Impetigo has not been linked to a risk of rheumatic fever

Ecthyma is an ulcerative pyoderma of the skin well known to be caused by group A beta-
hemolytic streptococci. Concomitant Staphylococcus aureus is often isolated from lesional
skin.  On occasion, S aureus alone has been isolated.  Because ecthyma extends into the dermis,
it is often referred to as a deeper form of impetigo.

Treatment for impetigo and ecthyma

Uncomplicated Comlicated

First line Second line First line Second line

Impetigo Mupirocin 2% β-lactamase- IV ceftriaxone IV

ointment resistant (daily dosing) ampicillin/sulbactam
- or - penicillin - or -
 retapamulin - or - IV cefuroxime
1% ointment first-
- or - generation
fusidic acid 2% cephalosporin
cream† - or -
clindamycin
- or -
macrolide‡

Ecthyma β-lactamase-
resistant
penicillin (e.g.
dicloxacillin)
- or -
first-
generation
cephalosporin
(e.g.
cephalexin)

Bacterial Foliculitis –
Follicular pustules, often arising on an erythematous base. Favors areas with terminal
hairs, such as the scalp and beard, as well as the upper trunk, buttocks and lower
extremities Bacterial culture of pustular contents most commonly reveals normal flora,
followed by Staphylococcus aureus Treatment depends on the particular type of
folliculitis.
Deep folicuilitis - resolutions - often arise the scars.
 Abscesses, furuncles and carbuncles
• Abscesses and furuncles (boils) are collections of pus that are “walled-off” from the
surrounding tissues
• Abscess - occur anywhere in or on the body,
• Furuncle, by definition, involves a hair follicle
• Carbuncle - A contiguous collection of furuncles
• Etiology - S. aureus
• Predisposing factors - chronic S. aureuscarriage, diabetes mellitus, obesity, poor
hygiene, and immunodeficiency states (e.g. chronic granulomatous disease,
hyperimmunoglobulin E syndrome)
• Treatment - for simple furuncles, warm compresses may promote maturation, drainage
and resolution. Larger or deeper fluctuant lesions typically require incision and drainage.
Systemic antibiotic therapy is recommended

Furuncules Carbuncles
 Blisterin distal dactilitis
• Group A Streptococcus spp. or S. aureus are usually the causative organisms.
• Localized - volar fat pad of a finger or, less often, a toe, with occasional involvement of
the nail fold or more proximal portion of the digit. Darkening of the skin - is often
observed for several days to a week before blister formation. The infection most
commonly occurs in children aged 2–16 years.
• Treatment - drainage and a 10-day course of an oral antistaphylococcal antibiotic are
recommended. Although topical therapy with mupirocin has been described, systemic
therapy can prevent development of new sites of infection as well as local extension.

Staphylococcal scalded skin syndrome

Ritter’s disease ▪ Pemphigus neonatorum
• SSSS - caused by hematogenous dissemination of the same exfoliative toxins that lead
to bullous impetigo when produced locally.

• SSSS is primarily a disease of infants and young children, who have decreased renal
toxin clearance (especially neonates) and/or a lack of toxin-neutralizing antibodies.

• Onset – signs of malaise, fever, irritability and severe tenderness of the skin. The
patient may have purulent rhinorrhea or conjunctivitis as a manifestation of the
underlying staphylococcal infection. Erythema typically first appears on the head
(accompanied by variable facial edema) and in intertriginous sites, often with
generalization within 48 hours. The skin subsequently develops a wrinkled
appearance owing to the formation of flaccid, sterile bullae within the superficial
epidermis - Nikolsky sign is positive. Classically, the flexural areas are the first to
exfoliate, leaving behind moist skin and thin, varnish-like crusting.

• Scaling and desquamation continue for the next 3–5 days, followed by re-
epithelialization without scarring. With proper treatment, SSSS resolves in 1–2
weeks, usually without sequelae. The mortality rate is 3% for children but >50% in
adults.

• Treatment - require hospitalization and parenteral antibiotics. Oral treatment with

a β-lactamase-resistant antibiotic (e.g. dicloxacillin, cephalexin) for a minimum of 1
week is usually sufficient for milder disease. Identification and decolonization of S.
aureus carriers (see Folliculitis section above) are important, especially in hospital-
acquired cases
 Toxic shock syndrome
• Etiology – St Aureus, group A Streptococci

• Fever: temperature >102°F (or >38.9°C)

• Rash: diffuse macular erythroderma

• Desquamation: 1–2 weeks after the onset of illness (especially palms and soles)

• Hypotension: systolic blood pressure <90 mmHg for adults (<5th percentile for
children)

• Involvement of three or more of the following organ systems: Gastrointestinal,

Muscular
Central nervous, Renal, Hepatic, Mucous membranes (erythema), Hematologic
(platelets <100 000/mm3)

• Treatment - severe cases of TSS require intensive monitoring and supportive therapy.
Hypotension can be treated with intravenous fluids and vasopressor agents. Foreign
bodies (e.g. surgical mesh, nasal packing, tampons) should be removed and abscesses
drained. Beta-lactamase-resistant antibiotics are used to eradicate the toxin-producing
staphylococci; MRSA is responsible for only a small proportion of TSS cases Some
advocate using antibiotics that suppress protein (and thereby toxin) production, such
as clindamycin, and administration of intravenous immunoglobulin (IVIg) may help
 to neutralize the toxin. In severe cases of shock unresponsive to antibiotics, low-dose
corticosteroids have been used.

Scarlet fever – Scarlatina

• Group A β-hemolytic streptococci - by streptococcal pyrogenic exotoxins (SPEs) types
A, B and C

• Clinical features - sudden onset of a sore throat, headache, malaise, chills, anorexia,
nausea and high fevers. Young children - may experience vomiting, abdominal pain
and seizures.

• Eruption begins 12–48 hours later as blanchable erythema on the neck, chest and
axillae

• Desquamation occurs after 7–10 days, most prominently on the hands and axille.
Possible complications - of scarlet fever and the underlying streptococcal infection
include: otitis, mastoiditis, sinusitis, pneumonia, myocarditis, meningitis, arthritis,
hepatitis, acute glomerulonephritis and rheumatic fever