Flashcards in skin 3: exotoxin-mediated, erysipelas and cellulitis Deck (56):
Staphylococcal Exfoliatin-toxin mediated diseases include:
Staphylococcal scalded skin syndrome (SSSS) including Ritter's Disease of the newborn
Scarlet fever-LIKE syndrome
Caused by *exfoliatin toxin* (ET) –producing strains of Staphylococcus aureus
ET causes an epidermal desquamation of superficial intraepidermal layers of
skin (*cleavage in epidermis*).
Produces Nikolsky sign and/or bullae; No inflammation or necrosis, no scarring unless 2o infection occurs
Epidermal necrosis - sloughing of large layers of skin. Sloughing with oblique pressure
flaccid, paper thin (thin-walled) white, serous fluid-filled sacks which rupture-->painful, moist, denuded erythematous lesions that dry in 1-2d to thin "varnish-like" light-brown crusted lesions
Occurs in infants, young children on exposed areas of face, legs.
*Bullae contains organism*
Toxin(s) and organism remain localized
*NO Nikolsky sign*
Staphylococcal scalded skin syndrome (SSSS) complex
Occurrences primarily in:
infants-children 5 years or younger
Usually a focal infection by ET-producing strains.
Dissemination of staphylococci is rare; Focal infection is contagious (toxin disseminates)
ET produced in the focal lesion spreads hematogenously resulting in skin lesions/*bullae which are sterile*
(diff than bullous impetigo: org in lesion)
syndromes – SSSS and Ritter's disease of the
Widespread, diffuse erythroderma (scarlatiniform rash).
Progresses in 1-3d to extensive in size, widely distributed, spontaneous, exfoliation of skin and/or bullae that progress as described above. *Positive Nikolsky sign*
Erythematous, dry, fissuring, peeling, bleeding lips often occur.
Within 5 d of onset, a fine, flaky, discolored, total-body desquamation occurs.
Purulent conjunctivitis may occur.
most severe form of SSSS
Ritter's disease of the newborn/neonate
Scarlet fever-Like Syndrome.
dx bullous impetigo, SSSS and Ritter's
Pyodermic staphylococcal infections diagnosed by culture and Gram- stain, also assay for elevated levels of anti-teichoic acid antibodies by gel diffusion
px bullous impetigo, SSSS and Ritter's
Usually rapid recovery with effective treatment
tx of bullous impetigo, SSSS and Ritter's
Supportive, i.e., fluid replacement and pain management.
MRSA are common in community and nosocomial outbreaks. For impetigo involving limited body surface area, topical antibiotics such as *mupirocin*.
For patients with systemic symptoms, oral antibiotics should be considered. Topical antiseptics such as hydrogen peroxide should NOT be used in the treatment of impetigo.
G+, chain-forming cocci; Group A, β-hemolytic. (GABHS).
Classification of streptococci is based on 3 independent groupings:
Lancefield serotypes AT.
T protein serotypes based on groups A, B, C, G.
M protein types (>90 serotypes).
S. pyo virulence factors
M protein (>90 types; antiphagocytic).
Toxins: streptococcal pyrogenic exotoxins (SPEA, B, C; etc. aka erythrogenic
S. pyo pathogenesis
Suppurative diseases (pus producing):
Pharyngitis and related infections vs. Integumental and soft tissue infections.
S. pyo Pharyngitis and related infections, rheumatic fever (RF), AGN, scarlet fever (SF):
-Lower numbered M types.
-Direct spread by droplet nuclei from person with pharyngitis or carrier
-Colder months of the year (winter and early spring).
-Highest incidence in 5-15 year old.
S. pyo integumental (impetigo, ecthyma) and soft tissue infections (AGN, SF)
-Higher numbered M types.
-Direct spread, agent colonizes skin surface, minor trauma or
insect bite allows for agent to cause infection. ---Also associated with poor hygiene
-Warmer months of the year
-Highest incidence in children less than 6 y-o-age.
S. pyo Non-suppurative diseases/sequelae/autoimmune disease
Rheumatic fever (RF) may follow pharyngeal infection.
Post-streptococcal Reactive Arthritis (PRSA).
Pediatric Autoimmune Neuropsychiatric Disorders Associated with
Streptococcal Infections (PANDAS).
Acute glomerulonephritis (AGN) may follow pharyngeal or
Exotoxin-mediated diseases (superantigens):
Streptococcal toxic shock syndrome (STSS): SEE TSS
Scarlet fever: Conditions required:
-Colonization by the etiologic agent - GAS.
-Must be a lysogenized strain bearing the α-tox phage that encodes for SPEs. Non-lysogenized strains do NOT produce SPEs.
-Lysogenized strain must produce sufficient amounts toxin, *not all do*. The extent of exotoxin production is determined solely by the bacteriophage so there is variation between lysogenized strains; partially determines patient S/S.
-Lysogenized strains may produce *one or more* SPEs at the same time.
-Lack of neutralizing immunity in host determines the clinical syndrome, outcome of infection:
1. presence or absence of immunity to specific M-type.
2. presence or absence of immunity to SPEs.
SPE are both ??
exotoxins and superantigens
Exotoxin-mediated diseases (superantigens): Clinical manifestations
A complication of some cases of streptococcal pharyngitis OR epidemic impetigo: S/S of either (see above) plus:
Systemic signs (via superantigen)
Exotoxin-mediated disease: Enanthem
a pronounced hyperemia of the entire pharynx with petechial lesions. White strawberry-->red strawberry-->raspberry tongue.
Exotoxin-mediated disease: Exanthem
Diffuse macular erythroderma-->a blanching
scarlatiniform (fine, red, punctate, “sandpaper-like” rash on an erythematous base) rash.
Rash first appears on the trunk and then spreads
peripherally to cover the whole body within hours or
Rash resolves with desquamation (particularly palms and soles) which occurs 1-2 weeks after the onset of illness.
organism is in mouth, throat
Scarlet fever ddx
any scarlet fever-like rash (scarlatiniform) associated with a sick child needs medical attention.
S. aureus are wound or skin infections; needs incision and drainage.
If it is caused by Panton- Valentine leukocidin–positive S. aureus strains: more serious disease!
Infectious mononucleosis; Kawasaki Disease.
GAS: Invasive Disease:
Only associated with strains of S. pyogenes that MAY elaborate SPEs.
Patient manifests with STSS and/or GAS necrotizing fasciitis.
Both STSS and GAS necrotizing fasciitis are uncommon infections
Erysipelas (St. Anthony's fire) vs cellulitis
both manifest as areas of skin erythema, edema, and warmth.
difference: erysipelas involves the upper dermis and superficial lymphatics, whereas cellulitis involves the deeper dermis and subcutaneous fat
if recurrent it is due to??
Most often in the young and elderly
Preceded by URT or skin infection caused by GAS
(may be secondary to bee sting)
Recurrent erysipelas is due to lymphatic obstruction.
A distinctive form of rapidly progressing (hours) superficial (may not involve subQ tissue)
Occurs on extremities (leg, feet, @ 80%) and face (over bridge of nose “butterfly”; cheeks). (looks like SLE)
Erysipelas clinical manifestations
Illness begins with systemic signs similar to that of cellulitis:
burning or itching at site of infection site followed by a rapidly spreading (over minutes/hours) erythema forms that is:
Bright red, Has a *sharply demarcated raised edge*, swollen, warm, hardened, painful rash, similar in consistency to an orange peel. ("peau d'orange")
Cellulitis agents G-/G+
Gram-positive cocci: S. pyogenes, S. aureus, S. pneumoniae
Gram-negative rods: mostly facultative anaerobes, some obligate anaerobes.
Cellulitis agents: atypical mycobacteria
Mycobacterium ulcerans: Buruli ulcer.
Mycobacterium haemophilum – cervicofacial lymphadenitis in children.
M. fortuitum, M. abscessus, M. chelonae (the ‘fortuitum complex’)
Cellulitis fungal agents
Systemic mycoses: blastomycosis, histoplasmosis, coccidioidomycosis
Mucormycosis (AKA zygomycosis) a group of ubiquitous fungi that include: Absidia, Mucor, Rhizomucor, Rhizopus.
Cellulitis epidemiology is important bc it
relates to tx coverage
Cellulitis after Exposure to water (fresh or seawater) predisposes to cellulitis with bacteremia as a common complication. Cellulitis is caused by:
Facultative anaerobic, G- rods,
Mycobacterium marinum – Fish tanks (fresh or salt water)*fish tank cellulitis*
M. fortuitum, M. abscessus, M. chelonae – pedicures
Vibrio vulnificus (salt water)-->hemorrhagic cellulitis.
Cellulits after Animal (mostly dogs and cats) bite and/or scratch predisposes to cellulitis caused by:
facultative anaerobic Gram-negative rods: especially *P. multocida*; Capnocytophaga canimorsus
is it cellulitis or necrotizing faciitis??
typically ddx via pain, but if diabetic neuropathy need more dx modalities
Infections in areas adjacent to oral cavity (head/neck soft tissues, sinuses, R.T.) or contaminated with oral secretions (bite and clenched hand aka fist wounds) predisposes to cellulitis caused by ??
Eikenella corrodens (formerly Bacteroides corrodens)
Cellulitis caused by Breaks in the skin caused by:
cuts and punctures; insect bites; skin diseases, e.g. tinea pedis, viral lesions, psoriasis, eczema, bed sores or other ulcers, burns
Classification of surgical wounds/post operative wound infection becomes obvious as ??
the suture line becomes reddened, tender
risk factors for cellulitis infections occurring within 72 hrs of surgery
venous insufficiency or lymphatic obstruction, i.e., breast conservation therapy/breast-sparing surgery (lumpectomy, axillary lymph node dissection, radiotherapy).
improper/lack of antibiotic prophylaxis, when appropriate
Etiology/agents of cellulitis infections occurring within 72 hrs of surgery:
-S. aureus: Infection occurs 2-3d post-surgery, Bacteremia is uncommon.
-β-hemolytic streptococci (GAS & GBS).
-Clostridium perfringens, type A
etiology of cellulitis infections occurring 10-30 days post-operative (Most common):
G- rods (mostly facultative anaerobes)
Cellulitis infections occurring 2 - 3 months post-operative:
prostheses, i.e., joint or heart valve
G+ cocci - coagulase negative staphylococci.
Cellulitis clinical manifestations often develop within a few days after the inciting event and include:
Systemic signs: fever, chills, malaise, leukocytosis
Local infection: Inflammation (*pain, erythema, edema, warmth*) with a *rapidly
advancing edge* that may or may not be elevated but it is *NEVER sharply demarcated*
Often suppurative, local abscess can develop and small patches of overlaying skin may undergo necrosis
The subcutaneous tissues usually can be palpated and are yielding
Lymphangitis, lymphadenitis may also occur
dx of cellulitis or erysipelas:
-Appearance of the affected skin.
-When cellulitis is associated with an open wound there is usually a purulent exudate which allows ID of etiologic agent by microscopic examination of Gram- stained smear.
-Palpation of soft tissue, X-ray, CT, MRI reveals the absence of gas pockets
-Blood culture: positive about ~ 5% of the time
-Clues based on patient's history
cellulitis clues based on pt hx that may help dx
Post-operative wound, Underlying disease (e.g., diabetes, cirrhosis, malignancy, URT).
Exposure to water.
Animal bite/insect bite
tx of cellulitis or erysipelas:
Surgical intervention is usually NOT needed for either cellulitis or erysipelas: but IV therapy is common – hence hospitalization
tx of cellulitis or erysipelas:: how to choose an abx
Select an abx efficacious against both staph and strep; let history and Gram-stained smear of purulent exudate or a positive blood culture be a guide as to the ddxl and abx usage.
1. Cefazolin-probenecid; Nafcillin; Ceftriaxone;a first generation cephalosporin
(e.g. Cephalexin); Clindamycin
tx of cellulitis or erysipelas: For MRSA or pt allergic to penicillin:
2. Vancomycin; Linezolid; Daptomycin; Tigecycline; Dalfopristin-quinupristin