Transcript Cellulitis - UMF IASI 2015

Bacterial Infections
of the Skin
General Considerations of Bacterial Diseases
• Two major forms: Primary vs. 2nd manifestation in the skin
• Natural resistance of the skin:
Integrity of the skin integument
Low pH
Antibacterial substances in seb secretions
FFA (linoleic and linolenic acids)
Immunoglobulins, cellular immunity, delayed hypersensitivity
Enhanced susceptibility of immunocompromised host Relative
Dryness of nl skin
Bacterial interference
Pathogenesis of Bacterial Infection of the Skin
• Pathogenicity of the microorganisms
Invasive potential (antiphagocytic surface component)
Toxin
Exotoxin
Endotoxin (LPS)
-TNF and IL1 by LPS activated
microghages
-Shwartzman rxn (DIC vs. Hem necrosis)
• Portal of entry
• Specific features of host inflammatory response
Classification of Bacterial Infection of the Skin
• Etiology seems more important
• Helpful classification:
Primary infxn (Pyodermas)
Secondary infxn
Cutaneous manifestations of systemic dz
Diagnostic Strategies
• Direct examination of aspirates and biopsies (Gm and Cx)
• Special culture material
Dephtheria
- Loeffler or tellurite agar
GNR
- EMB or MacConkey plate
M/G
- Chocolate agar or modified Thayer-Martin CO2
Anaerobic strep, clostridia, bactreroides – blood agar, O2 free
• Flourescent Ab
• Other Immunologic methods
• PCR
Antibiotic Therapy
• Dosage
• Toxicity
• Antibiotic resistance because of “ R” factor
• Topical antibacterial agents
Skin Infections Caused by
Gram-Positive Organisms
Staph skin infection:
Streptococcal Skin Infections
The two gram-positive cocci Staphylococcus
aureus and group A beta-hemolytic streptococci
account for the majority of skin and soft tissue
infections.
• S. aureus invades skin and
causes
–
–
–
–
impetigo,
folliculitis,
cellulitis, and
furuncles.
Elaboration of toxins by S.
aureus causes the lesions of
– bullous impetigo and
– staphylococcal scalded skin
syndrome.
• The streptococci are
secondary invaders of
traumatic skin lesions
and cause
–
–
–
–
impetigo,
erysipelas,
cellulitis, and
lymphangitis.
Staph skin infection:
• Two major groups of Staph:
coag + and coag • 30-50% healthy adults harbor
S. aureus
• Pathogenesis:
Cellular and extracellular
products - coagulase, leukocidin,
alpha toxin, exotoxins (TSST-1,
enterotoxins B/C, exfoliative
toxins A/B)
Surface adherence
Host factors
Staph Bacteremia and
Endocarditis
• Secondary bacteremia
(from a defined peripheral
focus of infxn), <10%
endocarditis
• Primary bacteremia (no
identifiable peripheral focus
yet repeatedly (+) bld Cx),
treated as endocarditis
• Janeway lesions, Osler’s
nodes, subungual splinter
hemorrhages,
subconjunctival hemorrhage,
Roth spots, endophthalmitis
Superficial pustular
folliculitis:
• = follicular or Bockhart’s
impetigo, impertigo of Bockhart
• Children: scalp; Adults: beard
area, axilla, ext, buttock
• Periporitis staphylogenes = 2nd
Staph infxn of neonatal miliaria
• Ddx - other infectious folliculitis,
noninfectious follicular disorders
Deep folliculitis:
• Sycosis barbae, Sycosis Vulgaris,
Barber’s itch
• Perifollicular, chronic, pustular,
recurrent staph infxn
• Ddx – dermatophytic folliculitis
(tinea barbae), pseudofollicular
barbae, herpetic sycosis
• Lupoid sycosis (sycosis lupoides):
a deep chronic form of pyogenic
folliculitis and perifolliculitis
Treatment for folliculitis
• Antibacterial soap
• Mupirocin oint topically
• 1st gen cephalo, oxacillin, cloxacillin,
dicloxacillin
• For acute inflammation, Burow’s sol diluted 1:20
• For chronic folliculitis: Drysol
• For blepharitis: antibiotic ophth oint
Furunclecircumscribed
perifollicular
abscess
Carbuncle: >2 confluent furuncles
Abscess
The best, most cost-effective way to prevent
hospital furunculosis is:
The best, most cost-effective way to prevent
hospital furunculosis is:
Treatment for furunculosis
• Warm compresses and oral Abx
• 1st gen cephalo, oxacillin, cloxacillin,
dicloxacillin
• Mupirocin oint to nares x 5 to prevent recur
• Suspect MRSA or even vanco-resistant strains
• The timing of I& D
• The cavity should be packed with iodoform or
Vaseline gauze
Treatment for furunculosisspecial locations
• External auditory canal: avoid irrigation and early
incision; apply mupirocin; give oral Abx and heat
application
• Nasal furuncles: hot saline compresses inside and
outside the nostril until softening; furuncles should
not be incised but steamed; local and oral Abx
• Upper lip and nose: danger of sinus thrombosis,
meningitis, and septicemia; prevent trauma w
dressing; local and oral Abx; incision as the last
resource
Chronic furunculosis
• Due to autoinoculation and intrafamilial spread
among carriers
• Daily antibacterial soap or chlorhexidine,
specially to axillae, groin and perianal area
• Eradicating nasal carriage state
- Mupirocin oint bid q 4wk
- Rifampin 600mg qd x 10d combined w
cloxacillin 500mg qid or clinda 150mg qd
for 3 mos
- Mupirocin oint bid inside nares
throughout the course of isotretinoin tx
Pyogenic paronychia:
• Staph is the major cause
of acute paronychia, other
bacterias including strep
pyogenes, Pseudomonas,
Proteus or anaerobes
• Chronic/recurrent form by
C. albicans
• Predisposing factors:
trauma-separation of
eponychium from nail plate,
chronic moisture
Treatment of paronychia:
• Prevent from trauma and keep dry
• I& D for acutely inflamed absecesses
• Oral Abx (semisynthetic penicillin or 1st
gen cephalosproin, if anaerobic, use
Augmentin
• For chronic paronychia: fungicide and
bactericide such as Neosporin soln,
Vioform, 2% thymol in acetone, Castellani
paint, oral azole
Staph Whitlow (Felon):
• Purulent infxn/abscess @ the
bulbous distal end of the finger
• S. aureus and HSV (recurrent,
hemorrhagic vesicles)
• Portal of entry: trauma,
parynochia
• X-ray to r/o osteomyelitis
• Surgical drainage of loculated
abscesses and IV Abx
Botryomycosis
• Rare pyogenic dz
• Nodular, crusted, purulent
lesions, sinuses discharge sulfur
granules
• Predisposing factors: trauma,
immuno-suppression, chronic
alcoholism, DM
• Skin, bone, liver
• Often genital areas
• The role of a foreign body
• Abx, surgical drainage and
excision
Nonbullous Impetigo
(Impertigo Contagiosa)
• Children and adults
• Face (around nares) and exts
• S. aureus > gpA strep, or both
• Bacteriocins produced by S.
aureus highly bactericidal to gpA
strep
• gpA beta-hemolytic strep
nephritogenic strains: type
49,55,57, and 60 strains and
strain M-type 2
• Tx: local and systemic Abx;
soak off the crusts, prophylactic
Abx oint
Bullous Impetigo
• Group 2 S. aureus phage type
71
• Exfoliatin A/B – serine
protease of desmoglein 1
• 51% pts had (+) Cx from nose
or throat
• Pemphigus neonatorum or
Ritter’s dz
• Topical mupirocin + P.O. Abx
5-10 d (dicloxacillin,
erythromycin, azithromycin,
Augmentin, cephalexin,
cefaclor,cefprozil,clindamycin)
Bullous Impetigo
1. What is the responsible phage
type?
2. What’s exotoxin?
3. What is the target of the bacterial
toxin on the skin?
4. If you see a vesicular separation
on H/E, what it the level of
separation?
Staph Scalded-Skin Syndrome (SSSS)
• Exfoliative (epidermolytic) toxin A/B
by S. aureus phage group II
• Serine protease cleaves desmoglein 1
• Children < 5 y/o, particularly neonates
• Generalized, superficial exfoliative dz,
formally known as Ritter’s dz or
dermatitis exfoliativa neonatorum
• Localized form = bullous impetigo
• Abortive form: may represent mild
form of toxic shock syndrome
SSSS
SSSS
H&E:
Bullous impetigo
Exfoliative cytology
TEN
Staph Toxic-Shock Syndrome (STTS)
Bulbar conjunctival hyperemia
Menstrual:
• TSST-1
Nonmenstrual:
• TSST-1
• Enterotoxin B/C
Staph scarlatiniform eruption
Recalcitrant, erythematous, desquamating
disorder (RED)
Recurrent toxin-mediated perineal erythema
Streptococcal Skin Infections
• Lancefield classification A-T by C carbohydrate Ag of cell wall
• GpA strep beta-hemolytic, sensitive to bacitracin
• Subtyping of gpA strep by M-protein
• Virulence factors
Cell surface molecules
Secreted proteins
• 10% asymptomatic carriers in nl population (oropharynx)
• Acute rheumatic fever – only 2nd to pharyngitis/tonsillitis
• Acute nephritis – skin or URT (different serotype)
Ecthyma
• Neglected impetigo extends into
dermis; an ulcerated staph or strep
pyoderma
• Lower ext of children, elderly,
DM
• Crusted, “punched out” ulcer
• Tx: same as for Staph impetigo;
several wks of Abx
Superficial Pyoderma in Nonintertriginous Skin
Impetigo, nonbullous
• Indistinguishable from that caused by S. aureus
• Half pts have both S. aureus and gp A strep
• GpB strep a/w impertigo in the newborn
• Tx:
Topical mupirocin
Penicillin
Erythromycin if allergic to PG
Practically, Tx should be directed at S. aureus
Strep Infxn in Intertriginous Skin Sites
Streptococcus intertrigo
Streptococcus intertrigoperianal strep cellulitis
You are asked to see a consult on the
floor, what is your impression?
Erysipelas
• Most common: gpA strep
• Occasionally, gps C, G, B strep, S.
aureus
• Recurrent erysipelas a/w saphenous
vein harvest and lymphedema
Cellulitis
• Most common: S. aureus
• Gp A strep, gps C, G, B strep, E.
Coli and other enterobacteriaceae
and anaerobes
• Extends deeper into subcut
• Ext leg > arm, thrombophlebitis
• Complicate surgical wound,
pressure ulcer, animal bites
Cellulitis: Differential Diagnosis
Disease
Description
Edema surrounding crusted lesion. Painless or itching. Animal
contact.
Affects diabetic patients with end-stage renal disease and
hyperparathyroidism who are receiving renal replacement
Calciphylaxis (calcific
therapy. Metastatic calcification leads to small vessel
uremic arteriolopathy)
vasculopathy. Early stage: presents with nonulcerating plaques
in the calves. Lesions eventually become necrotic and painful
ulcers develop.
A form of metastatic carcinoma with lymphatic involvement.
Seen on anterior chest wall in breast cancer and sites of distant
Carcinoma
metastasis. No fever, slow progression. If a suspected breast
erysipelatoides
infection does not resolve with antibiotics, mammography and
tissue biopsy are indicated.
Lesion sharply demarcated and constricted to the area of
exposure. Pruritus present, not in cellulitis. Topical steroids
Contact dermatitis (acute)
effective. Systemic corticosteroids are indicated for severe
cases. Secondary infection may complicate dermatitis.
Unilateral leg edema, warmth, or erythema. Tenderness along
Deep venous
involved veins. Can have low-grade fever, leukocytosis. Duplex
thrombophlebitis
ultrasonography diagnostic.
Anthrax (cutaneous)
Cellulitis: Differential Diagnosis
Disease
Description
Erythema migrans
Lyme disease rash that typically expands but clears in center. Often a
single or multiple lesions occur that are round and red and expand to
many centimeters but do not show central clearing.
Erythema nodosum
Most common panniculitis. Raised, painful, bilateral, tender lesions
located over both shins. Lesions may coalesce and resemble cellulitis.
Factitial
Mechanical or chemical manipulation of skin can produce an area of
erythema that resembles cellulitis.
Fixed drug eruption
A well-demarcated plaque that recurs at same site each time offending
drug is taken. Itching or burning not seen in cellulitis. Most commonly
affected areas are lips and genitalia.
Foreign-body
granulomatous reactions
Material injected into skin can stimulate an overlying erythema.
(silicone injections,
paraffin oils)
Cellulitis: Differential Diagnosis
Disease
Gouty arthritis (acute)
Insect stings or bites
and other
envenomations
Leukemia/lymphoma
Necrotizing fasciitis
Description
Joint inflamed with overlying erythema and warmth. May lead to
tendonitis and bursitis. Chills, low-grade fever, elevated
leukocyte count. Typically monoarticular, lower extremity, usually
first metatarsophalangeal joint or knee.
Swelling that can extend over a large area; peaks within 48
hours and lasts up to 7 days. No lymphangitis. Pruritus
distinguishes this lesion from infectious cellulitis. Envenomations
by marine animals cause a similar picture.
Lymphoma diagnosed after failure of antimicrobial therapy.
Persisting fever or generalized lymphadenopathy may suggest
the diagnosis.
A rapidly advancing erythema. Begins with fever and chills.
Vesicles and bullae may form and drain fluid. Painless ulcers
appear as the process spreads.
Disease
Description
Pancreatic
disease,Differential
either inflammatory
or neoplastic, may lead to
Cellulitis:
Diagnosis
panniculitis presenting as tender, red nodules located on pretibial
regions, thighs, or buttocks. Lupus panniculitis occurs on face and upper
extremities. α1-Antitrypsin deficiency may present as cellulitis on trunk
and proximal extremities, often precipitated by trauma. Panacinar
emphysema, noninfectious hepatitis, and cirrhosis should suggest the
Panniculitis
diagnosis. Protein electrophoresis reveals low levels of α1-antitrypsin.
Some patients respond to dapsone or α1-protease inhibitor concentrate.
Other forms of panniculitis are Weber-Christian disease, cytophagic
histiocytic panniculitis, post-steroid panniculitis, and nodular panniculitis.
Deep excisional biopsies rather than punch biopsy are required to
diagnose panniculitis.
A form of panniculitis; affects middle-aged women, associated with
Lipodermatoscle
venous insufficiency. Acute form resembles cellulitis. Painful, red,
rosis (chronic
indurated, edematous area in medial aspect of leg. Lasts a few months.
indurated
Superimposed cellulitis may occur. Compression therapy reduces
cellulitis)
venous hypertension and fluid extravasation.
Nonpitting edema, erythema, induration of an extremity. No fever, no
Lymphedema
response to antibiotics. May be complicated by infection, recurrently.
Lymphangioscintigraphy confirms diagnosis.
Pyoderma
gangrenosum
An ulcerative cutaneous disease. Ulcers may follow trauma. An atypical
form occurs on the hand. A red ulcer border may be misinterpreted as
infection.
DIAGNOSIS OF CELLULITIS
• Recognizing the distinctive clinical features (erythema,
warmth, edema, and pain) is the most reliable way of
making an early diagnosis.
• Isolation of the etiologic agent is difficult and is usually
not attempted.
• Fever, mild leukocytosis with a left shift, and a mildly
increased sedimentation rate may be present.
• Patients with cellulitis of the leg often have a preexisting
lesion, such as an ulcer or erosion that acts as a portal of
entry for the infecting organism.
Gangrenous Cellulitis
Type II
Type I
Type I
Gangrenous Cellulitis
Type II
Type I
Type I
C. perfringens, involving more superficial subcut
C. perfringens, involving muscle w/ 2nd changes in skin
C. septicum, hem. malignancy or colon ca,
100% mortatility
Necrotizing Fasciitis
NSAIDs may be
contraindicated
Type II necrotizing fasciitis
• Almost always gp A strep,
rarely C and G
• Gp B in newborns and
postpartum
• Rarely S. pneumoniae
• Usually healthy individuals
• The location is most often an
ext
• 2/3 bacteremia
• Often strep TSLS
Necrotizing Fasciitis
Type I necrotizing fasciitis
• A mix of facultative and anaerobes
• Often following Sx, bowel perf,
trauma in pts with diabetes and
malnutrition
• The location is often an ext, Abd,
perineum, or about op wounds
• Infxn in the thigh may be 2nd to an
intestinal source
• Crepitus
Necrotizing Fasciitis
Fournier’s gangrene
• Localized type I necrotizing fasciitis involving scrotum and
penis
• Men 50-60 y/o with underlying dz
• Purplish discoloration -> frank gangrene
Synergistic necrotizing cellulitis
• Anaerobes and facultative bacteria
• Involve all soft-tissue structures (muscle)
• Poor prognosis related to pt population
• Small area of necrosis/blister overlying widespread destruction
of deeper tissues, skin sinus draining necrotic fat
• Most common site is perineum
Progressive Bacterial Synergistic Gangrene
(Meleney’s Gangrene)
• Develop in proximity to wires or other foreign bodies
• Microaerophilic or anaerobic strep at the advancing margin
• S. aureus in the central, ulcerated area
• Removal of foreign bodies, excision of necrotic tissues, zinc
sulfate cream and Abx
Blistering distal dactylitis
• Gp A strep (majority)
• Occasionally gp B strep, S.
aureus
• Blister over the volar skin
pad of distal fingers/toes
Acute Lymphangitis
• Gp A strep (majority)
• Occasionally S. aureus; rarely, Psateurella multocida
or HSV
• A portal of entry and tender regional adenopathy
• Frequently lead to bacteremia
Gp A Strep Toxic Shock-like Syndrome
(TSLS) or Toxic Strep Syndrome
• Pyrogenic exotoxin (erythrogenic toxin) A > pyrogenic
exotoxin B/C, strep superAg, strep mitogenic exotoxin Z
• Young (20-50 y/o), healthy pts
• 80% soft tissue site of infxn
• over half develop bacteremia
• Near 50% mortality rate
• “Septic scarlet fever” – TSLS may be a more severe form
of scarlet fever
• Tx: extensive debridement, Abx, IV fluids, vasopressors,
IVIG
Erythrasma
• Corynebacterium
minutissimum – gram (+) rod
• More common in men
• Web spaces of feet, and
intertriginous areas
•Asymptomatic or puritic
• Tx: BP wash/gel,
clindamycin soln, azole cream