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Flashcards in L 70 Necrotizing soft tissue infections Deck (31):

Types and pathogens of necrotizing cellulitis

2 anaerobic groups:

1) Clostridium anaerobic: Clostridium perfringens

2) Nonclostridial anaerobic:
Bacteroides, Peptostreptococcus
These are obligate anaerobes that are often mixed with facultative anaerobes like coliform bacilli, staph, strep


What are the colifrom bacteria?

E. Coli


Signs and symptoms of Necrotizing Cellulitis

Thin, dark, sometimes foul smelling wound drainage and tissue gas
*Pain, swelling, and system toxicity
Crepitus skin
Sparing of deep fascia and muscles


What is Meleney's Synergistic Gangrene

Rare infection of post-operative patients
Interaction between S. aureus and microaerophilic streptococci


Necrotizing Fasciitis general features

Can spread from the subQ tissues, goes along fascial planes, does not infect muscle, is not contagious


Describe Type I necrotizing fasciitis

Type I is polymicrobic
Includes at least 1 anaerobic species: Bacteroides, Clostridium, Peptostreptococcus (all normal microbiota)
Combined with one or more facultative anaerobic strep or members of enterobacteriaceae (PESSKEY Strains)

Two locations:
1) Cervical (face, neck, mediastinum): Fusobacterium, strep, Bacteroides, spirochetes
2) Perineum: Anaerobes (Bacteroides, Clostridium, Fusobacterium) & facultative anaerobes E.coli, klebsiella


Risk factors for type I necrotizing fasciitis

Surgery/Trauma to introduce the bacteria
Diabetes, peripheral vascular disease (lower extremities)
Neonates (abdomen, perineum)


Fournier's Gangrene

Subtype of type I necrotizing fasciitis
A fasciitis of the genitalia


Type II necrotizing fasciitis

Monomicrobic or Streptococcal Gangrene
other beta-hemolytic strep
Alone or isolated with other species–S. aureus


Virulence factors in type II monomicrobic necrotizing fasciitis

GABHS having M-proteins 1 & 3


Causes of Type II necrotizing fasciitis

Can follow blunt trauma, bug bite, chickenpox, surgery, childbirth, IV drugs
Also hematogenous translocation


Other pathogens that can cause type II necrotizing fasciitis

Aeromonas hydrophilia – traumatic lesion in freshwater

Vibrio vulnificus – seawater injury


Type II necrotizing fasciitis risk factors

Patient often immunocompromised
No significant PMH
Any age group
History of skin injury: laceration, blunt trauma, surgery, burn, childbirth, IV drugs, varicella infection


Clinical manifestations overview for necrotizing fasciitis

Infects deeper tissues destroying muscle fascia and overlying subq
Spreads along muscle fascia because it has a poor blood supply and spares the muscle below
initially won't see much, but patient will complain of pain out of proportion to manifestation
Rapid progression over several days
Skin changes color, skin breaks down and forms bullae
Pain disappears from destruction of nerves (cutaneous anesthesia) precedes the skin necrosis


Manifestations of an advanced infection in necrotizing fasciitis

Fever, tachycardia, systemic toxicity
If systemic=>altered mental state
Malaise, myalgia, diarrhea, anorexia, hypotension
Putrid odor only if anaerobic (type I) and not strep


Necrotizing Fasciitis diagnosis

Surgery only way to confirm presence and extent
Tissue biopsy can be useful, but requires time
In surgery, tissue is necrotic, fascia is swollen with dull gray to yellow-green color, easy separation along fascial planes


Necrotizing fasciitis treatment

Surgery debridement to remove all damaged tissue
Broad spectrum antibiotics
Clindamycin: very good at preventing enzyme production in the bacteria that are the toxins that cause the tissue damage (strep, staph, clostridium)


Use of sterile fly larvae

Useful to eat and remove dead tissue, secrete antimicrobial byproducts, eat/kill bacteria


Description and cause of spontaneous gangrenous myositis

Aggressive infection of skeletal muscle
Caused by Strep that is attracted to bruised or damaged skeletal muscle by the increased production of vimentin


Spontaneous gangrenous myositis manifestations

Fever, exquisit pain, tenderness
Swelling of affected muscle with induration (hardening)
Overlying skin initially uninvolved, later becomes erythematous, warm, petechiae, bullae, vesicles

Progresses rapidly to other muscle and soft tissue
Hypotension and renal failure precede cutaneous manifestations by 4-8 hours
Signs of STSS
Elevated serum creatinin kinase
NO gas formation in the tissues


Spontaneous gangrenous myositis diagnosis

Immediate surgery
Findings surgical specimens
Numerous gram (+) bac in muscle


Spontaneous gangrenous myositis treatment

Aggressive surgical debridement


GAS gangrene causative agents

Also called Clostridial Myonecrosis
Caused by endorspore-forming anaerobic bacilli: Clostridium perfringens Type A (soil and human feces)
C. septicum–usually endogenous, cancer can be involved by releasing it from the gut
C. perfringens–usually exogenous, trauma or surgery


Initial progression of GAS gangrene

Short doubling time: 8-10 minutes


Toxins associated with gas gangrene

There are more than 20 virulence factors associated with clostridium, but ALPHA-Toxin (pohospholipase C, lecithinase?) is the major cause
Lyses lots of cell types
Triggers histamine release, platelet aggregation
Prevents extravasation of WBC's
Don't see PMNs in infected tissue

THETA-Toxin (Perfringolysin): causes direct vascular injury, cytolysis, hemolysis, may explain poor inflammatory response and absence of inflammatory cells

KAPPA-Toxin (collagenase): fascilitates necrosis and spread through tissue planes


Gas production in myonecrosis and GAS gangrene

Clostridia and other bac make in soluble H2 gas–useful to separate tissues and allow access to fresh tissue and nutrients, also collapses blood vessels to keep regions anaerobic


Myonecrosis clinical manifestations

Acute onset with sever pain at site of trauma/surgery
Pain from toxin mediated ischemia
Skin overlying the injury: Pale-bronze-purple/red, becomes tense & extensively tender, bullae clear, red, blue, purple

Rapid development of system toxicity: tachycardia, fever, multiple organ dysfunction syndrome, thin hemorrhagic exudate, sweet mousy smell (C. perfringens), (foul odor common with anaerobes)
Crepitus (not in type II necrotizing fasciitis)


Myonecrosis diagnosis

Muscle tissue does not bleed, does not contract when stimulated, grossly edematous, my have re-blue to black coloration
*NO immune cell infiltration because of alpha-toxin preventing extravasation, and theta-toxin lyses any cells that do get to the tissue

Microscopic: gram-variable bacillis at site, gram (+) in culture


What does clostridium do on blood agar?

Has double zone of hemolysis:
beta-hemolysis of theta-toxin, and incomplete alpha-hemolysis of alpha-toxin


Treatment of traumatic myonecrosis

Surgical debridement
Maintain vascular integrity
Delay primary suturing to maintain oxygen exposure
Initiate broad spectrum antibiotics
For C. perfringens specific: combination IV penicillin, clindamycin, or tetracycline
Tetanus booster if appropriate


Non-Clostridial myonecrosis

Bacteroides fragilis

G(+) S. aureus

Much better prognosis than clostridium caused