L 70 Necrotizing soft tissue infections

Question 1

Types and pathogens of necrotizing cellulitis

Answer 1

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

Question 2

What are the colifrom bacteria?

Answer 2

Citrobacter
Enterobacter
E. Coli
Klebsiella

Question 3

Signs and symptoms of Necrotizing Cellulitis

Answer 3

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

Question 4

What is Meleney’s Synergistic Gangrene

Answer 4

Rare infection of post-operative patients

Interaction between S. aureus and microaerophilic streptococci

Question 5

Necrotizing Fasciitis general features

Answer 5

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

Question 6

Describe Type I necrotizing fasciitis

Answer 6

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

Question 7

Risk factors for type I necrotizing fasciitis

Answer 7

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

Question 8

Fournier’s Gangrene

Answer 8

Subtype of type I necrotizing fasciitis

A fasciitis of the genitalia

Question 9

Type II necrotizing fasciitis

Answer 9

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

Question 10

Virulence factors in type II monomicrobic necrotizing fasciitis

Answer 10

GABHS having M-proteins 1 & 3

Question 11

Causes of Type II necrotizing fasciitis

Answer 11

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

Question 12

Other pathogens that can cause type II necrotizing fasciitis

Answer 12

Aeromonas hydrophilia – traumatic lesion in freshwater

Vibrio vulnificus – seawater injury

Question 13

Type II necrotizing fasciitis risk factors

Answer 13

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

Question 14

Clinical manifestations overview for necrotizing fasciitis

Answer 14

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

Question 15

Manifestations of an advanced infection in necrotizing fasciitis

Answer 15

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

Question 16

Necrotizing Fasciitis diagnosis

Answer 16

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

Question 17

Necrotizing fasciitis treatment

Answer 17

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)

Question 18

Use of sterile fly larvae

Answer 18

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

Question 19

Description and cause of spontaneous gangrenous myositis

Answer 19

Aggressive infection of skeletal muscle

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

Question 20

Spontaneous gangrenous myositis manifestations

Answer 20

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

Question 21

Spontaneous gangrenous myositis diagnosis

Answer 21

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

Question 22

Spontaneous gangrenous myositis treatment

Answer 22

Aggressive surgical debridement

Antibiotics–clindamycin

Question 23

GAS gangrene causative agents

Answer 23

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

Question 24

Initial progression of GAS gangrene

Answer 24

Short doubling time: 8-10 minutes

Develops

Question 25

Toxins associated with gas gangrene

Answer 25

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

Question 26

Gas production in myonecrosis and GAS gangrene

Answer 26

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

Question 27

Myonecrosis clinical manifestations

Answer 27

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)

Question 28

Myonecrosis diagnosis

Answer 28

Definitive–surgery 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

Question 29

What does clostridium do on blood agar?

Answer 29

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

Question 30

Treatment of traumatic myonecrosis

Answer 30

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

Question 31

Non-Clostridial myonecrosis

Answer 31

Anaerobes: Bacteroides fragilis Peptostreptococcus Aerobes: G(+) S. aureus Much better prognosis than clostridium caused