- 4.4 organisms per infection on average
Strep pyogenes (group A, beta-hemolytic)
Clostridial gas gangrene is less common but serious
MRSA being increasingly isolated
In bites, Pasturella, Capnocytophaga and in humans Haemophilus and
Water infections: Aeromonas, Vibrio sp., mycobacterium marinum.
Sites Common sites include perineal and perianal, peri-rectal
Also foot, lower extremities, esp in diabetic / PVD feet
Post-surgical wounds, pressure ulcers, bites, GI wounds after
Polymicrobial infections Often perineal, perianal, diabetics, bite wounds.
Both gram +ve and gram -ve, aerobic and anaerobic; GI contaminants
in context of perforations
Group A Beta-haemolytic Strep
Rapid and agressive with high mortality
Virulence factors and exotoxins: allows infx to spread rapidly
through otherwise healthy tissue and induce sepsis and shock.
In US, 60% of community staph isolates are now in the MRSA spectrum.
Also produces toxins that lead to direct invasion and can result in
• Type I–
of aerobic and anaerobic bacteria
occurring mostly after surgical
in patients with diabetes and peripheral vascular disease.
70-80%. Average of 3-4 organisms. Mixed aerobic and anaerobic
Staphylococci, Streptococci, Klebsiella,
Most patients have underlying illness – previous surgical procedures, diabetes,
PVD, cirrhosis, elderly
• Type II –
infection caused by group
A Strep (Strep
pyogenes). NF caused by
community-associated MRSA can
also cause type I NF. Clostridium perfingens
may also produce
mono-microbial NF. These patients are
often healthy and
infection occurs after
1. Blood supply to the soft tissues and fascia is relatively poor
and vulnerable to rapidly spreading infections.
2. Bacteria invade into soft tissues and spread along either the
superficial or deep fascial planes.
3. Microvascular thrombosis results from toxins and
polymorphonuclear leukocytes --> tissue ischaemia and necrosis.
4. Some organisms, eg. clostridium secrete toxins that cause
necrosis in other populations (see gas
5. In the immunocompromised there is often a synergistic bacterial
infection, where different species help create a perfect environment
for each other's growth.
virulence factors for Steprococcus pyogenes
(Pathogenesis of Type 2 NF)
proteins – antiphagocytic
• Exotoxin: Haemolysin, Streptolysin O and S and
Leukocydin: leads to cell
destruction and inflammation
•Exotoxin A, B or C –
also Act as a superantigen
which able to stimulated T-CellRespondent without antigen
by binding to MHC class II protein on APC. Lead to
production of IL-1. IL-6 and TNF-alpha leading to
toxic shock syndrome
• Exotoxin initiate the
vascular thrombosis and
inflammation. Its superantigen ability also initiate the immune response for MOFS and SIRS
pathogenesis of polymicrobial
necrotizing soft tissue
infection (Type I NF)
facultative organisms lower the oxidation-reduction potential of
microenvironment and promote anaerobes
anaerobes interfere with host
function, and allow aerobes to proliferate
(e.g. B. fragilis) produce B-lactamase to interfere with
exotoxins (C. perfringens
-alpha toxin, S.
pyogenes - haemolysin,
Streptolysin O and S, Leucocidin) cause
tissue digestion and act as
inflammatory process produces involves
local blood vessels leading to
obliterative endarteritis, necrosis of blood vessel walls and
small blood vessels
heparinase contributes to
increases due to the infection,
further impairing blood supply
leads to liqufactive
necrosis of fascia with
concomitant breakdown to skin, muscle and surrounding tissue.
Exotoxin: the toxin release from bacteria
that can damage the local host
Endotoxin: the toxin contained within the
Gram Negative bacteria that
only release once the bacteria is dead
Some pts exhibit few signs
Pain out of proportion to clinical signs is common.
Superficial spreading infection and necrosis Systemic
- tachycardia, hypotension, low urine output, high fluid
Few early skin features
Erythema, skin blistering
Progresses to blue-black discoloration, crepitus and dishwater grey
fluid discharge from wound.
- very high white cell counts and renal impairment at presentation
ABG = prognostic
- do not delay surgery for imaging
Radiology, when performed, may show gas in tissue planes
- may be helpful to show deep seated tissue abscesses as primary
- may simply show fat stranding in the superficial fat planes
Life threatening and early recognition is essential
- delay to therapy of 12h+ associated with mortality.
Broad spectrum ABx.
Treat up front with polymicrobial cover
– e.g. tazocin (piperacillin - tazobactam), Timentin, MRSA cover
Clindamycin (1200 mg IV every 6h) beneficial if high-virulence
wounds; has protein-synthesis inhibiting properties that prevent
Penicillin 24M Units / day
Surgical incision down to deep muscle fascia
- inspection of all tissue layers for necrotic tissue
Then wide debridement / tissue excision to bleeding edges
- together with antibiotics and systemic support.
--> all dead tissue must be excised
Explore tissue planes for extent.
- extensive oedema, dishwater grey fluid, and fluid collections
suggestive of spreading infection zones.
More than one operation commonly needed
- ie return to OR at 24h for inspection after saline-soaked packing
- serial dressing changes
Avoid VAC / negative pressure dressings until after resolution of
sepsis; may result in unrecognized progression.
- may need to involve plastics; often wise to consult early.
Hyperbaric oxygen therapy, IV immunoglobulins, extracorporeal plasma
exchange = experimental; no RCT evidence and not in routine use.