skin 16: clostridial myonecrosis Flashcards Preview

Micro > skin 16: clostridial myonecrosis > Flashcards

Flashcards in skin 16: clostridial myonecrosis Deck (30):

clostridial myonecrosis

(gas gangrene) An invasive, anaerobic infection of muscle

Characterized by:
-extensive local edema.
-massive tissue necrosis.
-variable degree of gas production.
-profound toxemia.


myonecrosis may follow

traumatic wounds, surgery (esp GI tract/colon surgery).


c. myonecrosis most common agent

C. perfringens, type A:
Non-motile, short, G+ rod.
*Histolytic strains produce exotoxins*
Widely distributed in nature, including human intestine.


other clostridial agents of myonecrosis

C. novyi: causes 20-40% of all cases

C. sordellii: rare agent

*C. septicum infections especially those in absence of trauma are highly associated with malignancy (cryptic malignancy) of the GI tract*


clostridium virulence factors

EXOTOXINS: Those species which are capable of producing clostridial myonecrosis produce one or more exotoxins.


C. perfringens, type A produces these exotoxins:

Phospholipase C (PLC; lecithinase, α toxin)
Perfringolysin (Theta [θ/H] toxin)
numerous degradative enzymes.
Hydrogen gas is produced during catabolic (fermentation) metabolism


Phospholipase C (PLC; lecithinase, α toxin):

-Cytotoxin (destroys cell membranes by cleaving lecithin, the major phospholipid in cell membranes, thus lysing cells).
-Causes a significant reduction in mean cardiac output.
-Potent inducer of TNF-a.


Perfringolysin (Theta [θ/H] toxin):

In low concentrations causes:
-Priming and degranulation of PMNs.
-PMNs to increase production of adherence molecules (FYI e.g.,
integrins [CD11/CD18] FYI).
-Endothelial cells to produce platelet activating factor (PAF, a proinflammatory autocoid), which mediates adherence of PMNs to endothelial cells and alters vascular integrity (makes vessels leaky), relaxes tension of vascular walls.

In high concentrations, causes the complete lysis of RBCs, PMNs.


Both Phospholipase C and Perfringolysin toxins cause ??

rapid (minutes) and irreversible vascular occlusion by inducing the formation of activated platelet aggregation in arterioles and venules. Soon after, these aggregates acumulate fibrin and neutrophils.


Medical significance: During infections by anaerobes (e.g., Clostridium perfringens, type A) which can cause gas gangrene, H2 gas ??

-is produced in significant amounts.
-is insoluble in tissue.
-tracks along fascial planes separating tissues (creating/causes access to
fresh tissue).
-collapses blood vessels (creating anaerobic conditions).


c. myonecrosis XR of affected tissue reveals ??

a feathery pattern of extensive gas
formation in subcutaneous tissues, along fascial planes and between major muscle bundles - pathognomonic for presence of hydrogen gas


Two basic requirements for the initiation of c. myonecrosis:

Clostridial contamination of tissue
Area of decreased redox potential


Clostridial contamination of tissue: Sources of clostridial cells:

Endogenous - C. perfringens, type A, is gut normal flora in 20  30% of population, so surgery or trauma resulting in ulceration of GI tract (bowl) will release agent.

Exogenous - C. perfringens, type A is a spore-former, and spores are present in soil (but in low numbers), so dirty, unclean wounds put person at risk.


Area of decreased redox potential:

Circulatory failure/impaired tissue perfusion (low O2 levels in area) due to
deep lacerating, crushing wounds which damage blood vessels, capillary beds.
Necrotic tissue (have acidic pH, makes available nutrients for bacterial
Other: Presence of foreign bodies, O2-utilizing bacteria (i.e., polymicrobic).


There are 2 separate aspects to this c. myonecrosis:

The local lesion (focal infection)
Systemic illness (Toxemia)


The local lesion (focal infection)

A vicious cycle of bacterial colonization->production of exotoxins and gas-> destruction of host tissue->invasion of healthy tissue


c. mynecrosis: absence of ?? at site of infection is common

-PMNs are killed directly in area of infection.
-A leukostasis of PMNs in vessels adjacent to infection site. (PMNs
are neutralized in areas around the infection site by adherence to endothelial cells causing damage to the blood vessels they adhere to).


c. myonecrosis: Location of initial, focal infection:

90% in extremities.
10% are trunk due to:
1. trauma.
2. surgery.
3. female reproductive tract.


Systemic illness (Toxemia):

Toxins enters bloodstream, resulting in shock and death.
Cardiac output drops and impaired circulation occurs.
Model: toxins promote distributive shock:
-directly due to vascular leakiness
-probably cause massive release of endogenous mediators (PAF, IL-1,
TNF-α) which increases vascular leakiness.
-Occurs in many (50% of all) individuals with clostridial gas gangrene.


The distinguishing characteristic of clostridial gas gangrene is ??

a short incubation period; 8h-3d after injury/infection, usually less than 24 hours.


c. myonecrosis manifestations:

Acute onset and a fulminant course (an exception to general clues for diagnosis of anaerobic infection).


c. myonecrosis local effects at affected site:

skin color is copper/black.
Severe pain, which becomes progressively worse.
local edema.
thin, hemorrhagic exudate, which may have foul or sweet odor.


c. myonecrosis systemic effects

low-grade fever
toxemia with tachycardia
hypotensive shock


c. myonecrosis complications

Bacteremia is an uncommon, rare feature; but when it occurs, rapid intravascular hemolysis may result in nephrosis with death due to renal failure.

Infection of the uterus may result in:
-induced abortion
-prolonged labor
frequently results in death due to:
-secondary kidney failure.


c. myonecrosis dx
is gas dx??

*Clinical signs and symptoms are of primary importance*. Gas per se, is not diagnostic:
Non-clostridial gas gangrene is more common than clostridial myonecrosis:


c. myonecrosis, gram stain??

Gram stain is of limited value – many wounds contain C. perfringens type A: Expect G+ rods, few (if any) white or red cells.


c. myonecrosis, culture??

Culture is of limited value – many wounds contain C. perfringens type A, even histolytic strains, yet few wounds develop gas gangrene.
-Typical double zone of hemolysis on sheep blood agar (α then β hemolysis).


c. myonecrosis radiology

*X-rays of affected tissue reveals a *feathery pattern* of extensive gas formation in
subcutaneous tissues, along fascial planes and between major muscle bundles*

Radiographic techniques visualize/determine the extent of the gas pocket.


clostridial myonecrosis tx

Meticulous care of traumatic wounds:
surgical debridement and excision of all non-viable tissue, delay primary suturing.
Probably amputation as soon as possible.
Antibiotic therapy.
Hyperbaric oxygen therapy (reduce toxin production?).
Antitoxins to C. perfringens exotoxins are available but are efficacious only when
administered prophylactically, NOT after infection is established.


For non-clostridial myonecrosis/other soft tissue infections (cellulitis, necrotizing fasciitis or myonecrosis) treatment depends upon:

location of infection.
severity of infection.
etiologic agent/agents:
a. Gram-negative rods.
b. Streptococci.
c. Staphylococci.
d. Bacteroides sp. and other anaerobic bacteria.

but overall, amputation is LESS LIKELY to be necessary.

Decks in Micro Class (61):