Mid - Anaerobes

Front 1

Toxin produced by C. perfingens

Back 1

α-toxin: This toxin increases vascular permeability, resulting in massive hemolysis and bleeding and tissue destruction (myonecrosis)
β-toxin: Necrotizing activity, responsible for lesions in necrotizing enteritis
θ-toxin: Heat and oxygen labile hemolysin; cytolytic
Enterotoxin: Heat-labile, produced during phase transition from vegetative cells to spores and released when cells are lysed. Binds to the brush border membrane of the small intestine and disrupts transport and membrane permeability

Front 2

Toxin produced by C. tetani

Back 2

Tetanolysin: unknown
Tetanospasmin: blocks the release of neurotransmitters for inhibitory synapses causing excitatory. leads to spastic paralysis
synaptic activity to be unregulated.

Front 3

Toxin produced by C. botulinum

Back 3

Botulinum: preventing release of the neurotransmitter acetylcholine

Front 4

Toxin produced by C. difficile

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Toxin A (Enterotoxin): Produces chemotaxis of PMN’s, induces cytokine production, hypersecretion of fluid, and hemorrhagic necrosis
Toxin B (cytotoxin); Induces polymerization of actin with loss of cellular cytoskeleton.

Front 5

Clostridium difficile colitis

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Alteration of the normal gut flora with antibiotics favors C. difficile. The disease occurs if the organism proliferates in the colon and produces its toxins, an enterotoxin (toxin A) and cytotoxin (toxin B).
C. difficile diarrhea usually begins 5 to 10 days into antibiotic treatment. It may be mild and watery or bloody and accompanied by abdominal cramping, leukocytosis, and fever. Severe cases may be associated with an intense inflammatory response. The colonic mucosa becomes studded with inflammatory plaques, which coalesce into an overlying “pseudomembrane” composed of fibrin, leukocytes, and necrotic colonic cells.

Front 6

Clostridial myonecrosis (Gas gangrene)

Back 6

C. perfringens produces a wide range of wound and soft tissue infections. Clostridial myonecrosis develops in traumatic wounds with muscle damage after contamination with dirt or foreign material containing C. perfringens. Low oxidation-reduction potential in a wound favors spore germination and multiplication resulting in production of toxins (α-toxin and θ-toxin), which promotes vascular permeability and edema. Intense pain and a sense of heaviness or pressure develops at the site of injury within 1 to 4 days after inoculation, and progresses rapidly to extensive muscle necrosis and shock, frequently within 2 days of onset.
Myonecrosis must be treated with surgical debridement and high dose penicillin.

Front 7

Tetanus

Back 7

C. tetani forms spores and is often found in soil. The soil is introduced into wounds contaminated with soil or foreign bodies. In an area of low oxidation-reduction potential, such as a necrotic wound, C. tetani multiply locally and elaborate Tetanospasmin. Tetanospasmin blocks the postsynaptic inhibition of spinal motor reflexes resulting in spasmodic contractions of both protagonist and antagonist muscles.
Treatment of tetanus requires debridement of the primary wound and treatment with metronidazole to eliminate remaining vegetative bacteria, passive immunization with human tetanus immunoglobulin to bind free tetanospasmin, and vaccination with tetanus toxoid.

Front 8

Treatment of botulism

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Treatment involves intensive supportive measures (mechanical ventilation), elimination of gastrointestinal carriage of organism (gastric lavage, metronidazole), and botulinum antitoxin to bind circulating toxin.

Front 9

Anaerobic cocci

Back 9

In normal flora of skin, mouth, intestinal and genitourinary tracts

Peptostreptococcus (most common)
– P. magnus: chronic bone and joint infections, especially prosthetic joints
– P. prevotti and P. anaerobius: female genital tract and intraabdominal
infections

Front 10

Clostridial perfringens soft tissue infections

Back 10

Crepitant cellulitis
Fascitis
Myonecrosis