Clostridium

Question 1

Clostridium are Gram ___ Large/Small Rods/Cocci that Do/Do Not produce spores.

Answer 1

(+), Large, Rods, Do

Question 2

Clostridium are Aerobes/Facultative Anaerobes/Anaerobes

Answer 2

STRICT anaerobes

Question 3

What are the environments for normal Clostridium flora?

Answer 3

soil (spores), GIT, feces

Question 4

What are groupings of different spp of Clostridia according to mode and site of action? State the spp for each grouping.

Answer 4

Neurotoxic
-Cl. tetani, Cl. botulinum
Histotoxic
-Cl. chauvoei, Cl. novyi type B, Cl. septicum
Enterotoxic
Enteropathogenic
-Cl. perfringens, Cl. difficile

Question 5

How do hosts rank in suspetibility?

Answer 5

Human & horses > ruminants & pigs > carnivores > Birds completely resistant

Question 6

How would you diagnose Cl. tetani on a slide?

Answer 6

Characteristic ‘drumstick’ shape -> round part is spore

**If looking at plate easy to miss b/c bacteria spread across plate

Question 7

What is special about the Cl. tetani vaccine?

Answer 7

The neurotoxin Tetanospasmin is antigenically uniform meaning it will not change and therefore the same vaccine can be used around the world

Question 8

How do hosts acquire Cl. tetani?

Answer 8

Open wounds. If only vegatative bacteria can still form spores in the wound.

Question 9

Pathogenesis: Describe the structure and MO of tetanospasmin. Please include a description of the specific way the toxin works.

Answer 9

• A light chain (toxic) and a heavy chain (receptor binding) joined by a disulfide bridge.
• Toxin binds irreversibly to motor neuron and ascends to CNS via axon
• Toxin blocks pre-synaptic transmission of inhibitory signals by hydrolyzing proteins of vesicles containing NT’s (synaptobrevins) resulting in Spastic paralysis -> all m.’s in contraction. Some inhibitory NT’s are GABA, glycine.

Question 10

Describe the epidemiology of Cl. botulinum.

Answer 10

The germination of endospores, growth of vegetative cells and toxin production all occur in: rotting carcasses, decaying vegetation and contaminated canned food. Dz from ingestion of preformed neurotoxin which is absorbed and circulated in blood.

Question 11

What are the types of Cl. tetani toxin and who are effected?

Answer 11

Types C & D: Domestic animals

Types A, B & E: Humans

Question 12

What is the pathogenesis of Cl. botulinum?

Answer 12

Toxin synthesized as a single chain but must be cleaved into a light chain and heavy chain to increase potency. The toxin acts on at peripheral neuromuscular junctions. Binds to stimulatory neuron and prevents release of ACh resulting in flaccid paralysis. Eventual death from paralysis of respiratory m.s.

Question 13

Compare and contrast tetanospasmin and Cl. botulinum toxin.

Answer 13

Toxin structure:
1. Tetani- H and L chains
2. Botulinum- Single chain cleaved into H and L chains
Site and MO
1. T- Prevents CNS inhibitory n.s NT release
2. B- Prevents PNS stimulatory n.s NT release
Results:
1. T- Spastic paralysis
2. B- Flaccid paralysis

Question 14

What are the histotoxic clostridium species of importance?

Answer 14

Cl. chauvoei AKA Black Leg
Cl. novyi Type B AKA Black’s Dz
Cl. septicum AKA Braxy or Malignant Edema

Question 15

What are the two types of Clostridium histotoxic infections?

Answer 15

1. Endogenous- Result of activation of dormant spores in muscle and liver
2. Exogenous- Introduction of clostridia into wounds

Question 16

Describe the overall pathogenesis of histotoxic clostridium species.

Answer 16

Tissue Injury-> Necrosis and decrease O2 tension (ie. anaerobic conditions) that is req’d for germination and vegetative replication from spores that are dormant in tissue-> Endotoxins produced by bacteria causes further proliferation and tissue damage

Question 17

What is the pathogenesis of Cl. chauvoei (Black Leg)?

Answer 17

1. Commensal or ingestion of bacteria
2. Relocation to m.
3. Bruising
4. Spore germination & toxin production
5. Symptoms: Hemolysis, crepitation (gas gangrene bubbles popping), necrosis, gas gangrene in large m. grps

Question 18

What is the pathogenesis of Cl. novyi Type B (Black’s Dz)?

Answer 18

1. Commensal or ingestion of bacteria
2. Relocation to liver
3. Fluke migration sets up anaerobic conditions
4. Spore germination & toxin production
5. Symptoms: Edema, shock, necrosis-> Necrotic Hepatitis

Question 19

What is the pathogenesis of Cl. septicum that causes Braxy?

Answer 19

1. Injury to abomasum (usually via frozen feedstuffs)
2. Colonization by commensal/ingested bacteria
3. Toxin production
4. Localized mucosal hemorrhage and necrosis
5. Toxemia

Question 20

What is the pathogenesis of Cl. septicum that causes Malignant Edema?

Answer 20

1. Wound is inoculated with clostridia
2. Toxin production
3. Cellulitis and myositis (malignant edema)
4. Gangrene

Question 21

What are the control methods for histotoxic clostridium?

Answer 21

• Antibiotics usually ineffective unless given early

- Vaccination is multicomponent: bacterin, toxoid, adjuvent

Question 22

What are the types of toxins Cl. perfringes produces and in general, what do these toxins do and/or who are ?

Answer 22

• Type A- alpha toxin, Enterotoxemia in chicks, humans, cows, sheep, dogs and horses, gas gangrene
• Types B, D, E- Enterotoxemia in sheep. D causes pulpy kidney in lambs
• Type C- beta toxin, Enterotoxemia in pigs, cattle, sheep (struck)

Question 23

Where is Cl. difficile normally found when it infects man? Is it found in animals?

Answer 23

1. In hospitals. Antibiotic associated diarrhea in man from toxin. Antibiotics are used the in hospital but clear out normal flora and CD floods in causing pathology.
2. Yes, it is also found to infect horses, hamsters, guinea pigs and neonatal pigs all causing enteritis.