Bacillus/ Clostridium Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

What kind of bacteria is Bacillus?

A
  • Gram positive large rods
  • Produce resistant spores
  • Aerobes/ Facultative anaerobes (Clostridia are straight anaerobes)
  • Grow rapidly producing colonies @ 24 hours.
  • Can use many substrates to grow.
  • Most are non pathogenic envrionmental organisms.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the main species of Bacillus of Veterinary Importance?

A
  1. B. anthracis- anthrax in cattle, man
  2. B. cereus- food poisoning, eye, soft tissue infection (man), Mastitis (cattle)
  • Emetic form
  • Diarrheal form
  1. B. liceniformis- sporadic abortion in cattle.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Species infection variation of Anthrax:

What species is highly susceptible?

Species moderately susceptible?

Species comparitvely resistant?

Species totally resistant?

A
  1. This is a worldwide endemic affecting virtually all mammals.
  2. Ruminants are highly susceptible and can develop a rapidly fatal septicemia.
  3. Pig, horses moderately susceptible.
  4. Carnivores are moderately resistant.
  5. Birds totally resistant.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Anthrax Epidemiology:

Most important factor in Anthrax persistance?

When do outbreaks occur?

How is infection acquired?

A
  • **Endospore formation most important factor in persistance of anthrax in the environment and spread to other animals. **
  • Endospores are EXTREMELY resistant and can survive in the environment (soil) for decades.
  • Outbreaks usually occur in herbivores when pasture contaminated by spores…this is why ruminants are HIGHLY susceptible.
  • These spores are brought to the surface by flooding, excavation, subsidence, earthworm activity.
  • Infection is acquired by ingestion of spores either by inhalation or skin abrasian which is more common in man.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the infectous process of B. anthrax.

A
  1. Endospores in the environment are brought to the soil surface (flooding, excavating, earthworm activity).
  2. These spores are ingested (grazing, drinking) or inhaled.
  3. The spores germinate inside the herbivore and multiply in the lymphatics and spleen.
  4. Vegetative forms (sexually active-asexual) are released in massive numbers into the ruminants blood in the final hours of its life.
  5. This causes an overwhelming septicemia and the animals begins to bleed from every orifice.
  6. Vegetative forms are shed at death in hemorrhagic excudate from the nose, mouth, anus.
  7. These vegetative form sporulate when exposed to O2 and become the notorious resistant endospores than can last for decades in the environment.
  8. Spores can infect cutaenously (man), pulmonary infection, gastrointestinal infection (infected meat, water, vegetables)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Anthrax Pathogenesis:

What are its virulence factors? Where are they encoded and how are they regulated?

A
  1. Virulence factors:

**a. poly-d-glutamic acid capsule

b. complex toxin**
2. Both virulence factors are encoded on plasmids.
3. The expression of these virulence factors are regulated by host temperature and CO2.
4. The poly-d-glutamic acid capsule inhibits phagocytosis.
5. The complex toxin consists of three anitgenic components ( protective antigen, edema factor, lethal factor) and the protective antigen acts as the binding moeity for edema/lethal factor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Anthrax Pathogenesis continued:

Edema Factor- What virulence factor is this a component of? How does it work?

Lethal factors-What virulence factor is this a component of? How does it work?

What effects will these antigenic factors have on tissues?

A
  • Edema factor:
  • One of the antigenic components of the complex toxin.
  • Calmodulin dependent adenylate cyclcase increase cAMP causes build up fo fluid in tissue as well as inhibits neutrophils.
  • Lethal factor:
  • Antigenic component of the complex toxin.
  • Lethal toxin is a zinc metalloprotease plus Protective Antigen which acts as a binding domain.
  • Lethal factor stimulates macrophages to release IL-1 beta and TNF alpha and cleaves MAP kinase (this is responsible for the inflammatory response, but without cannot kill anthrax)
  • Tissue swelling (edema), darkening of the tissue, necrosis.
  • When the lethal factor induces the release of the cytokines IL-1 beta and TNF- alpha from the macrophages they induce signs of shock and eventually death.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is characteristic of anthrax just before death?

A

A MASSIVE septicemia, bactermia occluding the vasculature, overwhelming the body. Death occurs. Bleeding from orifices. Spread of infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How can we diagnose Anthrax?

A
  • Carcasses are bloated & DO NOT EXPERIENCE rigor mortis.
  • Bleeding ensues from the mouth, anus, nose.
  • Blood is collected from the animal and stained with polychrome methylene blue and will show BLUE BACTERIA WITH PINK CAPSULES… This is called a McFadyeans capsule stain. (unique to anthrax)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is anthrax characteristic appearance on blood agar?

A

Medusa head colonies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 3 forms of anthrax disease in man?

A
  1. Cutaneous-endospores enter abraded/ damaged skin
  2. Pulmonary- woolsorters disease- via inhalation of spores
  3. Intestinal via ingestion by infected meat, vegetation, or water.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How can we control anthrax?

A
  • Do not open carcass. this will facilitate spore fomration and environmental contamination.
  • Annual vaccination.
  • Burn infected carcasses AWAY from water sources.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What kind of bacteria is Clostridum?

Discuss any enzymes, toxins, and sensitivities.

A
  • Gram positive large rods
  • Resistant spores (similar to bacillus)
  • Strict anaerobes (tell me how im sposed to breath with NO AIR)
  • Grow VERY rapidly (similar to bacillus)
  • Produce VFA
  • Contain enzymes including proteases, saccharases.
  • Produce 2 toxins:

**1. tetanus toxin on plasmid.

  1. Botulism toxin on lysogenic phage.**
    * Antimicrobial sensitive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where is Clostridia found? What are the 3 types of Clostridium?

A
  • Found in soil, alimentary tract of animals, and in feces.
    1. Neurotoxic clostrida
    2. Histotoxic clostridia
    3. Enteropathogenic/ enterotoxemia clostridia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Neurotoxic Clostridia:

Most susceptible?

Moderately susceptible?

Comparitively resistant?

Resistant?

A
  1. Horses/ Humans.
  2. Ruminants/ pigs
  3. Carnivores
  4. Poultry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the characteristic shape of clostridium when staining?

A

Drumsticks.

17
Q

What two toxins does Clostridium produce and where are they found?

A
  1. Tetanus toxin: found on plasmid
  2. Botulism toxin found on lysogenic phage.
18
Q

Tetanus:

Toxin produced?

Where is toxin found?

How does infection occur?

What produces the toxin?

A
  1. Neurotoxin **tetanospasmin. **
  2. It is a plasmid encoded toxin
  3. Infection occurs when endospores are introduced into tissue (traumiatized or not) from soil and feces.
  4. Vegetative bacteria develop from the spores in the wound.
  5. Vegetative bacterial forms produce the toxin tetanospasmin.
19
Q

Tetanus Pathogenesis:

What comprises the tetanus toxin tetanospasmin?

A
  • The tetanus toxin consists of two chains joined by a disulphide bridge.
  • The light chain- toxic and the **heavy chain **
  • Irreversibly binds to ganglioside receptors on the motor neuron terminals and transported to the CNS via intraxonal flow.
  • Tetanospasmin blocks pre synaptic transmission of inhibitory signals (NT’s) such as GABA, glycine therefore causing SPASTIC PARALYSIS.
  • Bound toxin is not neutralized by antitoxin.
  • Toxin acts on opposing muscle groups.
20
Q

Botulism:

What is the associated toxin?

How does infection occur?

What toxin types produce outbreaks in domestic animals?

What toxin types produce outbreaks in humans?

A
  • Different antigenic forms of the neurtoxin (types A-G)
  • Germination of endospores, growth of vegetative cells, and toxin production occurs in rotting carcasses, decaying vegetation, contaminated canned food.
  • Type C/ D- Domestic Animals
  • Types A/B/E- Humans
21
Q

Botulism Pathogenesis:

A
  1. Neurtoxins of C. botulinum are the most potent biolgical toxins known.
  2. The botulinum toxin is synthesized as a single polypeptide chain and is then nicked by a bacterial protease to produce two chains.
  3. The toxin is absorbed from the GI tract and ciruclates in blood.
  4. Acts at nueromuscular junctions of cholinergic nerves and peripheral autonomic synapses. (vs. CNS in Tetanus)
  5. Remains at the junction.
  6. Irreversible interference with acetylcholine (blocks the fusion and release of acetylcholine from the pre synaptic nerve terminal at the neuromuscular juntion) resulting in FLACCID PARALYSIS (vs. spastic in clostridum tetanus)

Acetylcholine is a stimulatory signal that is being blocked by BT… VS. GABA/ glycine which are inhibitory signals that are being blocked by Tetanus Toxin.

  1. Death occurs because of flaccid paralysis of respiratory muscles.
22
Q

Tetanus Toxin (tetanospasmin) vs. Botulism Toxin (antigenically variable)

A

These toxins are very similar in structure despite having opposing effects on the body.

Opposing effects are due to acting on different receptors in the body.

Both toxins are Zinc dependent metalloproteinases.

Proteins (synaptobrevins) clamp the vessicle to the Pre synaptic membrane.

Clostridial toxins inhibit vessicle release by cleaving peptide bonds in these proteins.

Each toxin has a specific locus of activity.

23
Q

Histotoxic Clostridia:

A

The migration from the GIT to the tissues has no clinical symptoms until tissue damage occurs. Then reduced oxygen levels producing an anaerobic environment allow germination and vegetative proliferation.

Local Necrosis produced by exotoxins of replicating vegeative bacteria allows further proliferation and tissue damage.

  • Ingested endospores are excreted however some may leave the intestinal tract and enter the tissue where they will lie dormant.
24
Q

Histotoxic Clostridial Endogenous Infections:

Give examples and how they occur.

A
  • Black leg, infectious necrotic hepatitis, bacillary hemoglobinura, results from:
  • -> **ACTIVATION OF DORMANT SPORES IN THE MUSCLE OR LIVER. **
25
Q

Histotoxic Clostridial Exogenous Infections:

Give examples and how they occur.

A
  • Gas gangrene (myositis) results from **introduction of clostridia into wounds. **
  • Anaerobic environment of necrotic tissue allows replication, and toxin production.
26
Q

Histotoxic Clostridia:

C. chauvoei

A
  • Endogenous Infection
  • Blackleg
  • Commensal/ Ingestion
  • Relocalization to muscle
  • Bruising from trauma
  • Spore Germination and Toxinogenesis
  • Hemolysis, Crepitation, Necrosis.
27
Q

Histotoxic Clostridia:

C. novyi

A
  • Endogenous infection
  • Black’s Disease
  • Commensal/ ingestion
  • Relocalizes to liver
  • Fluke Migration (F. hepatica) causing damage to liver parenchyma
  • Spore germination and proliferation/ toxinogenesis.
  • Edema, shock, necrosis.
28
Q

Histotoxic Clostrida:

C. septicum (endogenous)

A
  • Injury to abomasum (hardware)
  • Colonization by commensal/ ingested C. septicum
  • Germination, proliferation, toxinogenesis.
  • Localized muscosal hemorrhage and necrosis.
  • Toxemia
  • Braxy (inflammatory disease in abomasal lining in sheep)
29
Q

Histotoxic Clostridia:

C. septicum (exogenous)

A
  • Wound
  • inoculation with clostridia
  • Toxinogensis
  • Cellulitis, myositis, edema
  • Gangrene (tissue death)
30
Q

How to control Histotoxic Clostridia?

A

Vaccine:

  1. Bacterin (killed organism)

+

  1. Toxoid (toxin inactivated with formaldehyde)

+

  1. Adjuvent
31
Q

Enteropathogenic & Enterotoxigenic Clostridia:

C. perfringens (type A-E)

Predisposing factors?

A
  • Replicates in intestinal tract and elaborate toxins wihch produce both localized and systemic effects.
  • Predisposing factors: inappropriate husbandry, dietary changes, local environmental influences.
  • Cause local and systemic effects.
  • The pattern of toxin production varies with each individual type and determines clincal syndrome observed.
32
Q

C. perfringens TYPE A

Toxin produced?

Diseased caused?

A
  • alpha toxin, Enterotoxin
  • Necrotic enteritis in chickens.
  • food poisoning in man.
33
Q

C. perfringens TYPE B

Toxin?

Disease caused?

A
  • Beta toxin
  • has effect on gut, ovewhelms, septicemia.
  • Lamb dysentery.
34
Q

C. perfringens TYPE C:

Toxin?

Disease caused?

A
  • Beta toxin
  • Piglets: hemorrhagic enteritis.
  • Calves- Enterotoxemia
  • Sheep- Struck
35
Q

C. perfrigens TYPE D:

toxin?

Disease Caused?

A
  • Epsilon toxin
  • Pulpy kidney in fat lambs
  • Sheep- Enterotoxemia.
36
Q

Clostridium difficile

How is this acquired?

What species does it affect and what disease does it cause in those species?

A
  • Anitbiotic associated diarrhea in man (hospital aquired-toxin mediated)
  • Pseduomembranous colitis in man
  • Necrotizing entercolitis in Horses
  • Diarrhea in Hamsters/ guniea pigs
  • Enteritis in neonatal pigs.