Clostridia Flashcards

1
Q

2 Types of Anaerobes

A
  1. Aerotolerant
  2. Obligate/Strict
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2
Q

Why do obligate anaerobes not tolerate any amount of oxygen?

A

they lack the enzymes to detoxify reactive oxygen species (superoxide dismutase, catalase, peroxidases)

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3
Q

How are you able to culture strict anaerobes?

A

use a reducing agent in the medium

packets in the lab, something to absorb oxygen, reduce hydrogen peroxide, thioglycolate or metallic iron

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4
Q

Anaerobiosis

A

Eh (standard reduction potential) falls below 150mV, anaerobes are able to grow

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5
Q

Examples of Conditions which lower Eh values

A

Loss of vascular supply to tissue
Trauma, foreign bodies
Acid production
Tissue necrosis

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6
Q

Are aerotolerant anaerobes gram positive or negative?

A

gram positive

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7
Q

Are obligate anaerobes gram positive or negative?

A

gram negative

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8
Q

Are anaerobe present in normal flora?

A

yes, they actually make up the majority

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9
Q

Are anaerobes opportunistic?

A

yes! think that they’re normally present (endogenous) and then shit happens

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10
Q

Do anaerobes cause infection on their own?

A

sometimes, but most are mixed infections

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11
Q

Clostridia

A

large gram positive rods, most are motile, non-encapsulated, spore forming

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12
Q

Which Clostridia species is NOT motile?

A

C. perfringens

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13
Q

Blackleg disease organism

A

Clostridium chauvoei
(also C. novyi, septicum, or sordelli)

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14
Q

Blackleg Disease Pathogenesis

A

C. chauvoei produces Phospholipase C (alpha toxin) which degrades phosphatidylcholine, which is the most abundant phospholipid on cell membranes

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15
Q

Signs of Blackleg

A

gas gangrene in muscle tissue, myositis, gram positive bacteria in exudate

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16
Q

Malignant edema organism (clostridial myositis)

A

Clostridium septicum

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17
Q

Clostridium septicum pathogenesis

A

wounds, fractures, etc, but also due to IRRITATED STOMACH LINING by eating dry or icy feed; alpha toxin breaking down cell membranes

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18
Q

Braxy

A

name of C. septicum infection in sheep

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19
Q

Which Clostridium species causes red water disease (hemoglobinuria)?

A

Clostridium hemolyticum

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20
Q

Clostridium hemolyticum pathogenesis

A

liver flukes cause liver infarcts (tracts/necrosis in the liver), bacteria grows and produces alpha toxin which then spreads systemically

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21
Q

2 Groups of Disease-Causing Clostridia

A
  1. Invasive group
  2. Non-invasive group
22
Q

Which two Clostridia species are non-invasive?

A

C. tetani and C. botulinum

23
Q

Tyzzer’s Disease is caused by what organism?

A

Clostridium piliforme

24
Q

Toxin which mediates Tyzzer’s disease?

A

Iota toxin

25
Appearance of C. piliforme on TEM
slender, thin, and long with peritrichous flagella
26
2 Types of Disease Caused by C. piliforme
1. Necrotizing hepatitis 2. Hemorrhagic enteritis
27
hemorrhagic enteritis
results in melena, diarrhea, and black color caused by the oxidation of iron
28
Diagnosis of Tyzzer's (necrotizing hepatitis) on histopathology
long slender cells with a fuzzy appearance, lots of filaments in weird arrangements in hepatocytes on Giemsa staining
29
Tyzzer's on Necropsy
disseminated small gray-white necrotic lesions with suppurative inflammation
30
Clostridium perfringens
non-motile Clostridia species which causes enterotoxaemia (usually due to overeating)
31
enterotoxaemia
toxin in blood from the gut
32
Most common toxinotype of C. perfringens?
Type A
33
C. perfringens in horses
causes necrotizing myositis, often associated with IM Banamine injection; causes gas; make incisions to expose bacteria to air
34
Pulpy Kidney (Overeating) Disease
occurs in sheep due to Type D C. perfringens which produces lethal epsilon toxin
35
Is C. perfringens a strict or aerotolerant anaerobe?
STRICT anaerobe
36
Why is Type D C. perfringens linked to overeating?
the organism thrives on sugars and starches in the upper portion of the GI tract
37
C. perfringens (Type D) Clinical Signs
colic, muscle tremors, convulsions, frothing, nystagmus, teeth grinding
38
3 Toxins Produced by C. tetani
1. Tetanolysin 2. Tetanospasmin 3. Non-spasminogenic Toxin
39
Tetanospasmin
potent A-B neurotoxin that blocks the release of inhibitory neurotransmitters (GABA and glycine)
40
GABA
chief inhibitory neurotransmitter in the CNS, ensuring muscle relaxation by inhibiting motor neurons
41
tetanic spasm
spastic paralysis, muscles are unable to relax due to the inhibition of GABA
42
2 Forms of Botulism
1. Food-borne 2. Infant
43
Food-borne botulism
intoxication (NOT infection) of preformed botulinum toxin
44
Infant botulism
non-invasive infection of C. botulinum in young infants who have consumed solid foods containing botulinum spores
45
C. botulinum pathogenesis
inhibits excitatory NT Ach in the PNS leading to flaccid paralysis, leading to respiratory arrest
46
Target of Botulinum vs. Tetani
Botulinum = PNS Tetani = CNS
47
DO botulinum and tetani have the same MOA?
yes - essentially the toxin degrade the SNARE proteins which are necessary for the fusion of the vesicle at the synapse for NT release
48
4 Gram-Negative Anaerobic Rods
1. Fusobacterium necrophorum 2. Dichelobacter nodosus 3. Prevotella melaninogenicus 4. Bacteroides fragilis
49
Can gram-negative anaerobic bacteria sporulate?
no!
50
Only gram-negative anaerobic bacteria which can cause disease?
Fusobacterium necrophorum (this is the primary invader which must come first)
51
Bacteriodes fragilis affects what species?
humans (can be domestic animals but not the point)
52
Main disease caused by the gram-negative anaerobic bacteria discussed in class?
FOOT ROT!