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
Q

Appearance of C. piliforme on TEM

A

slender, thin, and long with peritrichous flagella

26
Q

2 Types of Disease Caused by C. piliforme

A
  1. Necrotizing hepatitis
  2. Hemorrhagic enteritis
27
Q

hemorrhagic enteritis

A

results in melena, diarrhea, and black color caused by the oxidation of iron

28
Q

Diagnosis of Tyzzer’s (necrotizing hepatitis) on histopathology

A

long slender cells with a fuzzy appearance, lots of filaments in weird arrangements in hepatocytes on Giemsa staining

29
Q

Tyzzer’s on Necropsy

A

disseminated small gray-white necrotic lesions with suppurative inflammation

30
Q

Clostridium perfringens

A

non-motile Clostridia species which causes enterotoxaemia (usually due to overeating)

31
Q

enterotoxaemia

A

toxin in blood from the gut

32
Q

Most common toxinotype of C. perfringens?

A

Type A

33
Q

C. perfringens in horses

A

causes necrotizing myositis, often associated with IM Banamine injection; causes gas; make incisions to expose bacteria to air

34
Q

Pulpy Kidney (Overeating) Disease

A

occurs in sheep due to Type D C. perfringens which produces lethal epsilon toxin

35
Q

Is C. perfringens a strict or aerotolerant anaerobe?

A

STRICT anaerobe

36
Q

Why is Type D C. perfringens linked to overeating?

A

the organism thrives on sugars and starches in the upper portion of the GI tract

37
Q

C. perfringens (Type D) Clinical Signs

A

colic, muscle tremors, convulsions, frothing, nystagmus, teeth grinding

38
Q

3 Toxins Produced by C. tetani

A
  1. Tetanolysin
  2. Tetanospasmin
  3. Non-spasminogenic Toxin
39
Q

Tetanospasmin

A

potent A-B neurotoxin that blocks the release of inhibitory neurotransmitters (GABA and glycine)

40
Q

GABA

A

chief inhibitory neurotransmitter in the CNS, ensuring muscle relaxation by inhibiting motor neurons

41
Q

tetanic spasm

A

spastic paralysis, muscles are unable to relax due to the inhibition of GABA

42
Q

2 Forms of Botulism

A
  1. Food-borne
  2. Infant
43
Q

Food-borne botulism

A

intoxication (NOT infection) of preformed botulinum toxin

44
Q

Infant botulism

A

non-invasive infection of C. botulinum in young infants who have consumed solid foods containing botulinum spores

45
Q

C. botulinum pathogenesis

A

inhibits excitatory NT Ach in the PNS leading to flaccid paralysis, leading to respiratory arrest

46
Q

Target of Botulinum vs. Tetani

A

Botulinum = PNS
Tetani = CNS

47
Q

DO botulinum and tetani have the same MOA?

A

yes - essentially the toxin degrade the SNARE proteins which are necessary for the fusion of the vesicle at the synapse for NT release

48
Q

4 Gram-Negative Anaerobic Rods

A
  1. Fusobacterium necrophorum
  2. Dichelobacter nodosus
  3. Prevotella melaninogenicus
  4. Bacteroides fragilis
49
Q

Can gram-negative anaerobic bacteria sporulate?

A

no!

50
Q

Only gram-negative anaerobic bacteria which can cause disease?

A

Fusobacterium necrophorum (this is the primary invader which must come first)

51
Q

Bacteriodes fragilis affects what species?

A

humans (can be domestic animals but not the point)

52
Q

Main disease caused by the gram-negative anaerobic bacteria discussed in class?

A

FOOT ROT!