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DVM2: Veterinary bacteriology/mycology > Gram + anaerobes > Flashcards

Gram + anaerobes Flashcards

1
Q

Clostridium spp. morphology + metabolic requirements/characteristics

A

Large gram + rods

Anaerobic, spore-forming, motile

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2
Q

Clostridial diseases by species (12)

A 
C. tetani - tetanus
C. botulinum - botulism
C. perfringens - enterotoxaemia/haemorrhagic enteritis, malignant oedema, lamb dysentery
C. novyi - malignant oedema, big head, black disease 
C. haemolyticum - bacillary haemoglobinuria
C. septicum - braxy, malignant oedema
C. chauvoei - black leg
C. spiroforme - enterotoxaemia
C. villosum - cat fight abscess
C. difficile - enterocolitis
C. colinum - necrotic enteritis
C. piliforme - acute hepatic necrosis
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3
Q

Which Clostridia spp possess neurotoxins? (2)

A

C. tetani - spastic paralysis

C. botulinum - flaccid paralysis

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4
Q

Pathogenesis of tetanus

A 
Local infection of wound by spores
> infection/necrosis = ↓ redox potential/↓ [oxygen]
> spore germination/growth 
> exotoxin disseminates via blood/nerves
> binds to pre-synaptic membrane of inhibitory neurons 
> blocks GABA/Gly release 
> tetanic spasm 
> respiratory paralysis/death
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5
Q

Tetanus VFs (3)

A

Tetanospasm (exotoxin) = Zn endoproteinase activated by bacterial proteases (unstable in GIT)

Tetanolysin (haemolysin)

Non-spasmogenic toxin

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6
Q

Tetanus route of infection

A

Deep wounds

  • anaerobic environment required for spore germination
  • tetanospasm is destroyed in intestine
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7
Q

Tetanus immunity

A

Ab mediated immunity to toxin > toxoid vax/passive immunity

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8
Q

Tetanus tx

A

Penicillin - may not reach wound in necrotic tissue

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9
Q

Tetanux dx

A

clinical observations = tetanic muscle spasm

hard to find wound + can’t demonstrate toxin

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10
Q

Tetanus source of infection

A

Common in environment

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11
Q

Botulism source of infection

A

Ubiquitous in poor quality food

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12
Q

Species susceptibility to tetanus

A

Horse > pig/rum/carn

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13
Q

Species susceptibility to botulism

A

Rum > others

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14
Q

Pathogenesis of botulism

A

Agent multiplies in feed
> cell lysis = toxin release
> toxin ingestion
> toxin cleaved by trypsin in GIT + absorbed
> binds NMJ = blocks ACh release
> flaccid paralysis (can’t initiate muscle contraction)
> Respiratory paralysis/death

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15
Q

Botulism VFs (1)

A

7 distinct toxins (A-G)

  • C/D are most animal cases = obligate intestinal parasites
  • Zn-endoproteinase cleaves synaptobrevin in peripheral nn.
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16
Q

Botulism immunity

A

Anti-toxin Ab > toxoid vax (type C/D toxins)

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17
Q

Botulism epidemiology (2)

A

Multiplies in carcasses, ↓ quality/poorly stored feed, spoiled silage, decomposing plant material

Outbreaks in water birds dt ingestion of decomposing plant material/snails eating it

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18
Q

Botulism route of infection

A

Oral

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19
Q

Botulism Dx (2)

A

food/GIT specimens inoculated into mice

ELISA on serum

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20
Q

Invasive Clostridial spp.

A

C. chauvoei
C. novyi (type A/B)
C. septicum
C. perfringes

21
Q

Malignant oedema - agent

A

Clostridium perfringes type A

± C. chauvoei, C. novyi type A, C. septicum

22
Q

C. perfringens toxins (4)

A

Alpha = splits lecithin in cell wall

Beta = intestinal inflamm/mucosal sloughing
- destroyed by trypsin

Epsilon = ↑ permeability of gut epithelium/ brain endothelium TF necrotising
- activated by trypsin/pepsin

Iota = cytotoxin

23
Q

Malignant oedema - pathogenesis

A

C. perfringens type A

Wound contamination by spores
> germination in anaerobic conditions
> alpha toxin elaboration = muscle damage
> further replication
> exotoxins absorbed into circulation = endothelial damage
> hepatic/muscle damage

24
Q

Clostridial enterotoxaemia - agent + source of infection

A

C. perfringens type D

Commensal of intestine > overgrows w ↑ undigested starch contents

25
Q

Clostridial enterotoxaemia - pathogenesis

A

C. perfringens type D

Change in food = ↑ undigested starch
> proliferation of agent
> epsilon toxin accumulates = ↑ GI permeability
> toxin absorbed into circulation
> ↑ vasc perm of brain = focal symmetrical encephalomalacia
> renal tubule dmg = glycosuria
> death w hypovolaemia + pulmonary oed/hydropericardium

26
Q

Pulpy kidney

A

Post-mortem change dt rapid autolysis following death from clostridial enterotoxaemia

27
Q

Haemorrhagic enteritis - agent

A

Clostridum perfringens type B/C

28
Q

Haemorrhagic enteritis - pathogenesis

A

C. perfringens type C

Agent binds to jejunal mucosa
> Beta toxin elaborates (if no trypsin)
> necrosis/sloughing of mucosa
> haemorrhagic enteritis

29
Q

Malignant oedema/enterotoxaemia/haemorrhagic enteritis - immunity

A

Toxoid (type B + D) = protective Ab to types A-D

Enterotoxaemia requires Ab in circulation
Enteric dz requires Ab in intestinal lumen (colostrum)

30
Q

C. perfringens dx (3)

A

serum/intestinal contents inoculated into mice to demonstrate toxin presence

ELISA

Lots of agent in upper SI

31
Q

C. novyi types + associated dz’s (2)

A

C. novyi type A = malignant oedema including big head (rams dt fighting)

C. novyi type B = black disease (infectious necrotic hepatitis)

32
Q

C. novyi VFs (1)

A

Alpha = lethal, ↑ capillary permeability causing oedema

33
Q

Black disease (infectious necrotic hepatitis) - agent + pathogenesis

A

C. novyi type B

Agent ingested + spores lodge in liver
> local hepatic necrosis dt F. hepatica larval migration (or other causes)
> ↓ redox = spore germination/multiplication
> toxin elaborate = further local necrosis
> toxins enter circulation
> ↑ vasc perm + muscle dmg (incl heat) + congestion

34
Q

Black disease - immunity

A

Toxoid of type B = Ab protective against C. novyi type A + B

35
Q

Black disease - dx (2)

A

Focal hepatic necrosis

Evidence of F. hepatica migration

36
Q

Braxy - agent

What other disease does this agent cause?

A

Clostridium septicum

Also malignant oedema

37
Q

Braxy - pathogenesis

A

C. septicum

Eating frozen pasture = dmg to abomasal wall
> local replication of agent
> toxaemia

38
Q

Blackleg - agent + route of infection

A

Clostridium chauvoei

oral route (ingested)

39
Q

Blackleg - pathogensis

A

C. chauvoei

Ingestion + replication in intestine
> spores reach muscle via circulation (no external wounds)
> Muscle damage (bruising) = anaerobic conditions/↓ redox = germination/replication
> local muscle dmg dt toxins
> toxins enter circulation = lameness, fever, depression, death

40
Q

Blackleg - immunity (1)

A

Ab against bacterin (cells) + toxin

41
Q

Blackleg - dx

A

agent demonstrated by fluorescent Ab staining of muscle smears (ddx pos-mortem invasion)

42
Q

Enterocolitis in horses, rabbits, guinea pigs - agent + clin signs

A

Clostridium difficile

Toxin elaboration = GI epithelial necrosis/inflamm > severe diarrhoea + necrotising enteritis

43
Q

Enterocolitis (eq/rabbits) - risk factors/associations

A

C. difficile

Broad-spectrum antibiotic use = overgrowth of agent dt destruction of competing flora

Assoc w tx for rattles

44
Q

Enterocoloitis - tx (2)

A

Metronidazole

Vancomycin

45
Q

Tyzzer’s disease (foals) - agent/morphology/habitat

A

Clostridium piliforme - gram neg

Obligate intracellular parasite of hepatocytes, epithelial cells, GI SM cells

46
Q

Tyzzer’s disease (foals) - disease

A

C. piliforme

Acute hepatic necrosis + necrotic enterocolitis

47
Q

Cystitis/pyelonephritis in sows - agent + morphology

A

Actinobaculum suis - gram + anaerobic, pleomorphic rod

48
Q

Cystitis/pyelonephritis in sows - source of infection

A

A. suis

Carried by boars in prepuce > infection of sows during coitus > ascending UTI

Urease + = NH3 prod’n > mucosal ulceration + haemorrhagic cystitis

49
Q

Cystitis/pyelonephritis in sows - tx

A

penicillin

DVM2: Veterinary bacteriology/mycology (9 decks)

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