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VET 413: Infectious Disease/Immunology > Bacteriology - Clostridium > Flashcards

Bacteriology - Clostridium Flashcards

1
Q

is clostridium aerobic or anaerobic

A

anaerobic

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2
Q

is clostridium gram positive or negative

A

positive

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3
Q

is clostridium rods or cocci

A

rods

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4
Q

how do clostridium cause disease

A

release of toxins

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5
Q

enterotoxemia

A

toxins that are generated in the intestines and absorbed into circulation to act on distant organs

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6
Q

is C. perfringens endogenous

A

yes - most have C. perf in gut without causing disease

culturing it does NOT always indicate disease - requires typing or toxin ID

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7
Q

C. perfringens type A

A

alpha toxin only
- produced in all clostridial types; does not cause disease in most animals

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8
Q

can C. perfringens type A cause disease

A

yes but rarely; caused by over production of alpha toxin leading to intravascular hemolysis

Yellow Lamb disease
- anemia, icterus, depression, diarrhea

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9
Q

how to diagnose C. perfringens type A disease

A

culture w/ typing AND colony count - must be >10^6 CFUs/gram

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10
Q

C. perfringens type B

A

alpha + beta + epsilon toxins

causes Lamb Dysentery - rarely diagnosed in US

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11
Q

C. perfringens type C - toxins & signalment

A

alpha + beta toxins

occurs in NEONATAL ruminants, horses, pigs, humans

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12
Q

beta toxin

A

highly necrotizing - causes necrotizing enteritis

inactivated by TRYPSIN

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13
Q

pathogenesis of C. perfringens type C

A
  1. ingestion of C. perfringens type C
  2. proliferates in intestines
  3. lack of trypsin (ex. neonates - colostrum inactivates trypsin)
  4. beta toxin remains active
  5. necrotic enteritis
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14
Q

clinical signs of C. perfringens type C

A

hemorrhagic diarrhea
neurologic signs
sudden death

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15
Q

diagnostics for C. perfringens type C

A

toxin ELISA for beta toxin

culture w/ typing, histology, clinical signs are all suggestive but not diagnostic

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16
Q

C. perfringens type D - toxins and signalment

A

alpha + epsilon toxins

occurs in ADULT sheep and goats

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17
Q

epsilon toxin

A

increases vascular permeability

activated by TRYPSIN

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18
Q

pathogenesis of C. perfringens type D

A
  1. excess carbohydrate ingestion
  2. carbohydrates do not get fermented in rumen
  3. starch enters directly into SI
  4. promotes C. perf type D growth
  5. production of epsilon toxin
  6. travels to brain, heart, lungs, etc
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19
Q

clinical signs of C. perfringens type D

A

sheep: neurologic disease, respiratory difficulty
- NO diarrhea

goats: neurologic disease, alimentary disease, or BOTH
- can have diarrhea

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20
Q

diagnosis of C. perfringens type D

A

toxin ELISA for epsilon toxin

culture w/ typing, clinical signs are suggestive

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21
Q

C. perfringens type E

A

alpha + iota toxins

not a significant cause of disease in animals

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22
Q

C. perfringens type F

A

alpha + CPE (CP enterotoxin)

causes food poisoning in humans
- not a significant cause of disease in animals

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23
Q

C. perfringens type G - toxin and signalment

A

alpha + NetB toxins

occurs in poultry

24
Q

NetB toxin

A

causes necrotizing enteritis

main predisposing factor is coccidiosis (Eimeria)

25
Q

clinical signs of C. perfringens type G

A
  • loss of production
  • depression
  • diarrhea
  • sudden death
26
Q

diagnosis of C. perfringens type G

A

combination of clinical signs, histology, and culture w/ typing

NO toxin test for NetB

27
Q

C. difficile toxins and signalment

A

toxin A, toxin B, CDT

occurs in horses, pigs, rabbits, hamsters
- horses: all ages
- pigs: neonates

28
Q

what is the main predisposing factor for C. difficile

A

antibiotic therapy +/- hospitalization

29
Q

clinical signs of C. difficile

A

horses: diarrhea +/- hemorrhage, colic

pigs: diarrhea +/- hemorrhage, colic, mesocolonic edema

30
Q

diagnosis of C. difficile

A

toxin ELISA for toxins A, B, or both

culture w/ typing, histology, and clinical signs are suggestive

31
Q

C. piliforme signalment

A

horses, rabbits, rats, hamsters, cats, others

32
Q

clinical signs of C. piliforme

A

Tyzzer Disease - ‘triad of lesions’

  • intestines (colitis)
  • liver (hepatitis)
  • heart (myocarditis)

can cause neurologic signs from hepatic encephalopathy

33
Q

diagnosis of C. piliforme

A

histology, PCR

34
Q

paeniclostridium sordelli clinical signs

A

hemorrhagic and necrotizing enteritis

35
Q

paeniclostridium sordelli diagnosis

A

rule out other causes of enteric disease, then:
- culture
- PCR
- IHC

36
Q

C. colinum

A

Quail Disease

causes ulcerative colitis

37
Q

C. spiroforme

A

Rabbit Enterotoxemia

causes hemorrhagic cecum

38
Q

what causes Black Leg

A

clostridium chauvoei

39
Q

Black Leg species affected

A

cattle
sheep (rare)

40
Q

Black Leg toxins

A

C. chauvoei toxin A (CctA)

41
Q

pathogenesis of Black Leg

A

ENDOGENOUS infection - does not require a cut

  1. spores ingested in soil and absorbed in intestines
  2. enters circulation and travels to muscle
  3. engulfed by muscle macrophages
  4. spores remain dormant in muscle
  5. blunt trauma occurs and reduces O2 causing spores to germinate
  6. produces CctA toxins
  7. muscular necrosis, toxemia, shock
42
Q

lesions in Black Leg

A

muscle necrosis of skeletal AND cardiac muscle

43
Q

what causes gas gangrene

A

C. septicum, chauvoei, novae, perfringens, and Paeniclostridium sordelli

44
Q

Gas Gangrene species affected

A

sheep, goats, cattle, horses, pigs

45
Q

pathogenesis of Gas Gangrene

A

EXOGENOUS infection - requires a cut

  1. spores or bacteria in soil enter through external wound
  2. reduction in O2 induces spore germination
  3. release of toxins
  4. muscle or SQ necrosis, toxemia, shock
46
Q

lesions of Gas Gangrene

A

muscle or SQ necrosis
- NO cardiac muscle; skeletal only

47
Q

diagnosis of gas gangrene

A

culture, PCR, FAT, IHC

48
Q

what clostridium species cause hepatitis

A

C. novyi and C. haemolyticum

49
Q

hepatitis type B - disease and species

A

infectious necrotic hepatitis in sheep

can occur in cattle and horses

50
Q

hepatitis type D - disease and species

A

bacillary hemoglobinuria in cattle

can occur in sheep and horses

51
Q

what are the toxins produced by C. novyi and C. haemolytica

A

C. novyi - alpha + beta toxin
C. haemolytica - beta toxin only

52
Q

pathogenesis of Clostridial hepatitis

A
  1. spores ingested from soil and absorbed in intestines
  2. travels in circulation to liver
  3. engulfed by hepatic macrophages
  4. spores remain dormant in liver
  5. liver damage causes reduced O2
  6. spores germinate and release toxins
  7. hepatic necrosis, toxemia, shock
53
Q

what is the predisposing factor for clostridial hepatitis

A

fasciola hepatica

54
Q

clinical signs of clostridial hepatitis

A
  • depression
  • sudden death
  • hemoglobinuria and icterus (type D only)
55
Q

diagnosis of clostridial hepatitis

A

culture, PCR, FAT, IHC

VET 413: Infectious Disease/Immunology (38 decks)

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