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

Bacteriology - Clostridium Flashcards

(55 cards)

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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

Study These Flashcards
A

alpha + NetB toxins

occurs in poultry

24
Q

NetB toxin

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A

causes necrotizing enteritis

main predisposing factor is coccidiosis (Eimeria)

25
clinical signs of C. perfringens type G
- loss of production - depression - diarrhea - sudden death
26
diagnosis of C. perfringens type G
combination of clinical signs, histology, and culture w/ typing NO toxin test for NetB
27
C. difficile toxins and signalment
toxin A, toxin B, CDT occurs in horses, pigs, rabbits, hamsters - horses: all ages - pigs: neonates
28
what is the main predisposing factor for C. difficile
antibiotic therapy +/- hospitalization
29
clinical signs of C. difficile
horses: diarrhea +/- hemorrhage, colic pigs: diarrhea +/- hemorrhage, colic, mesocolonic edema
30
diagnosis of C. difficile
toxin ELISA for toxins A, B, or both culture w/ typing, histology, and clinical signs are suggestive
31
C. piliforme signalment
horses, rabbits, rats, hamsters, cats, others
32
clinical signs of C. piliforme
Tyzzer Disease - 'triad of lesions' - intestines (colitis) - liver (hepatitis) - heart (myocarditis) can cause neurologic signs from hepatic encephalopathy
33
diagnosis of C. piliforme
histology, PCR
34
paeniclostridium sordelli clinical signs
hemorrhagic and necrotizing enteritis
35
paeniclostridium sordelli diagnosis
rule out other causes of enteric disease, then: - culture - PCR - IHC
36
C. colinum
Quail Disease causes ulcerative colitis
37
C. spiroforme
Rabbit Enterotoxemia causes hemorrhagic cecum
38
what causes Black Leg
clostridium chauvoei
39
Black Leg species affected
cattle sheep (rare)
40
Black Leg toxins
C. chauvoei toxin A (CctA)
41
pathogenesis of Black Leg
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
lesions in Black Leg
muscle necrosis of skeletal AND cardiac muscle
43
what causes gas gangrene
C. septicum, chauvoei, novae, perfringens, and Paeniclostridium sordelli
44
Gas Gangrene species affected
sheep, goats, cattle, horses, pigs
45
pathogenesis of Gas Gangrene
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
lesions of Gas Gangrene
muscle or SQ necrosis - NO cardiac muscle; skeletal only
47
diagnosis of gas gangrene
culture, PCR, FAT, IHC
48
what clostridium species cause hepatitis
C. novyi and C. haemolyticum
49
hepatitis type B - disease and species
infectious necrotic hepatitis in sheep can occur in cattle and horses
50
hepatitis type D - disease and species
bacillary hemoglobinuria in cattle can occur in sheep and horses
51
what are the toxins produced by C. novyi and C. haemolytica
C. novyi - alpha + beta toxin C. haemolytica - beta toxin only
52
pathogenesis of Clostridial hepatitis
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
what is the predisposing factor for clostridial hepatitis
fasciola hepatica
54
clinical signs of clostridial hepatitis
- depression - sudden death - hemoglobinuria and icterus (type D only)
55
diagnosis of clostridial hepatitis
culture, PCR, FAT, IHC

VET 413: Infectious Disease/Immunology (38 decks)

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