Clostridium - made a table instead Flashcards

1
Q

what is the causative agent of botulism?

A

Clostridium botulinum

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2
Q

where are the endospores of botulism found?

A

distributed in soils and aquatic environments

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3
Q

what are the 7 types of toxins of C. botulinum?

A

A, B, C, D, E, F, & G

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4
Q

When choosing an antitoxin for botulism what is most important for it to be an effective treatment?

A

antitoxin must match toxin

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5
Q

what type of paralysis is seen with C. botulinum?

A

flaccid paralysis

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6
Q

Describe the botulism endospores

A

oval subterminal endospores, bulge mother cells

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7
Q

what is the most common toxin in cattle and what part of the cow contains the toxin?

A

bones and meat contain BoNT

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8
Q

what is shaker foal syndrome?

A

in horses from type b
foal found dead or progressive symmetric motor paralysis

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9
Q

How does the botulinum neurotoxin cause disease?

A

enter cystosol of host cell and cleaves SNARE proteins required for membrane fusion of synaptic vesicles and cell membrane > blocks AcH release

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10
Q

what are clinical manifestations of C. botulinum?

A

tongue, jaw, and tail flaccidity
incoordination and knuckling fetlocks
flaccid paralysis

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11
Q

How is botulism diagnosed?

A

eliminate other possible causes
history, clinicals signs, ID of toxin in serum/tissue before death

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12
Q

why is the toxin not useful in dead carcaccases?

A

environmental organism used to deregulate dead carcasses > false positive

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13
Q

why are you likely unable to culture C. botulinum from non-toxicoinfection cases?

A

cant grow in gut well
toxin is what is important for disease not the bacteria

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14
Q

what does PCR detect for botulism?

A

toxin genes
requires bacteria from culture or patient

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15
Q

How is C. botulinum treated and controlled?

A

evacuation of stomach and purging for recent ingestion
polyvalent antiserum - binds unbound toxin, serotype specific

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16
Q
A
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17
Q

what diseases does C. chauvoei cause?

A

blackleg
clostridial myositis
black quarter

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18
Q

what hemolysis does C. chauveoi have?

A

B hemolysis

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19
Q

where is C. chauveio found?

A

naturally in intestinal tract of animals

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20
Q

How does C. chauveio enter tissues?

A

likely ingested, organism crosses epithelial layer in GI tract to enter tissues

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21
Q

Is C. chauveio an endogenous or exogenous disease?

A

endogenous disease - disease may occur without a wound

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22
Q

what is the virulence factor for C. chauveio? what does it do?

A

CctA : Clostridium chauvoei toxin A > perforates host cell membrane

23
Q

What age of cattle is blackleg most commonly found?

A

well-fed 6m-2yr most commonly

24
Q

How is blackleg cause in sheep?

A

C. chauvoei-associated gas gangrene
wound infections > follows injury

25
What generates lesions in blackleg? Describe lesions
CctA dry, dark, emphysematous
26
what are the clinical manifestations of blackleg?
gangrenous cellulitis & crepitant myositis acute development lameness, edema, crepitation
27
How is blackleg diagnosed?
28
How is blackleg treated?
vaccinate susceptible animals and treat prophylactically with penicillin for up to 14 days
29
How is blackleg controlled?
vaccination - Bacterin (killed bacteria) vaccine produced with local, previously identified clostridial strains of C. chauvoei in cases where toxoid vaccine is ineffective
30
what is the causative agent of infectious necrotic hepatitis (black disease)?
C. novyi
31
Where is C. novyi found?
worldwide soil borne organism often present intestine and liver of herbivores
32
what is the key virulence factor for black disease?
TcnA - lethal, necrotizing, activates GTP binding proteins leading to edema
33
What species is C. novyi type B found?
sheep and cattle
34
How are sheep and catle infected with C. novyi Type B?
endospores ingested and migrate to Kupffer cells in liver where they remain dormant
35
How is the liver injured with C. novyi type B?
fluke migration - tissue is anoxic so endospores germinate
36
What clinic signs are seen with black disease?
rarely observed and cattle simply found dead
37
How is black disease diagnosed?
liver lesions - grayish yellow gross lesions - fluke tracts contain large gram + rods in liver
38
Postmortem how does c. novyi contaminant liver?
GI tract
39
How is C. novyi type B controlled?
prophylactic vaccination w/ bacterin - toxoid combination control fluke and other hepatopathic agents
40
How often do animals have to be vaccinated for C. novyi type B?
long term immunity - 1 vaccination
41
what is the causative agent of bacillary hemoglobniuria (red water disease)?
C. haemolyticum
42
what type of disease is red water disease?
acute, infectious toxemic disease
43
what species does red water disease infect? where?
ruminants - rocky mtn, pacific coast, gulf of mexico
44
How are ruminants infected with C. haemolyticum?
grazing in pastures infested with liver flukes encysted on vegetation
45
what is the virulence factor of C. haemolyticum?
B-toxin - hemolytic and necrotizing phospholipase C
46
How do liver flukes contribute to C. haemolyticum infection?
young liver flukes excyst in duodenum > burrow through intestinal wall then migrate to and enter liver > damage creates anaerobic tissue > C. haemolyticum can grow
47
what leads to hepatocyte necrosis and endovascular thrombosis with C. haemolyticum?
toxin production by vegetative growth
48
what are the clinical manifestations with a subacute infection of C. haemolyticum?
fever, jaundice, anorexia, abdominal pain, rapid deep breathing, decreased milk production, blood in feces and urine
49
How is red water disease diagnosed?
clinical history necropsy - lesions (infarcts) in liver
50
How is C. hameolyticum confirmed?
C. haemolyticum in liver infarction
51
How is red water disease treated?
Antibiotic treatment likely ineffective antitoxin
52
How is C. haemolyticum controlled?
vaccination seasonal - 1 dose prior to dry season constant protection - semiannual vaccination
53