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Bacteria > Clostridia L5 > Flashcards

Clostridia L5 Flashcards

1
Q

Are clostridium species gram positive or gram negative?

A

Gram positive

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2
Q

Are clostridium species rods or cocci?

A

Rods

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3
Q

Can clostridium species survive in aerobic conditions?

A

No- they’re obligate anaerobes.

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4
Q

Are clostridium species spore forming?

A

Yes

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5
Q

What is the typical shape of clostridium species?

A

Drumstick shape or Grama’s slippers.

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6
Q

What is the clostridium species responsible for Tetanus?

A

C. tetani

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7
Q

What is the clostridium species responsible for Botulism?

A

C. botulinum

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8
Q

What toxaemia group are C. tetani and C. botulinum?

A

Neurotoxic

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9
Q

What clostridium species is enterotoxic, how many types does it have and what one is relevant in NZ?

A

C. perfringens
Types A, B, C, D, E
In NZ Type D causes disease.

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10
Q

Are clostiridal disease contagious?

A

No

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11
Q

What do clostridium species play an important role in?

A

Putrefaction

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12
Q

What are the 4 common histotoxic clostridium species?

A

C. chauvoei
C. novyi
C. septicum
C. sordelli

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13
Q

What are the hosts for histotoxic clostridium species?

A

Cattle, sheep, humans, horses

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14
Q

What are the common hosts for C. tetani?

A

Humans, horses and pigs are highly susceptible. Cattle, sheep, dogs, cats and goats are less susceptible.

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15
Q

What are the hosts for enterotoxic clostridium species?

A

Humans, sheep, cattle

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16
Q

What type of paralysis does C. tetani cause?

A

Rigid paralysis

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17
Q

What type of paralysis does C. botulinum cause?

A

Flaccid paralysis

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18
Q

What is the neurotoxin that causes the clinical signs of Tetanus?

A

Tetanospasmin

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19
Q

When is tetanospasmin released?

A

When the bacteria lyse, such as during spore germination or during vegetative growth.

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20
Q

Where does tetanospasmin toxin act?

A

CNS- peripheral nerve terminals, spinal cord, the brain and the sympathetic nervous system.

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21
Q

How does tetanospasmin act?

A

Blocks inhibitory impulses by interfering with the release of neurotransmitters.

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22
Q

How many phases are there of clinical disease with tetanus?

A

4 phases

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23
Q

What phase of clinical disease with tetanus causes constricted pupils, tight lips, erect ears, inability to open its jaws sunken eyes and/or sensitivity to light?

A

Phase I

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24
Q

What phase of clinical disease with tetanus causes erect tail, sawhorse stance, difficulty swallowing, walking stiffly and with difficulty?

A

Phase II

25
Q

What phase of clinical disease with tetanus causes muscle tremors or spasms, inability to walk and seizures?

A

Phase III

26
Q

What phase of clinical disease with tetanus can possibly have HR below 60bpm or HR above 140bpm, high BP or low BP or respiratory arrest?

A

Phase IV

27
Q

What is the treatment of tetanus?

A

Controlling muscle spasms, stopping toxin production, and neutralizing the effects of the toxin.
Tetanus immune globulin (passive immunisation)
Large doses of antibiotics to stop toxin production.

28
Q

What type of immunization is provided by annual tetanus toxoid vaccine?

A

Active immunisation.

29
Q

What are the hosts for C. botulinum?

A

Humans and animals. (not zoonotic)

30
Q

How is C. tetani acquired?

A

Penetrating wounds that heal over creating an anaerobic environment.

31
Q

How is C. botulinum acquired?

A

Food-borne.

32
Q

What form produces the toxin for C. botulinum?

A

Vegetative form

33
Q

Where are C. botulinum present?

A

Intestinal tract, soil, freshwater and marine sediments throughout the world.

34
Q

What are common clinical presentations for Botulism?

A 
Cattle:
Acute form- sudden death
Subacute form- stiff gait, ruminal atony, ataxia, sternal recumbency, dropped head, saliva drools, tongue stays out to side when pulled.
Birds:
Twisted neck, dropped head.
35
Q

What preventions are there for botulism?

A

Prevention of decomposing rodent/bird carcasses in the feed.
Immunization of at-risk animals using type-specific toxoid.
Addition of food additives (nitrates) and stringent production processes prevent spore germination in food.

36
Q

What clostridium species causes black leg?

A

C. chauvoei

37
Q

What clostridium species causes malignant oedema?

A

C. septicum
C. novyi
C. sordelli

38
Q

What clostridium species causes black disease?

A

C. novyi (Type B)

39
Q

How do C. chauvoei get into the host to cause disease. And what disease it cause?

A

Spores are ingested and transported via macrophage to tissues.
Blackleg

40
Q

How do spores of C. chauvoei come out of dormancy?

A

The muscle has to be damaged creating an anaerobic environment. Germination causes toxin production- toaxaemia.

41
Q

What age group of animals is likely to be affected by black leg?

A

Well conditioned, fast-growing <2 year old animals.

42
Q

What are the signs an animal has died from blackleg?

A

Sudden death.
Lying on side with affected limb extended.
On PM muscles have areas of black.

43
Q

What are clinical signs of Malignant oedema?

A

A large, cold swelling, that pits.

Pyrexia (fever), dullness, inappetence.

44
Q

Where is malignant oedema located on an animal?

A

In the connective tissues.

45
Q

What is the origin of malignant oedema?

A

Exogenous - puncture wounds that have sealed over creating an anaerobic environment.

46
Q

What are clinical signs of Black Disease?

A

Rapid onset of disease, depression and reluctance to move, +/- abdominal pain.
Absent rumen sounds.
Death within 48 hours

47
Q

What is black disease associated with?

A

Liver fluke

48
Q

How does liver fluke lead to black disease?

A

Causes damage in liver causing an anaerobic environement. So if they have ingested C. novyi and it was transported to the liver, they can replicate in the anaerobic environment.

49
Q

What causes Enterotoxaemia (Pulpy Kidney) and Gas Gangrene?

A

C. perfingens

50
Q

What is Enterotoxemia Type D referred to as?

A

“Classic” overeating disease.

Pulpy Kidney Disease

51
Q

Is Pulpy Kidney Disease the most common sheep disease in the world?

A

Yes

52
Q

What animal (species, age/growth) does Enterotoxemia commonly strike?

A

Sheep.

Largest, fastest growing lambs in the flock.

53
Q

What causes Enterotoxemia?

A

It is caused by a sudden change in feed that causes the organism to proliferate causing a toxic reaction.

54
Q

What are the clinical manifestations of Enterotoxemia?

A

Sudden death particularly if consuming high concentrate rations.
Lambs over 1 month age.

55
Q

What cause the Pulpy Kidneys of Enterotoxemia?

A

Autolysis of the kidney.

56
Q

What findings are there in the rumen and guts of an animal with Enterotoxemia?

A

Plenty of grain in rumen.

Haemorrhagic enteritis.

57
Q

How can we control Clostridial Diseases?

A

Vaccination with multivalent vaccine.

Convexin-10 or ‘5 in 1’

58
Q

What does clostridial vaccines contatin?

A

Antigens (toxoids)

59
Q

When should sheep be vaccinated for clostridial diseases?

A

Replacement ewes at weaning and booster 4-6 weeks.

Booster prior to lambing.

Bacteria (1 decks)

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