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Ruminants > Clostridial diseases > Flashcards

Clostridial diseases Flashcards

1
Q

What kind of bacteria are Clostridia?

A

Gram positive, anaerobic, spore-forming rods

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2
Q

What are examples of protein exotoxins?

A

Botulinum toxin, tetanus toxin, epsilon toxin

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3
Q

What are examples of exoenzymes?

A

Collagenase, proteinase, hyaluronidase, lecithinase

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4
Q

What are the most common routes of clostridial toxin entrance to the body?

A

Ingestion of preformed toxins, production in the GI tract, production in infected tissues/wounds

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5
Q

Which types of Clostridium cause neurologic disease?

A

Tetani, botulinum, perfringens type D

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6
Q

What types of Clostridium cause enterotoxemia?

A

Perfringens types A, B, C, and E

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7
Q

What types of Clostridium cause gas gangrene and malignant edema?

A

Chauvoei, septicum, sordelli, novyi type A and D

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8
Q

What types of Clostridium cause liver lesions?

A

Novyi type B, hemolyticum

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9
Q

Where is Clostridium tetani found?

A

In the soil and in the intestinal tract of herbivores

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10
Q

What are common routes of infection for Clostridium tetani?

A

Puncture wound of feet or soft tissues, uterus after calving, castration site (especially with elastrator bands), tail docking sites, infected umbilicus

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11
Q

What unique signs are associated with tetanus in ruminants?

A

Vaginal bruising, necrosis, retained placenta

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12
Q

What unique signs are associated with tetanus in yearling cattle?

A

Infection of tooth alveoli

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13
Q

Describe the pathophysiology of tetanus

A

Inoculated spores germinate in anaerobic conditions. In this process, they produce toxins and release them upon cell lysis. This can happen immediately after introduction of the spores or months later if an additional traumatic episode occurs.

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14
Q

What are the three toxins produced by tetanus?

A

Tetanolysin, tetanospasmin, non-spasmogenic toxin

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15
Q

Describe tetanolysin

A

Oxygen-sensitive hemolysin that destroys phagocytes and causes tissue necrosis; primarily allows for maintenance of infection

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16
Q

Describe tetanospasmin

A

A lipoprotein exotoxin that diffuses into the vascular system and binds with presynaptic motor end plates causing neurological effects by releasing glycine (so muscles cannot be relaxed)

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17
Q

Describe non-spasmogenic toxin

A

Produces over-stimulation of the sympathetic nervous system causing tachycardia, sweating, and hypertension

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18
Q

What clinical signs are associated with tetanus?

A

Stiffness, tremors, third eyelid prolapse (except in sheep), bloat, rigid paralysis, difficulty eating/chewing, respiratory arrest, death

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19
Q

How is tetanus treated?

A

With procaine penicillin G, local injection of antitoxin, debridement +/- acepromazine for sedation and relaxation

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20
Q

How can tetanus be prevented?

A

Vaccinate ewes prior to lambing and vaccinate lambs when they are tail docked/castrated and booster 2 to 4 weeks later

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21
Q

Why are ruminants more resistant to botulism than horses?

A

Botulism toxins are partially destroyed in their rumen

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22
Q

Where are the botulism types usually found?

A

B- decaying vegetable matter
C and D- intestinal tract of carcasses of rodents, birds, and cats

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23
Q

Describe the pathophysiology of botulism

A

Toxins act at presynaptic cholinergic neuromuscular junction and postganglionic parasympathetic nerve endings to block the release of acetylcholine. Toxin binding is irreversible so function only returns after regeneration occurs.

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24
Q

What are the four sources of botulism toxin?

A

Forage poisoning, carrion associated, wound associated, toxicoinfectious

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25
Q

Describe forage poisoning

A

Seen in adults following ingestion of preformed toxin in spoiled feed materials (grains, silage, hay), usually type B

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26
Q

Describe carrion-associated botulism

A

Animals exposed to carcasses of rodents, small mammals, and birds or poultry litter contract type C and D; most common source of botulism

27
Q

Describe wound botulism

A

Infection of a wound with type B toxin. Bacteria sporulates and releases toxin under anaerobic conditions. Rare

28
Q

Describe toxicoinfectious botulism

A

More common in young animals due to ingestion of bacterial spores from the environment and sporulation in the GI tract (shaker foal syndrome); rare in ruminants

29
Q

What clinical signs are associated with botulism?

A

Progressive flaccid paralysis, especially of the limbs, throat, and tongue

30
Q

How can botulism be fatal?

A

By arrest of the respiratory tract

31
Q

How is botulism diagnosed?

A

Clinical signs, serum or GI content bioassay, PCR assay for type B, analysis of feed

32
Q

How is botulism treated?

A

Supportive therapy, polyvalent antitoxin (expensive, only works before toxin has bound to receptors)

33
Q

How can botulism be prevented?

A

Prevent animals from eating rotten vegetables or carcasses

34
Q

What are names for the disease caused by Clostridium perfringens type D?

A

Enterotoxemia, overeating disease, pulpy kidney

35
Q

Which species are most affected by Clostridium perfringens type D?

A

Mostly sheep (growing lambs), somewhat goats, virtually non-existant in cattle

36
Q

Describe the pathophysiology of C. perfringens

A

Proliferates with consumption of rapidly digestible carbs and produces non-toxic prototoxin that is cleaved by trypsin to form epsilon toxin. Epsilon toxin causes intestinal permeability, vascular edema, hyperglycemia, and damages the nervous system

37
Q

What clinical signs are associated with C. perfringens?

A

Sudden death, clonic convulsions, muscle tremors, opisthotonus

38
Q

What group of animals are predisposed to developing enterotoxemia?

A

Rapidly growing lambs

39
Q

How is enterotoxemia diagnosed?

A

Hyperglycemia and glucosuria, pulpy kidney on necropsy, perivascular edema, hemorrhage, and focal malacia, intestinal contents can be cultured

40
Q

How is enterotoxemia treated?

A

Usually not treated. Hyperimmune serum is available but it’s always too late.

41
Q

How is enterotoxemia prevented?

A

Vaccinate maiden ewes, vaccinate and booster lambs, reduce feed intake to lambs at risk, give antitoxin to all lambs if outbreak begins

42
Q

Describe focal symmetric encephalomalacia; what causes it?

A

Disease caused by Clostridium perfringens type D in sheep that causes aimless wandering, inability to eat, focal symmetrical encephlomalacia. Can occur at any age, sporadic.

43
Q

What causes hemorrhagic bowel syndrome?

A

Clostridium perfringens type A alpha toxins

44
Q

Which animals are usually affected by hemorrhagic bowel syndrome?

A

High producing dairy cows in early lactation

45
Q

Describe the pathophysiology of hemorrhagic bowel syndrome

A

Unclear; probably C. perfringens type A proliferating with excess starch and creating the toxin which induces segmental hemorrhage leading to obstruction from blood clot

46
Q

What clinical signs are consistent with hemorrhagic bowel syndrome

A

Decreased milk production, anorexia, tachycardia, tachypnea, dehydration, blood loss, shock, intestinal obstruction, right-sided intestinal distension, colic signs, scant to no feces with blood in rectum

47
Q

How is hemorrhagic bowel syndrome diagnosed?

A

Ultrasound can confirm intestinal distension, right flank abdominal explore will confirm diagnosis, necropsy will have intraluminal blood clot. Culture can be supportive.

48
Q

How is hemorrhagic bowel syndrome treated?

A

Medical therapy- fluids, antibiotics, NSAIDs, blood transfusion
Surgical therapy- R&A, enterotomy, disruption of clot- more successful than medical treatment

49
Q

How is hemorrhagic bowel syndrome prevented?

A

Vaccine available but ineffective, maximize feed management

50
Q

Describe gas gangrene

A

Myonecrosis following bruising of muscle tissue or deep wound

51
Q

Describe malignant edema

A

Cellulitis of connective tissue

52
Q

What is the causative agent of blackleg?

A

Clostridium chauvoei

53
Q

Which species develop blackleg?

A

Cattle and occasionally sheep

54
Q

Describe the pathophysiology of blackleg

A

Endogenous spores are in muscle tissue and germinate when anaerobic conditions present themselves (trauma). The spores undergo vegetative multiplication and release alpha, beta, gamma, delta, and edema factors which cause necrotizing myositis and systemic toxemia

55
Q

What clinical signs are associated with blackleg?

A

Found dead, lameness and firm swelling of the affected muscles, depression, fever, subcutaneous emphysema, tachycardia

56
Q

What are the causative agents of malignant edema?

A

C. septicum (most common), sordelli, chauveii, perfringens, novyi

57
Q

Describe the pathophysiology of malignant edema

A

Wound is inoculated with soil with clostridial spores. C. septicum germinates and malignant edema develops rapidly as gelatinous fluid swells and extends. Toxins cause destruction of adjacent leukocytes, increased capillary permeability, and systemic toxemia

58
Q

What clinical signs are associated with malignant edema

A

Swelling with edema and emphysema around a wound, fever, depression, lameness

59
Q

How is malignant edema diagnosed?

A

Differentiate from blackleg, aspirate tissue to reveal gram positive rods. Pathology shows gelatinous edema. Fluorescent antibody tests can be diagnostic.

60
Q

How is malignant edema treated?

A

Usually not discovered until it’s too late. Treat with penicillin at high doses, debride, lavage with hydrogen peroxide

61
Q

How is malignant edema prevented?

A

Proper hygiene, vaccination

62
Q

Describe “big head”

A

Disease caused by C. novyi type A, seen in rams 6m-2y secondary to fighting wounds of the head; specific type of malignant edema

63
Q

Describe “braxy”

A

Clostridial abomasitis of sheep from C. septicum. Rare in the US. Caused by abomasal epithelium injury. Results in necrotizing hemorrhagic abomasitis with edema and emphysema.

64
Q

Which vaccines are recommended for cattle in fluke and non-fluke areas?

A

Fluke- 8-way, 2 injections before weaning
Non-fluke- 4-way, complete 2 injections before weaning

Ruminants (10 decks)

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