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Clostridial diseases Flashcards

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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
Describe forage poisoning
Seen in adults following ingestion of preformed toxin in spoiled feed materials (grains, silage, hay), usually type B
26
Describe carrion-associated botulism
Animals exposed to carcasses of rodents, small mammals, and birds or poultry litter contract type C and D; most common source of botulism
27
Describe wound botulism
Infection of a wound with type B toxin. Bacteria sporulates and releases toxin under anaerobic conditions. Rare
28
Describe toxicoinfectious botulism
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
What clinical signs are associated with botulism?
Progressive flaccid paralysis, especially of the limbs, throat, and tongue
30
How can botulism be fatal?
By arrest of the respiratory tract
31
How is botulism diagnosed?
Clinical signs, serum or GI content bioassay, PCR assay for type B, analysis of feed
32
How is botulism treated?
Supportive therapy, polyvalent antitoxin (expensive, only works before toxin has bound to receptors)
33
How can botulism be prevented?
Prevent animals from eating rotten vegetables or carcasses
34
What are names for the disease caused by Clostridium perfringens type D?
Enterotoxemia, overeating disease, pulpy kidney
35
Which species are most affected by Clostridium perfringens type D?
Mostly sheep (growing lambs), somewhat goats, virtually non-existant in cattle
36
Describe the pathophysiology of C. perfringens
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
What clinical signs are associated with C. perfringens?
Sudden death, clonic convulsions, muscle tremors, opisthotonus
38
What group of animals are predisposed to developing enterotoxemia?
Rapidly growing lambs
39
How is enterotoxemia diagnosed?
Hyperglycemia and glucosuria, pulpy kidney on necropsy, perivascular edema, hemorrhage, and focal malacia, intestinal contents can be cultured
40
How is enterotoxemia treated?
Usually not treated. Hyperimmune serum is available but it's always too late.
41
How is enterotoxemia prevented?
Vaccinate maiden ewes, vaccinate and booster lambs, reduce feed intake to lambs at risk, give antitoxin to all lambs if outbreak begins
42
Describe focal symmetric encephalomalacia; what causes it?
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
What causes hemorrhagic bowel syndrome?
Clostridium perfringens type A alpha toxins
44
Which animals are usually affected by hemorrhagic bowel syndrome?
High producing dairy cows in early lactation
45
Describe the pathophysiology of hemorrhagic bowel syndrome
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
What clinical signs are consistent with hemorrhagic bowel syndrome
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
How is hemorrhagic bowel syndrome diagnosed?
Ultrasound can confirm intestinal distension, right flank abdominal explore will confirm diagnosis, necropsy will have intraluminal blood clot. Culture can be supportive.
48
How is hemorrhagic bowel syndrome treated?
Medical therapy- fluids, antibiotics, NSAIDs, blood transfusion Surgical therapy- R&A, enterotomy, disruption of clot- more successful than medical treatment
49
How is hemorrhagic bowel syndrome prevented?
Vaccine available but ineffective, maximize feed management
50
Describe gas gangrene
Myonecrosis following bruising of muscle tissue or deep wound
51
Describe malignant edema
Cellulitis of connective tissue
52
What is the causative agent of blackleg?
Clostridium chauvoei
53
Which species develop blackleg?
Cattle and occasionally sheep
54
Describe the pathophysiology of blackleg
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
What clinical signs are associated with blackleg?
Found dead, lameness and firm swelling of the affected muscles, depression, fever, subcutaneous emphysema, tachycardia
56
What are the causative agents of malignant edema?
C. septicum (most common), sordelli, chauveii, perfringens, novyi
57
Describe the pathophysiology of malignant edema
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
What clinical signs are associated with malignant edema
Swelling with edema and emphysema around a wound, fever, depression, lameness
59
How is malignant edema diagnosed?
Differentiate from blackleg, aspirate tissue to reveal gram positive rods. Pathology shows gelatinous edema. Fluorescent antibody tests can be diagnostic.
60
How is malignant edema treated?
Usually not discovered until it's too late. Treat with penicillin at high doses, debride, lavage with hydrogen peroxide
61
How is malignant edema prevented?
Proper hygiene, vaccination
62
Describe "big head"
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
Describe "braxy"
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
Which vaccines are recommended for cattle in fluke and non-fluke areas?
Fluke- 8-way, 2 injections before weaning Non-fluke- 4-way, complete 2 injections before weaning

Ruminants (10 decks)

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