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540 (cow class) > Clostridia & Anthrax & Toxins > Flashcards

Clostridia & Anthrax & Toxins Flashcards

1
Q

clostridia are what type of bac t ?

A

gram + rods, anaerobic
form spores

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1
Q

what should be considered as a ddx for all cases of sudden death?

A

Clostridial disease

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2
Q

true or false: clostridia can be transmitted between animals

A

false.

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3
Q

what is the cause of clinical disease of clostridiosis?

A

exotoxins

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4
Q

what are the clostridiosis risk factors?

A
  • age: young>adult, FTPI
  • species (horses = tetanus) (C. perfringens type D lambs > calves)
  • beef > dairy
  • injuries (esp umbilical cord or castration)
  • environment (soil disturbance)
  • nutrition (sudden diet change)

the dead calves are the heavier calves!! the healthy ones in good BCS die bc they’re eating more

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5
Q

how do you diagnose clostridiosis?

A

necropsy ;)

culture (FAT & PCR), ELISA (exotoxin ID)

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6
Q

are there clostridial vaccines?

A

yes. most are killed bacterin, require booster annually

anaphylaxis = risk factor

make sure tetanus is in there!

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7
Q

what are the neurotoxic clostridia?

A

C. tetani, C. botulinum

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8
Q

what are the histotoxic clostridia?

A

C. septicum, C. chauvoei, C. haemolyticum/C. novyi type D, C. novyi, C. sodellii, C. perfringens

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9
Q

what are the enterotoxin clostridia?

A

C. perfringens, C. sodellii, C. piliforme, C. difficile

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10
Q

who is affected by C. tetani, what predisposing factors is it associated with, and what does it do to the body?

A

who: all species, not birds
predisposing factors: wounds
what: spastic paralysis due to tetanospasm (inhibits inhibitors)

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11
Q

what are the C/S of tetanus?

A

pyrexia, sweating, opisthotonus, convulsions, muscular stiffness, muscle tremor, ataxia, prolapse of 3rd eyelid, ears erect and tail head out, limbs become rigid

bloat is a common early sign

progresses to recumbency prior to death

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12
Q

what is the tx for tetanus?

A
  • antitoxin available
  • penicillin + NSAID + sedatives (acepromazine)
  • keep animals in dark, bedded sheds
  • but, generally euthanize
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13
Q

what does C. botulinum do to the body and what predisposing factor is it associated with?

A

what: flaccid paralysis (inhibit Ach release)
PF: eating toxin from decaying matter

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14
Q

what are the C/S of botulism?

A

sudden death, progressive muscle weakness, reduced muscle tone, difficulty swallowing, tongue paralysis, resp failure due to diaphragm paralysis = death

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15
Q

how do you dx tetanus?

A

C/S, hx
no pathognomonic lesions

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16
Q

how do you dx botulism

A

C/S, hx
no pathognomonic lesions

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17
Q

how do you tx botulism?

A

usually euthanize

but there is an antitoxin + supportive therapy option

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18
Q

what disease does C. chauvoei cause?

A

Blackleg (clostridial myositis)

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19
Q

what are the predisposing factors for blackleg?

A
  • 2-24mo, warm season
  • damage to muscles

(ingest spores, GIT–>muscle, lay dormant, trauma = low O2, replication, Toxin A production)

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20
Q

what are the C/S of blackleg?

A

sudden death
pyrexia, severe lameness, edema, crepitus (emphysema)

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21
Q

clostridial diseases cause ___ decomposition of the carcass.

A

rapid!

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22
Q

how do you dx black leg? what are you looking for?

A

necropsy!!!

black rancid gas filled muscle
(limbs, heart, tongue, diaphragm, longissimus)

culture & FAT to confirm

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23
Q

how do you tx black leg

A

penicillin and fasciotomy
herd tx and vaccination at same time
avoid injuries while handling

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24
Q

what disease does C. septicum cause?

A

malignant edema/gas gangrene
“big head” in bighorn sheep

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25
Q

what predisposing factor is associated with malignant edema?

A

damage to muscles

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26
Q

what are the C/S of malignant oedema?

A

localized swelling around injury –> oedematous and emphysematous wound

pyrexia and rapidly toxemic

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27
Q

how do you dx malignant edema?

A

necropsy!
gram stain, PCR, FAT

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28
Q

what are you looking for on necropsy with malignant edema?

A

cellulitis and/or necrotizing myositis

gas gangrene, edema, hemorrhage present, cellulitis

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29
Q

how do you treat malignant edema?

A

Abx, fasciotomy

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30
Q

what disease does C. novyi type B cause?

A

Black disease (infectious necrotising hepatitis)

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31
Q

what predisposing factor is associated with black disease (infectious necrotising hepatitis)?

A

damage to liver by migrating fluke

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32
Q

what are the C/S of black disease?

A

sudden death

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33
Q

you have a cow with black disease in for necropsy. what do you expect to find?

A

increase in serous or blood-tinged fluid in body cavities, hepatic lesions (pale yellow to white irregular necrotic areas surrounded by dark red to black hyperaemia)

evidence of fluke migration

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34
Q

what disease does C. haemolyticum cause?

A

bacillary hemoglobinuria (red water)

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35
Q

what predisposing factor is bacillary hemoglobinuria assoc with

A

liver fluke migration

summer and autumn

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36
Q

what are the C/S of bacillary hemoglobinuria

A

anemia, hemoglobinuria, arched back, recumbency, resp distress, death

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37
Q

what is the primary lesion on necropsy for bacillary hemoglobinuria?

A

hepatic necrosis (red/brown liver)
icteric carcass

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38
Q

what type of hemolysis does bacillary hemoglobinuria cause?

A

intravascular hemolysis

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39
Q

what disease does C. perfringens type A cause?

A

hemorrhagic enteritis

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40
Q

what predisposing factors are there for hemorrhagic enteritis?

A

young animals, sudden diet change (high starch)

41
Q

what are the C/S of hemorrhagic enteritis?

A

abdominal distension, colic, diarrhea, depression, anorexia, sudden death

42
Q

true or false: C perfringens is a commensal in the GIT of cattle

A

true

43
Q

what are you looking for in necropsy for hemorrhagic enteritis

A

… hemorrhagic enteriris lol

enteritis, abomasitis, hemorrhage, mucusal ulceration

44
Q

how do you tx hemorrhagic enteritis?

A

penicillin and supportive care
early dx is key!!!!

45
Q

what disease does C. perfringens type D cause?

A

overeating disease or pulpy kidney

46
Q

what predisposing factors are assoc with C. perfringens type D

A

young animals, overeating, diet change (high grain rations, high protein + starch diets), stress

47
Q

what are the C/S of pulpy kidney?

A

sudden death in rapidly growing well-fed calves
if found alive, then dead within 5 hours due to necrohemorrhagic enteritis, may show CNS signs and depression

48
Q

how do you dx pulpy kidney?

A

necropsy, ELISA, histo

49
Q

how do you prevent pulpy kidney?

A

vax, diet mgmt

50
Q

what are you looking for on necropsy for pulpy kidney?

A

necrohemorrhagic enteritis, excessive pericardial fluid + glucosuria, friable “pulpy” kidneys, encephalomalacia, cerebral vermix herniation, pulmonary edema

51
Q

true or false: anthrax is a reportable disease

A

true ya bishhhhh

52
Q

what is the bacteria that causes anthrax?

A

Bacillus anthracis

53
Q

true or false: if you suspect anthrax, you should cut open the animal so that the birds can have something to eat while you wait on diagnostics :)

A

no dont do that :)
don’t open the carcass :)
bird will die :(

54
Q

who is most at risk for anthrax?

A

herbivores! cattle!

55
Q

when should you suspect anthrax in an animal

A

animal found dead with…
- non-clotting blood or blood-tinged secretion from all natural orifces
- animal bloat fast after death
- no rigor mortis

56
Q

where is anthrax endemic that’s close to home:(

A

Wood Buffalo National Park

57
Q

if you do open an animal with anthrax, what do you expect to find?

A

swollen spleen and serosanguinous fluid in all body cavities

58
Q

what should you do if you suspect anthrax in a dead animal?

A
  • DO NOT OPEN CARCASS!
  • nick ear or remove and bag –> bring to lab
  • sample blood, microscopic exam, look for “trains” of organisms, SNAP test available
59
Q

what do anthrax little guys look under da microscope?

A

rod bac t surrounded by capsule visible in blood smears

60
Q

is there zoonotic risk with anthrax?

A

only from spores, not from animal to animal

61
Q

when should you suspect Toxicosis?

A
  • acute illness in a group of animals
  • simultaneous appearance of signs
  • similar signs and of similar seveity
  • signs appear after a shared event
  • incidents assoc w environment, diet, water
62
Q

what organs are most commonly affected by poisons?

A

liver, kidney, brain

63
Q

what is the antidote for lead toxicosis?

A

Ca-EDTA + thiamine

64
Q

what is the antidote for nitrate toxicosis?

A

methylene blue

65
Q

what is the antidote for organophosphate toxicosis?

A

atropine

66
Q

what is the antidote for cyanide toxicosis?

A

sodium thiosulfate

67
Q

why does lead be poisoning da cows?

A

decrease heme synthesis, interfere with GABA transmission, Ca absorption, Na/K ATPase pumps –> alters nerve and muscle transmission

68
Q

what are the C/S of lead toxicosis?

A

GIT and neuro signs basically
- ataxia, blindness, salivation, wandering, bruxism, muscle tremors, seizures

69
Q

what happens if you have a subclincla lead toxicosis cow?

A

absorb lead into bone –> uh oh! lead in da calf’s milk!!! oh no!!!

70
Q

how do you dx lead toxicosis?

A

whole blood, liver/kidney/brain, feed or suspected source

71
Q

how to you tx lead toxicosis?

A

thiamine + Ca-EDTA
rumentotomy to remove lead source

72
Q

copper tox is more common in what species?

A

sheep

73
Q

what are the C/S of copper toxicosis?

A

acute: gastroenteritis with colic, d+, dehydration –> dead within 3 days (not as common)

chronic: weak, depressed, poor appetite, hemolysis, hemoglobinuria, icterus (more common (high liver Cu)

74
Q

how do you dx Cu tox?

A

chem liver profile, Cu analysis (liver and kidney), feed analysis

75
Q

what are the C/S of selenium toxicosis?

A

acute: sudden death, weak with rapid progression to cardiogenic shock, abd. pain, low RR, low HR, pulmonary edema, garlic odour on breath

chronic: hair and hoof abnormalities

76
Q

what causes acute and chronic selenium toxicosis? what is the max limit of selenium?

A

acute: iatrogenic
chronic: plants (locoweed), supplements

5mcg/g

77
Q

how do you dx selenium tox?

A

blood and hair Se
kidney and live

78
Q

how do you treat selenium toxicosis?

A

remove exposure, low Se diet, hoof care

79
Q

nitrate toxicosis comes from where? when?

A

plants or water
common in spring

80
Q

what is the mechanism of nitrate toxicosis?

A

nitrate –> goes to nitrite in rumen –> blood –> oxidizes Fe –> methmeglobin –> cannot bind O2 –> anoxia

81
Q

what are the C/S of nitrate tox?

A

acute death, ataxia + tremors, excessive salivation, d+, cyanotic mm, resp distress, brown color to tissues and blood

82
Q

how do you dx nitrate tox?

A

frozen ocular fluid, whole blood

83
Q

how do you tx nitrate tox?

A

methylene blue 1%

84
Q

what is the mechanism for Urea/NPN toxicosis?

A

urea + urease (rumen) –> ammonia –> increase rumen pH –> blood –> liver –> brain –> neuro signs

85
Q

what are the C/S for urea/NPN toxicosis?

A

acute death, ataxia, incoordination, PU, salivation, seizures, bloat

86
Q

how do you dx urea tox/

A

frozen ocular fluid, food/water samples

87
Q

how do you tx urea tox?

A

triage animals (if they pee and poo, better px)

decrease ammonia formation

88
Q

what are the ionophores that we should prolly know?

A

monensin and lasalocid

89
Q

what is the mechanism behind ionophore toxicosis?

A

increase Na + Ca intracellular influx –> Ca enzyme activation + lipid perox (membrane damage) –> muscle necrosis

90
Q

what are the C/S of ionophore tox?

A

anorexia, loose stool, weakness, depression, dyspnea, extreme exercise intolerance, SQ edema, pica, jugular pulse, muscle damage, hydrothorax/ascities, pulmonary/hepatic congestion

91
Q

how do you tx ionophore tox

A

none :(
you can remove feed, but cardiac damage chronic

92
Q

what is the mechanism behind Na toxicosis /water deprivation

A

no H2O –> neutron increase Na –> Na/K pump impairment // access to H2O –> increase intracellular water –> CNS edema

93
Q

what are the C/S of Na tox / water deprivation/

A

centrally unaware, opisthotonus, CNS signs similar to Pb
anorexia, D+, abnormal gait

94
Q

how do you dx Na tox/ water deprivation

A

brain (fresh and fixed), sample ater

95
Q

how do you tx Na tox/water deprivation?

A

give water but just a lil bit :)

96
Q

how do organophosphates cause disease?

A

AchE inhibitors

97
Q

what are the C/S of organophosphates?

A

muscarinic (DUMBBELLS –> salivation, urination, defecation, colic)

nicotinic (tachycardia, weakness, tremors, muscle twitching, hypertension, paralysis)

98
Q

how do you dx organophosphate tox?

A

blood + brain (looking for lower AchE activity)

99
Q

how to you tx organophosphate tox?

A

if you catch it early, give atropine

540 (cow class) (32 decks)

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