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VMS4008 > Sudden death & PME in production animals > Flashcards

Sudden death & PME in production animals Flashcards

1
Q

What sudden death categories are there?

A
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2
Q

How do we rule out anthrax?

A
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3
Q

What clostridial diseases in sheep and cattle?

A
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4
Q

Describe clostridial diseases (general)

A
  • Gram +Ve, obligate anaerobes
  • Spore forming
  • Survive a long time in the environment
  • Infection
  • Wound contamination
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5
Q

Pathophysiology/ entry of clostridial dx?

A
  • Ingested spores localise in muscle/ liver/ spleen
  • Spore entry- wounds, ingested or dormant state in gut
  • Environmental conditions become anaerobic- tissue injury, high
    carbohydrate diet, liver damage promotes growth
  • Species have specific toxins released which have various effects
  • Toxins cause widespread tissue damage and spread.
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6
Q

What strain of clostridial causes blackleg?

A

clostridial chauvoei

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7
Q

Describe blackleg?

A
  • Youngstock
  • Unknown trigger
  • Risk- turnout
  • Clostridial myositis
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8
Q

SIgns & presentation of blackleg?

A
  • Extensive swelling, black necrosis of muscle,
    stiffness and severe lameness, rapid death
  • Usually big muscle masses
  • Or found dead
  • Cardiac blackleg has been reported
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9
Q

What causes MAlignant Oedema?

A
  • Mixed clostridial infection
  • C Septicum, C. novyi, C chauvoei
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10
Q

CLS of Malignant Oedema

A
  • Clinical signs 48 ours after infection
  • Severe swelling, limb- or head in sheep,
  • Pyrexia
  • More likely to be found alive
  • Wound infection
    Deep puncture wounds
    Dirty injection
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11
Q

Key differences between blackleg and malignant oedema?

A
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12
Q

Clostridial enterotoxaemia -> causes?

A

Pulpy kidney -> C.perfringens TYPE D

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13
Q

Describe etiology of C.perfringens / pulpy kidney

A
  • GI tract commensals
  • Live in the soil
  • Overfeeding/change in diet
  • Enterotoxaemia
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14
Q

PAthophysiology of pulpy kidney?

A

beta-toxin (type B & C) causes haemorrhagic eneteritis and ulceration

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15
Q

Who gets affected by ulpy kidney?

A

rapidly growing animals

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16
Q

What factor in Pulpy kidney/ Cperfringens

A

Anaerobic conditions in
abomasum/SI and large amount of
fermentable carbohydrates

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17
Q

What GI signs can we see with closiridial enterotoxaemia?

A
  • D+
  • Dysentery
  • Acute abdominal pain
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18
Q

Neurological signs of clostridial enterotox?

A
  • Bellowing
  • Aimless running
  • tetany
  • Opisthotonus
  • Dx is often fatal
  • Sudden death
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19
Q

How do we diagnose clostridial enterotoxaemia?

A
  • Intestinal contents
  • Faecal smear
  • Toxin isolation
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20
Q

Post mortem signs of clostridial enterotoxaemia?

A
  • Good condition animals
  • Rapid PM changes esp kidneys
  • Hydropericardium
  • Hydrothorax
  • Ascites
  • Pulomonary oedema
  • Subendocardial haemorrhages on left
    ventricle
  • Haemorrahgic enteritis or gas filled
    green intestines
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21
Q

What type of clostridial causes lamb dysentry?

A

C perfringens type b

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22
Q

Describe Lamb Dysentry?

A
  • Necrotising emphysematous enteritis
  • Lambs < 3 weeks old
  • Lethargy, diarrhoea, sudden death
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23
Q

Lamb Dysentery risk factors?

A
  • Risk factors -> Ewe not vaccinated, FPT, dirty lambing
    pen
  • Other causes of poor colostrum quality
24
Q

What causes tetanus?

A

C. tetani

25
Q

Describe pathophysiology of tetanus?

A
  • Spore contamination of wounds
  • Neurotoxin production reaches CNS via
    peripheral nn
  • Incubation period: days to > four weeks
  • Usually sporadic
26
Q

Diagnosis of Tetanus?

A
  • CLS
  • Classic tetanus is seldom confused with other diseases
  • No lab test for the live animal
  • PM non specific (pronounced muscle rigidity)
27
Q

What CLS of tetanus

A

Stiffness, reluctance to move, elevated tail
head/stiff held out tail, lockjaw, protruding
third eyelid, easily excitable

28
Q

Tx and control of tetanus?

A
  • Penicillin
  • Tetanus antitoxin
  • NSAIDs
  • Wound management
  • Muscle relaxants (e.g. Xylazine)
  • Dark, quiet surroundings, ample bedding
29
Q

Pathophysiology C.Botulism?

A
  • Intoxication
  • Ingestion of pre-formed Cl. botulinum toxins in spoiled or contaminated food and water
  • Neurotoxins cause flaccid motor paralysis
  • Incubation period – few hours to 14 day
30
Q

Context of botulism?

A
  • Partucularly associated with poultry waste
  • Often an outbreak situation
    Zoonotic
31
Q

Subacute CLS? Botulism

A
  • Lingual paralysis
  • Dysphagia
  • Ataxia
  • Muscle weakness
  • Laboured breathing
  • Recumbency
  • Constipation
  • Death
  • Occasional recovery in 3-4 weeks
32
Q

Peracture CLS?

A
  • Sudden onset, rapid paralysis
  • Death within 12-18 hrs
33
Q

Acute CLS?

A
  • Progressive muscular paralysis
  • Recumbency
  • Death
34
Q

Diagnosis of Botulism?

A
  • Clinical signs
  • No readily available test for botulinum
    toxin
  • Demonstration of toxins in serum, liver or
    feed
  • History may reveal access to poultry waste
    etc.
35
Q

PM findings in botulism?

A
  • Flaccid paralysis
  • Non-specific findings
  • Decaying animal carcass in rumen?
36
Q

Tx for botulism?

A
  • Symptomatic treatment
  • Fluid therapy
  • Nursing
  • NO antimicrobial therapy
37
Q

Prevention of Botulism?

A

Remove carcasses before applying poultry
waste to pasture

38
Q

What causes Black Disease (rare)

A

C.novyi

39
Q

Who does C.novyi affect?

A

Cattle, sheep and goats

40
Q

What does C.novy cause ?

A
  • Necrotic hepatitis
  • Associated with liver fluke
    infestation in the liver
  • More likely at times of high
    fluke activity
41
Q

C.novyi pathophysiology?

A
  • Spores ingested from the
    environment, travel to the liver.
  • Can remain in the liver without
    ill effect until damage to the
    liver occurs
  • Onset of disease rapid
42
Q

Signs of Black Dx ?

A
  • Sudden death
  • Systemic signs
  • High fever, depression,
    anorexia, abdominal pain
  • Jaundice, anaemia,
    haemoglobinuria (B.H.)
  • Subcutaneous oedema
43
Q

Diagnosis on PM of Black dx?

A

anaemic infarcts in liver, pathogen isolated in liver

44
Q

PMEs in general?

A
  • Client expectations and communication
  • Within 24 hours of death
  • Severe autolysis is going to impede results
  • Possible notifiable disease?
  • If suspect then notify APHA and stop PM
45
Q

When not to do a PME?

A
  • Significant clinical importance (e.g. where a large number of animals have been lost or for highvalue animals)
  • Presenting with unusual or unspecific clinical signs –Where notifiable or zoonotic diseases are suspected -> Anthrax!
  • Legal or forensic cases
  • Those associated with a client complaint
  • Where there may be a public health concern (e.g. open farm, lead toxicity)– Neurological, which may require brain and/or spinal cord removal (which is difficult in the field)
46
Q

Approach to PME?

A
47
Q

Step 1?

A
  • Fleece and skin
  • Eyes, mouth, nose, ears
  • External genitalia
  • The perineal area
  • Udder
  • Feet
  • Umbilicus
48
Q

Step 2?

A

Subcut tissues

49
Q

Step 3? Abdomen

A
  • Spleen
  • Liver
  • Stomachs
  • Intestine
  • Uterus
  • Kidney
  • Bladder
50
Q

Step 4 -thorax?

A
  • Tongue, larynx
  • Oesophagus
  • Trachea & bronchi
  • Lungs
    Heart
51
Q

Step 5?

A

HEAD ->
- Brain
- Eyes
- teeth
- Tympanic bullae

52
Q

Step 6? other

A
  • Joints
  • Bones
  • Skeletal muscle
53
Q

Step 7 ?

A

SPINAL CORD

54
Q

Histology?

A
  • Tissue samples about 1cm
  • Should be mixed with formalin
    10x the size of the sample
  • Put into formalin instantly
  • Take several samples from
    each organ
  • On the margin between
    normal and abnormal tissue
55
Q

What samples to take if no visible PM lesions?

A

VMS4008 (42 decks)

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