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PRODUCTION 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?

25
Describe pathophysiology of tetanus?
* Spore contamination of wounds * Neurotoxin production reaches CNS via peripheral nn * Incubation period: days to > four weeks * Usually sporadic
26
Diagnosis of Tetanus?
- CLS - Classic tetanus is seldom confused with other diseases - No lab test for the live animal - PM non specific (pronounced muscle rigidity)
27
What CLS of tetanus
Stiffness, reluctance to move, elevated tail head/stiff held out tail, lockjaw, protruding third eyelid, easily excitable
28
Tx and control of tetanus?
* Penicillin * Tetanus antitoxin * NSAIDs * Wound management * Muscle relaxants (e.g. Xylazine) * Dark, quiet surroundings, ample bedding
29
Pathophysiology C.Botulism?
* 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
Context of botulism?
- Partucularly associated with poultry waste - Often an outbreak situation Zoonotic
31
Subacute CLS? Botulism
* Lingual paralysis * Dysphagia * Ataxia * Muscle weakness * Laboured breathing * Recumbency * Constipation * Death * Occasional recovery in 3-4 weeks
32
Peracture CLS?
* Sudden onset, rapid paralysis * Death within 12-18 hrs
33
Acute CLS?
* Progressive muscular paralysis * Recumbency * Death
34
Diagnosis of Botulism?
* 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
PM findings in botulism?
* Flaccid paralysis * Non-specific findings * Decaying animal carcass in rumen?
36
Tx for botulism?
* Symptomatic treatment * Fluid therapy * Nursing * NO antimicrobial therapy
37
Prevention of Botulism?
Remove carcasses before applying poultry waste to pasture
38
What causes Black Disease (rare)
C.novyi
39
Who does C.novyi affect?
Cattle, sheep and goats
40
What does C.novy cause ?
* Necrotic hepatitis * Associated with liver fluke infestation in the liver * More likely at times of high fluke activity
41
C.novyi pathophysiology?
* 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
Signs of Black Dx ?
* Sudden death * Systemic signs * High fever, depression, anorexia, abdominal pain * Jaundice, anaemia, haemoglobinuria (B.H.) * Subcutaneous oedema
43
Diagnosis on PM of Black dx?
anaemic infarcts in liver, pathogen isolated in liver
44
PMEs in general?
* 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
When not to do a PME?
* 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
Approach to PME?
47
Step 1?
- Fleece and skin - Eyes, mouth, nose, ears - External genitalia - The perineal area - Udder - Feet - Umbilicus
48
Step 2?
Subcut tissues
49
Step 3? Abdomen
- Spleen - Liver - Stomachs - Intestine - Uterus - Kidney - Bladder
50
Step 4 -thorax?
- Tongue, larynx - Oesophagus - Trachea & bronchi - Lungs Heart
51
Step 5?
HEAD -> - Brain - Eyes - teeth - Tympanic bullae
52
Step 6? other
- Joints - Bones - Skeletal muscle
53
Step 7 ?
SPINAL CORD
54
Histology?
* 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
What samples to take if no visible PM lesions?

PRODUCTION VMS4008 (34 decks)

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