4.6 Sudden Death in Farm Animals

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20 Terms

1
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important public health concerns

must be sure anthrax is not the cause

notifiable disease

last seen in UK 2015

call APHA if suspicious

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history

number/groups/fields/ages affected

progression of signs (if any)

vaccination & worming history

management-> recent treatments, changed fields or feed, unusual weather events

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environmental examination

observational skills very important

likely if suspected toxicity

<p>observational skills very important<br><br>likely if suspected toxicity</p>
4
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distance/ individual animal examination

individuals clearly sick or affected

if all normal, consider optimal use of time

<p>individuals clearly sick or affected<br><br>if all normal, consider optimal use of time</p>
5
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post-mortem examination

best if conducted closest to time of death

on the spot diagnosis

collect samples for further analysis

<p>best if conducted closest to time of death<br><br>on the spot diagnosis<br><br>collect samples for further analysis</p>
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data analysis & decision making

lots of animals at risk-> quick & decisive

management changes-> feeding/field

control program-> vaccination, worming

treatment of individuals?

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reporting back

discuss actions before leaving farm

report lab results & follow-up

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causes of sudden death

infectious: septicemia/toxemia (pneumonia), anemia (liver fluke, haemonchus)

toxicity (plant or chemical):
inadvertent, iatrogenic

nutritional: metabolic disease, bloat, CCN, white muscle

other: climate, trauma

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infectious: septicemia or toxemia

common, usually bacterial

in environment or commensals

predisposed by management factors-> good nutrition i.e. clostridial disease, high stocking density i.e. salmonellosis, pneumonia, flood i.e. leptospirosis

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infectious (septicemia/toxemia) diagnosis

history esp. vaccination status & management

clinical signs noted

changes in mm color

PME

<p>history esp. vaccination status &amp; management<br><br>clinical signs noted<br><br>changes in mm color<br><br>PME</p>
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clostridial vaccination protocol

adult ewe: primary injection then 4-6 weeks late, booster 4-6 weeks prior to lambing (maximizes colostral antibody levels)

young lambs: maternal antibodies last up to 12 weeks (clostridial)

weaned lambs: from 8 weeks old, if short time to slaughter is vaccination sensible?

<p>adult ewe: primary injection then 4-6 weeks late, booster 4-6 weeks prior to lambing (maximizes colostral antibody levels)<br><br>young lambs: maternal antibodies last up to 12 weeks (clostridial)<br><br>weaned lambs: from 8 weeks old, if short time to slaughter is vaccination sensible?</p>
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infectious: anemia

acute fascioliasis, haemonchosis

should be obvious premonitory clinical signs BUT infrequent or cursory inspection

diagnosis: history esp. parasite control, clinical signs, pale mm, PMR more useful than FEC or blood testing

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toxicity: plant

diagnosis: history esp. access to toxic plants, all deaths in same field etc., search of field, PME- presence of leaves in rumen, variety of PME signs

ex: yew, oleander-> access to old house site, prunings put into field, storm bringing down boughs

<p>diagnosis: history esp. access to toxic plants, all deaths in same field etc., search of field, PME- presence of leaves in rumen, variety of PME signs<br><br>ex: yew, oleander-&gt; access to old house site, prunings put into field, storm bringing down boughs</p>
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toxicity: mineral

selenium, copper

iatrogenic-> accidental over-supplementation, animals fed wrong type of feed

death usually very rapid

diagnosis: history of supplementation or feed change, Se-> blood selenium levels, Cu-> Cu levels, PME

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toxicity: others

lead, cyanide, etc.

access to random stuff, calves in old buildings (lead paint), accidental access to pest poisons, medicated feed given to wrong animals

<p>lead, cyanide, etc. <br><br>access to random stuff, calves in old buildings (lead paint), accidental access to pest poisons, medicated feed given to wrong animals</p>
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metabolic disturbances

hypocalcemia, ketosis, hypomagnesemia

obvious in frequently observed animals...

<p>hypocalcemia, ketosis, hypomagnesemia<br><br>obvious in frequently observed animals...</p>
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nutritional imbalance

change in GIT function, ex: acidosis, bloat, gut torsion

deficiency in essential nutrients, ex: intrinsic due to change in microflora (CNN), extrinsic (water deprivation)

water deprivation can lead to salt toxicity as well-> abnormal pain & regurgitation, nervous signs (ataxia, circling, blindness, seizures, aggression)

<p>change in GIT function, ex: acidosis, bloat, gut torsion<br><br>deficiency in essential nutrients, ex: intrinsic due to change in microflora (CNN), extrinsic (water deprivation)<br><br>water deprivation can lead to salt toxicity as well-&gt; abnormal pain &amp; regurgitation, nervous signs (ataxia, circling, blindness, seizures, aggression)</p>
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climatic

lightning, hypothermia

lightning rare, climatic conditions suggestive!

hypothermia reasonably common esp. young lambs & sheep after shearing

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trauma

foreign bodies, falling off cliffs, etc.

rare for more than 1 animal to be affected

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dealing with sudden death

diagnosis

prevent further cases asap, infectious (change husbandry, antibiotics, vaccination, anthelmintic as appropriate), toxicity (remove from source, therapy as appropriate), metabolic (treat as appropriate, changes to husbandry for remainder of animals), nutritional (change diet, therapy as appropriate)