non-infectious diseases Flashcards

(37 cards)

1
Q

downer cow definition

A

a cow that has been on the floor that has not gotten up in a while
many metabolic diseases present with downer cows as a sign

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2
Q

what are the main metabolic diseases in cattle

A

there are 4 main metabolic diseases of cattle
fatty liver disease:
ketosis
hypocalcemia (milk fever)
hypomagnesaemia (staggers)
however, there are only 2 main metabolic diseases in
the risky period is usually 2-8 weeks after calving sheep:
pregnancy toxaemia ( twin lamb disease)
hypocalcemia
these usually happen before lambing

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3
Q

how to deal with a downer cow?

A

approach
take a history
consider aetiology
like metabolic diseases
or toxaemia/ infections
periparturient injury
examination
and finally treatment and management

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4
Q

some of the history questions to ask

A

what happened at the time of calving?
assisted or natural?
how long since calving?
treated with anything? (like calcium)
how long has the cow been recumbent?
is she trying to get up?
is she always laying on the same leg

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5
Q

what are the metabolic reasons for a cow to be down?

A

low calcium
low magnesium
low phosphate
hypokalaemia ( low potassium)
fatty liver disease
acidosis

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6
Q

what are the infectious causes of a cow being down?

A

mastitis (infection of the udder)
metritis (inflammation/ infection of the uterus)
peritonitis (infection of the peritoneum/ abdomen)
rupture of the uterus so all of the uterus material is in the abdomen
inhalation pneumonia
botulism (caused by clostridium botulinum) causes nerve damage

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7
Q

what are some periparturient injuries that can cause downer cows?

A

obturators paralysis
fractured leg or pelvis
sciatic paralysis
haemorrhage

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8
Q

are there any calving-related issues?

A

vaginal prolapse
dystocia
ring womb
uterine torsion/ twisted uterus
uterine tear
nerve paralysis
uterine prolapse (after calving)

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9
Q

what is the issue with dystocia?

A

means difficult calving
may be due to deformities
feto-maternal disproportion, small pelvis, big calf
presentations of the calf or lamb may not be normal
uterine inertia, no contractions
could be due to low calcium
low oxytocin
over or under stretched

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10
Q

how can dystocia be treated?

A

calcium injections can help with contractions and open the cervix
assisted delivery can help using aids
C-section
embryotomy/ foetotomy if the calf is dead, so you can cut it up for the benefit of the cow
euthanasia of the cow and cut the calf out if the cow is beyond help, must shoot

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11
Q

how to conduct an examination of a downer cow?

A

examine the cow systematically
check for evidence of the etiologies listed
also, check for any unexpected surprises you might see

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12
Q

downer cow diagnosis

A

perform biochemistry to assess the levels of Ca+, P and Mg in the blood serum

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13
Q

treatment of a downer cow

A

treat the primary cause if possible and known
ensure the cow is comfortable and lying in a nice position
turn cow regularly and massage dependent limbs
if no fracture, consider hoisting for 20 minutes, twice a day
provide food and water
analgesia (a drug to relief pain)

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14
Q

what is the outcome of a downer cow?

A

normally the cow will be fine.
however, the cow will be euthanised if:
there is a fractured limb
cow keeps rolling flat out on the same side
groans persistently, stops eating or drinking

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15
Q

ovine pregnancy toxaemia

A

also known as twin lamb disease
there is a severe energy deficiency in ewes
most common in:
lowland flocks
multiparous ewes ( having more than 1 child)
ewes in the last month of gestation

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16
Q

what is the aetiology of pregnancy toxaemia?

A

follows periods of severe energy shortage
could be because of poor energy roughage
insufficient concentrates
high foetal demand, for example, quads
clinical signs often show after a stressful event
other factors could be fat ewes, lameness or temporary lack of appetite like with hypocalcemia.

17
Q

what is the pathology of twin lambs disease?

A

severe energy deficiency leads to increased fat mobilisation and fatty infiltration, particularly in the liver

18
Q

early clinical signs of pregnancy toxaemia

A

the ewe will stand with the group but not eat
blindness and separation from the group
dull and depressed
easy to catch but hyperaesthetic to stimuli

19
Q

what are the clinical signs on examination?

A

poor body condition
poor mammery development
distended abdomen
lack of menace response
but pupillary reflex present
head pressing into a corner and star gazing
recumbency
death after 5 to 10 days if untreated

20
Q

differential diagnosis of pregnancy toxaemia

A

ruminal acidosis
listeriosis
hypocalcaemia
impending abortion
cerebrocortical necrosis (CCN)
copper poisoning

21
Q

how to diagnose pregnancy toxaemia?

A

signs and history as always
biochemistry
PME
high BHB levels in serum/ eye fluid help diagnosis

22
Q

how to treat pregnancy toxaemia?

A

turnout to good pasture
oral electrolyte and propylene glycol
intravenous glucose
glucocorticoid (steroid)
caesarean section- it is expensive but get the lambs
guarded prognosis (not enough information for a decision)

23
Q

what is cerebrocortical necrosis (CCN)?

A

also known as polioencephalomalacia
a neurological disease of weaned lambs
but can occur in older animals

24
Q

the pathogenesis of cerebrocortical necrosis

A

deficiency in thiamine ( vitamin B) due to thiaminase activity in the rumen
the disease may be triggered by a change in the diet, altering the rumen microflora
which can result in the proliferation (rapid increase) of thiaminase-producing bacteria.
thiamine is produced by the microflora and is important for glucose production.
usually sporadic (infects individuals) but can get outbreaks
in lambs, often only seen 2 weeks after diet change, e.g. movement of pasture or routine anthelmintic treatment

25
the clinical signs of cerebrocortical necrosis
blindness sheep isolate aimless wandering stargazing when standing still depression anorexia ataxia (affected co-ordination) and proprioceptive deficits hyperaesthetic recumbency death within a week
26
the diagnosis for CCN
history and signs will give you tentative results only definitive way to know is PME and histology
27
cerebrocortical necrosis treatment
high doses of thiamine, frequently during the early stages of the disease the response is usually rapid sight will return last
28
how to remember differential diagnosis
D egenerative A nomolous M etabolic N neoplastic or utritional I nfectious, nflammatory, diopathic, atrogenic, mmune-mediated, nherited T raumatic or oxic V ascular
29
neoplasia
a malignant cancerous growth treatment: removal of the tumour may mean the removal of the surrounding tissue
30
examples of degenerative diseases in sheep
white muscle disease delayed swayback
31
white muscle disease in sheep
degenerative muscle disease in sheep, usually affecting new-born and fast-growing lambs caused by a deficiency of selenium and/or vitamin E also known as stiff lamb disease contractile components of the muscle degenerate immediate regeneration occurs after a single vitamin E/ selenium treatment when heart is affected, will cause blood stained discharge from the nose
32
delayed swayback in sheep
a degenerative neuronal disease affecting lambs from birth to 6 months associated with copper deficiency in pregnant ewes affected lambs (after 3 weeks old) have incoordination of hind limbs lamb is still able to kick and appetite is not affected there is no treatment prevention may include copper supplementation which is risky
33
nutritional disease
to do with too much or too little of something too much gives toxicity like copper too little could be calcium, energy, magnesium abrupt changes in diet could cause disease like bloat in cattle CCN could be caused due to change in diet
34
cobalt deficiency
also known as pine in sheep usually reflects low soil concentrations but may be further complicated by diet cobalt is further essential for B12, manufactured by gut microflora
35
clinical signs of Pine in sheep
usually in grazing lambs after weaning lethargy poor appetite poor wool poor growth poor BCS even though nutrition is adequate blocked tear ducts associated with white liver disease hepatotoxic disease, adequate cobalt levels seem to protect photosensitisation anaemia/emaciation
36
diagnosis of cobalt deficiency
based on clinical signs and local history of the disease supported by low plasma/ vitamin B12 in the liver PME is non-specific severely emaciated (thin or weak) carcase enlarged, pale, fatty friable liver
37
treatment of cobalt deficiency
diet supplementation combined anthelmintics or cobalt drenches top dressing pasture with cobalt salts