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Clinical Endocrine, Metabolic and Dermatology > Metabolic Diseases of the Cow > Flashcards

Metabolic Diseases of the Cow Flashcards

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1
Q

What is the given definition of Metabolic Diseases in Cattle?

A

A manifestation of the cows inability to cope with metabolic demands of high production

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2
Q

What are the most commonly affected farm animals by Metabolic Disease?

A
  • Dairy cattle

- Pregnant Ewes

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3
Q

What are the top 7 production diseases of cattle?

A
  • Hypocalcemia
  • Hypomagnesemia
  • Ketosis
  • Acidosis
  • Mastitis
  • Lameness
  • Reproductive Disease
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4
Q

What are the top 4 Metabolic Diseases of Cattle?

A
  • Hypocalcemia
  • Hypomagnesemia
  • Ketosis
  • Acidosis
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5
Q

What are the effects of Hypocalcemia?

A
  • Reduce immune cell function -> infections
  • Reduced smooth muscle contraction -> teat sphincter wont close, leading to mastitis
  • Retained fetal membranes -> metritis
  • Infertility
  • Reduced DMI -> leading to Neg Energy Balance -> ketosis
  • Loss of BCS -> loss of fat pads in the foot -> lameness
  • Drop in fertility and expression of estrus
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6
Q

What is the most common presentation of hypocalcemia in cattle?

A

Periparturient hypocalcemia

a.k.a Milk Fever

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7
Q

What are the normal ranges of Calcium, Phosphorus and Magnesium in the cow?

A

Ca = 2.1 - 2.5 mmol/L

P = 1 - 2.5 mmol/L

Mg = 0.65 - 1.3 mmol/L

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8
Q

What are the risk factors that predispose a dairy cow to Milk Fever?

A
  • Age = 3rd + lactation
  • Breed = Channel Island Breeds (Jersey + Guernsey)
  • Overconditioning = High BCS cows eat less during the post-parturient period, intake less Calcium from diet and thus cant absorb from intestines
  • Genetics = certain cows/ lines will have repeat offences
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9
Q

What are the main causes of Hypocalcemia in dairy cattle?

A

DIETARY!

  • High Calcium in dry cow diet. Should be around 30g/cow/day. If above this then the mechanisms for bone resorption become relaxed
  • Suboptimal Mg in dry cow diet = Lack of Mg reduces sensitivity to PTH and reduces secretion of PTH in response to hypoCa
  • Excessive/ High DCAD Diet = Dietary Cation-Anion Difference (Na + K) - (Cl + S)

High DCAD causes alkalization, which reduces tissue sensitivity to PTH

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10
Q

What are the stages and associated clinical signs of Milk Fever in the dairy cow?

A

Stage 1: excitement phase (lasts 30mins - 2 hours)

restless, paddling, more vocal, inappetent

Stage 2: sternal recumbency (8 - 12 hours)

dull, depressed, swan neck, ‘calf sleeping posture’, low temperature, constipated, low RR, tachycardia (80 - 100bpm) but muffled heart sounds

Stage 3: lateral recumbency

comatose, death (usually due to the relaxation of the esophageal sphincters and inhalation of rumen contents causing asphyxiation/ drowning)

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11
Q

What factors can indicate Milk Fever in the dairy cow?

A
  • History
  • Clinical signs: recumbency within 24 - 48 hours post calving
  • Response to treatment
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12
Q

What are the Differential Diagnosis for Milk Fever in cattle?

A

Excitation Phase can look like:

  • Hypomagnesium tetany
  • Nervous ketosis
  • BSE (bovine spongiform encephalopathy)

Recumbent Phase can look like:

  • Peracute toxemic mastitis
  • Toxemic metritis/ peritonitis
  • Uterine haemorrhage
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13
Q

What are the 3M’s of a dull, recumbent cow post calving?

A

Metritis

Mastitis

Milk Fever

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14
Q

Why is sub-clinical hypocalcemia an issue on a herd level ?

A

Cattle are hypocalcemic but arent showing clinical signs, but are at risk of:

  • Suffering (animal welfare issue)
  • Uterine inertia = take longer to calve down which increases calf mortality
  • Retained placenta
  • Displaced Abomasum
  • Reduced Feed Intake = can lead to LDA and ketosis
  • Mastitis
  • Delayed ovulation post calving
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15
Q

What is the treatment of Milk Fever in dairy cattle?

A
  • IV dose of 2g Ca/ 100kg of BW given slowly through a 14G needle and a flutter valve
    e. g. 400mL of 40% Calcium borogluconate IV

Caution: will cause arrhythmia if given too quickly

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16
Q

How can you prevent Milk Fever?

A
  • Adequate Mg in the Dry cow diet = 15-20g Mg/cow/day for the last month of pregnancy
  • Silage low in K+
  • <5% Calcium in dry cow diet
  • optimal BCS pre-calving
  • Avoid metabolic alkalosis = add acidic salts to the dry cow diet e.g. NH3Cl or CaCl
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17
Q

What diets or feeds can predispose a non-parturient cow (or even bull) to hypocalcemia?

A
  • Lush pasture, causing diarrhea and electrolyte imbalance
  • Sugar beet tops + carrots + potatoes
  • Barley poisoning
  • High grain diets
  • Fusarium spp = estrogenic mycotoxicosis
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18
Q

What are the 3 main differences between cattle and sheep when it comes to hypocalcemia ?

A

Cattle:

  • Occurs 24 - 48 hours post-calving
  • High Ca demand in colostrum and milk
  • Tx: ~400mls of 40% Calcium borogluconate

Sheep:

  • Occurs 3-4 weeks before laming
  • High Ca demand from calcification of fetal bones
  • Tx: 50 - 80mls of 20% Calcium borogluconate
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19
Q

What is the definition of a Downer Cow?

A

Any cow which is down in sternal recumbency for more than 24 hours with NO EVIDENCE of a systemic disease, or clinically apparent structural injury, which would prevent it from rising

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20
Q

What are the 3 main causes of Downer Cow Syndrome?

A

1) Hypocalcemia
2) Calving paralysis = paralysis of the hind leg(s) due to constant pressure on the Obturator nerves as the calf passes through the pelvic canal
3) Spinal injury

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21
Q

What is the time frame for a cow being down where we begin to worry, and why?

A

6 - 12 hours

Muscle and nerve damage

  • Pressure on the sciatic nerve caudal to the proximal femur
  • Muscle tear and haemorrhage as the animal struggles to rise
  • Renal damage associated with myoglobinuria
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22
Q

What is the general prognosis for a Downer Cow and how can it be measured?

A
  • Most downer cows will rise within 4 days
  • Cows down for 7+ days have a poor prognosis
  • Can measure with biochemical indicators (CK and AST)
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23
Q

What kind of nursing care/ treatment is required for Downer Cows?

A

Outside: a small, sheltered paddock on flat dry ground
Inside: 0.5m of straw bedding cleaned daily

Important:

  • Feed and give fresh water 2x a day
  • 2x daily teat disinfection (higher risk of mastitis being on the ground)
  • Move animal from side to side and assist in getting up
  • NO antibiotics unless indicated with a wound or additional known/ suspected infection
  • NSAID/ pain control = Ketoprofen 10% (low meat withdrawal time and zero milk)
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24
Q

What are the 2 main roles of Magnesium in the body?

A
  • Intracellular signalling

- Nerve transmission

25
Q

Where in the ruminant GI is the majority of Mg absorbed?

A

Rumen

26
Q

Why is Mg homeostasis difficult to maintain in all ruminants (cows, sheep, goats etc.)?

A

They have no feedback mechanism to regulate Mg, therefore what they need has to be taken in daily through feed

27
Q

What factors might decrease the absorption of Mg within the Rumen?

A
  • Concentration of Mg in feed
  • Rumen pH (high pH = low absorption)
  • Reduced transit time (e.g. lush high-moisture pasture)
  • Dietary Na+ (low = low Mg absorption)
  • Dietary K+ (high = low Mg absorption)
28
Q

Where in the ruminant is the majority of Mg lost?

A

Kidneys

Limited reabsorption from the kidneys through PTH stimulation

29
Q

When is Hypomagnesaemia a concern during the year in Ireland?

A

Can occur year round

With lowest blood levels recorded in March - April (first 2 weeks following turnout onto pasture)

30
Q

What risk factors are associated with Hypomagnesaemia in cattle?

A
  • Age: 4-7 years old
  • Stage of Lactation: first 2 months
  • Stress: excitement, transportation, cold wet weather, sudden changes in husbandry
  • Dietary:
  • less Mg availability in grass than in silage
  • type of fertilizer used on pasture
  • grass species (Ryegrass has lower Mg content than Clovers)
  • cereals are high in K+ and low in Mg
  • seasonality: spring rapid growth pasture = low Mg and shorter transit time
  • Rumen Degradable Protein: high levels will increase ammonia and increase pH, thus reducing Mg absorption
31
Q

What are the clinical signs associated with Hypomagnesaemia?

A
  • Sudden death/ found dead = peracute
  • Acute lactational tetany = stop eating, muscle twitching, fall to the ground, nystagmus, muscular spasms, frothing from the mouth, Opisthotonus (spasms and arching of head, neck and spine)

Note: Tachycardia but VERY LOUD pounding sounds (tachy in hypocalcemia but muffled and quiet heart sounds)

32
Q

How can Hypomagnesaemia be diagnosed in cattle?

A
  • History
  • Clinical Signs
  • Response to treatment
  • Serum Mg (not usually used though)
  • PM difficult to diagnose: need a fresh (up to 72hr) sample of vitreous/ aqueous humour sample
33
Q

What are the Differential Diagnosis for Hypomagnesaemia?

A
  • Stage 1 Excitable hypocalcemia
  • Nervous ketosis
  • BSE
  • Lead Poisoning
34
Q

What is the normal range for Mg in a Blood Biochemistry?

A

0.7 - 1.25 mmol/L

35
Q

What is the treatment for Hypomagnesaemia?

A

EMERGENT!
- Convulsing = sedate (5 - 15mL of 20% sodium pentabarbital slow IV) OR use Diazepam

  • +400mL of 20% Calcium borogluconate-Mg Hypophosphate solution slow IV
  • +400mL of 25% MgSO4 sol. sub-cutaneously

Caution: Must monitor heart continuously!

Once the animal is sedated and given the above drugs;

  • Place in sternal
  • Provide shelter (animal should rise in 12 hours)
  • Give 60g of MgO orally

Note: if not up in 24 hours = poor prognosis

36
Q

How can Hypomagnesaemia be prevented in a herd?

A
  • Be aware of risk periods;
  • 6-8 weeks after going to grass in spring
  • Winter milk herds on lush autumn pasture
  • Sept-March in out-wintered sucklers
  • Any animal undergoing transit

-Provide 30g/Mg/cow/day during these risk periods

Note: oral supplementation is unpalatable. Feed with concentrates or molasses to entice, salt licks, Mg bullets, in drinking water

  • Avoid K+ fertilizers in the autumn for spring pasture
  • Supply salt licks
  • Avoid stress
37
Q

Hypomagnesemia in Calves

A
  • Not common

- Calves 2-6 months old, on a milk diet: milk is low in Mg thus need another source of it

38
Q

What is another name for Bovine Ketosis?

A

Acetonemia

39
Q

What are the clinical signs associated with Bovine Ketosis?

A
  • Marked decrease in milk yield
  • Weight loss
  • Selective inappetence
40
Q

When does Bovine Ketosis most commonly occur?

A

Within the first 6 weeks post-calving, when milk production is highest

41
Q

What are the different types of Bovine Ketosis?

A
  • Primary/ Lactational Ketosis: Type I + Type II
    Type I: w/in 4-6 weeks post-calving
    Type II: w/in first 3 weeks post calving
  • Secondary Ketosis: associated with a sick animal not eating
  • Alimentary Ketosis: poor silage quality, leading to high levels of Butyric acid -> Beta hydroxybutyrate -> ketosis
  • Starvation Ketosis: Not fed, break down fat stores -> ketone production
  • Ketosis due to Cobalt Deficiency
42
Q

What are the risk factors associated with Bovine Ketosis?

A
  • Age: common in heifers, and older
  • BCS at calving: overconditioned animals will suffer from ketosis
  • Dry Period Length: longer dry period, more likely to develop ketosis
  • Excessive Protein in ration: ration should not exceed 180 - 190g CP/kg DM
  • Bidirectional association with other diseases: Milk fever, RFM, lameness, hypomagnesemia
43
Q

What are the signs we look out for in animals with Subclinical Ketosis?

A
  • Reduced feed intake
  • Ketonuria
  • Reduced milk yield
  • Reduced levels of milk protein
  • Increased incidence of endometritis and LDA
  • Infertility
    note: these signs will be very subtle and difficult to distinguish
44
Q

What are the clinical signs associated with Primary/ Lactational Ketosis (Dull Form)?

A
  • Rapid decrease in milk yield over 2 - 3 days
  • Selective inappetence: wont eat concentrate! Very unusual for a healthy cow
  • Rapid marked weight loss
  • Decreased Rumen-reticular activity: increased chances of displaced abomasum
  • Heart sounds heard on rumen auscultation: very unusual
  • Ketone smell on the breath or milk
45
Q

What are the differential diagnosis of Primary/ Lactational Ketosis (Dull Form)?

A
  • Simple indigestion
  • LDA, RDA, fatty liver syndrome
  • traumatic-reticular pericarditis
  • Pyelonephritis
  • Diabetes Mellitus (very rare though!)
46
Q

What are the clinical signs associated with Primary/ Lactational Ketosis (Nervous Form)?

A
  • Excessive licking: licking gates, bars, walls
  • Rapid chomping/ chewing
  • Hyper-reactive to stimuli
  • Twitching
47
Q

What are the differential diagnosis of Primary/ Lactational Ketosis (Nervous Form)?

A
  • Stage 1 Hypocalcemia
  • Subacute hypomagnesemia
  • BSE
  • Rabies
  • Pruritic conditions
48
Q

How can Bovine Ketosis be diagnosed in cattle?

A
  • Ketonemia: BHB, Acetone and Acetocetic Acid
    Can measure BHB only?
  • Ketonuria: Dipstick
  • Milk Ketones: less sensitive but more specific
49
Q

What is the normal BHB levels (mmol/L) for a lactating and dry cow?

A
  • Lactating: <1.0 mmol/L

- Dry Cow: < 0.6 mmol/L

50
Q

What is the Subclinical threshold for BHB levels (mmol/L) for a cow?

A

1.2 OR 1.4 mmol/L

depends on what part of the world you are

51
Q

What is the treatment and prognosis for Bovine Ketosis?

A
  • Good prognosis
    1) 400mL 50% glucose IV: rapidly improves oxaloacetate levels
    2) + Corticosteroids (e.g. Dexamethesone) IV: rapidly improves oxaloacetate levels
    3) + Propylene glycol orally: improve rumen propionate

225g BID for 2 days, then 110g SID for 2 days

+/- B vitamins (Cobalt/B12) even in non-deficient cases

52
Q

What are the steps of Fatty Liver development in the cow?

A
  • Mobilization of fat stores
  • Liver has 2 pathways to deal with NEFA’s
  • Oxidation pathway becomes quickly overwhelmed leading to ketone production and ketosis
  • Esterification pathway becomes overwhelmed next, VLDL’s cant be exported quick enough and accumulation of fat droplets (TAG’s) occur in the liver
53
Q

What are the knock on effects of fatty liver syndrome (accumulation of TAG’s in the liver)?

A
  • Decreased gluconeogenesis
  • Decreased ureagenesis
  • Further lipogenesis
  • Increased levels of ammonia, NEFA and ketones
54
Q

What are the effects on Production of the cow, with fatty liver syndrome?

A

Increased prevalence of:

  • Milk fever, retained placenta, mastitis
  • Delayed uterine involution
  • Disruption in synthesis of steriodogenic hormones (progesterone and LH)
  • Lower levels of Insulin and IGF-1: important factors as they DO influence fertility in the cow
55
Q

What are the risk factors associated with Fatty Liver Syndrome in cattle?

A
  • Management: inadequate space, poor transition diet and poor silage conservation
  • Genetic: some lines are at higher risk than others
  • Age: more common in older cows
  • Winter calving: late lactation they are on pasture in the spring with lush grass and are more prone to gaining weight, as well as during the dry period. They are then more likely to be overconditioned come winter when they calve again and go into a Neg Energy Balance
56
Q

What are the clinical signs associated with Fatty Liver Syndrome in Cattle?

A
  • Inappetance
  • Weak rumen contractions
  • Prolonged recumbancy
  • Ketosis + Ketonuria
  • +/- Hepatic encephalopathy
  • +/- Secondary diseases: hypocalcemia, LDA, RFM and Metritis
57
Q

How can Fatty Liver Syndrome be diagnosed?

A
  • Clinical signs
  • Blood analysis: GGT, AST, GLDH liver enzymes
  • Liver Biopsy
  • Ultrasound: most reliable, will see hyper-echoic
58
Q

What is the treatment for Fatty Liver Syndrome and the prognosis?

A

Prognosis Poor

Tx: same as ketosis

1) 400mL 50% glucose IV: rapidly improves oxaloacetate levels
2) + Corticosteroids (e.g. Dexamethesone) IV: rapidly improves oxaloacetate levels
3) + Propylene glycol orally: improve rumen propionate

225g BID for 2 days, then 110g SID for 2 days

+/- B vitamins (Cobalt/B12) even in non-deficient cases

+/- Insulin (Zn protamine): 200 - 300units BID

Clinical Endocrine, Metabolic and Dermatology (17 decks)

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