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- most dystocias will be seen in the afternoon or evening
- Most (90%) of early morning calls will be milk fever in dairy practice
- Avg Jersey cow 300d milking = 4500L
- Toxic mastitis, metritis or dehydrated cow will not produce much milk
- Parturient hypocalcaemia in cows is most common manifestation of
   hypocalcaemia in cattle
- Also see hypocalcaemia in feedlot beef steers in pathological numbers
- Hypocalcaemia occurs when total Ca < 2.1 mmol/L
           o OR ionised plasma calcium < 1.1 mmol/L
- Ionised calcium is the biologically active calcium
- 50% of total calcium is bound to protein therefore if hypoalbuminaemic,
   will also likely to be hypocalcaemic
           o This occurs in Johne’s disease
- In lactation, up to 70g/day calcium from the cow is diverted into the milk
   she produces
- 1kg of colostrum takes 2.5g calcium from the blood
- Decreased intestinal calcium absorption occurs via
           o Oxalated
           o Fats
           o Mg fluoride
           o Low P
- Decreased bone resorption of calcium occurs via
           o High calcitonin
           o Age
- Increased calcium bone resorption occurs via
           o Acid blood pH
           o Youth
           o Oestrogen
           o High 1,25(OH)2D3
- Increased calcium intestinal absorption occurs via
           o Acid lumen pH
           o High calcium
           o High 1,25(OH)2D3
- Aetiopathogenesis of milk fever
           o Decreased smooth muscle contractility
           o Decreased vascular contractility
           o Decreased GIT contractility
           o Decreased cardiac muscle contractility
           o Decreased skeletal muscle contractility
           o Decreased neurotransmitter function  affects other endocrine
           o Decreased apocrine gland function  get a dry muzzle
- Effects of hypocalcaemia include
           o Muscular weakness
           o Decreased gut motility
           o Decreased thermoregulation
           o CVS collapse
-   CSx you won’t expect to see in milk fever
           o Agalactia
           o Pyrexia (most of the time  exception is a hot day or where cow
               has been lying in sun for some time)
           o Strong normal heart sounds
           o D+
-   Differential diagnosis i.e. first things to rule out
           o Toxic mastitis
           o Obstetric paralysis
           o Hip luxation
           o Salmonellosis
           o Parturition e.g. twinning, uterine torsion
-   Treatment
           o Calcium replacement – calcium propionate is good for milk
               fever (and also for ketosis)
           o Glucose/dextrose supplement and Mg and P
           o Supportive treatment
           o If don’t strip the udder out for 48hours there is a greater risk of
                   Are already at an increased risk of mastitis because of
                      milk fever interfering with humoral immunity and
                      because cow is usually sitting in faeces and/or dirt
-   CSx if treatment/diagnosis was correct
           o Sweat beads on muzzle
           o Steam rising from coat
           o Eructation
           o Tremor
           o Standing
           o Cardiac changes – nb. These can be difficult to interpret
-   Standing
           o 60% will get up within 30 mins
           o 75% will get up within 2 hours
           o 10% will get up within 24 hours
           o 15% don’t get up!
-   Cows that are about to calve get udder oedema and flank oedema


-   Pregnancy toxaemia – twinning most likely but unable to be likely to
    without assistance
-   Blood glucose should be low but may come back up again
-   Ketones in the urine
-   Other thing to look at is feed – if this is poor can be pretty certain in preg
-   Has a poor prognosis
-   Treatment – glucose, induce calving with dextrose, consider giving
    prostaglandins also

-   Typical Volatile Fatty Acids (VFAs)
-   Acetate : propionate : butyrate
-     70         20          10            - for high forage diets
-     60         30          10            - for high starch diets
-   VFAs provide 60-80% glucose ?
-   Ketone bodies are impt water soluble fat derived metabolites
          o Produced mainly in the liver
          o Good energy source as long as they aren’t the only energy
          o Most ketone bodies are
                   Acetone
                   Acetoacetate
                   Butyrate          If can’t enter the
                                          Kreb’s cycle

        Actetate                         Acetyl CoA
        Butyrate                                                        Can go into Kreb’s
                                                                         cycle but only if
                                                                        there are sufficient
                                                                            levels of –
      Propionate                        Oxalo-acetic

               Therefore the
             limiting factor is

-   If acetyl CoA can’t enter the Kreb’s cycle, it is formed into aceto-acetate
-   Fat is also mobilised  increased free fatty acids, increased triacylglycerol

-   3 syndromes
          o Hepatic lipidosis
          o Ketosis/Pregnancy toxaemia
          o Fat cow syndrome
-   Hepatic lipidosis
-   Present in all high producing cows to some degree so can be a normal
    state i.e. not necessarily a disease state
-   Fatty liver occurs when the increase in TGs exceeds the rate of hydrolysis
    into VLDL etc
-   Ruminants have a low rate of TG metabolism
-   Accumulation of TG in the liver occurs  impaired hepatocyte function 
    VLDL production impaired and conversion of propionate to glucose is
    also impaired
-   Ketosis
-   Ketosis is usually associated with some degree of fatty liver
-   Dairy cow in ketosis will fix herself in time if no intervention but in
    meantime there will be decreased milk production etc
-   Cow with preg tox will not fix herself because can’t just get rid of the
-   Subclinical ketosis is common
-   1-5% incidence in winter housing period in all dairy cows in UK
-   Commonly seen as a 2˚ disease  i.e. 2˚ to LDA, metritis, mastitis
-   Fat cows are predisposed to ketosis at calving
-   CSx
           o Eating in paddock but not eating grain
           o Firm dry faeces
           o Depressed
           o Have lower plasma calcium
                   - Therefore reduced rumen contraction, frequency and
           o Temp and other cardinal signs usually normal
           o Some cows show neurological signs
                   - Sudden onset
                   - Delirium
                   - Circling
                   - Blindness ***
                   - Etc
-   All tests for ketones in the urine only detect aceto-acetate
           o Most cows have a large % of ß-hydroxybutyrate ad some don’t
                even have appreciable levels of aceto-acetate
           o Therefore tests are only ~ 85% sensitive
-   Fat Cow Syndrome
-   All cows inappetant in last week of calving
-   But in the fat cow, there is an accumulation of TAG in liver and kidneys
    and even in the lungs
           o Therefore will see an increase in liver enzymes and BUN
-   Generalised fatty degeneration of the parenchymised organs
- Treatment of Fat cow, hepatic lipidosis, ketosis, preg tox etc
 - 500ml of 50% IV glucose/dextrose solution
          o Essential in all cases showing CNS signs
          o Additional Tx often needed to prevent relapse
          o Large proportion is excreted in the urine  reduced insulin
 - Glycerol or propylene glycol (pink stuff)
          o 200mL BID for 1 day, then 100mL BID for 3 days
          o Results in elevated blood glucose 4 hours after treatment
 - Glucocorticoids
          o E.g. dexamethasone
          o Hyperglycaemic agents i.e. increased blood glucose level ~ 24
             hours after treatment
          o Reduced milk yield occurs in healthy cows therefore impact in
             sick cow?
          o Value in fatty liver questionable
                  Increased adipose lipolysis
                  Increased hepatic TG secretion
 - Insulin
          o Off label use
          o Expensive!
          o Decreases blood glucose levels


-   Nasal plane dry – indicates dehydration or pyrexia
-   Also has slightly reddened area inside nose
-   DDx
          o Septicaemia***
          o Meningitis – CSx – blindness, head pressing, stupor, coma
-   Organisms responsible
          o Strep ***
          o Staph
          o Sometimes coliforms
          o Occasionally Pasteurella spp.
-   Prognosis is guarded
-   Treatment
          o IV fluids and antibiotics
          o 40-50kg calf needs ~ 4-5L fluids
          o Hartmann’s because calf is likely to be acidotic
          o Then give oral lectade etc
          o Antibiotics – best is trimethoprim/sulf or Chlorphenicol
-   Need to know if calf is from a heifer or a cow
          o If from heifer  colostrum could be an issue
           o If from a cow  better colostrum donors
                   But, high producing cows can leak colostrum


-   DDx – craniolateral dislocation of hip
-   Worth treating
-   Prognosis is good


-   DDx
             o Obturator nerve paralysis (calving paralysis)***
             o Sciatic nerve – but usually causes a weakness of whole leg
-   Prognosis is good
-   If left for 2-3 days  prognosis is poor


-   Alternating between sternal and lateral recumbency indicates cow is in
-   DDx
            o Abortion
            o Calving
            o Possible uterine torsion if calving
-   Do vaginal examination to confirm
-   If not calving, need to identify if has a closed cervix to be sure of this
            o Should only be able to fit one finger through cervix at best
-   Treatment
            o Roll cow
            o Caesarean if not successful


Discuss factors that you consider to be impt in the epidemiology of hypomagnasaemic
tetany (grass tetany) in dairy cattle and briefly discuss the pathogenesis of this
condition in cattle.

-   Epidemiology
          o Plant factors - 5
          o Animal factors - 4
          o Environmental factors – 3
-   Pathogenesis
          o Low serum Mg
          o Low serum calcium or decreased serum calcium
          o Mg level in CSF

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