Metabolic diseases

Transition period

3 weeks before calving and 3 weeks after calving

when most metabolic problems occur in dairy cows

significant changes in energy demand/metabolism, endocrine status, feed intake, predisposition to disease

Early lactation

80% of disease in dairy cattle, 60% of losses

Last 3 weeks antepartum

feed intake decreases by 25-50% but energy demand of fetus is increased

udder development, lactogenesis, glucose requirements increase by 30%

Onset of lactation

feed intake decreases, glucose requirements increase by 75%

where negative energy balance starts through lipomobilisation

Physiologic adaptations in early lactation

in a negative energy balance, increased energy demand and secretions, increased lipolysis

rumen - increased hypertrophy and resorption

liver - increase in size and blood supply, increased gluconeogenesis and ketogenesis

muscle - proteolysis

Lipolysis

triglycerides broken down to fatty acids → sent to liver → fatty acid oxidation → energy

Ketosis

common metabolic disease of dairy cows

management disease → incidence varies greatly by farm

significant economic loss

demand for glucose by fetus or mammary gland exceeds what is available resulting in a negative energy balance or absorption and production of ketone bodies exceeds their use leading to elevated ketone bodies, free fatty acids, unesterified fatty acids

Pathophysiology of ketosis

lack of carbohydrates → increased fat mobilization → increased ketone body formation

adipose stores energy as triglycerides → can be mobilized to NEFAs → Krebs cycle → lipoprotein

Ketone bodies

important alternative energy source, spares glucose

small amount of ketones normal in lactating cows and pregnant ewes/does

Primary (Type I) ketosis

insufficient dietary intake, hypoglycemia

responds well to treatment

Secondary (Type II) ketosis

secondary to disease-induced inappetence ± fatty liver immediately post-partum

over conditioned cows, transient hyperglycemia, high blood insulin

treatment often unsuccessful if primary disease not detected

Subclinical ketosis

elevated ketone bodies with few to no clinical signs

30-50% of cows in early lactation, high risk for post-partum disease

Clinical ketosis

10-15% of cows

elevated ketone bodies with clinical signs

Risk factors of ketosis

first 6 weeks of lactation

high milk yield, higher parity, overconditioning

genetic factors

problems during previous transition periods

Clinical signs of ketosis

gradual loss of appetite leading to inappetence, decreased milk production, ruminal hypomotility, mild dehydration, dullness/depression, weight loss, altered CNS function (rare)

normal TPR

Diagnosis of ketosis

subjective - odor on cow’s breath

definitive - test for ketones in blood, urine, or milk

blood test best and most sensitive indicator, urine overly sensitive, milk low sensitivity but high specificity

Treatment for ketosis

primary ketosis - increase availability of glucose and carbohydrates

secondary ketosis - find and address underlying disease

propylene glycol PO for max 5 days

increased dietary intake

IV dextrose, glucocorticoids, insulin

Prevention of ketosis

avoid over-conditioning at calving, slow introduction of lactation ration early, minimize stress in transition period, ionophores, monitor closely for concurrent disease and subclinical ketosis, herd monitoring (blood, urine, milk)

Hepatic lipidosis (fatty liver)

physiological response to negative energy balance → lipomobilization

rate of hepatic triglyceride formation exceed oxidation of fatty acids and release of very low density lipoproteins → liver becomes overwhelmed with movement of NEFAs

Subclinical hepatic lipidosis

fatty liver

indicator of suboptimal adaptation, predisposition for further disease

fertility/milk yield decrease, immunosuppression, inflammation

Clinical hepatic lipidosis

severe liver disease

decreased liver function, hepatic encephalopathy

increase in postpartum diseases, increased losses

Diagnosis of hepatic lipidosis

increase NEFAs, intra-abdominal palpation, liver biopsy/necropsy (best)

Insulin

controls blood glucose concentration

favors cellular uptake of glucose, lipogenesis and glycogen synthesis

decreases lipolysis and hepatic gluconeogenesis

Glucagon

increased lipolysis and hepatic gluconeogenesis

decreased lipogenesis

Volatile fatty acids

main energy source in ruminants, fermented carbohydrates

acetate - most of them, fat synthesis, ketogenic

propionate - glycogenic

butyrate - ketogenic

Pregnancy toxemia

metabolic disease of small ruminants and beef cattle

ketosis associated with late pregnancy (last 2-6 weeks)

increased energy demand from fetuses, negative energy balance, decreased rumen fill

lower morbidity and higher mortality compared to fatty liver in cattle

Risk factors of pregnancy toxemia

sheep more sensitive than goats

multiple fetuses, poor quality feed, over-conditioned animals or very poor BCS, availability and quality of feed, stress

Pathophysiology of pregnancy toxemia

40% decline in rumen volume in final 6 weeks of pregnancy

dietary intake decreases spending on number of fetuses

30-40%of glucose goes to feto-uterine unit

Clinical signs of pregnancy toxemia

anorexia, depression, separation from herd, weakness, recumbency

neuro signs - blindness, tremors, circling, star gazing

concurrent disease process - pneumonia, GI parasitism

Differentials for pregnancy toxemia

hypocalcemia, hypomagnesemia, mastitis, enterotoxemia, listeriosis, polioencephalomalacia, anemia/parasitism, copper toxicosis

Diagnosis of pregnancy toxemia

ketone assessment - blood or urine

ultrasound to determine number of babies

chemistry and blood gas - metabolic acidosis, hypocalcemia, hypokalemia, hypoglycemia, azotemia, ± increased liver enzymes

Treatment of pregnancy toxemia

exogenous energy source - oral propylene glycol, IV dextrose, corticosteroids, insulin

removal of energy demand - emergency C-section, induce labor

supportive care and ancillary treatments - IV fluids, vitamin B1, physical therapy, antimicrobials and antiparasitics if warranted

Prevention and control of pregnancy toxemia

appropriate BCS prior to breeding and during gestation, high quality forage and increased grain, record keeping for breeding date, pregnancy diagnosis by ultrasound, herd checks

Protein-energy malnutrition

disease of pregnant beef cattle

malnutrition, negative energy balance due to decreased quality and quantity of feed

prevention - make sure cows going into 3rd trimester have good BCS and are fed high-quality forage and grain

4M’s of recumbent cow

mastitis metritis, musculoskeletal/neurologic, metabolic

metabolic - hypocalcemia, hypokalemia, hypomagnesemia, hypophosphatemia

Calcium basics

from - bone or diet

loss - bone growth, fetus, lactation

homeostasis - bone resorption, kidneys, resorption in small intestine

PTH and Vitamin D increase ionized calcium

calcitonin decreases ionized calcium

mostly extracellular

Calcium function

neuromuscular - transmission of nerve impulses, excitation of skeletal and cardiac muscle for contraction

CNS - neurotransmitter release

enzymatic reactions, second messenger molecule, glucose regulation (insulin release)

Hypocalcemia (milk fever)

occurs within 24-48 hours after calving → onset of lactation pulls approximately ten times the ECF calcium content into milk within several hours → depletion as serum Ca so rapid that hormonal controls can’t keep up → blood calcium drops so low that muscle and nerve function are compromised → paresis

usually occurs pre-partum for beef cattle and small ruminants

Risk factors for hypocalcemia

older cows, Jerseys and Guernsey, high BCS, poor nutrition, high-producing cows, high calcium dry cow diets, within 72 hours of parturtion, hypomagnesemia, metabolic alkalosis

Metabolic alkalosis in hypocalcemia

diet affects blood pH → pH alters conformation of PTH receptor, decreases bone resorption, decreases renal reabsorption, kidneys don’t make vitamin D

need to create compensated metabolic acidosis pre-calving

Dietary cation-anion difference

in dry period should be -100 - -150 mEq/kg, need more anions than cations

add anionic products slowly to total mixed ration, usually unpalatable and may reduce feed intake

Stage 1 hypocalcemia

influence on nerve conduction - hypersensitivity, irritable

influence on neuromuscular strength - weight-shifting, weakness

influence on cardiac muscle - tachycardia

might be missed, stage 2 ensues rapidly S

Stage 2 hypocalcemia

sternal recumbency - head tucked, S-shaped neck

flaccid paralysis, muscle fasciculations, tachycardia, weak cardiac contractility

ejection volume drops, blood pressure drops → vasoconstriction

poor perfusion - subnormal rectal temperatures, cold extremities

mild bloat, GI stasis, dry feces

slow PLR

Stage 3 hypocalcemia

lateral recumbency, progressive loss of consciousness, coma → death

severe bloat, severe tachycardia, heart sounds very quietD

Diagnosis of hypocalcemia

clinical signs and history, biochem/blood calcium

Treatment of hypocalcemia

calcium borogluconate IV - 1 bottle slowly over 15 minutes, monitor for tachycardia or bradycardia and arrhythmias, can give second bottle SQ to cover ongoing losses

oral calcium - drench or bolus, avoid aspiration, calcium very caustic

supportive care - hobbles, good footing, keep cow sternal, offer water and fod, roll if recumbent, hygiene and udder control

Complications of hypocalcemia

flaccid paralysis - bloat, aspiration pneumonia

recumbency - muscle compression, muscle rupture, skeletal injuries, peripheral nerve damage

Prevention for hypocalcemia

create compensated metabolic acidosis (urine pH 6.2-6.8)

oral calcium treatment at time of calving

Phosphorus basics

structural function at tissue, cellular, and molecular levels

component of phospholipids, phosphoproteins, nucleic acids, ATP

main source from diet

homeostasis - PTH, vitamin D, calcitonin

resorption in small intestine

Causes of hypophosphatemia

intestinal absorption - persistent anorexia, hypovitaminosis D, marginal diet during increased needs, malabsorption

increased renal excretion - diuresis, hypocalcemia

shift from extracellular to intracellular - glucose infusion, refeeding syndrome

Post-parturient hemoglobinuria

severe acute hypophosphatemia in first 4-6 weeks of lactation

high producing multiparous cows

clinical signs - depression, weakness, anorexia, drop in milk yield, anemia, hemoglobinuria, icterus

association vs causation?

Treatment of hypophosphatemia

restore dietary requirements, treat hypocalcemia, phosphorus supplementation (IV or oral), blood transfusion if needed

Potassium basics

most potassium in intracellular space

main intake through nutrition

part of ingested potassium will be excreted by kidneys

no regulatory feedback mechanism

resorption through rumen

Causes of hypokalemia

decreased intake - anorexia, disease, deficiencies, ration, environment

losses - aldosterone, renal disease, temperature, drugs, toxins

other abnormalities - diarrhea, third space loss, alkalosis, mineralocorticoids, diuretic drugs

Clinical signs of hypokalemia

do not always correlate with serum potassium

severe depression, recumbency, muscle tone severely reduced, abnormal neck posture (S-shaped), tachycardia, GI stasis

Differentials for hypokalemia

GI stasis, botulism, hypocalcemia, cervical trauma

Treatment of hypokalemia

address any pre-existing disease, oral supplementation (most effective), IV infusion of potassium chlorideP

Prevention of hypokalemia

monitor closely for anorexia and post-partum disease

use mineralocorticoids with caution

Magnesium basics

mostly in skeleton

cofactor for enzymes, need for function of PTH receptor, responsible for neuromuscular transmission, cofactor of acetylcholinesterase

regulation - aldosterone

resorption in rumen and intestines

most forages do not have required amount of Mg, need to supplement

Hypomagnesemia

usually lactating animals

usually occurs in spring and fall, grazed upon lush pastures high in potassium and nitrogen but low in Mg

Clinical signs of hypomagnesemia

lateral cow with stiff legs

anorexia, nervousness, decreased milk production, hyperexcitability, tetany, convulsions

Treatment of hypomagnesemia

IV Mg therapy - usually combo Ca/Mg

oral Mg administration