Calf Management

Clinical Exam of a Calf

• Systematic approach

• Describe 10 differences from adult cattle

Systematic Approach: Similar to cows

1. Distance

2. Back

3. Left

4. Head and neck

5. Right

Differences to Adult Cattle: No udder, rumen auscultation, rectal OR vaginal exam in calves

1. History (milk intake easier than pasture intake)

2. Behaviour (more playful)

   • Normal: Adequate reaction to acoustic and optical stimuli, very BAR

   • → Adequate reaction → Delayed reaction → Reaction to ONLY painful stimuli (eg. venipuncture) → No reaction to painful stimuli

3. Symmetry (underdeveloped rumen → different to adult abdomen shape)

4. Faeces VERY important to examine

   • Rub perineum to stimulate defaecation (may not be observed if very liquid and shoots out)

5. Palpate navel

6. Palpate joints

7. Pinging still important

8. Reflexes: Suckling and palpebral

   • Suckling = Strong → Weak → Absent/chewing movements

     • Management: Small teat openings and more frequent feeds to satisfy innate desire to suckle

     • Test with fingers (should be painful) + observe tail wag

   • Palpebral = Eyelids closed immediately and fully → Delayed closure → Delayed closure and NOT fully → NOT closed at all

9. Strength and posture

   • Normal: Calf standing by itself → after encouragement → Steady after lifting → Unsteady but can correct position if forced → Unsteady and unable to correct position → Sternal recumbency → Lateral recumbency

   • Encourage standing by rubbing hair over the back in the opposite direction

10. Ears (more prone to ear infections

TPR of calves

RR = 24 - 36/min

HR = 80 - 100 bpm

T = 38.5 - 39.5˚C

List 9 DDx for calf disease

1. Diarrhoea

2. Navel ill

3. Calf pneumonia

4. Rumen drinking/acidosis

5. Joint ill

6. Meningitis/salt poisoning/PEM (see “Systemic Diseases”)

7. Abomasal disease (ulcers, bloat and displacement)

8. Calf diphtheria

9. Other

   1. Atresia ani/colonic aplasia

   2. Contracted flexor tendons

   3. Bovine neonatal pancytopenia

Overview of Umbilical Diseases

• Normal umbilicus structure

• Describe normal umbilicus involution

• 5 Types of umbilical diseases

• Recommendations for umbilical care

Structure:

1. Urachus = To bladder

2. ONE umbilical vein = To liver

3. TWO umbilical arteries = To aorta (snap back after birth)

Normal Involution:

1. Umbilical cord ruptures at birth ~4 fingers away from skin

   • Rupture at skin = Risk of infection

2. Dries out within 4d (determine age or signs of infection)

3. Sloughs off at ~14d

4. Scab present until 3 - 4w

Types of Umbilical Diseases:

1. Uncomplicated umbilical hernia

2. Complicated umbilical hernia

3. Umbilical remnant infection (infected vein, arteries or urachus)

4. Umbilical abscess/chronic omphalitis

5. Urachal cyst/rupture

Umbilical Care: ASAP after birth before AND after transport

• Iodine/chlorhexidine spray/dip to completely cover navel

• Handle navel gently and as little as possible

• Repeat ≥SID until navel dries out

Navel Ill

• 5 Risk factors

• Diagnosis (2)

• 6 Clinical signs

• 5 Sequelae

• 2 Treatments of umbilical infections

• 2 Treatments of umbilical abscess

Risks:

1. Poor/no navel treatment

2. Insufficient colostrum intake

3. Low calf pick-up frequency (2x minimum and 4x ideal)

4. Poor general hygiene (calf pen, calving paddocks and trailer)

5. Overstocking

Diagnosis: History and general clinical exam (fever and inappetence) →

1. Further examination of umbilicus

   1. Distance Examination

      • Length? Dry? Smell? Fistula? Discharge?

   2. External Umbilicus

      • Size

      • Texture

      • Pain

      • Hernial ring

      • Reduction possible?

   3. Internal Navel Palpation = Palpate intra-abdominal structures

      • Size

      • Texture

      • Pain

      • Adhesions

2. Further diagnostics

   1. Probe/cannulation

   2. U/S = Evaluate extra- and intra-abdominal structures

Clinical Signs:

1. Swelling

2. Discharge

3. Pain (hunched/flinching when umbilicus pinched)

4. Damp

5. Hernia

6. Severe = Pyrexia, septicaemia, lethargy and inappetence

Sequelae:

1. Septicaemia

2. Liver abscess

3. Meningitis

4. Joint ill

5. Spinal abscess

6. Endocarditis

Treatment of Umbilical Infection:

1. Broad-spectrum AB and NSAIDs for 3 - 5d

2. Surgical intervention

Treatment of Umbilical Abscess:

1. Drain abscess (thin-walled and large)

2. Surgical extirpation (thick-walled and small)

Umbilical Hernia

• Aetiology

• 3 Examples of complicated umbilical hernia

• 3 Treatments of uncomplicated umbilical hernia

• Treatment of complicated umbilical hernia

Aetiology: Congenital or following infection (consider genetics)

Complicated Umbilical Hernia:

1. Non-reducible and/or infected

2. Hard to feel hernial ring

3. Systemic signs of depression/colic

Treatments when Uncomplicated:

1. Do nothing when 1.5 - 3.5cm

   • 90% of hernias with diameter of 1.5cm - 3.5cm close within 65 days

2. Keep hernia reduced with hernial clamps/elastrator ring/abdominal support bandage

3. Surgical intervention

Treatment when Complicated: EMERGENCY surgical intervention

What is the most likely DDx for a female calf with pulsing urination?

Urachal cyst/fistula

Overview of Bronchopneumonia

• Prevalence in NZ

• Aetiology

  • Viral (5)

  • Bacterial (6)

• Risk factors

• Pathogenesis

Prevalence: Relatively rare in NZ due to outdoor housing (vs. intensive dairy systems)

• More common cause of death in feedlot cattle

Aetiology: MULTIFACTORIAL = Stress + virus + bacteria

• Virus

  1. Infectious bovine rhinotracheitis (BHV-1)

  2. Parainfluenza virus (PI-3)

  3. Bovine viral diarrhoea virus (BVDV)

  4. Bovine respiratory syncytial virus (BRSV)

  5. Bovine coronavirus (BCoV)

• Bacteria

  1. Mannheimia haemolytica = G- aerobe

  2. Pasteurella multocida = G- facultative anaerobe

  3. Histophilus somni = G- facultative anaerobe

  4. Mycoplasma bovis = No cell wall

  5. Trueperella pyogenes = G+ facultative anaerobe

  6. Fusobacterium necrophorum = G- anaerobe)

Risks:

1. Purchase calves from auctions or markets

2. Mix calves from different sources (peak mortality ~16d after arrival in feedlot)

3. Weather conditions at arrival

4. Transport → Reduced mucociliary clearance and dry bronchial mucus → Suppressed immune system

5. Crowding

6. Other diseases

7. Climate/season: Poor ventilation, humidity, draught, cold stress, ammonia

8. Poor colostrum management

Pathogenesis:

1. Viruses and stressors damage alveolar macrophages and local ciliated epithelium

2. Results in suppressed immune system

3. Calves either heal OR become further infected

4. 2˚ bacterial infection results in respiratory disease

5. Further infection with Trueperella pyogenes → abscess OR Fusobacterium necrophorum → necrosis

6. Results in death

Diagnosis of Bronchopneumonia

• Clinical signs

• 7 Methods of diagnosis

Clinical Signs: DART

1. Depression

2. Anorexia

3. Respiratory character change (cough and dyspnoea)

4. Temperature elevation

5. ± Agalactia in cows

Diagnosis: Individual and group PE →

1. Thoracic U/S = ID presence and severity of lung consolidation

   • +ve: Gold standard

     1. Changes occur within hours

     2. On-farm and real-time

     3. Helps with prognosis and treatment triage

     4. ID re-aeration of lungs = Treatment success

     5. Lung consolidation associated with reduced ADG and lower CWT

2. CBC/biochemistry = Acute inflammation and FPTi

3. Nasal swabs = Superior for acute viral isolation

4. Transtracheal wash for culture and sensitivity

5. Radiographs with portable unit → Cranioventral lung lobe consolidation

6. Bronchoalveolar lavage and sterile sample

   1. Bacterial culture

   2. PCR

   3. MALDI-TOF MS

   4. Next generation sequencing

7. PM ± Culture of lesions

Lung U/S and presence of cough = #1 parameters to determine WHICH calf needs treatment to cure

Treating Bronchopneumonia

• Treatment

• Prognosis

• 4 Sequelae

Treatment: EARLY! Late therapy = #1 reason for treatment failure

1. Antibiotics for 3 - 4 days: Requires G- negative with good lung penetration

   • Penicillin

   • Florfenicol

   • Enrofloxacin

   • Tulathromycin

   • Cephalosporins

   • Oxytetracycline

2. NSAIDs

Prognosis: Fair to grave depending on severity and response to treatment

• Response to treatment often after 12 - 24hr

  • Treat 2 days after recession of fever

  • Check U/S

Sequelae:

1. Chronic lung injury

2. Pulmonary abscess

3. Ear infection

4. Chronic, recurrent bloat (swelling of mediastinal LN)

Chronic Bronchopneumonia

• 2 Clinical signs

• Pathogenesis

• Treatment

Clinical Signs:

1. Initial acute bronchopneumonia (MAY or may not have been treated)

2. Poor growth rates and chronic weight loss despite treatment

Pathogenesis:

1. 2˚ infection with Pasteurella multocida/Trueperella pyogenes → Fibrinosuppurative abscess → Congested OR Fusobacterium necrophorum → Necrotic tissue walled off

   • Difficult for antibiotics to penetrate

2. Extension of inflammation to pleura → Pleuropneumonia → Pleural effusion and adhesions

   • Common with Histophilus somni

Treatment: Cull (poor prognosis)

Rumen Drinking/Acidosis

• Normal physiology of the oesophageal groove

• 4 Aetiologies (+ examples)

• Pathogenesis

• 6 Clinical signs

• 5 Treatments

• 3 Methods of prevention

Normal Physiology: Suckling reflex linked to closure of the oesophageal groove

• Rumen drinking = Insufficient closure of oesophageal prevent milk from bypassing the rumen

Aetiologies:

1. Primary suckling weakness

   1. Difficult calving

   2. Se deficiency

   3. CNS problem (BVD)

   4. Dummy calve syndrome

   5. Prematurity (insufficient lung development)

2. Secondary suckling weakness due to illness

3. Iatrogenic = Drenching/forceful feeding of milk

4. Overloaded abomasum → Reflux of milk into rumen

Pathogenesis: Similar to adult rumen acidosis

1. Fermentation of milk in rumen

2. Increased lactate (D-/L-)

3. Drop in rumen pH

4. Blood acidosis

5. Rumenitis and bacterial translocation

6. Dehydration

Clinical Signs:

1. No/poor suckling reflex, weak and depressed

2. Pale faeces

3. Poor doer

4. Rough coat with alopecia

5. Full rumen with slushing sounds on ballottement

6. Teeth grinding and arched back

Treatment:

1. Eliminate and treat underlying cause

2. Flush rumen

3. Bicarbonate PO(15 - 30g in cold water)

   • IV if acidosis present

4. ± IV dextrose for maintenance requirements (400g dextrose/40kg calf/24hr) if not good suckling reflex present

   • Do NOT offer milk until good suckling reflex present

5. ± Oral antibiotics for severe rumenitis (poor prognosis) → Yoghurtised milk or rumen transfaunation

Prevention:

1. Gentle and patient calf husbandry (avoid negative association)

2. Never drench or force feed milk/MR (first colostrum is ONLY exception)

3. Disease monitoring

2 Ways to ID a premature calf

1. Incisors have not completely broken through

2. Very soft cartilage (rolled up ears)

Joint Ill

• 2 Aetiologies

• 5 Clinical signs

• 4 Methods of diagnosis

• 7 Treatments

Aetiologies:

1. Haematogenous spread (eg. navel ill or pneumonia)

2. Traumatic (puncture, decubitus 2˚ to contracted flexor tendons)

Clinical Signs:

1. Distended joints (painful as joint capsule highly innervated)

2. Calor, rubor, dolor (inflammation)

3. Increased/decreased mobility

4. Muscle atrophy

5. General symptoms: Fever, anorexia

Diagnosis: Orthopaedic exam of ALL joints →

1. U/S with linear transducer (5 - 7.7 MHz)

   • Diagnosis of arthritis, bursitis, abscess, haematoma

   • Normal synovial cavities in cattle DIFFICULT/IMPOSSIBLE to visualise via U/S (very small amount of normal synovial fluid)

     • → Effusion that is easily visualised = Pathology

2. Joint tap to examine synovial fluid (do NOT joint tap if phlegmone present (inflammation of soft tissue)

   • Cloudy, turbid and watery

   • TP > 4g/dL

   • > 30,000 WBC/mm³

3. Radiography

4. Arthroscopy

Treatment:

1. Broad-spectrum AB (≥10 days and ideally 14 days)

2. Intra-articular antibiotics ± local anaesthesia

3. NSAIDs (ketoprofen or carprofen)

4. Joint lavage q2 days 3 - 5 times

   • Only if no fibrin present

5. Bandage

6. Box rest

7. Traumatic/open joints/multiple joints affected → Euthanasia (difficult to treat)

Abomasal Ulcers

• 3 Aetiologies

• 5 Clinical signs

• PM

• 5 Treatments

Aetiology:

1. Stress/pain-related

2. Weather

3. Cl. perfringens type A???

Clinical Signs:

1. Melaena and occult blood

2. Anaemia

3. Acute death with perforation

4. Teeth-grinding

5. Dipping mouth into water trough

PM: Superficial, haemorrhagic and'/or perforating ulcers

Treatments:

1. Blood transfusion

2. Antacids

3. NSAIDs?

4. Surgery

5. Oral AB?

Abomasal Bloat

• 5 Risks

• 3 Clinical signs

• Diagnosis

• 5 Treatments

Risks:

1. Feeding amount (>3L/meal)

2. Feeding frequency (once per day)

3. Milk temperature (cold milk)

4. Schedule

5. Milk quality

Clinical Signs:

1. Abdominal distension vs. severe colic

2. Dehydration

3. Diarrhoea

Diagnosis: Ballottement and U/S

Treatments:

1. Gastric tube → ± Administer vegetable oil or surfactant to pop bubbles in the frothy foam produced to remove gas

2. NSAIDs

3. Buscopan (anti-spasmodic)

4. Roll calf on back and relieve gas with needle (toggle principle)

5. Surgery

Abomasal Displacement in Calves

• Aetiology

• 3 Treatments

Aetiology: Poor milk quality, volume and feeding interval

Treatments:

1. Rolling (LDA)

2. Abdominal surgery with full GA in left lateral recumbency (right flank approach)

3. Empty abomasum out as content often cause

4 Ways to prevent abomasal disease in calves

1. Smaller volume feeds more frequently (15 - 20% BWT/24hr over 6 feeds daily)

   • Ensure small teat hole to prevent rapid consumption

2. High milk quality (derived from milk proteins) and yoghurtised milk

3. Gradual transition between milk products

4. Feed cold milk

Atresia Ani/Colonic Aplasia

• Aetiology

• 5 Clinical signs

• 2 Treatments

Aetiology: Congenital and linked to early rectal pregnancy palpation of embryo (membrane slip?)

Clinical Signs:

1. No anus (obvious)

2. No defaecation (apart from meconium)

3. Full abdomen

4. Colic

5. Anorexia after few days

Treatments:

1. Surgery

2. Euthanasia and PM

Bovine Neonatal Pancytopenia (BNP)/Bleeding Calf Syndrome

• Signalment

• Aetiology

• Pathogenesis

• 3 Clinical signs

• Treatment

• Prevention

Signalment: Calves <3m

Aetiology: Associated with BVD vaccination of mothers (PregSure) and also genetic contributions?

Pathogenesis: Antibody-mediate immunopathic process

• Allo-Ab directed against WBC derived from colostrum

Clinical Signs:

1. Generalised bleeding disorder

2. Fever

3. Death

Treatment: Symptomatic treatment usually NOT successful → Euthanasia

Prevention: Stop using this vaccine (no longer used)

Contracted Flexor Tendons

• Aetiology

• Signalment

• 4 Treatments

• Complications

Aetiology: Congenital (different grades of severity)

Signalment: Large male calves predisposed

Treatment:

1. Physiotherapy

2. Hoof extensions

3. Casts/splints

4. Surgery

Complications: Decubitus and arthritis

Describe 4 challenges of NZ calves

1. All calves born during SHORT but INTENSE calving period → High pressure on limited staff and resources

2. Born in contaminated and muddy paddocks outside in cold/wet weather

   • → Slippery paddocks which make it difficult to stand and suckle → Reduced colostrum intake

   • → Increased energy demands to maintain body heat → Weaker calves upon arrival at calf shed

3. Calves raised in groups (vs. individual pens)

   • → High calf-to-calf contact → Increased rate of disease transmission

   • → Smaller calves forced to compete with larger, stronger calves for feed and space

4. More calves born than what sheds can accomodate → Calves turned onto pasture when only a few weeks old to make room for younger calves

6 Causes of calf diarrhoea (+ timing)

1. E. coli (enterotoxic K99 = ETEC): 0 - 5d

2. Rotavirus/coronavirus: 5 - 15d

3. Nutritional (iatrogenic): 0 - 3w

4. Cryptosporidiosis: 5 - 35d

5. Salmonella spp.: 10d - 3m

6. Coccidiosis (Eimeria spp.): ≥21d

Reason for clinical disease = Adverse relationship between resistance of calf and infectious pressure

3 Impacts of calf scours

1. #1 cause of calf death (birth → 3w) in many countries

2. $$$ (one case ~$150 treatment)

3. Labour intensive for farmers/calf rearers

5 Steps of calf scours outbreak investigation

1. ID scale of problem (numbers affected/died)

2. Verify signalment (age) and clinical signs

   • Dirty backside/tail

   • Inappetence, lethargy, hunched/arched back

3. Confirm vaccination status of herd → Contact MSD Animal Health if Rotavec

4. Assess for dehydration and acidosis (blood gas analysis)

5. Brix test colostrum

6. Blood test 12 healthy calves for FPTi

7. ± Faecal culture/examination

8. ELISA TIMING important (eg. -ve result in sick calf or +ve result in healthy calf)

9. PM of freshly dead calves and histopathology

   • Small and large intestine → Fix in formalin ASAP (autolysis <30 min)

     • BOTH = Coronavirus

     • Small intestine ONLY = Rotavirus

       • Cryptosporidium in small intestine ONLY

Enterotoxigenic E. coli (ETEC), K99

• Age

• 3 Clinical signs

• Pathogenesis

Age: <3 - 5d

Clinical Signs:

1. Rapid onset of depression and recumbency with profuse scours

2. Rapid loss of >12% BWT in fluids

3. Death due to hypovolaemic shock within 12 - 24hr

Pathogenesis:

1. Bacteria adhere to enterocytes in small intestine

2. Enterotoxins produces which increases Cl- secretions

3. Net increase of fluid into intestinal lumen (secretory diarrhoea)

4. → Dehydration, acidosis and hypersecretion

   • NO mucosal damage)

Rotavirus/Coronavirus

• Age

• 3 Clinical signs

• Pathogenesis

Age: 5 - 15d

Clinical Signs:

1. Moderately depressed

2. Often continue to drink milk

3. Scours last ~3d (± chronic with some coronavirus scours)

Pathogenesis:

1. Secretion of viral enterotoxin

2. Vasoactive agents from damaged cells → Activation of enteric nervous system

3. Villous atrophy and crypt cell hyperplasia in small intestine

4. Destruction of enterocytes in colon (coronavirus)

5. → Malabsorption due to reduced SA

Cryptosporidiosis

• Age

• 4 Clinical signs

• Pathogenesis

Age: 5 - 35d

Clinical Signs:

1. Emaciation with persisting scours regardless of treatment

2. D-lactic acidosis

3. Death due to hypoglycaemia (even after resolution of scour) due mucosal damage → Malabsorption

4. Deaths more likely in cold spells and if milking restricted

Pathogenesis:

1. Protozoan parasite inhabits brush border of enterocytes

2. Villous atrophy, fusion and crypt cell hyperplasia

3. Prostaglandin-mediated anion secretion (Cl- or HCO3-)

4. Malabsorption and hypersecretion

Salmonella spp.

• Age

• 4 Clinical signs

Age: 10d - 3m

Clinical Signs:

1. Fever

2. Depression → Recumbency and coma

3. Rapid weight loss

4. Death due to septicaemia (vs. hypovolaemic shock)

Coccidiosis

• Age

• PPP

• Source

• 4 Risks

• 5 Clinical signs

• Diagnosis

• Treatment

• 4 Methods of prevention

Age: >21d (5 - 8w)

• <12m but rare

PPP: 18 - 21d

Source: Oocysts persist in environment

Risks:

1. Inconsistent use of monensin → Delay or influence onset of disease

2. High challenge (overcomes in-feed coccidiostats)

3. Discontinued meal too soon after weaning

4. Stress (eg. weaning or weather)

Clinical Signs:

1. Abdominal apin

2. Scours

3. Tenesmus

4. Haematochezia

5. Severe dehydration

Diagnosis: Faecal smear or FEC

Treatment: Baycox (toltrazuril) 15mg/kg PO

Prevention:

1. Calf meal with coccidiostat (monensin) until ≥3w post-weaning

2. Strategic use of Baycox = Single drench at 4 - 5 weeks of age

3. Hygiene = Position water troughs to prevent faecal contamination

4. Steam clean calf houses annually

Nutritional (Iatrogenic) Scours

• Age

• 4 Causes

• 3 Clinical signs

• Prevalence

Age: <3w

Causes:

1. Milk contamination (malfunction of pasteuriser)

2. Milk replacer incorrectly mixed

   • Should be of high quality with actual milk proteins

3. Rapid diet change

4. Change in temperature or volume of milk

Clinical Signs:

1. BAR

2. Good appetite

3. Gradual weakness and emaciation if diet not corrected

Prevalence: Uncommon and overdiagnosed cause of calf scours

List 2 main problems with calf diarrhoea

1. Dehydration

2. Blood acidosis

8 Steps of managing calf scours outbreak

1. Stress zoonotic risk (esp. Salmonella, Crypto and E. coli)

2. Discuss treatment of affected calves

3. Discuss 3Qs of colostrum management → ID areas for improvement

4. Discuss biosecurity (”all-in, all-out”), ID and isolate sick calves and hygiene

5. Observe calf pens and bedding and ID areas for improvement

6. Calculate feed requirements (12 - 15% BWT in milk in first months)

7. Advise preventative vaccination

8. Report and review annually → Keep it simple and achievable

   • Keep records (IDs, dates and treatments)

   • Monitor FPT and disease diagnosis

5 Treatments for individual calf scours

1. Fluid therapy

2. Buffer

3. Continue milk feeding (milk withdrawal NOT recommended → No improvement of clinical outcome)

   • → Malnourishment and weight loss

   • Milk necessary for energy and nutrients required for recovery of intestinal mucosa

   • High-energy ORS cannot prevent -ve energy balance in calves

4. ± Antibiotics (routine use NOT recommended)

   • Indication: Systemic involvement (marked depression, anorexia and fever) with risk of bacteraemia

     • 95% of infectious calf scours caused by rotavirus/coronavirus or Cryptosporidium

   • Susceptibility tests from faecal samples NOT reliable

5. NSAIDs (meloxicam) → Improved food intake and weight gain

ONE: DEHYDRATION

• 2 Causes

• 3 Clinical signs

  • %Dehydration

  • Volume of fluid deficit for a 40kg calf

• Blood test

• Treatment

Causes: Diarrhoea → Negative intestinal net fluid balance (secretion > absorption)

1. Lack of fluid intake

2. Excessive fluid loss

Clinical Signs: Tacky MM not a quantitative measure

Clinical Signs	% Dehydration	Volume in 40kg calf
None	< 5%	≤ 2L
Delayed skin tent Neck or upper eyelid (esp. beef calves with excess neck skin) Less reliable in geriatric patients with reduced collagen and skin elasticity	5 - 7%	3L
Sunken eyes	8 - 10%	4L
Comatose	>10%	5L

Blood: Increased HCT/PCV

Treatment: FLUIDS

1. Maintenance = 50 - 80mL/kg/d → 2L in 40kg calf

2. Existing deficit (%dehydration)

3. Ongoing losses = 5 - 10% BWT/d depending on severity

TWO: ACIDOSIS

• 2 Causes

• Pathogenesis of D-lactic acidosis in calves

• 4 Clinical signs

• 3 Blood tests

• Treatment

Causes:

1. Loss of buffer (bicarbonate) in faeces

2. Accumulation of organic acids (eg. D-lactate) in blood

   • Rumen drinking

   • Neonatal calf diarrhoea

Pathogenesis: Vicious cycle

1. Malabsorption results in fermentation of readily fermentable CHO in rumen/intestines

2. Increased production of D-lactate

3. Absorption of D-lactate and depletion of HCO3- buffer

4. Favourable environment for lactic acid-forming bacteria

Clinical Signs: NO impairment of suckling reflex

1. Impaired palpebral reflex

2. Staggering, “drunken” gait or recumbency

3. Somnolence

4. Unphysiological postures white standing/lying

D-lactic acidosis is the main cause of clinical signs

Blood:

1. Low/negative BE

2. Low blood pH/HCO3-

3. Increased anion gap (accumulation of unmeasured anions eg. D-lactate)

Treatment: Buffer = Bicarbonate AND fluids to increase D-lactate excretion

• Bicarbonate (mmol) = BWT (kg) x Base deficit (mmol/L) x 0.6

  • OR “rule of thumb” Amount of bicarbonate (g) for 40kg calf = Base deficit x 2

Severity of acidosis	Clinical signs	Approximate BE	Required amount of bicarbonate (g)
Mild	Standing securely Palpebral reflex mildly delayed	-10mmol/L	20g
Moderate	Standing insecurely (can be pushed over) Palpebral reflex delayed and incomplete	-20mmol/L	40g
Severe	Recumbent/unable to stand Very delayed/absent palpebral reflex	-30mmol/L	60g

3 Methods of Fluid Therapy Administration

• Indication

• Dosing

• Options

1. Oral Rehydration Solution (ORS)

   • Indication: Begin ASAP after scours identified BEFORE clinical signs of dehydration

     • Standing with suckled reflex → Bottle feed

     • Weak calves that cannot suckle but CAN lift head → Oesophageal tube

     • Weak and recumbent → AVOID (aspiration risk)

   • Dosing: 1 - 2L EXTRA daily in addition to milk

     • BUT NOT within 2 - 4hr of milk feeding (bicarbonate impairs milk clotting in abomasum)

     • Continue until scours stop and animal is fully rehydrated

   • Options:

     • Must include Na+, glucose, glycine/alanine, K+ and buffer

     • Acidotic calf → Dilute 20 - 30g sodium bicarbonate in water and drench

       • Citrate/propionate/acetate → Metabolised by liver to bicarbonate

       • Bicarbonate orally → Neutral abomasal pH → Increased risk of bacterial infection

2. Intravenous Fluids

   • Indications:

     1. Severely depressed, recumbent, with no suckle reflex

     2. Dehydration >8% and prolonged anorexia (>24hr)

     3. Metabolic acidosis with increased D-lactate and L-lactate in blood

   • Dosing: Run first bag at shock rates (80mL/kg/hr) → 2nd bag at 50mL/kg/hr

     • Cephalic vein #1

     • Correct deficits over 4 - 6hr

     • Discontinue IV once calf can hold head up

   • Options:

     1. 250 - 750mL of 8.4% sodium bicarbonate (depending on degree of acidosis)

        • Acidotic, recumbent calves respond to IV sodium bicarbonate (within 1hr → Suckle)

     2. 2 - 5L of 0.9% NaCl or Hartmann’s (depending on degree of dehydration and state of patient)

3. Milk Feeding

   • Indication: ALWAYS continue milk feeding with electrolyte solution

     • Calves require high level of energy for size + little fat reserves if food is withheld

     • ORS insufficient source of energy and protein

   • Dosing: NEVER tube feed milk → Rumen drinker

     • 8am: 2L milk

     • 12pm: 2L electrolytes

     • 4pm: 2L milk

     • 8pm: 2L electrolytes

     • Provide ad lib access to electrolyte solution AND fresh water overnight → Self-rehydration

List 8 calving management factors

1. Environmental Management = Calving paddocks

2. Calving Paddock Checks

3. Transport to Calving Shed

4. Environmental Management = Calving shed

5. Colostrum

6. Vaccination

7. Hygiene

8. Well-Trained Staff

ONE: Environmental Management = Calving Paddocks

6 Recommendations

1. Adequate shelter belt (guarded from wind and rain)

2. Free draining soils (reduce mud)

3. Easy access for farm staff

4. Avoid calving cows on crop → Wet and muddy

5. Move springers onto new grass breaks 2x daily

6. Teat-spray springers

TWO: Calving Paddock Checks

3 Actions

1. Check ≥BID (ideally QID) to ensure colostrum ingested ≤12hr after birth AND reduce number of calves in trailer

2. ID and assist with calving complications

3. Record births

THREE: Transport of Calves to Shed

8 Recommendations

1. Handle calves with care to reduce stress and pain

2. Bend knees when lifting calves

3. Maintain watchful eye on dam and keep calf between you and her

4. Ensure all calves can lie down comfortably (prevent overloading → trampled navels)

5. Drive slowly to maintain stability and allow newly calved cows to follow behind

6. Line trailer with easy clean, non-slip material

7. Regularly disinfect trailer → Allow to dry in sun to reduce bacteria

8. Spray navel before AND after loading/unloading from trailer

FOUR: Calf Shed

11 Recommendations

Calf pens are fit for purpose and well-maintained

1. Divide calf pens with solid dividers to avoid direct contact between calf pens (perspex ideal as easy to clean and allows calves to see each other)

2. Bedding is comfortable, clean and dry

   • Exposed concrete, bare earth and mud are NOT acceptable bedding types

3. Adequate ventilation (no ammonia smell), but draft-free at calf level

   • High ceilings and adequate air flow

4. Minimum 1.5m² per calf and maximum 10 - 20 calves per pen

5. Access to plenty of fresh water

6. Adequate good quality feed (meal) → Rapid development of rumen

7. “All in/all out” system = Calves of similar ages kept in batches and moved together through the sheds

8. Keep bobby calf pens away from replacement pens

9. No free lying water, mud, drains or effluent near calf sheds

10. Isolate sick calves ASAP → Recovered calf pen NOT into normal calf pen due to prolonged shedding

11. Use washing station and change gloves after sick pens

FIVE: Colostrum Management

• Definition

• Importance

• 4 Advantages of good colostrum management

• Describe 3 Q’s of colostrum management

• 7 Recommendations

Definition: Colostrum = 1st milk produced by cow post-calving which is high in Ab and nutrients

• Colostrum = Gold colostrum + transition milk

  • Gold colostrum = 1st milking of cow post-calving

  • Transition milk = Milk produced over the next ~4 days (2nd - 8th milking) which contains higher level of Ab and immune cells but NOT at the level necessary for passive transfer of immunity

    • Useful for feeding calves between ≥ 2 - 4 days (local immunity) but NOT newborn calves

• Components = IgG + WBC + growth factors + nutrients (CHO, proteins and fat)

Importance: Quality and quantity of Ab provided by colostrum within first 12hr of life determines effectiveness of calf’s immune response until calf’s immune system becomes functional

• IgG is NOT transferred via the bovine placenta → Calves born with naive immune system → Insufficient immune response to bacteria/viruses typically encountered in environment

+ve: Continue even after calf becomes immunologically mature

1. Faster GR → Targets met earlier (less energy expended on disease)

2. Produce more milk in future lactation?

   • Little long-term effects: No difference at pregnancy testing OR lactation performance

3. Decreased health costs

4. Decreased morbidity and mortality rates (pre-weaning and post-weaning <1yr old respectively)

3 Q’s of Colostrum Management:

1. QUICKLY = ≤12hr → Effective passive transfer BEFORE gut closure to big IgG molecules

   • Calf can only absorb Ab in colostrum for SHORT time after birth

   • 12hr post-calving → Only 5% of available Ab in colostrum absorbed

   • 24hr post-calving → Gut closes = No further absorption of Ab

2. QUANTITY = 10 - 15% BWT before gut closure (4 - 6L/calf)

   1. Pick up calves minimum 2x daily

   2. Offer 2L fresh gold colostrum once in shed (stomach-tube if necessary)

   3. Feed/tube again a few hours later to ensure ≥10% BWT of colostrum is received within 12hr of birth

3. QUALITY = High Ab and low bacterial contamination

   • Measured IgG with Brix Refractometer

     • ≥22% → Acceptable for newborn calves

     • 19 - 21% → Feed to calves 2 - 4 days of age

     • <19% → Feed to older calves ONLY

   • Measure bacterial contamination with coliform concentration (ideally < 10,000 coliforms/mL) OR measure total bacteria (ideally <100,000 bacteria/mL)

     • BUT contamination of NZ colostrum is extreme (millions of coliforms and billions of bacteria) → <9% of farms

     • #1 reason for FPTi in NZ is poor quality of colostrum (NOT picking up calves and NOT tube feeding)

Recommendations:

1. Dump milk from scouring cows

2. Clean dirty teats before cupping

3. Avoid pooling colostrum

4. Store in covered containers (freezing OR potassium sorbate)

5. Use colostrum ASAP after milking

6. Disinfect calf troughs daily

7. Feed calves youngest → oldest → sick calves last

   • Use separate equipment for sick calves OR disinfect immediately after

List 5 factors affecting colostrum quality

1. Colostrum quality is inversely proportional to time between calving and first milk collection

   • More time → Decreased Ab

   • Get cows in and milk ASAP post-calving

2. Maternal nutrition and individual variation

   • Avoid pooling colostrum (individual variation) → Individual selection of colostrum based on Brix refractometer

3. Maternal vaccinations (appropriate timing)

4. Bacterial contamination → Reduced ability to absorb Ab + infection

   • Bind IgG preventing absorption OR bind pores that allow IgG to be absorbed in the GIT

   • Reduce contamination by disinfecting with hot water

5. Time of colostrum storage (reduced IgG when being stored)

   • Place lid on colostrum drum and store adequately

Colostrum Storage

• 3 Disadvantages of pooling/mixing colostrum

• 3 Acceptable methods of colostrum storage

• 2 Unacceptable methods of colostrum storage

• Storage of transition milk

-ve of Pooling Colostrum:

1. Dilute Ab levels → Reduced quality

2. Increased risk of bacterial contamination (esp. E. coli) → Reduced quality

3. Increased risk of disease transmission (eg. Johne’s disease and ETEC)

Acceptable Methods of Colostrum Storage:

1. Freezing → Reduce bacterial growth AND prolong lifespan of colostrum for up to 6 months

   • Thaw colostrum SLOWLY in bath of warm water (do NOT use a microwave)

2. Potassium sorbate (does NOT control M. bovis)

3. Colostrum preservatives (acid-base)

Unacceptable:

1. Pasteurisation (reduces bacterial contamination BUT mild decrease in IgG concentration depending on technique)

2. Yoghurtisation

Transition Milk Storage: CAN be mixed and stored in large containers

• Ideally refrigerated at 4˚C (not always possible on farm)

• Preserve with potassium sorbate = Bacterial growth inhibitor

Failure of Passive Transfer (FPTi)

• Definition

• 5 Causes

• 5 Risks

• Prevalence

• Diagnosis

Definition: Calf does not receive adequate Ab within first 12hr of life → Calf has little immunological protection from surrounding environmental pathogens

Causes:

1. Inadequate staffing to meet demands of calving period (picking up calves and teaching to drink is time-consuming and requires patience)

   • Esp. at end of calving period (and with calves that are NOT replacement)

2. Staff not educated on importance of colostrum and how to measure quality, feed effectively and within correct time frame

   • Esp. at beginning of calving period

3. Poor hygiene protocols → Bacterial contamination of colostrum

   • Esp. at end of calving period

4. Farmer does not measure quality of colostrum (individual variation AND influenced by dam vaccination)

5. Calf does not suckle from dams in the field

Risks:

1. Stage of calving

   • Peak of calving → Higher risk of FPTi (busier)

2. Older dams

   • Younger dams (heifers) have lower risk of FPTi in their calves

   • Older dams have pendulous udders making suckling very difficult (conformation issues) AND produce larger volumes of colostrum → Dilute IgG

3. Weak, sick, small calves

4. Region

   • Otago or Southland → Increased risk of FPTi

5. Left on mother for 24hr → Less likely to develop FPTi vs. those tube fed

   • #1 reason is poor quality of colostrum being fed to picked up calves (still pick up calves and tube feed BUT give higher quality colostrum)

Prevalence: 33% (19 - 40% worldwide)

Diagnosis: Evaluate serum TP as proxy for IgG concentration in calves

• Timing: Beginning and peak of calving time

• Calves: 12 healthy calves 24hr - 7d old

• Sample: Red top tube

• Results: TP > 52g/L → Successful transfer of immunity

  • Calculate % of sampled calves with FPTi

• Other Methods: Measure IgG in calf serum (RID or ELISA) OR measure GGT

List 12 history questions for a calf scours outbreak

1. Age of affected calves

2. Number of calves showing clinical signs

3. When did the outbreak start?

4. Any death?

5. Current treatment protocols

6. Current management protocols (sick pen)

7. Hygiene measures

8. Colostrum management protocol

9. Vaccination of dams for rota/corona/E. coli

10. Dedicated staff member for calf rearing?

11. Volume and frequency of feeding

12. Frequency of newborn calf pick up