Cattle 4 Flashcards
Diseases that occur 1-7 days of age the main one, what age, mortality and pathogenesis
Enterotoxigenic E. coli (<4 days)
- Calves < 4 days
○ High morbidity, low-high mortality (6-12 hours)
○ Pathogenesis
§ Not destroyed in abomasum
§ Colonise proximal part of small intestines
§ Receptor specific (F antigen) -> resistance at 48 hours - THEREFORE ONLY ABLE TO CAUSE ISSUE IN REALLY YOUNG ANIMALS
§ Produce toxins -> hypersecretion and malabsorption -> FAST DEHYDRATION
Enterotoxigenic E. coli at what age, transmission and clinical presentation
< 4 days old
○ Recirculation of disease
§ Infected between 12 hours and 4 days of age
§ Infected animals -> environmental contamination -> faecal-oral
□ Cleaning between batches of calves is very important
§ 6 months in soil, 3 + months in water
- Clinical presentation
○ Yellow-white, piperstream diarrhoea, malodourous
○ Defecation is involuntary - VERY SICK
○ Hypothermic, weak, anorexic, dehydration, death, within a few hours or found dead
Navel ill at what age generally occur, what is it, common in, causes and leads to and treatment
7-14 days of age
- Infection of the umbilical cord
○ Common in housed/intensively reared calves
○ Housing, faeca management, asepsis for umbilicus (iodine)
- Non-specific pathogens
○ Strep, E.coli, staph, pyogenes
- Umbilical infection -> abscess -> septicaemia
○ Local infection: omphalitis, omphalophlebitis
○ Septicaemia: urachitis, polyarthritis, meningitis
- Treatment
○ Lance the abscess
○ Antibiotics if severely sick and think systemic infection
Rotavirus at what age, how common, mortality and pathogenesis
(<7-10d)
- Most commonly diagnosed at this age
○ Often with others (crypto, E.coli, salmo)
○ Moderate to high morbidity, moderate mortality
- Pathogenesis
○ Enterocyte cell receptor SI -> internalised -> enterocyte loss -> villous atrophy
○ Normal secretion, decrease absorption = maldigestion, malabsorption
○ Self-limiting disease, cell regenerate
§ Need stress and poor hygiene to cause disease -> just pathogen alone will not result
Rotavirus at what age, transmission/reciruclatin and clinical presentation (two main types)
<7-10
- Recirculation of disease
○ Infected cows/calves excrete
○ Up to 50% calves are subclinical/carriers - source of new infection
○ Water > 2 weeks, up to 9months in faeces/effluent
- Clinical presentation
○ Mild case - rotavirus and cryptosporidium
§ Bright and alert, pasty yellow diarrhoea
○ Severe case - rotavirus and cryptosporidium
§ Dehydrated with systemic signs (unable to stand, sunken eyes, purulent nasal discharge)
Coronavirus at what age, how common, mortality and pathogenesis
(5-20d)
- Less common than rotavirus
○ Increasing prevalence
○ Low-moderate morbifity, low mortality
§ 15-20% lower than rotavirus
○ Often occurs with others (crypto, rotavirus)
- Pathogenesis
○ SI and LI enterocytes -> villous atrophy -> maldigestion, malabsorption +/- colitis (haemorrhage or mucoid)
Epithelial of nasal turbinates -> mild intestinal pneumonia
Coronavirus age, recirulation of disease and clinical presentation
5-20 days
- Recirculation of disease
○ Faecal-oral or respiratory route of infection
○ Sensitive to disinfection
- Clinical presentation
○ Faeces profuse, watery -> mucus, undigested milk curd +/- blood
○ Strain to defecate if colitis
Salmonella age, mortality, species common and pathogenesis
(7-10d)
- Overview
○ Moderate-high morbidity, low-high mortality
○ Salmonella typhimurium most common
○ Salmonella dublin - septicaemia in calves
§ Long terms carriers
- Pathogenesis (high infective dose requirement)
○ Reversible, attachment -> irreversible, receptor mediated binding (-> bacteriaemia -> lungs, meninges, joints)
○ Cell destruction -> haemorrhagic enteritis
○ Malabsorption, maldigestion, protein loss, fluid loss +/- bacteriaemia
Salmonella age, recirculation of disease and clinical presentation
7-10d
- Recirculation of disease
○ Infection <24 hours, incubation 24-48 hours, disease 7-10days old
○ Asymptomatic carriers (stress causes shedding)
○ Several years in environment
- Clinical presentation
○ >10 days old - VERY SICK
○ Acute septicaemia/enteritis -> chronic enteritis
○ Pyrexia (initially), anorexia, depressed, recumbent
○ Dysentery: smell necrotic, fresh blood, pieces of mucosa
Sequelae: poor growth, polyathritis, necrosis of ears/tail/digits
Cryptospordium age, mortality, species, lifecycle, pathogenesis, resistance and presentation
(4 day to 4 weeks)
- High morbidity, low mortality
- C. parvum (SI) and C. muris (Abomasum)
- Direct lifecycle - faecal oral route, PPP of 6 months
- Pathogenesis
○ Infection of enterocytes -> cell destruction -> mild villous atrophy -> malabsorption
§ Low mortality, high morbidity
- Age related resistance
○ Incidence of disease peaks 2-3 weeks post calving
- Clinical presentation
○ Diarrhoea: yellow, watery (like rotavirus), pasty, grey, mucoid/slimy
○ SIMILAR TO ROTAVIRUS
Coccidosis what age and results
- Typically a disease in older calves
○ Can affect calves as young as 3 weeks old - Corrugations of the colon -> diarrhoea
Respiratory disease in neonates at what age generally and the 3 types
generally older than 1 month of age
1) aspiration pneumonia
2) enzootic pneumonia (2-5 months)
3) mycoplasma (uncommon)
Aspiration pneumonia what age, result from and lead to
generally older than 1 month of age
- Incorrect stomach tubing
- Congenital defect - cleft palate
- Abnormal suckling
- respiratory disease
Enzootic pneumonia what age, pathogens, risk factors, lead to and clinical presentation (2 forms)
(2-5 months)
- Pathogens: ubiquitous, normal flora
○ Shipping fever complex
○ Stress, compounding effects of ‘normal’ flora
○ Moderate morbidity, low mortality
- Risk factors
○ Housed indoors, crowded, poor ventilation
- Bronchopneumonia
○ 1st viral pneumonia: P13, BoHV-1, BRSV
○ 2nd bacterial pneumonia: Mannheimia, Pasteurella, Fusobacterium
- Clinical presentation
○ Chronic form: bright, eating, slight mucoid nasal or mucopurulent oculonasal discharge, dry, hacking cough
○ Enzootic: harsh, dry cough, febrile, dull, inappetant, dyspnoea, tachypnoea +/- wheezing, crackling lung sounds
§ Treatment with NSAIDS but also environment - NURITION, HYGIENE, HOUSING
Mycoplasma in calves how common, risk factors, treatment and clinical presentation
- Mycoplasma spp ○ More common in dairy goats ○ Rare outbreaks in calves - Risk factors ○ Non-pasteurised bulk milk and colostrum ○ Direct contact, formites - Treatment ○ Antibiotics: tetracyclines, tylosin ○ NSAIDS: ketoprofen - Clinical presentation ○ Lameness (polyarthritis), mild conjunctivitis ○ Multifocal lobular pneumonia (+/- respiratory distress)
With all calf diseases what are the 2 main steps
- Treat what is in front of you -> antibiotics, NSAIDS, fluids
- Ensure doesn’t happen again -> talk to the farmer about preventative measures
○ Stocking rate, husbandry, hygiene, cleaning between batches, colostrum management
NUTIRITON, HYGIENE, HOUSING
Clinical examination of calves what needs to be done and normal parameters
generally not 5 station just targeted exam
- Standing within 1 hr (hypoxia/trauma)
- Suckle reflex present at birth, no menace (d-weeks)
- HR: 80-100bpm; RR: 24-26bpm, Temp: 38.5-39.5 degrees
- GIT exam: no rumen sounds, palpation > percussion
- Rectal exam:
○ Digital exam - faecal sample - feel rectal mucosa (coccidiosis)
- Umbilicus:
○ Moist - 2 days, falls off 10-14 d
Treatment/diagnostic and management plan for neonatal disease what are the main things involved
- What do I do right now?
○ Diagnosis, fluid therapy, antibiotics, heat - What needs to happen in the next few weeks?
○ Disinfection, quarantine, follow-up treatments - How do we prevent it from happening again
○ Management review
§ Minimise exposure
§ Maximise immunity
Diagnostic aids for neonatal disease and which diseases useful for
- Thorough history - age, # affected, progression - mortality and morbidity
- Clinical exam - straining, faeces, dehydration
- Faecal samples (3-4 affected calves)
○ Faecal floats - crypto, coccidia
○ Faecal culture - E.coli, salmonella
○ ELISA - rotavirus, coronavirus - INTERPRETATION - Post mortem (>1 representative animal)
○ Histopathology - crypto, coccidia, salmonella, rotavirus, coronavirus - Other
○ Respiratory: nasal swab, trans
What are the 3 main types of diarrhoea, main pathogen and results
- Exudative diarrhoea (salmonella)
○ Acute/chronic inflammation -> necrosis - Malabsorption (rotavirus)
○ Increase osmotic pressure -> fluid into lumen
○ Often destroy villous absorptive cells - Hypersecretion (E.coli)
○ Increase cellular secretion without cell damage
○ Na, C, and water into the lumen, can’t absorb
What needs to be done in the treatment of diarrhoea in calves
- Correct dehydration
- Correct the acidosis
- Correct the electrolyte loss
- Provide an energy source
- Maintain cardiovascular function
- Treat the causative agent
DONE VIA fluid therapy, nutrition and medications
Fluid therapy for sick calves what are the steps
1) how much
2) how to give
- oral or parenteral
3) which product
- isotonic with added sodium bicarbonate
- hypertonic saline followed by oral sodium biocarb
- hypertonic saline containing sodium bicarb followed by oral isotonic electrolytes
4) checking progress
In terms of fluid therapy for scouring calf how much needed and how to determine
(50kg calf) - Scouring, dehydrated calves require from 8.5 to 11 litres of fluid DAILY
§ Normal daily requirement = 3-4 L (maintenance: 60-80ml/kg/d)
§ Make up for ongoing losses = 1-3L (approx. 20-60ml/kg/d)
Make up for dehydration (and acidosis) - table in cue cards
giving oral fluids for scouring calves when give, when not give, how much at what frequency, how does milk come into this
(<8% dehydrated)
§ Suckle reflex weak to good – IF NOT GIVE IV FLUIDS
§ Give 1.5 to 2L at a time, 3-4 times a day
□ Often feed milk morning and night and then supplement this during the day
□ Ad lib access to water
§ Leave 4 to 6 hours after a milk feed
□ Feed milk at night
§ Do we need to withhold milk?
□ Rest the gut approach
□ Continue to give milk with ‘lytes as additional feed
§ MAINTAIN FLUID-MILK RATION PLUR ORAL LYTES WHERE POSSIBLE
§ IF DEPRESSED/REFUSE TO SUCKLE - WITHHOLD FOR <24 HOURS (2 FEEDs) AND SUBSTITUTE WITH HYPERTONIE ORAL ELECTROLYTE SOLUTION
Giving parenteral fluids to scouring calves when give, why give, ways to give, examples and how to give
§ If calf is unable to rise, no suckle reflex, inappetant § Isotonic vs hypertonic + oral fluid □ Hypertonic - no if severely dehydrated § IV, SC, IP □ IV most rapid followed by SC then IP □ PREFERRED when on farm is IV § Examples □ Lactated ringers solution □ Acetated ringer solution □ Isotonic sodium bicarbonate □ Hypertonic saline □ Hypertonic saline bicarbonate § How give □ Warm the fluids, gravity fed IV fluids, best to contain in small area, provide bedding, warmth and shelter □ Can hog tie the calves - tie their legs together so cannot move while occurring and pull it out □ Jugular or Auricular vein catheterisation - can glue or suture it in
In terms of choosing a production for fluid therapy in scouring calves what are the goals, how achieve and max rate over what time period
○ Goal § Correct dehydration - FLUID VOLUME § Correct the acidosis - BICARBONATE § Correct the electrolyte loss - Na, K, Cl, AA's § Provide an energy source GLUCOSE § Maintain cardiovascular function § Treat the causative agent ○ Max rate: 80ml/kg/hr (30-50ml/kg/hr more common) - give over 4 hours
What are the 3 main options for products used for scouring calves, how give and main effects
1) Isotonic IVF with added sodium bicarbonate
□ Large volume, slow delivery
□ Approx. 10% calf BW over few hours (eg 4L for 40kg calf)
□ Homemade recipes available
2) Hypertonic saline IV immediate followed by oral sodium bicarbonate
□ 4-5ml/kg given over 4 mins
□ Rapid volume resuscitating, alkalising effects slowly
3) Hypertonic saline containing sodium bicarb IV immediate followed by oral isotonic electrolytes
□ 8.4% solution, 1mEq.ml bicarb
□ Rapid volume resuscitation and correction of acidosis
□ More expensive
Checking progress of fluid therapy for calves, what looking for and what if not responding
- If calf can suckle after initial resuscitation then switch to per-oral
- Urination in 30-60mins
- Improvements
○ Mental status
○ Hydration status
○ Restoration of suckle reflex
§ If not: check for septicaemia/omphalitis/pneumonia
○ Stand within a few hours of IVFT - Can repeat the IV fluid therapy but if not responding to the second something else really wrong
Treating the causative agent in treatment of scours in calves what is the main thing used and other treatments (details of these)
1) antibiotics
2) anti-inflammatories
§ Corticosteroids - limited use in diarrhoea and calves - already secreting glucocorticoids - ALREADY STRESSED
§ NSAIDS - eg. Meloxicam, flunixin - some benefit - dehydrated so be careful -> if possible give fluids first
3) halocur (crytosporidium parvum) - oral drench for calves age 1-21days - good for outbreak situations
4) baycox (coccidosis)
§ Oral treatment and prevention of coccidiosis - prevention is best
§ Up to 9 months of age
Antibiotics for calf scouring indications and selection
○ Indications
§ Diarrhoea PLUS systemic signs including decrease suckle
§ Blood/mucus in faeces (bacteraemia)
§ Documented FPT
§ Bacterial disease
§ Viral disease- NOTHING IN AUSTRALIA AT THE MOMENT - supportive treatment only
§ Diarrhoea syndrome - E.coli overgrowth, 30% bacteraemic
○ Antimicrobial selection
§ Target E.coli in SI, bacteraemia
§ Gram negative activity
§ Septicaemia: bactericidal
In terms of antibiotic options for calf scours list examples of bacteriocidal and bacteriostatic
○ Bacteriocidal compounds (esp. septicaemia - NEEDS TO KILL QUICKLY)
§ Third generation cephloporins (ceftiofur)
§ Aminoglycosides (neomycin)
§ Broad spectrum penicillin (amoxcillin, ampicillin)
§ Potentiated sulphonamides (TMPS)
○ Bacteriostatic compounds - slows the growth
§ Sulphonamides
§ Tetracyclines
Vaccines for prevention of calf scours what are the 3 main ones, what used for, what vaccinate and when
1) E.coli (Bovilis E)
§ Vaccinate dams late in gestation
§ Transfer of anti-K99 (F5 antigen) -> block binding
2) S. Dublin and S. Typhimurium (Bovilis S)
§ Dams vaccinated 8 and 3 weeks pre-calving
§ Conflicting reports
§ Partial protection, but incomplete
3) Rotavirus/coronavirus (rotavec corona)
§ Vax neonates; modified, live, oral formulation at birth
§ Vax dams: modified live/inactivated - SC infection
§ Conflicting reports - efficacy unknown
Prognosis for milk, severe and septicaemia scours and what needs to be done in all cases that resolve
- Mild to moderate disease ○ Oral fluids, AB's - good prognosis - Severe disease ○ Aggressive IV fluids, good nursing - can survive - Septicaemia ○ Poorer prognosis ○ Risk of polyarthritis if they survive - All cases that resolve ○ Reduced GR due to intestinal malabsorption (temp/perm) ○ Need quality nutrition
What are the 7 steps in the management of calf scouring outbreak
- Triage
- Categorise/group by severity
- Practical treatment/management plan
○ Resuscitation, fluids -> need to development plan with farmer - give prognosis - Reduce further contamination
- Reduce exposure
- Decontaminate areas
- CLIENT COMMUNICATION at the end of the visit
In terms of client communication for calf scours outbreak what is important
- Summarise in 3 points
- Write instructions down (clinic handouts)
- Empathise (it is more work)
- Explain why/importance
- Follow up phone call
CASE - - Scouring calves 1-3 weeks of age - Morbidity 80-100% in some batches - Mortality 20% - Mucoid/bloody scour through to coloured water - Temperature subnormal or normal - Collapsed calves approx. 10+% dehydrated What is the likely causes
- Viral - rotavirus or coronavirus
- Protozoal - cryptosporidium
Several calves: moderate skin tenting, recumbent, moderately depressed…
What is their likely dehydration status?
What is the best resuscitative fluid therapy to supply (assume 40 kg LWT)
- ~9% dehydrated
- 3.6 L bicarb & Hartmann’s IV - 0.09 x 40 = 3.6
Diagnostic appraoch to urinary tract disease 6 main things can do
- Get a good history
- Look at the environment
- Observe the animal at rest
- Observe urination (aka micrturition)
- General clinical examination
○ Including urinary tract
§ External - vulva, escutcheon
□ Crystals, bleeding, puss
§ Internal - kidney, ureters, bladder contents and wall - Blood samples - not so often
○ Blood urea nitrogen (in plasma)
§ Indicates renal perfusion or renal insufficiency
§ Limited application due to time and cost
What are the 3 main ways urinary disease manifests and things within
1) Abnormal urination ○ Stranguria (straining, painful) ○ Pollakiuria (frequent) ○ Polyuria (excessive volume) ○ Oliguria (reduced volumes) ○ Anuria (absent) 2) Abnormal appearance/contents of urine ○ Colour: from colourless to chardonnay § Normally clear ○ Clarity: clear and transparent § Normally DON'T have floaties ○ Smell: like cow's urine ○ pH: 7-9 ○ Protein/ketones/blood: nil or trace ○ Specific gravity - 1.020 - 1.050 3) Non-specific "sick cow"
Dysuria what are the 4 main causes
- Cystitis
- Pyelonephritis
- Obstructive urolithiasis
- Vaginitis
Cystitis what main clinical sign, pathogen, other signs, how occurs, what more common in and treatment
Dysuria
- E.coli
- Frequent urination +/- pain or discomfort
- Either ascending or descending infection
- Most common in females - short broad urethra - easier to ascending infection
- Penicillin - to prevent secondary infection of Corynebacterium renale (loves the urine)
Pyelonephritis pathogen, how occurs, clinical signs, diagnosis, treatment and prognosis
- Corynebacterium renale et al
- Ascending infection (hygiene, venereal)
- Haematuria, pyuria, painful microturition
- Painful kidney, colic
- culture
- Prolonged treatment required - penicillin
- Prognosis guarded
Urolithiasis main causes, what result in, what most common i and treatment
Dysuria
- Obstruction to flow
- Most common in males (esp steers)
- Struvites, silicates, Ca carbonate, oxalates
- Increase concentrate feeding, increase silicate pastures
- Decrease water intake -> in cold areas where water freezes over
- Urethrostomy or salvage slaughter
○ Salvage procedure, backwards urine - no longer breeding animal
Vaginitis main clinical sign, cause, treatment
- Usually secondary to calving trauma
- Often resolves without intervention
- Bruising, laceration - if torn stitch them
- Treatment with penicillin IM
- Also IBR (bovine herpes 1)
Abnormal contents or appearance of urine what are the 3 main looks
- Red urine (redwater) ○ Haematuria - red with clots ○ Haemoglobinuria - red without clots - may need to spin ○ Myoglobinuria - Proteinuria - Pyuria
Red urine what are 6 main causes
1) bracken fern poisoning
2) post-parturient haemoglobinuria
3) bacillary haemoglobinuria
4) leptospirosis
5) rape/kale poisoning
6) copper poisoning
Bacillary haemoglobinuria what pathogen, how common, results in
- Cl. Haemolytic (Cl. Novyi Type D)
- Uncommon
- Toxaemia, dark red/brown urine
- Rapid death
Leptospirosis 2 main serovars, how transmitted, age, importance and control
- Leptospira serovar pomona
- Leptospira serovar hardjobovis
- Enters mucous membranes or damaged skin, localises in kidneys, spread in urine
- Affects both calves and adults
- Zoonosis (esp… hardjobovis)
- Best control is vaccination
Leptospirosis pomona maintenance host, what occurs in calves and adults and differentials
- Maintenance host is pig
- Cattle are accidental hosts
○ More acute, severe, higher titre - Calves
○ Environmental exposure - wet, alkaline
○ Acute fever, petechiae, depression, haemolytic anaemia and haemoglobinuria
○ High case fatality, after 2-3 days
○ Treatment - streptomycin - Adults
○ Haemoglobinuria uncommon
○ Usually seen as sudden drop in milk production
○ May cause septicaemia and late abortions - Differential
○ Can look like cold water toxicosis -> if cows drink cold water can get red looking urine
Leptospirosis hardjobovis what is the main host, what occurs in adults and main issue
- Host adapted to cattle, so cattle have less obvious clinical signs, more chronic, carriers, lower titre
- Adults
○ Affects pregnant or lactating cows
○ Mild drop (yellow/orange udder secretion)
○ Abortion may follow - ZOONOSIS
○ Most significant consequence is zoonotic disease -> ongoing BAD flu like symptoms
○ No human vaccine
○ SO VACCINATE THE COWS
Copper poisoning how acute and chronic occur with signs for each
- Acute poisoning occurs by accidental exposure to Cu salts
- Chronic poisoning may occur on copper rich soils or in areas exposed to industrial contamination
- Acute
○ Gastrointestinal signs (diarrhoea, abdominal pain)
○ Fluid accumulation
○ Eventual intravascular haemolysis - Chronic
○ Only haemolytic and icteric signs
Proteinuria what are the 2 main causes and causes within
- Toxic nephrosis - caused by acorns
- Infection
○ Chronic infection may lead to glomerulonephritis +/- amyloidosis
○ Haematuria, haemoglobinuria, myoglobinuria and very alkaline urine will show as +ve proteinuria on dipstick
Pyuria what is it, treatment
- Pus in the urine is indicative of inflammation in the urinary tract
Treatment - Antibiotics should be chosen on the basics of culture if possible
- Prolonged therapy may be required - higher up biliary system the more prolonged the therapy
- Ancillary treatment have a role
define down cow, downer cow and downer cow syndrome
- “Down cow” = A recumbent cow
- “Downer cow” = A cow down in sternal recumbency for 12-24+ hrs without obvious signs of specific cause
- “Downer cow syndrome” = The pathology that is secondary to prolonged recumbency
What position is normal for cow to be in and what not normal and why
Sternal recumbency
- Most fore-weight borne by sternum
- Most hind-weight borne by underlying hind limb
○ normally reposition themselves alternating hind limb
Lateral recumbency
- Regurgitation and subsequent Aspiration
○ a serious potential complication
- Risk of positional bloat -> if fluid over oesophageal opening will not eructate and remove the gas
What are the 4 main causes of down cows and causes within
- Musculoskeletal/ Neurological ○ Fractures ○ Dislocations ○ 1° Neuropathies ○ 2° Myopathy/Neuropathy - Toxaemia ○ Acute, severe mastitis ○ Enteritis (eg Salmonellosis) ○ Grain overload ○ Peritonitis ○ Metritis ○ Abdominal catastrophes - Metabolic ○ Milk fever (hypoCa) ○ Grass tetany (hypoMg) ○ Both (hypoCa + hypoMg) ○ Pregnancy toxaemia ○ Fatty liver syndrome - Miscellaneous ○ Parturition ○ Exhaustion ○ Emaciation ○ Haemorrhage ○ Hypothermia ○ Severe systemic disease
What is history is important to obtain for a down cow case
- Age & Breed? ○ Middle-age, heifer, older cow ○ Jerseys - more predisposed to metabolic disease - Onset & duration of recumbency? ○ Depends on how frequent observation - Diet (current and previous)? - Parturition (If? When? How?) - Expectations (Intended use)? - Treatments already given? (What? How? How much? When?)
Clinical examination of a down cow what are the 4 main steps
- Observation of posture, responses
- Physical examination (don’t take shortcuts!)
○ Full clinical examination -> - Characterise as: Musculoskeletal/Neuro, Systemic or Metabolic
- If Musculoskeletal/Neuro: Thorough targeted MS/N exam
○ Downer cow unwilling or unable to stand due to primary musculoskeletal disease or injury
○ May be secondary to prolonged recumbency from primary disease (eg acute mastitis) which is more apparent than 2° injury from prolonged recumbency or attempting to stand
In characterising a down cow how to differentiate between musculoskeletal/neuro, systemic or metabolic cause
Presentation ○ Musculoskeletal/Neuro § Typically bright & alert § In sternal recumbency § Able to ‘creep’ ○ Acute Systemic/Toxic § Sunken eyes & depressed § Sternal, or Lateral if more severe § Observation of mastitis, metritis, peritonitis ○ Metabolic § Depressed or Hyper-responsive/Aggressive § Cardiac signs - HR, strength, rhythm on BOTH sides
During the examination of a down cow what also need to be doing
- Assessment and prompt treatment
- Improves chances of getting her up
- Need 2+ people to restrain, turn & roll
○ Use cow head to lever - Consider the DDx list as you are examining
- Consider taking pre-treatment samples
○ Lithium heparin blood for Ca, Mg, P, CK (not EDTA!)
○ Useful retrospectively if poor response - PROP UP COWS THAT ARE IN LATERAL RECUMBENCY (move neck closer, move back legs under and prop against something to prevent from going back down)
Posture for down cows what are 4 main ones and most common causes of those positions
- Frog legged
○ Femoral n. injury; Pregnancy toxaemia - Splay legged
○ Pelvic #; Hip dislocn; Muscle rupture; Obturator n. - Sternal recumbency
○ Musculoskeletal; Mild MF; Mild toxaemia - Lateral recumbency
○ Severe Milk Fever; Severe systemic/toxic disease
In terms of differential diagnosis for why a downer cow is down what is the first steps
Mental status
- normal
- abnormal
- > dull and depressed
- > hyperactive - grass tetany
Normal mental status on a down cow what is the next things to look at and things within
§ Structural damage
□ skeletal issues - broken legs or dislocated hips
□ No skeletal deformity - neurological defects
® Forelimb -> radial paralysis
® Hindlimb -> obturator, sciatic, femoral
§ No structural damage
□ Positive on ketone urea - pregnancy toxaemia
□ Negative ketonuria -
Abnormal mental status dull and depressed downer cow what looking at after this to determin cause
□ HR fast ® Mucous membrane brown - nitrate/nitrite poisoning ® Mucous membrane normal ◊ HR weak and hydrated - milk fever ◊ HR strong and dehydrated - toxic ® Mucous membrane pale - anaemic
If a cow has been in prolonged recumbency what can this indicate and possible causes
- Prolonged recumbency can indicate: ○ Inadequate treatment ○ Misdiagnosis ○ Relapse ○ Concurrent disease or injury - incomplete diagnosis - Prolonged recumbency is due to: ○ Advanced toxaemia/shock ○ Severe back/vertebral/upper limb pain ○ Spinal cord injury ○ Myopathy (usually secondary
Lifting cows for examination what are the main things used and the aim
1) Tail lift -> lifting and stabilising as she gets up
Tend to go forward when lift them
2) bagshaw hip clamps - Need to put on tight enough otherwise will fall out of
Want to put high enough so support when she stands
3) slings
4) cow jack
5) pelvic lifter - combination of hip clamps and contraction underneath so lift up
6) moo mobile
- The point is to bring her up and then let her take her OWN weight
IF when you lift her up she buckles on her knees and refuses to get up what is needed and why is this occurring
Need a chest strap
- Either doesn’t want to or have nerve damage
- Put strap underneath her chest and wrap around onto prongs on the tractor and lift up again with the hip clamps on as well
- This time front is brought up whether she likes it or not and then can see whether she will stand - if so no nerve damage
What are the 3 main parts of the musculoskeletal exam
1) back examination (while in sternal)
2) lumbosacral ligament examination
3) limb examination (roll into lateral)
Back examination in musculoskeletal examination what is involved
○ Obvious swellings along back
○ Palpate for pain between transverse processes
§ Blunt probe, scissor handles, vacutainer tube
○ Palpate spinous & transverse processes
§ Misalignment (relate to adjacent segment)
§ Push down on dorsal process (if unstable… BAD)
§ Abnormal sound/movement when rolled
§ Fractured thoracic – sacral vertebrae with paralysis
□ leads to ‘dog-sitting’ when trying to stand
□ Curvature of the spine
□ Differences in the position of vertebra to each other or movement of vertebrae
Lumbosacral ligament examination how common, what is done and what must not be done if diagnosed
○ Not common
§ First:
□ Hands on tuber coxae and apply forward and downward pressure. Assess for movement
§ Then:
□ Tuber coxae and rectal touching disc btw L6 & S1
§ Must not be lifted by pelvis if diagnosed -> just put extra strain on the ligament
Limb examination as part of the musculoskeletal exam what is invovled
(roll into lateral) ○ Check for dislocated hip, leg or pelvic fractures, ruptured muscles/tendons ○ Nerve function ○ Manipulate each limb ○ Assessing Nerve & Motor function
As part of the limb examination how to test the nerve function
§ Obturator (L5-L6)
□ Passes through pelvis then through obturator foramen
□ -> medial thigh muscles… adducts hind limb
§ Femoral n (L4 - L6)
□ Innervates quadriceps to draw hind limb forward
§ Sciatic . (L6 - S2)
□ Passes through pelvic canal initially, then around head of femur, then divides into peroneal and tibial
® Vulnerable to get the sciatic nerve
□ Peroneal -> anterior and lateral aspects of foot
□ Tibial -> caudal and medial
Manipulation of each limb during musculoskeletal exam what need to do
§ Get in lateral recumbency -> on each side
□ She needs to feel comfortable -> NOT ON CONCRETE
§ Ability to extend and flex to full extent
§ Abduct in normal range
§ Crepitus or laxity in hip/stifle -> hand on greater trochanter and moving forward and back and around for crepitus
§ To ensure no hip dislocation
□ Ensure the 3 points (greater trochanter, tuber coxa, tuber sacrale) of the hip are in a triangle with ratio of 1:2
□ As move leg backwards greater trochanter will move forwards and bring forward will go backwards
□ With leg slightly forwards and flexed push caudal to greater trochanter and leg will go into extension
§ Cruciate rupture (pain on stifle flexion)
§ Palpate full leg for heat/swelling
Assessing nerve and motor function as part of the limb examination during the musculoskeletal exam
§ Sensory nerve function (18g needle - stab with this)
□ Coronary rim of hoof (skin above coronary band)
□ Response? (none; muscle twitch; react; withdraw)
§ Deep pain (hoof testers)
□ Squeeze interdigital (normal strong kick response)
§ Patellar reflex (hoof testers in lateral)
□ Leg flexed (poor; normal; exaggerated)
□ Exaggerated reflex is a poor prognostic sign
§ Motor function
□ Stimulate cow to stand (making an effort?)
□ Use mechanical lift and assess her input
Diagnosis of limb and spinal fractures and when consider euthanasia
- Limb fractures & dislocations
○ Relatively easy – crepitus, instability, asymmetry
○ Fractures of femoral neck or shaft
○ Dislocation of hip or hock - frog leg stance - Spinal fractures
○ standing soon after injury, but deteriorate
○ Consider euthanasia if:
§ Patellar reflex exaggerated (uncommon?)
§ Vertebral rotation
Diagnosis of obturator and sciatic nerve injury
- Obturator n. injury
○ Lateral abduction of hip (uni or bi) - frog leg stance
○ Usually associated with dystocia.
○ Assess hip! - Sciatic n. Injury
○ Common with dystocia
§ Generally improvement after 2-3 weeks after caving and past this won’t get much improvement
○ Mild ataxia to recumbency with complete paralysis
○ Uni or bilateral – tend to sit on the worst leg
○ Sensory nerve deficit in downer cows
§ Knuckling of the fetlock, sliding forward with her hindlimb
Diagnosis of femoral nerve and radial nerve paralysis/injury
- Femoral n. Injury
○ Trauma to lumbar region
§ eg bulling
○ Depressed patellar reflex? Normal pain response
○ Mild stumbling when lifted
§ Legs move forward as trying to stand
○ Severe - frog legged - Radial n. paralysis
○ No sensation of anterior coronet
○ Flexion of fetlock joint (when lifted)
§ Assessing muscle tone -> as move legs around is there passive movement - if no tone - flaccid
§ Extensive test -> can feel the pain but cannot extend the leg
§ Negative extensive and negative tone - POOR PROGNOSIS
How to determine the prognosis of musculoskeletal/neural injuries
- Accurate prognosis is difficult but important
○ History and clinical presentation
○ Accurate diagnosis of cause and severity
○ Effectiveness of treatment
○ Access to nursing care, weather, cow attitude
Calving paralysis prognosis when good, guarded and poor
○ Good:
§ Deep pain; Full Tibial sensation; Full/Part Peroneal
○ Guarded:
§ Deep pain; Tibial/Peroneal sensation reduced/absent
○ Poor:
§ No Deep pain; Absent Tibial and Peroneal sens.
○ Patella reflex sluggish in moderate to severe
○ Euthanasia if in both legs?
femoral nerve injury prognosis when good, very poor and what to do in certain situations
○ Key features are patellar reflex & sitting posture
○ Depressed patellar reflex. If PR exaggerated -> spinal
○ Fractures of vertebral facets -> hopeless
○ Good: able to sit normally but legs out when standing
○ Very poor: legs always in frog leg
○ Cows will crawl initially but this increases damage
§ Confine these cases to minimise secondary injury - but don’t restrict
Prognosis for obturator and lumbosacral injury
- Obturator n. injury
○ Prognosis always guarded due to 2° hip dislocation
○ Can put on Hobbles to prevent the legs from getting too far apart as this is where the issues is
§ Cannot bring legs back together - Lumbosacral injury
○ Good to Guarded – do not lift!
Prognosis for non-responsive milk fever and radial nerve injury
- Non-responsive milk fever
○ Prognosis dependent on duration & muscle damage
○ Physiotherapy (electrostimulation?) - passive movement of the legs - Radial n. injury
○ Improve with time… Treatment & nursing
What are some poor prognostic signs with down cows - EXAM
- Recumbent for hours on hard surface - compartment syndrome
- Unable to maintain sternal recumbency
- Pronounced abduction of one or both hind legs - DOING THE SPLITS
○ Likely to dislocate hip, break legs or femoral head - Attempt to rise with front legs only
- No attempt to rise at all even when encouraged
- Extended hind legs so that sitting on stifles
- Rigid extension of hind legs (hind claws at elbows)
- Not eating or drinking
- inability or reluctance to correctly nurse the cow
What are the 4 main things involved with treatment for down cow
- Need to quickly address initial cause
- NSAIDs: First 24 hours (for up to 3 days?)
- Treat the underlying condition
- Nursing:
Nursing for downer cow what is involved
○ Clean, dry bedding (eg 300 – 400 mm deep hay) - COMFORTABLE BEDDING
§ Don’t want pressure points leading to pressure sores
○ Access to feed (good quality hay) & water
○ Turn cow 6 – 10x daily and strip milk (place calf in there to suckle) - worried about mastitis
§ Often lay on damaged leg so need to rotate
○ Effective lifting 1 – 2x daily
§ with some weight bearing
○ Confine if femoral n. injury
○ How long to persist?
§ Depends on cow response, not just time
how to move and roll and cow
Moving a down cow
- Place into the tractor (bucket) with head halter
○ Don’t hip with hip clamps and expect to walk to the area
- Move into a nursing area from the paddock
Rolling a down cow
- If cow cannot roll itself then need to roll 3-6 times a day
○ Hamstring damage
- Tuck the hindlimbs in and push the cow from the side (down low over the pelvis) and then pull the hindlimbs out on the their side
- Can also use the tail and move it the way want to roll
Lifting down a cow how done and when no worth it
- Hip clamps
○ Place on pelvis - put on firmly and pick up via the tractor - If standing effectively then leave for a few minutes and check back frequently so ensure cow hasn’t sat back down and then suspended full weight on the hip clamps which is bad as described below
○ The frequency of lifting is dependent on how long the cow remains standing each time - If not taking any weight then NOT WORTH LIFTING as will put pressure on the pelvis - will become sore and won’t want to get up
○ Leave for a few days and hopefully stronger and will stand
Housing the down cow, caring for it and assessing it what is involved
Housing the down cow
- Large bedding under cover and restrict to the area of bedding - so cannot move off the hay
- 12 foot gate squared area of 30cm of soft bedding
- 30 times greater survival rate in a good nursing environment compared to paddock
Caring for the down cow
- Feed and water is vital
○ Good quality Lucerne hay
○ Water can be hard -> move likely to drink when they are lifted on the hip clamps
- Hygiene and good teat disinfectant is important when hand milking the cow - can also place with calf so it can milk
○ Also removal of faeces to help reduce chance of mastitis
Assessing the down cow
- Ensure no green muck coming out of their mouths if in lateral recumbency -> if so possible that aspiration pneumonia or bloat
When is the transition period and what used for
- The Transition period is 4 weeks before to 4 weeks after calving
○ This period is a major focus for farmers, vets and advisors - Can be used to prevent milk fever
○ Low calcium diet -> calcium being reabsorbed off bone before calving so when it needs to be done after calving can occur quickly and adaptive
When is the transition period important
Grey area after calving-> taking back stored fat - ALWAYS LOSE CONDITION AFTER THEY CALVE
- At the beginning of lactation not able to eat enough to get enough energy
○ NEED TO HAVE THE STORES to reduce the reduction in the body energy stores
○ WHERE THE TRANSITION PERIOD IS IMPORTANT -> provides the stores
- At some point in lactation able to store energy and eat enough energy
○ Positive energy balance -> occurs 1-3months after calve depending on the diet fed
What can bad transition period result in
- Hypocalcaemia and downer calves
- Hypo-magnesiuma
- Ketosis and fatty liver
- Udder oedema and mastitis
- Abomasal displacements
- RFM/metritis
- Time to first service and fertility
- Subsequent production levels
What are the 4 main aims of the transition period - EXAM
- Reduce ruminal disruption - lactic acidosis, ruminal acidosis
- Minimise macromineral deficiencies - calcium, magnesium and phosphorus - requirement increase dramatically when producing milk
- Minimise lipid mobilisation disorders - ketosis, fatty liver
- Avoid immune suppression - trace elements (zinc, iodine, vitamin E and vitamin D)
How to ensure the aims of the transition period is achieved and what are the components of the diet
To ensure these aims are meet
- Achievable targets for cow health problem -> standard target that should aim and if not then need to reassess transitional diets
Components of an integrated transition diet to consider are:
- energy and protein;
○ Too much energy and not enough protein -> stored as fat
§ Not if body is metabolising fat
- Macrominerals and DCAD;
- microminerals;
- rumen modifiers; and
- buffers and other possible additives
What are the 4 main metabolic conditions that lead to a downer cow
- Milk fever
- Grass tetany
- Pregnancy toxaemia
- Fatty liver
Calcium where found, what does the test detect, what level an issue
- Plasma Calcium:
○ Free Ca (45-50%) Hormonally regulated and available for use
§ More is available at lower blood pH
○ Bound to proteins (40-45%) “Already in use”
○ Bound to non-proteins (5-10%) “Already in use” - Blood tests measure total calcium!
○ (This means that blood Ca++ Should be read in conjunction with Total Protein) - Reference ranges vary
○ In general <2mmol/L is worrisome - High Ca++ unusual in cattle
Calcium regulation how controlled 4 main ways
- Arterial Ca++ levels sensed by parathyroid glands which secrete PTH
- PTH Stimulates intestinal absorption and renal reabsorption of Ca++
- Short and long term effects (cells produced in the villi have calcium absorption switched on so longer term effects are better - lifespan of 9 days - once those 9 days are up the PTH has been turned off - reduced calcium absorption in new cells -> cyclic effect and possible recurrence of milk fever at this point - Some effects mediated via converting Vitamin D to active form.
- Calcium resorption from bone is slower in older cows - Low blood Mg++ reduces PTH secretion and also tissue sensitivity to PTH
Parturient hypocalcaemia what is it, clinical signs and cause
metabolic disease with paresis & hypocalcaemia:
- Weakness
- Recumbency
- Depression of consciousness
- Can be fatal
- Common disease of dairy cattle (can occur in beef cows)
○ Called severe problem if > 3% of the herd, or cows <5yo affected
- Sudden increase in Ca requirement with onset of lactation
○ Colostrum 2.3g Ca/kg; Milk 12.g Ca/kg
○ Onset of lactation increases calcium requirement by 2-4 fold
- Subclinical hypocalcaemia is very common
DCAD what is it, equation and therefore way does it measure
- More properly DCAB (B=Balance)
- Diets are electrically neutral, with a balance of cations and anions
- Strong Ions are ones that are highly bioavailable and not metabolized
- DCAD theory DCAD = (Na + K) –(Cl + S)
○ Lower DCAD the lower the pH the buffer and more protected of metabolic disease - Less is more …
- “Anionic salts” added to the diet
- Very small changes in blood pH
- Measurable changes in urine pH
DCAD how measured, what is normal levels
measured via Urine pH
- Easy to measure
- Holstein cows should be between 6.2 and 6.8, Jerseys 5.8 -6.3.
○ There are various differing recommendations for this
What are the 6 main risk factors for milk fever - EXAM
- Parturition –most milk fever occurs around parturition. (also transport)
- Transport -> reduction in the feed -> drop in dietary calcium
- Age –Mostly > 5yo
- Milk Production
- Breed - Jerseys more susceptible
- Dry period nutrition –diet (blood pH) and body condition
