Cattle 4 Flashcards

1
Q

Diseases that occur 1-7 days of age the main one, what age, mortality and pathogenesis

A

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

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2
Q

Enterotoxigenic E. coli at what age, transmission and clinical presentation

A

< 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

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3
Q

Navel ill at what age generally occur, what is it, common in, causes and leads to and treatment

A

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

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4
Q

Rotavirus at what age, how common, mortality and pathogenesis

A

(<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

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5
Q

Rotavirus at what age, transmission/reciruclatin and clinical presentation (two main types)

A

<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)

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6
Q

Coronavirus at what age, how common, mortality and pathogenesis

A

(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

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7
Q

Coronavirus age, recirulation of disease and clinical presentation

A

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

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8
Q

Salmonella age, mortality, species common and pathogenesis

A

(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

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9
Q

Salmonella age, recirculation of disease and clinical presentation

A

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

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10
Q

Cryptospordium age, mortality, species, lifecycle, pathogenesis, resistance and presentation

A

(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

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11
Q

Coccidosis what age and results

A
  • Typically a disease in older calves
    ○ Can affect calves as young as 3 weeks old
  • Corrugations of the colon -> diarrhoea
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12
Q

Respiratory disease in neonates at what age generally and the 3 types

A

generally older than 1 month of age

1) aspiration pneumonia
2) enzootic pneumonia (2-5 months)
3) mycoplasma (uncommon)

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13
Q

Aspiration pneumonia what age, result from and lead to

A

generally older than 1 month of age

  • Incorrect stomach tubing
  • Congenital defect - cleft palate
  • Abnormal suckling
  • respiratory disease
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14
Q

Enzootic pneumonia what age, pathogens, risk factors, lead to and clinical presentation (2 forms)

A

(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

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15
Q

Mycoplasma in calves how common, risk factors, treatment and clinical presentation

A
- 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)
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16
Q

With all calf diseases what are the 2 main steps

A
  1. Treat what is in front of you -> antibiotics, NSAIDS, fluids
  2. Ensure doesn’t happen again -> talk to the farmer about preventative measures
    ○ Stocking rate, husbandry, hygiene, cleaning between batches, colostrum management
    NUTIRITON, HYGIENE, HOUSING
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17
Q

Clinical examination of calves what needs to be done and normal parameters

A

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

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18
Q

Treatment/diagnostic and management plan for neonatal disease what are the main things involved

A
  • 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
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19
Q

Diagnostic aids for neonatal disease and which diseases useful for

A
  • 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
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20
Q

What are the 3 main types of diarrhoea, main pathogen and results

A
  1. Exudative diarrhoea (salmonella)
    ○ Acute/chronic inflammation -> necrosis
  2. Malabsorption (rotavirus)
    ○ Increase osmotic pressure -> fluid into lumen
    ○ Often destroy villous absorptive cells
  3. Hypersecretion (E.coli)
    ○ Increase cellular secretion without cell damage
    ○ Na, C, and water into the lumen, can’t absorb
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21
Q

What needs to be done in the treatment of diarrhoea in calves

A
  • 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
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22
Q

Fluid therapy for sick calves what are the steps

A

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

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23
Q

In terms of fluid therapy for scouring calf how much needed and how to determine

A

(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

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24
Q

giving oral fluids for scouring calves when give, when not give, how much at what frequency, how does milk come into this

A

(<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

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25
Q

Giving parenteral fluids to scouring calves when give, why give, ways to give, examples and how to give

A
§ 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
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26
Q

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

A
○ 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
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27
Q

What are the 3 main options for products used for scouring calves, how give and main effects

A

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

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28
Q

Checking progress of fluid therapy for calves, what looking for and what if not responding

A
  • 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
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29
Q

Treating the causative agent in treatment of scours in calves what is the main thing used and other treatments (details of these)

A

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

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30
Q

Antibiotics for calf scouring indications and selection

A

○ 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

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31
Q

In terms of antibiotic options for calf scours list examples of bacteriocidal and bacteriostatic

A

○ 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

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32
Q

Vaccines for prevention of calf scours what are the 3 main ones, what used for, what vaccinate and when

A

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

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33
Q

Prognosis for milk, severe and septicaemia scours and what needs to be done in all cases that resolve

A
- 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
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34
Q

What are the 7 steps in the management of calf scouring outbreak

A
  1. Triage
  2. Categorise/group by severity
  3. Practical treatment/management plan
    ○ Resuscitation, fluids -> need to development plan with farmer - give prognosis
  4. Reduce further contamination
  5. Reduce exposure
  6. Decontaminate areas
  7. CLIENT COMMUNICATION at the end of the visit
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35
Q

In terms of client communication for calf scours outbreak what is important

A
  • Summarise in 3 points
  • Write instructions down (clinic handouts)
  • Empathise (it is more work)
  • Explain why/importance
  • Follow up phone call
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36
Q
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
A
  • Viral - rotavirus or coronavirus

- Protozoal - cryptosporidium

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37
Q

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)

A
  • ~9% dehydrated

- 3.6 L bicarb & Hartmann’s IV - 0.09 x 40 = 3.6

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38
Q

Diagnostic appraoch to urinary tract disease 6 main things can do

A
  1. Get a good history
  2. Look at the environment
  3. Observe the animal at rest
  4. Observe urination (aka micrturition)
  5. General clinical examination
    ○ Including urinary tract
    § External - vulva, escutcheon
    □ Crystals, bleeding, puss
    § Internal - kidney, ureters, bladder contents and wall
  6. Blood samples - not so often
    ○ Blood urea nitrogen (in plasma)
    § Indicates renal perfusion or renal insufficiency
    § Limited application due to time and cost
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39
Q

What are the 3 main ways urinary disease manifests and things within

A
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"
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40
Q

Dysuria what are the 4 main causes

A
  • Cystitis
  • Pyelonephritis
  • Obstructive urolithiasis
  • Vaginitis
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41
Q

Cystitis what main clinical sign, pathogen, other signs, how occurs, what more common in and treatment

A

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)
42
Q

Pyelonephritis pathogen, how occurs, clinical signs, diagnosis, treatment and prognosis

A
  • Corynebacterium renale et al
  • Ascending infection (hygiene, venereal)
  • Haematuria, pyuria, painful microturition
  • Painful kidney, colic
  • culture
  • Prolonged treatment required - penicillin
  • Prognosis guarded
43
Q

Urolithiasis main causes, what result in, what most common i and treatment

A

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

44
Q

Vaginitis main clinical sign, cause, treatment

A
  • Usually secondary to calving trauma
  • Often resolves without intervention
  • Bruising, laceration - if torn stitch them
  • Treatment with penicillin IM
  • Also IBR (bovine herpes 1)
45
Q

Abnormal contents or appearance of urine what are the 3 main looks

A
- Red urine (redwater) 
○ Haematuria - red with clots 
○ Haemoglobinuria - red without clots - may need to spin 
○ Myoglobinuria 
- Proteinuria 
- Pyuria
46
Q

Red urine what are 6 main causes

A

1) bracken fern poisoning
2) post-parturient haemoglobinuria
3) bacillary haemoglobinuria
4) leptospirosis
5) rape/kale poisoning
6) copper poisoning

47
Q

Bacillary haemoglobinuria what pathogen, how common, results in

A
  • Cl. Haemolytic (Cl. Novyi Type D)
  • Uncommon
  • Toxaemia, dark red/brown urine
  • Rapid death
48
Q

Leptospirosis 2 main serovars, how transmitted, age, importance and control

A
  • 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
49
Q

Leptospirosis pomona maintenance host, what occurs in calves and adults and differentials

A
  • 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
50
Q

Leptospirosis hardjobovis what is the main host, what occurs in adults and main issue

A
  • 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
51
Q

Copper poisoning how acute and chronic occur with signs for each

A
  • 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
52
Q

Proteinuria what are the 2 main causes and causes within

A
  • 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
53
Q

Pyuria what is it, treatment

A
  • 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
54
Q

define down cow, downer cow and downer cow syndrome

A
  • “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
55
Q

What position is normal for cow to be in and what not normal and why

A

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

56
Q

What are the 4 main causes of down cows and causes within

A
- 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
57
Q

What is history is important to obtain for a down cow case

A
- Age &amp; Breed?
○ Middle-age, heifer, older cow
○ Jerseys - more predisposed to metabolic disease 
- Onset &amp; 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?)
58
Q

Clinical examination of a down cow what are the 4 main steps

A
  1. Observation of posture, responses
  2. Physical examination (don’t take shortcuts!)
    ○ Full clinical examination ->
  3. Characterise as: Musculoskeletal/Neuro, Systemic or Metabolic
  4. 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
59
Q

In characterising a down cow how to differentiate between musculoskeletal/neuro, systemic or metabolic cause

A
Presentation
○ Musculoskeletal/Neuro
§ Typically bright &amp; alert
§ In sternal recumbency
§ Able to ‘creep’
○ Acute Systemic/Toxic
§ Sunken eyes &amp; 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
60
Q

During the examination of a down cow what also need to be doing

A
  • 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)
61
Q

Posture for down cows what are 4 main ones and most common causes of those positions

A
  • 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
62
Q

In terms of differential diagnosis for why a downer cow is down what is the first steps

A

Mental status

  • normal
  • abnormal
  • > dull and depressed
  • > hyperactive - grass tetany
63
Q

Normal mental status on a down cow what is the next things to look at and things within

A

§ 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 -

64
Q

Abnormal mental status dull and depressed downer cow what looking at after this to determin cause

A
□ 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
65
Q

If a cow has been in prolonged recumbency what can this indicate and possible causes

A
- 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
66
Q

Lifting cows for examination what are the main things used and the aim

A

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

67
Q

IF when you lift her up she buckles on her knees and refuses to get up what is needed and why is this occurring

A

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
68
Q

What are the 3 main parts of the musculoskeletal exam

A

1) back examination (while in sternal)
2) lumbosacral ligament examination
3) limb examination (roll into lateral)

69
Q

Back examination in musculoskeletal examination what is involved

A

○ 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

70
Q

Lumbosacral ligament examination how common, what is done and what must not be done if diagnosed

A

○ 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

71
Q

Limb examination as part of the musculoskeletal exam what is invovled

A
(roll into lateral) 
○ Check for dislocated hip, leg or pelvic fractures, ruptured muscles/tendons 
○ Nerve function
○ Manipulate each limb 
○ Assessing Nerve &amp; Motor function
72
Q

As part of the limb examination how to test the nerve function

A

§ 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

73
Q

Manipulation of each limb during musculoskeletal exam what need to do

A

§ 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

74
Q

Assessing nerve and motor function as part of the limb examination during the musculoskeletal exam

A

§ 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

75
Q

Diagnosis of limb and spinal fractures and when consider euthanasia

A
  • 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
76
Q

Diagnosis of obturator and sciatic nerve injury

A
  • 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
77
Q

Diagnosis of femoral nerve and radial nerve paralysis/injury

A
  • 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
78
Q

How to determine the prognosis of musculoskeletal/neural injuries

A
  • 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
79
Q

Calving paralysis prognosis when good, guarded and poor

A

○ 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?

80
Q

femoral nerve injury prognosis when good, very poor and what to do in certain situations

A

○ 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

81
Q

Prognosis for obturator and lumbosacral injury

A
  • 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!
82
Q

Prognosis for non-responsive milk fever and radial nerve injury

A
  • 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
83
Q

What are some poor prognostic signs with down cows - EXAM

A
  • 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
84
Q

What are the 4 main things involved with treatment for down cow

A
  • Need to quickly address initial cause
  • NSAIDs: First 24 hours (for up to 3 days?)
  • Treat the underlying condition
  • Nursing:
85
Q

Nursing for downer cow what is involved

A

○ 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

86
Q

how to move and roll and cow

A

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

87
Q

Lifting down a cow how done and when no worth it

A
  • 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
88
Q

Housing the down cow, caring for it and assessing it what is involved

A

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

89
Q

When is the transition period and what used for

A
  • 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
90
Q

When is the transition period important

A

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

91
Q

What can bad transition period result in

A
  • 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
92
Q

What are the 4 main aims of the transition period - EXAM

A
  1. Reduce ruminal disruption - lactic acidosis, ruminal acidosis
  2. Minimise macromineral deficiencies - calcium, magnesium and phosphorus - requirement increase dramatically when producing milk
  3. Minimise lipid mobilisation disorders - ketosis, fatty liver
  4. Avoid immune suppression - trace elements (zinc, iodine, vitamin E and vitamin D)
93
Q

How to ensure the aims of the transition period is achieved and what are the components of the diet

A

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

94
Q

What are the 4 main metabolic conditions that lead to a downer cow

A
  1. Milk fever
  2. Grass tetany
  3. Pregnancy toxaemia
  4. Fatty liver
95
Q

Calcium where found, what does the test detect, what level an issue

A
  • 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
96
Q

Calcium regulation how controlled 4 main ways

A
  1. Arterial Ca++ levels sensed by parathyroid glands which secrete PTH
  2. 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
  3. Some effects mediated via converting Vitamin D to active form.
    - Calcium resorption from bone is slower in older cows
  4. Low blood Mg++ reduces PTH secretion and also tissue sensitivity to PTH
97
Q

Parturient hypocalcaemia what is it, clinical signs and cause

A

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

98
Q

DCAD what is it, equation and therefore way does it measure

A
  • 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
99
Q

DCAD how measured, what is normal levels

A

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

100
Q

What are the 6 main risk factors for milk fever - EXAM

A
  1. Parturition –most milk fever occurs around parturition. (also transport)
  2. Transport -> reduction in the feed -> drop in dietary calcium
  3. Age –Mostly > 5yo
  4. Milk Production
  5. Breed - Jerseys more susceptible
  6. Dry period nutrition –diet (blood pH) and body condition