Farm Repro and Neonatal Flashcards

1
Q

What are congenital issues?

What is the aetiology?

What are some examples?

A

Abnormalities in structure and function at birth

Aetiology- genetic or environment

Examples-
CV- PDA, VSD
Urogenital- patent urachus
Musculoskeletal- contracted tendons, dwarfism
Neurological

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2
Q

Dystocia is commonly due to neonates being oversized

What outcomes does this cause?

What are the consequences?

A

Oedema, bruising, fractures
Hypoxia-
compression of umbilical cord, premature placental separation
Acidosis-
metabolic- lactic acid due to tissue hypoxia, respiratory- poor lung function

Consequences- failure to nurse and reduced passive transfer

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3
Q

How long should it take a calf to be in sternal recumbency?

What can be used for the diagnosis of problems in newborn calve?

A

should be less then 5 minutes- if over 9 increases chance of death

Diagnosis- thermometer, stethoscope, blood gasses (less so)

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4
Q

What are the ABCs of resuscitation?

What are the other techniques?

A

Airways-
intubate, laryngoscope, sternal recumbency, pull the tongue out, pass tube

Breathing-
ambubag, blow down tube

Circulation-
fluids

Other techniques- cold water down the ear, rub with straw, acupuncture on philtrum, doxapram

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5
Q

What are common perinatal physiological problems?

A

Inactivity/lethargy- standing and sucking essential

Hypothermia- calfs temp drops to 39 in 30 mins, should not go lower then this

Hypoxaemia- numerous aetiologies

Hypoglycaemia

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6
Q

How much colostrum should be fed in the first 24 hours and why?

A

Minimum of 5% at each feeding (2-3l)
First feed within 2h and again 6-12 hours
=10% within 12 hours

The concentration of immunoglobulins and permeability of the calve gut decreases rapidly within the first 24 hours

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7
Q

What does colostrum contain?

A

Fat and protein- 50% more fat 4x more protein (immunoglobulin)

Vitamins and minerals-
fat-soluble vitamins A, D, and E (<8x), Vit B12 8x
Macrominerals/Micro (Ca, P, Mg)(Cu, Fe, Zn)- 2-20x more

Immune cells

Others- growth factors, enzymes, cytokines

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8
Q

What are the 4 Qs of colostrum intake?

A

Quality

Quantity

Quickly

sQueaky clean

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9
Q

Why do a lot of calves not have sufficient passive transfer?

A

High merit dairy cows have poor quality colostrum- dilution effect, calf need more

Conformation- big teats

Supervision- 34% of calves don’t suck within 6 hours

Bad calvings-
acidotic calves, do not suck enough

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10
Q

How should colostrum donors be selected?

A
  1. Health dams- negative for diseases (Johne’s), prolonged residence at farm
  2. No pre-calving milking or milk loss
  3. Only first milking colostrum should be given initially
  4. Use colostrum from one dam per calf
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11
Q

What affects the quality and quantity of colostrum?

How is colostrum quality monitored for?

A
  • When the colostrum is collected- decrease in IG with time
  • Breed of cow
  • Parity
  • Pre-partum nutrition
  • Length of dry period
  • Pre-milking
  • Abortion/induction
  • Masitis

Brix refractometer- >22%= 50g/l
Colostrometer
let cool- 20 degrees

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12
Q

How is colostrum pasteurised?

What are the pros and cons?

A

60 degrees for 60 mins

Pros-
Bacterial reduction- Mycobacterium avium subsp. paratuberculosis, Salmonella spp., Escherichia coli etc
improved efficiency of IgG absorption

Cons-
not sterilisation
kills leucocytes
Costs- labour

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13
Q

What should be considered when collecting colostrum for freezing?

What are the pros and cons?

A

Collect from first milking only
Only freeze good quality
Collect from lowest risk heifers (Johne’s)

Pros-
free, farm-specific antigens

Cons-
cost of storage

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14
Q

How are colostrum replacers produced?

What are the pros and cons?

A

Spray drying colostrum or concentrate whey from cheese

Efficacy of absorption is not as good as natural

Expensive

Less tailored to individual farms

Better then nothing!

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15
Q

How can failure of passive transfer be defined?

A

Serum IgG <10mg/ml- 55g/l

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16
Q

What are the common infectious diseases of neonatal ruminants?

What are the epidemiological considerations?

A

Diarrhoea
Joint ill
Navel ill
Septicaemia
Bloat- rumen and abomasal

Epidemiological considerations-

1) the reservoir
2) modes of transmission and agent characteristic
3) incubation period
4) Period of communicability

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17
Q
A
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18
Q

What cleaning should be done for prevention of infectious diseases in neonates?

A
  1. removal of organic material
  2. destruction of microbes follows first-order logarithmic decay
  3. Contact time, temperature, pH, water content/hardness,
  4. Smooth surfaces preferable
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19
Q

What can be used for diagnosis in a neonate?

A
  • Demeanor
  • Suck reflex
  • TPR
  • faeces
  • Navel
  • hydration staus
  • Acid-base staus
  • CNS signs
  • Abdominal distension
  • Abdominal signs
  • chest sounds
  • CSF tap
  • ZST/TP
  • PM
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20
Q

What is the route of infection of navel ill?

What can be infected?

What is a key sign?

What are the sequelae?

What are the risk factors?

A

Infection via navel or oro-respiratory route

May involve umbilical arteries, veins, urachus

Key sign- hard swollen navel

Sequalae- peritonitis, septicaemia, polyarthritis

Risk factors- pathogen load, patent navel, immune status of calf

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21
Q

How is navel ill diagnosed and treated?

A

Diagnosis-
clinical examination- swollen and hard, check for a hernia
Probe
Ultrasound- peritonitis, extension up the vessels

Treatment-
antibiotics
drainage
surgery- remove infected, if veins poor prognosis

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22
Q

What is joint ill a sequel to?

What are the risk factors?

What are the signs?

What is the prognosis?

How is it treated?

A

Sequel to navel ill usually

risk factors- hygiene at calving, FPT

Single or multiple joints- swollen painful

Prognosis- poor, depends on joint affected

Treatment-
reduce bacterial load
antibiotics- 2 weeks course following improvement, begin with IV
Joint lavage- useful but often hard to do
NSAIDs
Antibiotic impregnated beads- ‘home made’- methyl methacrylate, antibiotic impregnated, place in or around joint, remove in 4 weeks

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23
Q
A
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24
Q

What is bacteriaemia and septicaemia?

A

Bacteraemia-
bacteria in blood
2nd to mucosal damage- rumen acidosis, gum disease

Septicaemia-
bacteria multiplying in blood
concurrent endotoxaemia
fatal

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25
What agents commonly cause septicaemia? What is a prime determinant? When is it more commonly seen? What are the clinical signs? How is it treated?
E.coli Actinomyces Staph Salmonella The prime determinant is the lack of colostral antibody Usually seen from 1-5 days of age Clinical signs- non-specific, collapsed, shocked, very congested conjunctive, CNS sometimes Treatment- rarely successful antibioits, NSAIDs, corticosteroid, fluid therapy, supportive nursing
26
27
What agent causes calf diptheria? What is the signs? What factors increase infection How is it treated?
Fusiformis necrophourm Oral lesions- sore mouth, salivation and foul smell, ulcerative lesions Dirty buckets- poor hygiene Tx- penicillin
28
What can cause abdominal swelling in young calves?
Abomasal bloat- typically calves 1-2 weeks old will die within 6 hours causes?- clostridium, poorly mixed MR L sided swelling- free gas in abomasum R sided swelling- abomasal again Atresi coli- gradual distension over the first few days- total absence of faces- euthanasia
29
How should a swollen calf be approached?
Full clinical exam Pass stomach tube- wont resolve abomasal If distention resolved- rumen bloat Listen to guts before and after passing tube- pings, splashing
30
What can cause rumen bloat?
Rumen drinkers- Milk goes to rumen Failure of closure of oesophageal groove Ferments- metabolic acidosis risk factors- feed hygiene, worn teats Poor rumen development- pot bellies
31
How is abomasal bloat and ruminal bloat treated?
Abomasal- sedate and roll onto the back .16 gauge needle into 'ping' Ruminal bloat- relieve distension with a tube
32
What are the 5 major agents that cause calf scours?
Rotavirus Coronavirus Crytposporidia K-99 E.coli Salmonella
33
What is the mechanism of action of rotavirus and coronavirus? How does this cause scours?
Damage to intestinal lining Malabsorption of milk- fluid and electrolyte loss dehydration, acidosis and death
34
What E.coli causes characteristic simple scours in calves? How does it cause scours? Therefore how can it be treated?
E.coli K-99 Attaches to the gut wall and secretes a toxin that affects the intestinal lining of cells- the toxin causes hypersecretion of water and electrolytes- diarrhoea Treatment- the E.coli doesn't infect or damage the cells, the calve dies by dehydration and acidosis therefore early oral fluid is the key to success
35
What are the effects of Salmonellosis and Clostridia on the gut and peripherally? When does peak salmonella shedding occur? What are the signs? How is it treated?
Salmonellosis and clostridia- damage the gut tissue locally but also severe systemic inflammation from toxin release Peak shedding following stressors- calving Signs- diarrhoea ± mucous casts, dysentery, pyrexia, joint infections, pneumonia Treatment- aggressive antibiotic and antiinflammatory treatment
36
What are the host defences in diarrhoea of calves?
Passive immunity- local IgG and IgA adhering to mucosal surface, derived from colostrum- first and continued intake 'medical colostrum' then 'tonic colostrum' Healthy gut flora- suppressed growth of pathogens- competitive inhibiton Health mucosa- nutrition
37
What affects the epidemiology of the environment?
Pthogen load- space, time Cavling area- is it crowded Hygiene- environment, foodstuffs and utensils Inside v outside Single v group housing Cleaning protocols
38
What are the calf factors for scour infection?
Colostrum status- did the calf get enough at the right time Others- stress chilling nutrition Feeding routine- Hygiene, temperature, composition, bucket, teat Housing, comfort, warmth
39
How can scours exposure be minimised in dairy and beef?
Dairy- * clean calving * 'snatch calve' within 2-4 hours * Clean housing * Hygiene- at feeding * Hostpitalise sick calves Beef * Calve outside- tight calving period, flow system, sandhills system * Hospitalise sick calves
40
How can protection of scours be maximised in dairy and beef?
Dairy * 5% within 2 hours, repeat 6-12 hours * continue colostrum feeding for 4-10 days Beef * Adequate cow nutrition- feed for 3 weeks pre-calving * Frozen colostrum * Vaccinate dam
41
What can be the dam be vaccinated with in prevention of scours?
ETEC, rotavirus, coronavirus Vaccinare 3- weeks before calving Need to know calving date Works via colostrum/milk- colostrum management
42
What is the purpose of the sandhill system? Describe the sandhills system for beef cattle
Reduces- contact between younger and older calves Build up of pathogens Eliminates pathogen multiplier effect 1. Animals start on 1 pasture- cows that dont't calve move onto next 2. This means the calving cows have a fresh pasture 3. After 2 weeks the pastures of calves can be combined
43
What principles of sandhills can be applied to UK?
Turn out asap Segregate cow/calf pairs by age 7-10 days spread of calves Can mix at 4 weeks of age Abolishes pathogen multiplier effect
44
When does coccidiosis occur in calves? What increases incidence? What are the signs? What are the treatment and diagnosis?
Usually older calves \>21 days Poor hygiene- especially near troughs Dark scour ± blood- tenesmus- usually bright Treatment- sulfonamides, vocoxan Diagnosis- faecal oocyst count
45
What is necrotic enteritis? What causes it? What are the signs? How does it appear PM?
Affects 2-6-month-old suckers Usually sporadic cases Usually fatal Aetiology unknown Pyrexia, pale MMs, leucopenia, thrombocytopenia PM- necrotic lesions of gut and respiratory tract
46
What are the signs of peri-weaning scour syndrome? What needs to be looked at?
PAsty scour, poor growth -bloat, pot belly Look at feeding, management
47
What is diarrhoea?
Failure of net intestinal uptake of water and sodium such that the colon is overwhelmed
48
What does diarrhoea lead to in a calf?
Dehydration/hypovolaemia -pre renal failure and shock Metabolic acidosis- loss oh bicarbonate into gut L-lactic acid from tissues D-lactic acid from colonic fermentation Hypoglycaemia- starvation
49
How can dehydration by estimated?
Demeanor, eyeball recession, skin tent duration, increase in total protein With the failure of passive transfer- a dehydrated calf might show to be normal
50
What does Stewarts strong ion difference explain?
Explains the underlying physiology regulating acid-base balance Na, K, Cl, Protein, Unmeasured anions (Lactate, SO4, PO4, Oxalatate, Ketocacids) Strong ion difference (Na + K - Cl) = 35-45, decreases with acidosis Giving NaCl solution can cause acidosis as there is less Cl relative to Na
51
How can acid base be diagnosed in the lab?
Blood gas machine Harleco apparatus measures TCO2 pH meter
52
What kind of acidosis is this? What shows dehydration? What would cause a low HR?
Metabolic acidosis- low CO2 Increased PCV, urea show dehydration Low HR from increased K+
53
What are the therapeutic targets for fluid therapy in a diarrhoeic calf?
Hypovolaemia Matabolic acidosis Hypoglycaemia Pre-renal failure
54
What are the considerations of oral fluid therapy?
Can use commercial products or be homemade Typically around 5% BW or 2l Only use an oesophageal feeder if necessary- damaging- listeria Don't withhold milk replacer Seperate fluids with milk replacer
55
What are the major requirements for electrolyte solutions for oral dehydration?
1. Supply sufficient sodium to normalise ECF volume 2. Provide stubsances- glucose, citrate, propionate that facilitate absorption of sodium and water from the intestine 3. Provide an alkalinizing agent to correct metabolic acidosis, usually present in calves 4. Provide energy because most calves have diarrhoea are in negative energy balance
56
What are the advantages of the inclusion of VFAs in electrolyte solution of bicarbonate?
* Acetate and propionate facilitate sodium and water absorption in the calf small intestine, whereas bicarbonate does not * Acetate and propionate produce energy when metabolized * Acetate and propionate do not alkalinize the abomasum * Acetate do not interfere with milk clotting in calves
57
How should oral fluids be administered?
When- ASAP Route- teat and bucket best How much- 4-8 litres daily How often- little and often Milk as well
58
What are the advantages and disadvantages of oral fluid therapy?
Adv- * Feed the calf- maintain body condition, energy for immune response * Feeds the gut mucosa- assists in repair * Ensures intake of Ca, Mg, vitamins Dis- * May worsen diarrhoea via colonic overload * May worsen acidosis via colonic fermentation * May discourage farmer
59
How do IV fluids allow correction of Na and K?
Improves plasma volume Improving renal function- kidneys function Improves metabolic acidosis and corrects Na and K
60
What are volume expanding fluids?
Volume expanding fluid- isotonic Plasma like- Na, BIC, K NaCL- saline NaHCO3
61
What are hypertonic solutions? What other fluids can be used?
Sodium bicarbonate- 5% Sodium bicarbonate 8.4% Saline 7% Dextrose- glucose Colloids- uncommonly used
62
What should be given to dehydrated calves under and older a week? What should be given to a dehydrated calf unable to stand?
63
64
What are the following targets for dairy calf rearing?: Mortality Weaning weighy 3-month weight Service weight Calve time
Mortality less then 5% Weaning weight \>65kg 300kg service Calves at 24 months
65
To calve at 24 months When does the cow need to be served? What weight? What is the calving interval as an adult?
serve at 400 days Weigh at 400kg Birthweight at 40kg Grow 360kg Calving interval 400 days
66
What are the constraints of calve growth?
Disease- neonatal scours pneumonia- post weaning Sub-optimal nutrition Sub-optimal environment
67
What is lower critical temperature and what is a calves LCT?
Lowe critical temperature is the lowest temperature that an animal can wistand before using having to increase energy expenditure Calve 15-20 degrees depending on humidity
68
When should calves be weaned?
When eating 1.5kg daily for 2-3 days When at least 8 weeks old Weighing at least 65kg Can either dilute or reduce volume