BM - Kev Feedlot Flashcards
1
Q
General categories of stressors for cattle
A
- Physical
- Nutritional
- Environmental
- Physiological
- Psychological
2
Q
Stressors for cattle in different environments
A
- Property of origin: mustering, yarding, drafting, weighing, loading
- Cattle handling: poor cattle handling, electric prodding, yelling, chasing, overcrowding / forcing
- Feedlot: novel feed & adaptation, novel environment, overcrowded receiving pens, induction process, further commingling, dust, disease
- Saleyards: time off feed & water, commingling, noise, people, dogs, vehicles, abrasive yard surfaces
- Transport: time off feed & water, noise, commingling, injuries, environment & fumes
3
Q
In what state do cattle arrive to a feedlot? What are the first 2 priorities?
A
Tired, dehydrated, reduced rumen function, thirsty, hungry, frightened, disorientated & confused, bruised, injured
Priorities = get them eating and drinking
4
Q
Acclimation and stockmanship
A
- Make a good first impression
- Clean pen, clean water, extra water, fresh feed (GQ hay with 13% protein), good bedding
- Introduce to pen - take them to the feed and water
- Feeding and bunk management on time - ad lib feed for first few days
- Feed that meets cattle needs - quality commodities, bunk and water hygiene
5
Q
Backgrounding before feedlot entry
A
- Accumulating cattle
- Preparing for life at feedlot
- Bring up to feedlot entry weight
- Pre-vaccinate if at risk mob
- Bunk train
- Acclimate - to herd, new environment, new handlers
- Must have 4-6 weeks minimum!
6
Q
Principles for successful backgrounding
A
- Receive, rehydrate, rest, and acclimate
- Process, acclimate and bunk train
- Implant (low dose trenbolone acetate) if possible, need 6 weeks prior
- Comingle and grow (NOT fatten - won’t get fatter than 28% body fat)
- Sort, cominge, vaccinate or re-vaccinate
- Feeding - pasture, silage, grain or pellets
- Consistent growth at minimum 0.6kg/day
Tips:
- Select based on age, weight & frame
- If more than 7 purchase groups, need a minimum 4wks backgrounding after last group is added
- If big purchase groups (1-4 per paddock), need a minimum 2wks backgrounding
- Pre-vaccinate for IBR, MH, 5-in-1, BVD?
- Pink eye =waste of time for pink eye
- Pregnancy check heifers - do NOT abort within 4wks of feedlot entry (need ~8wks, let feedlot know if they are pgenant)
- Drench for fluke, worms and lice
- Cattle handling crucial! Handlers shape future cattle behaviour every day!
7
Q
BRD Risk Factors
A
- Presence of virus
- Weight and breed
- Change of address
- Region, feedlot capacity, season
- Purchase groups and size
- Filling pens
- Mixing and moving
- Transit time
- Stocking density
- Yard weaning = simple and effective way to reduce risk (½ the risk)
- Pre-vaccination
- Shared water troughs
BVS data - within first 6 weeks of induction, biggest exposure to IBR, then BVDV, then BRSV, then PI3. M. bovis exposure negligible.
8
Q
BRD Prevention
A
Limited vaccines:
- Intranasal IBR (rhinoguard zoetis)
- Killed pestivirus (pestiguard zoetis)
- MH killed (Bovilis MH MSD)
- MH modified live attenuated (Bovishield MH1 zoetis)
- MH & IBR killed (Bovilis MH & IBR MSD)
9
Q
Feedlot processing and induction
A
- Process when cattle are ready, within 3d allowing a 24h rest
- Do not give Tx without evidence! Minimise procedures.
- Fill starter pen ASAP (within 1d), and avoid add-on pens (last in, first out)
- Use clean needles to vaccinate, and put implant in middle ⅓ of ear
RULES:
- Hygiene
- Needle changes (every 25 head max)
- Injection site - neck only, 10cm b/w injections
- Implant in middle ⅓ of ear
Common issues: confinement & relocation anxiety (Tx = stockmanship), fear of humans, digestive problems (not eating, acidosis), lameness, injury
Goals: positive interaction b/w handlers and cattle, fix dehydration, restore rumen function, get them eating!
10
Q
Arrival & receiving diet
A
- Highly palatable with 13%+ protein (GQ hay) - chopped oaten hay, not lucerne
- High energy
- Limited starch or no starch
- Create rumination and establish microbial biome
11
Q
Matching nutritional program to recent nutritional Hx
A
- Rumen capacity limits feed intake in starter cattle for up to 7-14d
- After 48h off feed and water, cattle with higher pre-fasting DMI had higher post-fasting DMI
Trust → Confidence → Eating, drinking, resting, chewing cud → Reduced anxiety → Feel good hormones
12
Q
Critically Evaluating Alternative Handling Techniques
A
Study: 2115 calves from Florida, shipped to Colarado, randomised, “alternative” and control treatments applied.
- Wait until 90% calves wandering pen following initial rest period: loosely group cattle into pen corners, push cattle away from bunk and bring them back to it, do it AM and PM
- Each pen walked down drovers alley daily for 10d
Results:
- 0% GI mortalities cf 26% with traditional
- Labour cost per head $0.28
- Mortality cost per head $10.86
- Advantage per head $10.58
→ Acclimated cattle have reliably reduced digestive death loss
13
Q
Feedlot health problems
A
- Respiratory 66% - IBR, PI3, BRSV, Pasteurella, Histophilus
- Musculoskeletal 16% - infectious foot conditions, non-infectious, bullers
- GI 9% - non-eater, poor-doer, bloat, acidosis
- Other 9%
Reasons = 2 main issues - immune status and stress level.
- Immune status affected by active immunity, age, vax status, and stress load
- Factors contributing to health problems - cattle age, shrinkage, time off feed, source origin, breed, mgmt. prior to arrival, time in transit
- Pre-entry stressors - exhaust fumes, saleyards, commingling, injuries, transit time, transportation, temperament, weaning, mustering, crowing in yards, feed & water deprivation
14
Q
GI conditions and feed related problems
A
- Lactic acidosis and sequelae
- Alkalosis (non-eater)
- Feedlot bloat
- Urea toxicity (Ammonia toxicosis)
- Salmonellosis
- Internal parasites
15
Q
Lactic acidosis
- Causes
- Predisposing Factors
- Classification
- Clinical signs (individual and pen)
- Complications
- Pathogenesis
- Clinical Pathology
- Diagnosis
- Treatment
- Prognosis
A
- Causes = excess readily fermentable carbs, usually in early feeding period
- Predisposing Factors = feed stuff ups, change in diet acceptability, sudden change in / to grain, low roughage (<10%), too fast step up to grain, wheat has highest risk
- Classification = clinical (acute, mild, emergency) and subclinical (economic Dz)
-
Clinical signs (individual = emergency)
- 12-36h onset post-engorgement → ataxia, incoordination
- 24-48h → anorexia, rumen stasis, fluid distension, abdo pain, dehydration
- Later → profuse diarrhoea, some dead before this stage
- Severe cases (die) → recumbent 24-48h, quiet, weak, toxaemia, increased RR, often decreased body temp
-
Clinical signs (pen) = full range → dead, down, depressed, diarrhoea; acute laminitis
- Pen feed intake drops by 10% of more for 2d+
- >3% bubbly scours
- Complications (weeks later) = PEM, chronic rumenitis, abomasal ulceration (may perforate), liver abscessation, chronic laminitis, poor pen performance
- Pathogenesis = increase in CHO → increase in lactic acid producing bacteria (Strep bovis first) → decrease in pH dt acidic environ (good for more bugs to grow, until pH reaches 5 when they die) → rumen stasis → anorexia, no eating, no chewing → no buffer from saliva → drink more water to fix pH → rumen pH drops more and sloughs off → bacteria can enter bloodstream and go to liver → abscess formation
- Clinical Pathology = dehydration, rumen pH <5.5 = clinical acidosis but if 5.6-6.0 subclinical; elevated serum D-lactate (diagnostic >0.6)
- Diagnosis = Hx, CS, PM
-
Treatment (must consider severity, practicality, value of animals, and chance of success)
- Principles: increase rumen pH to 6-7, kill G- bacteria, electrolytes for acidosis, supportive therapy
- Prognosis (based on HR) = <100bpm fair, 100-120bpm guarded, 120bpm+ DIE
16
Q
Lactic acidosis Treatment
A
Mild cases: remove from feed, exercise cattle, and put on hay for saliva production
Moderate cases: hay, exercise, rumen pH correction, rehydrate with oral electrolytes, reduce G- bacteria, and bicarbonate in water
Severe cases: sharpen knife. Hero stuff = rumenotomy, rumen lavage. IVFT and bicarb (120g/L), aggressive supportive therapy)
- Role of exercise: stimulates rumen → encourages water & feed intake
- Antacids: sodium bicarb, Mg oxide / hydroxide, Mg carbonate, bentonite → 0.5-1g/kg
- Antibiotics: penicillin (1ml/20kg), oxytet (10-20mg/kg) → mix and stomach tube w/ 10L water
- Supportive Tx: C/steroids, anti-H2, Vit B1 (PEM), IVFT / oral FT
17
Q
Lactic Acidosis prevention strategies
A
- Buffers = sodium bicarb (true buffer from pH 6.2-6.5) has short DOA, little value as feed additive; Mg oxide is slow release pH increaser; Na bentonite not a buffer but absorbs water; Ca carbonate has high acid consumption, works best at 4.5-5.0pH; seaweed; acid buff celtic sea minerals used a lot in dairies, longer DOA dt honeycomb structure
- Rumen modifiers = directly modify balance of different microbe populations in rumen, and % of VFA’s
- Ionophores = work to reduce acid producing bacteria (Strep bovis, Lactobacillus) and restore consistent eating behaviour - Monensin (MUST dose correctly), Lasalocid (larger safety range), Narasin, Salinomycin
- AB rumen modifiers = Virginiamycin (G+ activity, reduces lactic acid production, reg for acidosis); Tylosin (combine w/ Monensin - reduces lactic acid production, controls liver abscesses)
- Lactic acid inhibition: IC50 = concentration needed to provide 50% inhibition of acid; Imax = maximum inhibition of lactic acid production → diff products have diff values)
- Yeasts = live yeast fed as byproduct or some commercially available
Prevention strategies
- Receival - hay
- Start diet max 50% grain
- Acclimation program
- Controlled step up - start <50% grain, take 14-21d to get to full ration
- Adequate roughage (50-100mm)
- Buffers and neutralising agents
- Rumen modifiers
- Yeasts & probiotics
Summary
- Ionophore +/- virginamycin 20ppm
- Gradual diet changes
- Bunk mgmt. - bunk space, allocation, step up max 10% on finisher diet
- Mixing
- Monitor fineness - dry roll vs. steam flaked vs. tempered
- Roughage - 5-10cm long (minimum 10% of ration)
18
Q
Bloat
- Cause
- Types
- Clinical Signs & Management
- Post Mortem
A
- Cause = assoc. w/ lactic acidosis, isolated cases from obstruction, ingestion etc.
- Types = gaseous (most common) and frothy
-
Clinical Signs & Management =
- Subclinical → no signs, poor performant
-
Mild → puffed out on left, not uncomfortable
- Tx = exercise, put on hay 1-2d
-
Moderate (bloat score 2) → uncomfortable, distended both sides
- Tx = remove from feed, NGT to relieve pressure, mineral oil (4L)
-
Severe (bloat score 3) → distressed, recumbent, likely to die → EMERGENCY Tx
- Tx = trochar (get rid of gas, move substrate on, kill bacteria), +/- rumenotomy
- PM = congestion in lungs, bloat line in oesophagus, massive rumen distension
19
Q
Polioencephalomalacia
- Causes
- Diagnosis
- DDx
- Treatment
- Control
A
- Causes = assoc. w/ acidosis, thiamine deficiency (acidosis → thiaminase producing bacteria)
- Diagnosis = Hx and CS (star gazing, appear blind, stumbling)
-
DDx = H. somni (aggressive), Vit A def., nervous coccidiousis, Pb poisoning, S toxicity
- All except S tox WILL NOT respond to thiamine Tx
- Submit formalin fixed cerebral cortex to lab
-
Treatment = thiamine 2-3g 2-3x per day IV or IM (inject slowly), Dex 0.5-1mg/10kg IV or IM (decreases brain swelling), supportive Tx (oral fluids and Vit B12)
- If unsuccessful, need to do PM - Tx should work if it is actually PEM (75% success). Add oxytet if it is H. somni.
- In feed Tx = Thiamine 250-350mg/head/day, if unprotected 30-40% bypass cf protected 70-75% bypass
- Control = control GIT problems, increase roughage in pen (increase pH), S-containing by-products (look for S in diet)
20
Q
Urea Poisoning
- Cause
- Clinical Signs
- Treatment
- Prevention
A
-
Cause = excess urea or NPN
- If pH 8.4 10% of NH3 is free cf pH 6.4 where 0.01% NH3 is free. Increased rumen pH increased free NH3. Urea + H2O → NH3 + CO2 (enters portal circulation).
- Clinical Signs = sudden 20-60min post ingestion - abdo pain, muscle tremor, salivation, pH>7.5, blood ammonia >1mg/dL
- Treatment = vinegar - 4L + 10-20L of water to stop free NH3 and reduce rumen pH
- Prevention = max 1% urea in diets, max 30% CP as NPN, mix feed properly, note rain on rations, adapt animal to high carbs before increasing urea
21
Q
Salmonellosis
- Cause
- Clinical Signs
- Post Mortem
- Treatment
- Prevention & Control
A
- Cause = Salmonella typhimurium - ubiquitous organism, shed from carriers, in contaminated feed and water, brought on by stress, faecal oral txm
- Clinical Signs = acute enteritis, colourful faeces, pyrexic, tenesmus, depressed & lethargic, nervous signs, can be secondary to other disease (→ immunocompromise)
- Post Mortem = SI and LI have fluid contents, check spleen and liver and mesenteric LN, evidence of resp Dz?
-
Treatment = culture first, treat with TMS 480 at 1.5ml/30kg IM SID for 5d, WHP 28d
- Mass Tx with sulfadimidine 400ppm for 5-10d but can have residue issues to make sure to flush out and don’t give to finisher cattle
- Electrostatic, faecal excretion so can contaminate pens!
- Prevention & Control = stress minimisation, acclimation, remove sources, QA systems, hygiene, hospital
22
Q
Coccidiosis
- Cause
- Clinical Signs
- Treatment & Prevention
A
- Cause = Eimeria protozoa (contagious)
- Clinical Signs = blood scours, straining, half moon on butt (scouring and twitching tail back and forth)
- Treatment & Prevention = TMS, Sulphadimidine, Amprolium, pen hygiene, ionophores, beef culture - probiotic
23
Q
Dead Rumen
- Cause
- Conditions
- Mgmt. of non-eaters
- Treatment
A
- Cause = severe dysfunction of rumen manifested by changes in microbial population of forestomachs and severe decrease or cessation of rumen motility
-
Conditions = non-eaters, severe simple indigestion, acute rumen acidosis, rumen alkalosis, rumen putrefaction
- Non-eater → Prolonged anorexia → decreased microbial activity → rumen dysfunction → rumen alkalosis
- Mgmt. of non-eaters = manage new arrivals properly; recognise, treat and manage affected animals
- Treatment = drench with organic acids to lower rumen pH, ketotic Tx (kickstart eating with propylene glycol - stimulant), present with hay (psychological issue - scared to eat)
24
Q
Feed & water deprivation & transport effects
- Effect on MO’s
- How to maximise DMI
- Acclimation
- Exercise
A
- Effect on MO’s = no effect on bacteria, protozoa decrease as time held off increases, and protozoa decrease as DMI decreases
-
How to maximise DMI = increase concentrate level → maximise performance and maximise health problems BUT all hay → poor performance and minimise health problems
- Free choice hay in first week (good grass hay) +75% concentrate results in reduced mortality and good rate of gain
- Acclimation = get them to eat properly! Remember issues - change of address, reduce fear of humans, teach to walk straight, stockmanship (stockman = leader).
- Exercise important! Esp. for pens not eating or drinking, stale pens, resp Dz pens.
25
Q
Incidence of BRD in terms of death / pull / cull rates
A
- Avg. death rate 1.18%, resp Dz death rate 0.52% → 44% from BRD
- BRD case fatality rate 3.4%
- Avg. pull rate 15.38%, resp Dz accounts for 72% of pulls → 11% from BRD
- Avg. cull rate 0.31%, resp Dz cull rate 0.07% → 23% from BRD
26
Q
When does disease occur in feedlots? relative to induction time
A
42% deaths by d42, peak day of death d34
72% pulls by d42, peak day of pull d27
45
Q
Process of animal going to hospital etc
A
