Feedlot Cattle Induction and Stressors

Feedlot Induction

• Ideally, cattle entering feedlots should be yard weaned, backgrounded, and run in pen lots on adjacent properties, receiving induction treatments before delivery.
• Many feedlot cattle, especially lighter ones for the domestic market, originate from distant saleyards.
• Bruising, inflammation, tissue protein mobilization, dehydration, and insufficient rumen substrate are common issues for newly arrived cattle

Common Stress Factors

• Mixing cattle from diverse sources.
• Novel feed and water systems.
• Introduction of new feedstuffs.
• Increased handling through yards.
• Various stimuli like machinery noise and vehicle movements.
• Dust exposure.
• Differing climatic conditions.
• These factors can lead to psychological disorientation, immunosuppression, and reduced gut function which emphasizes the importance of induction and handling in the first 40 days.

Initial Feedlot Arrival

• Provide highly palatable, high protein hay and clean water immediately.
• Legume hays are ideal, offered as biscuits in the feed trough, and large bales in hay racks in the pen.
• Limit hay availability to a maximum of 3 days, as prolonged provision dilutes nutrient intake and reduces performance.
• A smooth transition to a starter ration can be achieved by including the same legume hay, using its familiar smell to entice cattle.
• The timing of induction is crucial for health and performance; exhaustion and debilitation benefit from delayed induction with an adverse effect on performance after 3 days.
• Induction pens should accumulate over no more than 3 days, which affects management and buying practices.

Induction Procedures

• Individual visual ear tagging.
• Hormonal growth promotant administration.
• Anthelmintic use (with or without a flukicide, depending on origin).
• Clostridial vaccine.
• Possible vaccination against IBR (BHV1), Mannheimia haemolytica, and BVDV.
• Visual tags are still used by feedlot stockmen despite the use of automatic scanners and NLIS tags.

Hormonal Growth Promotants (HGPs)

• Most Australian feedlots accept cattle treated with HGPs, with a benefit:cost ratio of about 10:1.
• There are no human safety concerns using registered HGPs, as per the European Union's Scientific Working Committee, headed by George Lamming.
• A knockdown anthelmintic suffices since there is no parasite reinfestation in the feedlot.
• Flukicide use is debated; liver condemnations can cost $6/head+, but drenching may not help if scarring occurred before feedlot arrival.
• Older cattle develop fluke immunity, so flukicide economics are less favorable in bullocks.
• Some feedlots use flukicides on domestic cattle from fluke-prone areas like the NSW tablelands in the absence of adequate data, indicating a need for further research.

Infectious Bovine Rhinotracheitis (IBR)

• IBR is now considered separately from the Bovine Respiratory Disease (BRD) complex, as it is caused by a single organism.
• Bronchopneumonia can still occur without IBR.
• In Australia, a vaccine is available that is effective against IBR.
• Rhinogard vaccine prevents IBR, but not bronchopneumonia of BRD.
• BHV1 is the virus that causes IBR, which can kill cattle without significant secondary bacterial pneumonia.
• Rhinogard, a modified live intranasal vaccine, should be stored and handled according to label directions. A two-shot combined vaccine against Mannheimia haemolytica and BHV1 (Bovilis MH+IBR) is also an option.

Bovine Respiratory Disease (BRD)

• Unlike IBR, BRD is a stress-induced disease complex with viral initiators and bacterial pathogens.
• Mannheimia haemolytica is a bacterial cause of BRD, but vaccination alone has a limited effect on BRD incidence because it is only one of many bacteria, and the cost-effectiveness of vaccination needs to be assessed on feedlots.
• A study using 2500 animals showed injectable vitamin ADE at feedlot entry had no impact, supported by results from the National BRD Initiative.
• Responses to B-vitamin administration at induction are variable with health and/or performance responses to B vitamins at induction is unlikely except for vitamin B12 dosing of cobalt deficient cattle.
• There is no robust data to support drenching cattle with microbial inoculants at induction, but providing water, energy, and nitrogen/protein stimulates rumen microbe proliferation.

Lactic Acidosis

• Excessive consumption of readily fermentable carbohydrates leads to high volatile fatty acid (VFA) production, lowering rumen pH, and causing lactic acid producing bacteria.
• Associated diseases include feedlot bloat, laminitis, PEM, and liver abscessation
• High CHO intake leads to excess VFA production with the overgrowth of Streptococcus bovis and Lactobacillus spp.
• Increased lactic acid production, decreasing rumen pH to 5 or less.
• Death of cellulolytic bacteria and protozoa.
• Chemical rumenitis may precipitate liver abscessation (F. necrophorum and A. pyogenes), chronic rumen epithelium damage and reduced absorptive capacity and rarely, mycotic rumenitis (Mucor, Rhyzopus and Absidia)
• Rumen stasis occurs, and decreased salivation exacerbates bicarbonate production.

Clinical Signs of Lactic Acidosis

• Stilted gait
• Grey/dark green, bubbly, watery scours
• Anorexia
• Ruminal stasis
• Dehydration
• Recumbency
• Death in less than 24 hours.

Post Mortem Findings of Lactic Acidosis

• Low rumen pH, with cattle on roughage normally showing a pH of 6-7, and grain-fed cattle at 5.5-6.5 with pH less than 5 indicating lactic acidosis.
• Rumenitis with necrosis of papillae.

Lactic Acidosis Treatment

• Mild acidosis: observe for worsening, and remove from concentrates, placing onto hay.
• Anorexia, diarrhoea, depression, mild dehydration: remove from concentrates, and drench with 500g NaHCO3, 500g MgO, and 500ml paraffin oil in 8L of water.
• Acute, severe acidosis: poor response to treatment to be expected, and if treatment chosen, use IV fluids with bicarbonate and corticosteroids and rumenotomy.
• Prognosis based on heart rate: HR < 100 is fair, 100-120 is guarded, and > 120 is grave.
• Pen treatment: if bubbly scours exceed 3%, check feed processing/delivery; drop back one diet until faecal scores improve. A severe pen problem (10%+ bubbly scours); provide hay in racks.

Lactic Acidosis - Prevention

• Provide cattle access to hay upon arrival before induction.
• The starter ration should not contain more than 50% grain.
• Acclimate to full feed slowly (over 10-14 days, or up to 21 days).
• Add NaHCO3 to high grain diets at about 0.75%.
• Virginiamycin can be added to the diet at 20ppm (S4 and use must be targeted and justified).
• Change feeds gradually, increasing grain by no more than 10% during the step from higher roughage starter to higher grain finisher ration.
• Avoid fluctuating feed intake, keeping the feed trough filled during peak feeding times (sunrise/sunset), ensuring sufficient trough space, avoiding overcrowding, feeding more often during cold/wet/windy weather or when barometric pressure drops, and limiting feed allocation increase to 10% a day.
• Ensure rations are consistently mixed.
• Maintain grain milling targets, monitoring for fines in the ration.
• Ensure roughage is of sufficient chop length.

Feedlot Bloat

• Gaseous bloat: lactic acidosis → rumenitis → inflammation of eructation stimulating area → decreased eructation → fermentative gas builds up.
• Frothy bloat: lactic acidosis → gram positive bacteria form a thick slime with foaming properties, trapping gas and forming air bubbles.
• Legume ingestion causes proteins in leaves to result in stable foam formation.

Feedlot Bloat - Clinical Signs and Treatment

• Sub-clinical: decreased average daily gain (ADG) and decreased feed efficiency.
• Mild: distension on left side, observe for worsening.
• Moderate: uncomfortable beast with bilateral distension, remove from feed, pass a stomach tube to relieve pressure, and give paraffin &/or defoaming agent.
• Severe: beast in respiratory distress, in lateral recumbency, likely to die, place trocar into rumen from left side, and consider rumenotomy.
• Prevention: As for lactic acidosis.

Laminitis

• Commonly associated with lactic acidosis.
• Decreasing rumen pH leads to histamine release which causes constriction of blood vessels in the hoof laminae or local histamine production due to circulating endotoxin secondary to lactic acidosis. Absorption of histamine increases below rumen pH of 6, indicating marginal lactic acidosis.
• High-grade Bos indicus cattle are more susceptible.
• Clinical signs: "cats on hot bricks” – stilted gait.
• Treatment: salvage slaughter if feeding or watering is impaired.
• Prevention: As for lactic acidosis.

Polioencephalomalacia (PEM)

• Sulphites attack thiamine at the methylene bridge, cleaving the pyrimidine ring from the thiazole ring, accelerated by acidic conditions.
• Thiaminases are produced by bacteria such as Bacillus thiaminolyticus, Bacillus aneurolyticus and Clostridium sporogenes.
• Acidic rumen increases PEM likelihood by increasing thiaminase exoenzyme or thiamine destruction by bacterial sulphate reduction.
• Thiamine deficiency reduces the activity of transketolase and reduces ATP production, impairing the Na-K pump’s function and leading to sodium and water accumulation in the brain as well as resulting in the brain compressing the cranium.
• The worst affected regions of the brain are the frontal, parietal, and occipital areas of the cerebral cortex and the thalamus.

Agents Associated With PEM

• Very high grain rations.
• High molasses inclusion rates (>10%).
• High sulphide intake (e.g., bore water).
• Lactic acidosis (acid shocking of bacteria results in release of exoenzyme).

Clinical Signs of PEM

• Blindness (menace reflex may persist)
• Fine muscle fasciculations (around face and muzzle)
• Tremors
• Star gazing
• Recumbency (possible extensor rigidity)
• Normal cardinal signs
• Head pressing
• Death within 3-6 days of onset.

Diagnosis of PEM

• Clinical signs
• History
• Sudden onset
• High concentrate diets/dietary change
• Post-mortem: diffuse cerebral oedema, compression and yellow discoloration of the dorsal cortical gyri, cerebellar distortion.
• Submit liver, kidney and brain for differentiation.
• Treatment: 10mg/kg thiamine IV, followed by 5 similar doses every 3-6 hours anti-inflammatories. Successful treatment requires animals to be treated before becoming recumbent.
• Prevention: avoid sudden dietary changes and lactic acidosis, as well as monitor sulphur intake and increase roughage. Levels of 5-10 mg/kg feed have been suggested to address a problem.

Salmonellosis -Aetiology and Pathogenesis

• Stress-related, may be higher in response to inanition (intensively fed sheep)
• Involves Salmonella typhimurium, S. bovis-morbificans and S. dublin; they are ubiquitous in feedlots.
• Sources of infection: carrier animals, contaminated water such as water fowl and animal products are banned in ruminant feeding, and transmission occurs via a faeco-oral route.
• Acute enteritis develops due to invasion of the intestinal wall and ensuing inflammatory response. Salmonellae can also invade the mesenteric lymph nodes, with bacteraemia potentially leading to secondary hepatitis, splenitis and respiratory disease and increases the BRD fatality rate.

Salmonellosis Clinical Signs

• Bright green/yellow mucus with intestinal mucosa often with blood.
• Marked pyrexia (40°C+)
• Tenesmus and abdominal pain
• Lethargy and depression
• Can have terminal nervous signs such as incoordination and nystagmus

Salmonellosis Post-Mortem Findings

• Oedematous inflammation of the small and large intestines.
• Characteristic fluid intestinal contents.
• Splenic engorgement.
• Possible diffuse hepatisation of the lungs.

Salmonellosis Diagnosis and Treatment

• Clinical signs and faecal culture of salmonellae.
• Gross post-mortem: culture of salmonellae in mesenteric lymph nodes and possibly spleen, liver and lung. Trimethoprim-sulfa are also used.
• Can also remove clinical to clean pen, move healthy contacts in pen as well or provide feed medication such feed is Sulfadimidine 400 gm/tonne for 5-10 dd.
• Prevention: Minimise stress and time off feed, prevent faecal contamination, prevent water fowl from contaminating water, prevent pen-to-pen drainage and maintain clean pens (faeco-oral transmission via grooming)

Urea Poisoning (Ammonia Toxicosis)

• Aetiology and pathogenesis is rare, with intake of too much urea and urea + water = NH3 + CO2, and excessive free NH3 which can overwhelm the liver detoxification, which passes into the blood and causes an increase in blood and brain pH.
• Free NH3 passes from the rumen to the portal circulation; as rumen pH increases, more free NH3 is made available.
  • pH = 6.4 then 1/1000 of all NH3 is free
  • pH=8.4 then 1/10 of all NH3 is free

Urea Poisoning - Symptoms, Diagnosis and Treatment

• Symptoms: seen 20-60 minutes after ingestion. Severe abdominal pain → teeth grinding, muscle tremors, salivation, incoordination, weakness, dyspnoea, bloat, violent struggling and bellowing, short disease, and causes death in 4 hours by respiratory arrest due to ammonia intoxication.
• Diagnosis - rumen pH > 7.5 and blood NH3 concentrations usually increased to > 1 mg/dL
• Treatment - Prompt emptying of the rumen with a stomach tube or rumenotomy which is followed by stopping the formation of free NH3
• Lower rumen ph with Vinegar - 4L by stomach tube
• Lower rumen temperature - 10-20L cold water drench

Urea Poisoning - Prevention

• QA to guard against feed shed mixing errors, urea < 30% NPN is the ration and <1% urea also ensure troughs dont allow pools of Nitrogen

Bovine Respiratory Disease (BRD)

• A multifactorial disease with a variety of stressors, various viruses (Parainfluenza 3 (P13)/Pestivirus/Coronavirus) +/ bacteria ( Mannheimia haemolytica /Pasteurella multocida /Histophilus somni /Salmonellaspp / Trueperella pyogenes).
• Is a function of exposure of stressors + naïve cattle
• Clinical Signs - Depression/lethargy/Coughing/Nasal discharge/Anorexia/Pyrexia/Increased respiratory sounds
• Diagnosis - Clinical signs/Auscultation/Rectal temperature/Post-mortem

BRD Post Mortem and Treatment

• Red-grey regions of hepatisation and consolidation fibrinopurulent involvement + exudate of lung, occasional peritonitis (Histophilus somni), and lung absessiveness gives indication whether it was acute or chronic
• Treatment - Antibiotics ( OTC /Tilmicosin/Ceftiofur /Florfenicol/Tulathromycin) + meloxicam ( as inflammation)
• Prevention - avoid placement through saleyards within 12 days + backgrounding for conferment + Fill pens quickly (ideally within 1 day) + Minimise transport distance + Yard weaning+ Vaccinations (with modified live BHV 1 vaccine at feedlot entry ( MH or MH+IBR) Ensure high diet / mineral is provided such: >60IU/kg Vitamin E and provide Zinc to at 30 mg/kg + 45 mg/kg until 28 days.

Infectious Bovine Rhinotracheitis (IBR)

• Caused by Bovine Herpesvirus 1 (BHV 1, increasing stress can cause a "late break") and can result in failure of the lung to clear as BHV1 destroys the mucociliary escalator

IBR - Clinical Sign and Diagnosis

• Clinical Sign the same except with significant frothy salivation with extension of the neck ( not pathognomonic)
• Diagnosis - Clinical signs /Auscultation may indicate increased respiratory/Pyrexia/Post-mortem
• Post-mortem Findings- Necrotic tracheitis with secondary ventral lung lobes resembling an inhalation pneumonia.

IBR Treatment and Prevention

• Treatment - Antibiotics / NSAIDs (tolfenamic) Prevention As for BRD + vaccination with Rhinogard.

Atypical Interstitial Pneumonίa (AIP)

Aetiology - Common in Nth America, rare in Australian (linked in Nth America with melengesterol acetate + heifers) but is linked with irritate gases. Relevant gases in feedlots are Hydrogen sulphide, Ammonia , methane and dust + mouldy hay Is often caused by all active reaction

Necrotic Laryngitis

Aetiology - Caused by Fusobacterium necrophorum which enters the larynx via buccal/laryngeal wounds from coarse feeds or haematogenous spread/Clinical Signs - Dyspnoea, often with inspiratory stridor and marked pyrexia

Necrotic Laryngitis Treatment

• Procaine penicillin 12 mg/kg, oxytetracycline at 10mg/kg/ dexamethasone im or flunixine melumines 4.Musculoskeletal conditions Concrete Disease - Holding of catttle on a concrete surface + wear of the sole of the soft tissue (high mortality rate due to immobility) + prevention on buying patterns is key. The treatment is to remove catlle in grass + Antibiotics Transport and processing damages resolves in a week unless abrasions, swollen or lesions occurs Feedlot footrot

Feedlot Footrot

• Caused by Fusobacterium necrophorum /Bacteroides melaninogenicu
• Lesions occur due damaged: - wet muddy/Foreign bodies
• Clinical Signs: - Lameness/swells/necrotic small
• Treatment- OTC/ Penicillin is effective when early or pen medicate feed when over 6% prevalence/
• Prevention =Keep it dry

Bullers Aetiology and Pathogenesis

• Bullers are attractive to penmates, are multi-factorial, involve both riders and bullers and there is little bulking below 100 with dominance hierarchy. Incidence occur in late summer when cattle develop seromas and brushing
• Provide a buller pen for fast growth

Preputial Prolapse

• Primarily seen with heavy sheaths in Santa Getrudis and Barford cattle which can cause urine retention, and HGP are believed

Preputial Prolapse Treatment

• Anti-inflammation + penicillin or OTC or obstruction

Polioencephalomalacia

Neurological condition related to lactic acidosos

Listeriosis

• Neurological condition is caused Listermonoctogenes by spoiling spoiled silage which causes, and the occurs is not strict to silage Clinical Signs - fever and Head pressing /Unilateral facial paralysis /Ataxia + death due to respiratory failure
• Ensure the cerebellum and brain stem are included for analysis Prevention do not feed poor <5 pH of silage + prevent contaminants

Thromboembolic Meningoencephalitis (TEME)

• Caused by Histophilus somni which is transmitted via respiratory Clinical Signx: Sudden onset/ataxia/blindness

• Synovial fluid cloudy and may contain fibrinous flecks Tx: OTC

Clostridial Diseases

• Blackleg is caused by Clostridium chauvoei and causes gangrene of the muscles and Tetanus Cl and has 5:1 control

Botulism

• Cl. Botulinurn causes are flaccid paralysis.
• Feedlot are most likely get urolithiasis because steers have a arrow urethra + concentrates have high phosphorus

Heat Stress Aetiology

• High temperature over 42 + interruption to supply is the cause.
• Must have water cannon / shade for cooling and have a contingency plan.

Parasites

• Use a ivermectin of lactones to deworm Helminths + watch if liver fluke burdens

Coccidiosis

Caused by Eimerian and it’s rare due to the feed additives