Neonatal Calf Gastrointestinal Disease - PDF

N E O N ATA L CALF GASTROINTEST INAL DISEASE LUISA SOARES LMV, FHEA, MRCVS LECTURER IN PRODUCTION ANIMAL MEDICINE LEARNING OBJECTIVES By the end of this lecture should be able to Construct a differential diagnosis list based on clinical presentations associated wi...

N E O N ATA L CALF GASTROINTEST INAL DISEASE LUISA SOARES LMV, FHEA, MRCVS LECTURER IN PRODUCTION ANIMAL MEDICINE LEARNING OBJECTIVES By the end of this lecture should be able to Construct a differential diagnosis list based on clinical presentations associated with neonatal GI diseases and choose appropriate diagnostics. Determine appropriate medical and surgical interventions in the management and treatment of neonatal GI diseases in ruminants. Determine appropriate prognosis, based on an individual animal and a herd. Determine control measures appropriate for neonatal GI disease prevention. 2 W H AT W E A R E G O I N G T O C O V E R Diarrhoea Diphtheria Bloat Atresia coli and ani 3  CALF DIARRHOEA/ SCOUR 48.2% of pre-weaned calves affected by Diarrhoea * Up to 40% of calf deaths in the first six weeks of life are scour related. Need for rapid and appropriate treatment to ensure survival £123 per sick calf £36.91 per calf born Cause of death = dehydration, acidosis Damage to the guts results in reduced ADG *Johnson, K. F., Chancellor, N., & Wathes, D. C. (2021). A Cohort Study Risk Factor Analysis for Endemic Disease in Pre-Weaned Dairy Heifer Calves. Animals : an 4 open access journal from MDPI, 11(2), 378. https://doi.org/10.3390/ani11020378 AETIOLOGICAL AGENTS Nutritional Infectious Milk replacer Viruses: Quantity Rotavirus Quality Coronavirus Mixing (BVD) Temperature Bacteria Irregular feeding E.coli Poor weaning management Salmonella Clostridium Protozoa Stress Cryptosporidia Coccidia 5  Diarrhoea pathogens diagnosed on the farm (multiple options could be selected). Note: 49% of farmers did not use diagnostics or did not diagnose any pathogens for diarrhoea. Insights into UK farmers' attitudes towards cattle youngstock rearing and disease. Katharine Baxter-Smith and Robert Simpson. Livestock 2020 25:6, 274-281 https://doi.org/10.12968/live.2020.25.6.274 APHA 2012-2020. Scour causing pathogen identification in neonatal, pre-wean, post-wean groups. 6 DIARRHOEA Rotavirus and Coronavirus Picked up from calving pen then spread to other calves E. coli F5/ K99 1-3 days old picked up from calving pens F5 adhesion antigen + enterotoxin causes hypersecretion of Cl- and water into gut lumen Salmonella Neonatal or older – different presentations From carrier animals Colstridium perfringens Toxin α and β 7 DIARRHOEA Cryptosporidium Environmental pressures Excreted oocysts immediately infective Coccidia Weeks – months old Eimeria bovis/ zuernii/ alabamensis Exposure unavoidable Excreted oocysts need to sporulate in environment before becoming infective 8 9 HYPERSECRETORY VS MALABSORPTIVE Malabsorptive Crypto (villi), corona (villi), clostridium (mucosal necrosis), BVD (crypts) Rate of cell loss higher than cell replacement Reduction in small intestinal surface area for enzyme digestion and absorption of water and nutrients osmotic diarrhoea Hypersecretory Rota is both E.coli (villi damage as well), salmonella Pathogen secretes enterotoxin Chloride channels open Net secretion of chloride, sodium and water into intestinal lumen Overwhelms the absorptive capacity of the large intestine so increased fluid content of faeces 10 E N D R E S U LT → D E H Y D R AT I O N A N D M E TA B O L I C A C I D O S I S F R O M E I T H E R E L E C T R O LY T E I M B A L A N C E O R D - L A C T A T E B U I L D U P. 11 D - L A C TAT E A C I D O S I S Calves with Diarrhoea have damage to intestinal enterocytes allows undigested carbohydrates to reach the large intestine → acidification which favours growth of lactic acid producing gram positive bacteria. D-lactate also produced following ruminal drinking of milk, although at lower levels. Clinical signs of D-lactataemia: decreased palpebral reflex, broad based stance and ataxic movements due to the direct toxic effects on the brain. Signs associated with simple dehydration include a reduced suckle reflex, enopthalmus and an increased skin tent. Lorenz, I. & Gentile, A. (2014) d-Lactic Acidosis in Neonatal Ruminants. The Veterinary clinics of North America. Food animal practice. 30 (2), 317–331. 12 https://surrey.primo.exlibrisgroup.com/permalink/44SUR_INST/1tc3s1n/cdi_webofscience_primary_000339363000003CitationCount 13 HYPERKALAEMIA Diarrhoea causes hyperK+ due to acidaemia-induced dysregulation of internal K+ balance Confusing concept → potassium is lost from the body with Diarrhoea BUT potassium is used to buffer the high levels H+ in the blood, along with impairment of sodium/potassium ATPase which results in increased intracellular sodium and increased extracellular potassium → hyperkalaemia!! Hyperkalaemia = neuromuscular excitability and muscular weakness clinically an inability to stand and usually severe dehydration bradycardia Prompt response to fluid therapy treatment unlike calves suffering from D-lactataemia which takes time to leave the body. 14  DIAGNOSTICS FOR DIARRHOEA Enable correct treatment to be administered. Antibiotics Antiprotozoals Impossible to tell the exact cause of scours based on clinical signs and the nature of the scour alone. Rapid on farm diagnostics on faeces (“Rainbow test”) ELISA Lab PCR Faecal egg counts Haematology/ Biochem Which animals to sample? Acute cases Ideally not treated with ABs 15 T R E AT M E N T Considerations Suckle? Yes >Oral Rehydration Solutions No >IV fluids Oral feeds Continue milk Electrolytes as additional feeds Replace what has been loss Overcome continued losses #universityofsurrey 16 DECISION TREE FOR THERAPEUTICS 17 ORAL FLUIDS First generation ( e.g. rehydion gel) sodium, potassium and (insufficient) glucose. effective in treating dehydration associated with scour but cannot correct acidosis. Second generation (e.g. lectade plus) contain bicarbonate or bicarbonate precursor such as lactate, propionate or citrate very effective at treating dehydration and acidosis do not provide any energy to the calf Third generation (e.g. diakir plus) contain much higher concentrations of glucose to counter the energy deficit when milk feeding is stopped during treatment. Fourth generation (e.g. glutalyte) contain amino acid glutamine. used as both an energy source, as well as for protein synthesis, to facilitate sodium absorption from the small intestine and to help sustain the intestinal villus form and function. 18  IV FLUIDS Unable to stand, no suck reflex KEEP IT SIMPLE! “The kidney is smarter than the smartest vet” Perfuse the kidney and it will sort out 90% of acid- Base Deficit < 8 days old >= 8 days old base and electrolyte abnormalities Standing, strong suck 0 mmol 5 mmol Standing, weak suck 5 mmol 10 mmol Bicarbonate Sternal recumbency 10 mmol 15 mmol Often recommended in literature → RARELY needed Lateral recumbency 10 mmol 20 mmol Only use if severe D-lactic acidosis Hypovolaemic ➔ poor tissue perfusion ➔ lactate ➔ acidosis Alkalosis is more dangerous than acidosis Do not put into Hartmann’s – 0.9% saline 19  IV FLUIDS Dehydration as % BW IV fluid flow rate 5ml/kg/hr maintenance Provide half the deficit as a bolus, the other half over 6-8hrs Additionally, you can give 80ml/kg/hr for up to 30 minutes initially as a bolus (open the drip up). Example: 50kg calf with 10% dehydration 10% dehydration will result in a deficit of: 50 × 0.10 = 5 Litres Maintenance fluids for a calf = 50ml/kg/day = 2.5 Litres Ongoing losses approximately = 100ml/kg/day = 5 Litres Total 12.5 Litres over 24h Recommended reading: https://www.vettimes.co.uk/app/uploads/wp-post-to-pdf-enhanced-cache/1/practical-fluid-therapy-in-cattle-an-overview.pdf Hallowell, G. & Remnant, J. (2016) Fluid therapy in calves. In practice. 38 (9), 439–449. https://surrey.primo.exlibrisgroup.com/permalink/44SUR_INST/1tc3s1n/cdi_proquest_journals_1824985011 20 OTHER THERAPIES Specific Therapies Diagnosis necessary!! Antibiotics Not normally indicated (e.i. 10% cases) Only under veterinary guidance Antiprotozoals Cryptosporidia - Halofuginone Lactate Coccidia – Toltrazuril, Diclazuril, Decoquinate NSAIDs Meloxicam Reduce clinical signs 21 V A C C I N AT I O N Rotavirus, Coronavirus, E. coli F5 K99 adhesin Administer to cows/heifers pre-calving 12 – 3 weeks pre-calving Boost colostral antibodies Reduce incidence and severity of diarrhoea Reduce shedding of viruses 22 W H Y D O C A LV ES G E T D I A R R H O EA? ? 23 P O P U L AT I O N L E V E L I N V E S T I G AT I O N 1. Define the problem Calf scour 2. Define assessment criteria Diagnostic, therapeutic, prognostic 3. Collect information Environment, husbandry, group, records 4. Evaluation of problem Environment, lab samples 5. Define possible interventions Therapy, management, environment 6. Implementations Economic concerns vs welfare concerns 24  R I S K FAC TO RS Environmental risk factors Management risk factors Group size Mixing ages Stocking density Feeding practices Inter-batch disinfection Nutrition Dry bedding Milk feeding Concentrate provision Forage Cleanliness External stressors Management risk factors #universityofsurrey 25 M O N I TO R I N G C A LV E S A N D E F F E C T S O F CHANGES Body weights Growth rates Average daily gain Failure of Passive Transfer Total protein assessment of calves 50g/L TP >12g/L IgG Absorption Timing Presence of dam Metabolic disturbance Bacterial contamination Route of administration Quantity 3L within first 2h of birth 6L within first 12h https://ahdb.org.uk/knowledge-library/calf-management (accessed: October 2024) 27 HYGIENE HYGIENE! Faeco-oral route Regularly clean out and disinfect pens Quaternary ammonium based Kills cocci+crypto oocysts Ideally between groups Fresh, dry straw Low stocking densities Isolate scouring animals 28 #universityofsurrey 29 CALF DIPHTHERIA Fusobacterium necrophorum 2 forms Necrotic stomatitis – necrotic ulceration of the cheek Necrotic laryngitis – necrotic ulceration of the larynx Injury to mucosa → F. necrophorum infection Clinical signs: external swelling on the side of the mandible, or a lesion on the tongue. Foul smelling breathe, Cough, pyrexia, difficulty swallowing Diagnosis: Visual inspection of the oral cavity +/- speculum and light to visualise the larynx. 30 CALF DIPHTHERIA Treatment: Necrotic stomatitis- systemic administration of beta-lactams (penicillin usually sufficient for 3-5 days), tetracyclines, sulphonamides and macrolides Necrotic laryngitis- extended course ABs 2-3 weeks NSAIDs. Animals suffering dyspnoea may need a tracheostomy +/- steroids. Risk factors: Unhygienic environment, dirty shared feeding vessels, dry rough grazing or forage, erupting teeth, calves suffering from other concurrent upper respiratory diseases Good prognosis for necrotic stomatitis, Guarded for necrotic laryngitis 31 R U M I N A L T Y M PA N Y / B L O AT Accumulation of gas in the rumen most commonly seen 1–2 hours after feeding milk often associated with a pasty scour and bouts of colic Caused by feeding errors that lead to incomplete oesophageal groove closure. Incorrect temperature, bucket feeding, incorrect concentration Milk entering the rumen ferments and produces bloat with severe colic Also gorging on concentrates Treatment: passage of a stomach tube, or in extreme cases by trocar and cannula. NSAIDs will relieve the colic Prevent: address feeding practices 32  AT R E S I A C O L I A N D A N I Atresia ani Congenital absence of anus Lack of faeces Gradual development of abdominal distension Calves develop colic after ~3 days If rectum is present, there may be a soft bulge from pressure of accumulated faeces Can attempt treatment by incision Atresia coli Congenital intestinal aplasia and stenosis Calf develops progressive abdominal distension and colic. No Treatment - euthanasia 33 #universityofsurrey 34 35