Ruminant Gut Adult Non-Stomach Conditions PDF

A D U LT R U M I N A N T 3 : NON-STOMACH CONDITIONS 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 asso...

A D U LT R U M I N A N T 3 : NON-STOMACH CONDITIONS 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 non-stomach GI diseases and choose appropriate diagnostics Determine appropriate medical and surgical interventions in the management and treatment of the non-stomach GI disease in ruminants Determine appropriate prognosis, based on an individual animal and a herd Determine control measures appropriate for non-stomach GI disease prevention. 2 DIFFERENTIAL DIAGNOSES Infectious Obstruction Johne’s Disease Choke Bovine Viral Diarrhoea Caecocolic dilation and volvulus Salmonella Mesenteric torsion Winter Dysentery Other Parasitic Gastroenteritis Peritonitis Poisoning Acorn Yew #universityofsurrey 3  JOHNE’S DISEASE Chronic wasting disease chronic granulomatous enteritis and lymphadenitis Signs appear 2-5 years old After stressful event Clinical Signs Reduced production and fertility 10% decrease in My before clinical signs 20% decrease in MY after clinical signs Severe, progressive weight loss Intermittent diarrhoea No blood or mucous Submandibular oedema, emaciation and death 4  JOHNE’S DISEASE Diagnosis – No test 100% Ziehl-Neelsen staining of faecal smear or histo section Bacteriological culture of faeces 25% Se which increases when animal shedding to 74%, 100% Sp Faecal PCR Se increases with shedding to around 60%, 100% Sp Blood or milk ELISA - detect antibodies BUT not usually produced until late in dz, but still before shedding and clinical signs occur. 30% Se, 98% Sp Single herd test will detect 15-30% infected animals Repeat testing will ID up to 90% animals before they become clinical 1-2% False +ve when get down to low herd prevalence can make it difficult to manage Issues from TB testing and other mycobacteria exposure Don’t Johne's test within 6 weeks of TB test In the most optimistic scenario with 70% Se, 3/10 infected animals will return -ve test results 5  JOHNE’S DISEASE Control/ Prevention Minimum yearly testing Red cows – should be culled; start with most red If prevalence low then cull J4 (not J3) Combine with other data – milk yield, scour Protect calves from all manure and milk from amber cows Responsible sourcing of replacements – accredited free herds Calves more susceptible to infection: +ve animals calve in separate calving pen pinocytosis in the first 24hrs Either: oesophageal groove closure Raise calf for fattening – don’t keep as replacement takes bacteria straight to the Snatch calf for breeding before chance of faecal contamination abomasum Peyer's patches 9% of the MAP survives in faeces, so don’t spread on grazing fields surface area of intestine which Mains water have M cells that sample antigen 6 BOVINE VIRAL DIARRHOEA VIRUS Type I in UK, Type II in Europe Mucosal disease Various disease forms: Fatal disease of PI animals BVDv mutation into cytopathic form Acute disease Any animal Animals 6 –24 months old typically Small production losses Depressed Anorexic Lasts scour and Mucosal lesions: pneumonia Lips, gums, tongue, oesophagus, intestine Reproductive disease Diarrhoea: PI Foul smelling, blood, mucous Naïve dam infected 0-110 days Death in 5 –7 days Fetus is immune-incompetent Virus becomes established in tissues 7  BVD Diagnosis MDA can interfere with Ab testing until 4-5 months PCR for antigen Re-test 4 weeks later to distinguish PI from acute infection Ear notch testing for antigen ELISA or PCR Can’t test calves 3months May be worth testing specific cohorts Detection of carrier animals is difficult as often intermittently shedding for faecal culture Means you can't just say you are going to cull carriers 12  SALMONELLA Treatment Antimicrobials if septicaemic Control points for Salmonella TMPS (C+S important for resistance) Calving pen management May increase period of shedding Prompt removal of calf to reduce exposure Low stocking density Fluids – Oral/IV Regular bedding and cleaning out NSAIDs Pre-weaning management Good colostrum Don’t feed waste milk Keep separate from cows Can vaccinate Hygiene Reduces abortions and shedding Heifer management Avoid contact with mature cows Don’t graze on land that has had slurry on Quarantine ELISA screen purchased animals 13 WINTER DYSENTERY Acute and highly contagious Variable causing watery diarrhoea anorexia/depression/dehydration Housed, adult dairy cows Drop in milk production Normally winter Mild respiratory signs High morbidity but spontaneous recovery Probably Bovine Coronavirus 2-3 days Faeco-oral route Risk Factors Changes in diet Clinical signs Cold temperatures Acute onset explosive diarrhoea (+/- High stocking density dysentery) Poor ventilation Dark green – black Concurrent microorganisms May contain blood and mucous 14 WINTER DYSENTERY #universityofsurrey 15  WINTER DYSENTERY Diagnosis and Treatment Diagnosis: Exclusion of other pathogens BVD – absence of mucosal lesions Salmonella – Negative cultures Coronavirus ELISA?? Treatment Mostly spontaneous recovery after ~3-5 days Supportive therapy Fresh water, palatable feed, free-choice salt Fluids IV in most severely affected animals 16 PA R A S I T I C G A S T R O E N T E R I T I S - C AT T L E Ostertagia ostertagi Normally within first year grazing Two clinical syndromes: Type I Type II Late summer/early autumn Infective larvae ingested from autumn Ingestion and immediate maturation of onwards large numbers of larvae Arrested development L4 within Dry early summer → wet abomasal glands August/September Mass emergence late winter Sudden, profuse green diarrhoea Profuse unresponsive diarrhoea High morbidity, low mortality Poor treatment response Can lose up to 10% bdwt 17 PA R A S I T I C G A S T R O E N T E R I T I S - C AT T L E 18  P G E - C AT T L E Diagnosis, Treatment and Prevention Diagnosis Treatment History Type I: All anthelmintics (chose wisely to avoid Grazing pattern resistance!) Weather Type II: Group 3 anthelmintics (avermectin) Previous anthelmintic treatments Supportive therapy Faecal egg counts Prevention Type I High Grazing management Type II Probably absent Strategic anthelmintic treatments Pepsinogen levels Type I: ~3, 8 and 13 weeks post turnout Type II: Ivermectin at housing Faecal egg counts AHDB parasite control guide https://ahdb.org.uk/knowledge- library/parasite-control-guide 19 PGE - LAMBS Nematodirus battus Immature larvae L3 that cause the clinical signs Ingestion of infective L3 from the pasture – overwintered mass-hatch onto pasture following warm weather >10⁰C NADIS forecasts Development in the small intestine Clinical signs: Weight loss, diarrhoea, faecal staining around perineum, dehydration, death Usually spring in young lambs weather changes → outbreaks in older lambs later in season 20 21  PGE - LAMBS Diagnosis, Treatment and Prevention Diagnosis: FEC unhelpful 1 egg signifies a problem. Useful for monitoring treatment efficacy Clinical signs and Post-mortem Treatment: use of strategic benzimidazole anthelmintics (white drench) Control measures Not grazing next years lambs on the same pasture as last year due to carry over of pasture contamination Use of risk forecasts to predict mass hatchings of L3 22 ANTHELMINTICS Sustainable parasite control – sustainable use of anthelmintics Most products are POM-VSP Useful resources: SCOPS Know your anthelmintics groups https://www.scops.org.uk/internal- parasites/scops-know-your-anthelmintics- guide/ 23 ACORN POISONING Phenols and Tannins → Severe kidney damage Clinical Signs Anorexia, depression, weight loss Rumen stasis → foetid, tarry diarrhoea Death 4-7 days Sudden death Treatment – supportive Prevention – avoid grazing around Oak trees in Autumn 24 YEW POISONING toxic alkaloids – affect heart muscle Even more toxic after cutting Lethal dose of fresh plant material is 1-10g/kg BW Sudden death → very limited pathology Clinical signs Muscle tremors and incoordination Nervousness Difficulty breathing Vomiting and diarrhoea Convulsions Prevention – Prevent access! 25 CHOKE Oesophagus is obstructed by food or foreign objects → root vegetables Clinical signs: free-gas bloat, ptyalism/ nasal discharge of food + water. May present bloated and in distress or recumbent impedes eructation of ruminal gases, and free-gas bloat develops. Severe free-gas bloat may result in asphyxia expanding rumen puts pressure on the diaphragm and reduces venous return of blood to the heart. Diagnosis: inability to pass a stomach tube Treatment: trocar in left paralumbar fossa. solid objects (e.g, potatoes) may often be massaged free or spontaneously dislodge as their outer surfaces are softened by saliva Caution if attempt to push object down the oesophagus → oesophageal rupture 26  JEJUNAL HAEMORRHAGE SYNDROME Sporadic Disease Uncertain aetiology – C. perfringens type A Acute, localized, necrotizing, haemorrhagic enteritis of the small intestine that leads to development of an intraluminal blood clot Clot causes physical obstruction with proximal accumulation of intestinal fluid and gas and development of hypochloraemia, hypokalaemia, dehydration, and varying degrees of anaemia Progressive → Ischemia and necrosis extends through the intestinal wall, and within 24–48 hr, there is a fibrinous peritonitis, continued electrolyte imbalance, profound toxaemia, and death. Clinical signs sudden onset of abdominal pain, progressing to sternal recumbency, shock, and death Diagnosis made either during an exploratory laparotomy or at necropsy (may be able to see with U/S) Treatment: supportive Hospital cases may try laparotomy to remove blood clot 27 OBSTRUCTIVE DISORDERS Often unknown aetiology Altered intestinal motility Mesenteric or Caecocolic volvulus Ingestion of rapidly fermentable substrates Peritonitis adhesions Intussusception Clinical Signs Anorexic Reduced faecal output – mucous, blood tinged Sudden milk drop Cardiovascular effects Injected mucous membranes 28  OBSTRUCTIVE DISORDERS Diagnosis, Treatment and Prognosis Diagnosis: Treatment: Abdominal contour lower right for small Exploratory laparotomy intestine distension Right sided standard abdominal incision Auscultation pings and splashes Exploratory typhlotomy (caecum) Rectal examination dilated caecum in pelvis Supportive therapy Distended loops of intestines NSAIDs – risk of toxic shock on reduction Ultrasonography Right paralumbar fossa or Fluids – IV per rectum small intestinal distension Antibiotics – peritonitis, surgery increased peritoneal fluid Abdominocentesis haemorrhagic - strangulating obstructions Prognosis: Caecocolic volvulus 70-80% Small intestine volvulus 3g/dl NSAIDs Antimicrobial broad spec e.g amox-clav neutrophils (macrophages normal) Permeability of peritoneum increased Ultrasound free fluid in abdomen Diffusion into abscesses may be difficult abscesses Surgery?? Rectal examination lack of movement of Debridement, irrigation and drainage rectal wall (diffuse) Ultrasound guided Exploratory laparotomy Fibrin deposition rapid Prognosis - Guarded 33 #universityofsurrey 34