Equine Oral/Esophageal Dz PDF

654 ● ● Equine Oral/Esophageal Dz ○ Anatomy contributing to dental problems ■ Foals 6d, 6w, 6m rule ● Central, intermediate, corner incisors come in ■ Lower jaw 25% narrower, overgrowth where teeth don't contact ■ Canines males only ○ Malocclusion ■ Uneven tooth wear ■ Points, hooks, wave mouth, s...

654 ● ● Equine Oral/Esophageal Dz ○ Anatomy contributing to dental problems ■ Foals 6d, 6w, 6m rule ● Central, intermediate, corner incisors come in ■ Lower jaw 25% narrower, overgrowth where teeth don't contact ■ Canines males only ○ Malocclusion ■ Uneven tooth wear ■ Points, hooks, wave mouth, stepped molar arcade ○ Oral exam ■ 1-2x yearly for mature horses ■ Restraint, sedation, and speculum all critical ■ Palpate teeth, look at them all ■ Many dental dz prevented with care and diet ■ Wolf teeth vestigial PM1 ● Check top and bottom! ■ Retained premolars ○ Dental Sx ■ Many risks, $$, post-op complications ○ Esophageal obstruction (choke) ■ Risk factors ● masticatory/dental probs ● Stricture, diverticulum, perforation, esophagitis, neoplasia ● Cranial ⅔ striated mm, distal ⅓ smooth m ■ Clinical signs ● Nasal discharge (food, mucopurulent) ● Cough, pain, wt loss ■ Dx-NG tube, contrast esophogram ■ Tx ● May resolve on its own ● Gentle NG tube intubation ● Oxytocin to reduce skeletal m tone (proximal ⅓) ● Buscopan SM relaxation (distal) ● Sx esophagostomy ● #1 complication aspiration pneumonia ● Manage w/slow feeding, dental care, quality food ● Esophagitis Tx motility agents, (Bethanechol) ● Neoplasia= RARE Intro FA GI Dz/Individual Assessment ○ Anatomy/physiology ■ Rumen most of L side cow ■ Abomasum lower R quadrant ■ Omental curtain hangs over organs ■ Liver R side, spleen L side ○ PE techniques ■ Ballotment ■ ■ ■ ■ ● Auscultation Auscultation-percussion Sucussion Rectal palpation! ● Can feel lots of organs ○ GI system response ■ Low-threshold receptors INcrease rumen motility ● Pass stomach tube ■ High-threshold receptors DEcrease motility ■ Elevated Cl= abomasal reflux ○ GI clinical signs ■ Abd distension, pain, diarrhea, reduced fecal output ■ Wt loss, inappetence, bottle jaw Ruminant GI Dz ○ Exam ■ Gum color, pointed papilla ■ Intact palate Poison hemlock, nicotine ingestion ● Signs of regurg milk ■ Dentition ● Central incisors at 18mo (cattle show anecdote) ○ Dx= reportable, aggressive disinfection, insect control, zoonosis risk ■ Vesicular lesions ● Blisters, salivation ● Ddx FMD, VS ● 3-5d incubation, coronary band lesions ■ Malignant catarrhal fever ● Viral mainly in sheep ● Erosions, mucopurulent exudate ● Early corneal opacity ■ Bluetongue ● Sheep ● Hemorrhagic Dz in deer ● Photosensitization ■ Rinderpest globally eradicated ■ Contagious Ecthyma (ORF)= poxvirus ● Zoonotic target lesion ● Risk of condition loss w/discomfort ● PCR ● Scarification vxn, careful ■ Woody tongue ● Actinobacillus lignieresii, sulfer granules ● Tx sodium iodide ● Gram neg ■ Lumpy jaw ● Actinomyces bovis ● Gram pos ● Presumptive Dx ● Tx sodium iodide, Abx ● Poultry GI ○ Enteric Dz ■ Rotavirus ● Chickens may be subclinical ● Dilated intestines yellow, frothy, watery contents ● No vxn/tx ■ Reovirus ● Arthritic symptoms ■ Astrovirus ● Avian nephritis virus ● White chicks condition ■ Coronavirus ● Green-brown, watery frothy droppings in turkeys ● No vxn, tx ■ Clostridial ● Necrotic enteritis ■ Change in gut flora predisposed ■ Ballooned friable brown intestines ■ Prevention w/abx for coccidiosis ● Ulcerative enteritis ○ Clostridium colinum in quail ○ Chickens recover in 2-3wk ○ Neoplasia ■ Marek’s Dz= herpes ● All flocks assumed infected ● Enlarged nn, atrophic bursa, diffuse lymphoid tumors ■ Lymphoid leukosis ● Lifelong carriers shedding ● Bursal tumors ● Depopulation control ○ Nervous system ■ Encephalomalacia from Vit E deficiency ● Muscular dystrophy in mature birds ■ Avian encephalomyelitis ● head/neck tremors ■ Botulism= flaccid paralysis, no lesions ○ Systemic Dz ■ Fowl cholera ● Pastuerella multocida, v contagious ○ Swollen face/wattles ■ Salmonella ● Pullorum Dz ● Diffuse grey nodules ■ Fowl typhoid, paratyphoid ■ Colibacillosis ● E. coli ■ Erysipelas ● Acute sudden death ● Live vaccine 2-3wk split ■ ● ● Infectious bursal Dz (Gumboro) ● Immunosuppression ■ Gout ● Urate deposits ○ Parasitic Dz ■ Mites ■ Helminths ● Rotate ground, deworm ■ Coccidiosis ● E. tenella high mortality, bloody feces, cecal blood ■ Histomoniasis ● Liver and cecal target lesions ○ Pododermatitis Population FA GI Health ○ Infectious and non-infectious GI signs look the same ■ Root causes are multifactorial ● Nutrition, housing, normal flora, pathogens ○ Assessment=measuring=counting ■ Track by case definitions ■ Intervene early in an epi curve ○ Causes by life stage ■ Management of FA GI health ○ Rumen fermentation ○ ○ ○ ○ ○ ○ ■ VFA= cow for energy N=cow for protein Saliva as buffer Contractions ■ primary=mixing ■ secondary=eructation Health metrics ■ Appetite, production, contraction rate, rumen metrics, manure Cow-calf= 80%+ forage ○ ● ● Stocker= 35-65% grain ■ Avoid acidosis ○ Feedlot finisher= 80%+ grain ■ Diff rumen, manure ○ Lactating dairy= 50% grain, high dry matter ■ 3.5-4% milk fat in Holsteins ○ Non-lactating dairy= 80%+ forage and straw ■ Just barely maintaining to avoid preg issues ○ Displaced Abomasum ■ Nutritional cause ■ Subclinical ketosis, hypocalcemia ○ Beef cows don’t really get GI issues Forestomach Motility Issues ○ Clinical Signs ■ Papple= large L-shaped rumen ■ Abd fill in spite of poor appetite ○ Differentiate types ■ TRP (Hardware Dz) ● Feed magnet ● Reticulum juice v bad for the peritoneum ● Failed Withers pinch ■ Abomasal impaction (sand, poor quality feed) ● Oral fluids + mineral oil ■ Ruminal tympany (bloat) ● High, left, compressible ● V dangerous ● Tx stomach tube, feed low-bubble surfactant, relieve choke ● Plant ingestion or bacterial overproduction causes ○ Dx plan ■ High rumen CL=abomasal backflow ■ Lymphosarcoma (HULA locations) ○ Tx plan Displaced Abomasums ○ Anatomy ■ LDA= decreased motility and smaller rumen= shift L ■ *RDA= dilation, COUNTERCLOCKWISE rotation ● Fluid accumulation= v bad ○ Risk factors ■ RDA= Holsteins, early lactation, acutely off feed, dramatic production drop ■ LDA=Holsteins, recent calving, decreased production/eating ■ both= peri-parturient Dz, low fiber/high starch diet ● Milk fever, ketosis, metritis ○ Clinical signs ■ LDA= ketotic urine, ping on L ribs 13-18 ■ RDA= generally sick cow, decreased K, Cl on serum chem ○ Ddx ■ RDA= cecal dilatation ○ Tx plan LDA ■ Sx or Toggle, tx ketosis ● ● ○ ● ● ● R flank omentopexy Toggle placement on the side, tack outside the body ○ CHEAPER, FASTER Tx plan RDA ■ R flank laparotomy (deflate, untwist, tack to the body wall) ● Loss of motility poss ● Swoosh RIGHT Infectious enteric dz in cattle ○ Diarrhea as an indicator of GI health ○ Optimized growth= minimizing health problems ○ Managemental neonate diarrhea ■ Improper measurement of milk replacer=inconsistent nutrition ■ milk+grain= best rumen development ○ Infectious neonate diarrhea ■ E. coli ● 2-5d calves, dehydration/electrolyte derangement ■ Salmonella= bloody diarrhea ■ Coronavirus ● Calves <2wk ● Entire villus affected (crypts) ■ Rotavirus ● Calves up to 2wk ● Villus tip blunting ■ Cryptosporidium ● Zoonotic! ● 7-30d calves ● Mucoid diarrhea ● Acid-fast staining Managing infectious enteric dz in cattle ○ Presenting signs of enteric dz ■ Wt loss (chronic) ■ Sudden death (acute) ■ Abd distension (A) ■ Abd pain (A) ■ Reduced performance (C) ■ Pathogen locations ■ ETEC=jejunum ■ EHEC=colon ■ clostridium=abomasum, SI, colon ■ Rotavirus=SI ■ coronavirus=SI, colon ■ Crypto=ileum ■ coccidia=ileum, LI Eq gastric ulcers ○ EGUS in most broodmares, performance horses ○ Dx= response to Tx, endoscopy (only definitive) ○ Risk factors ■ Intense exercise, poor diet management (high concentrate) ○ Adults ○ ○ ○ ● ● ● ■ Foals ■ Path ■ ■ ■ Tx ■ Poor appetite, BCS, performance Colic, laying on back, bruxism Aggressive factors>defenses damage gastric lining Squamous mucosal lesions from increase acids (80% ulcers) Glandular mucosal lesions from impaired mucosal protection medication= control gastric acid (neutralizers, antisecretory), mucosal protectants ● Prostaglandins decrease acid ● Gastrogard=acid pump inhibitor ● Compounded omeprazole=bad for concentration, degradation ■ control= reduce training/stress, limit fasting, increase roughage, reduce grain ○ Duodenal ulcer/stricture ■ Foals, Tx gastrojejunostomy Abomasal disorders ○ Ulceration ■ Stress, diet, high grain ■ Hospitalized camelids high risk ■ Tx buffers, decrease acid production ○ tympany/abomasitis ■ >2wk bottle fed calves ■ Bacterial overgrowth C. perfringens type A ● Off feed w/o diarrhea, ‘slosh’ in abomasum ● Tx PPG PO, C. perf anti-toxin C&D ■ prevention=feeding management (small meals frequently) Ruminal acidosis ○ Risk factors ■ Sudden change in amount or type of CHO ■ Grain type fed, processing (moisture, particle size) ○ Ruminal changes ■ Excess starch & sugar= rapid fermentation ● Shift in microbial pop ● Increased lactate production= decreased pH ■ ACUTE= life-threatening ○ Clinical signs ■ Anorexia, bloat, watery diarrhea, death ○ Dx=Rumen pH <5, no living protozoa in rumen fluid ○ Tx=Stop fermentation & remove VFAs ■ Evacuate contents, +/- give PPG ■ Neutralize rumen pH, feed hay ○ Sequelae= liver abscessation Eq Small intestine ○ Gastric impaction ■ Dry feed, decreased water-> coke at Tx ○ Gastric neoplasia ■ SCC ● ● ■ Chronic wt loss, anemia, colic ■ Endoscopy ○ Anterior enteritis (AE) ■ Marked inflammation of SI ■ Adult horses on a high level of nutrition ■ Large nasogastric reflex ■ Dx intestinal distension on US, tap peritoneal fluid, explore ■ Tx decompress tube, fluid & electrolytes IV, flunixin meglumine ○ IBD ■ Thickened bowel, enlarged mesenteric LN; failure to absorb glucose ■ Path~ altered immune response ■ Tx steroids, good high-energy feeds ○ Intestinal neoplasia ■ Wt loss and r/o everything else ■ Grave prognosis ○ Lawsonia intracellularis ■ Equine proliferative enteropathy ■ Lethargy, edema, colic, wt loss, diarrhea ■ Dx thickened SI wall on US, hypoproteinemia ■ Tx clarithromycin, doxycycline ○ Equine coronavirus ■ Fecal-oral, self-resolving in 1wk ● Farm outbreaks ~3wk Equine Colitis ○ Enterocolitis sequelae ■ Sudden massive fluid loss, electrolyte imbalance ■ Gram negs in gut>>endotoxin sources, v sensitive ■ Poss hyperammonemia ○ Stress triggers ○ Foals-Pasty diarrhea associated with bacteremia ○ Salmonella=zoonotic ■ Should always be ruled out ○ Clostridium= normal flora ■ Send good amount of feces fast for ID ○ Tx ■ Correct fluid/electrolyte loss, tx endotoxemia ● Tx for loss, ongoing losses, and maintenance ● No IV sodium bicarb ● Plasma expanders for decreased pressure ○ Other plasma goodies help ● Endotoxins set off inflammation ○ Steroids, flunixin ○ Ice those feet Equine liver dz ○ Hepatic insufficiency= 80% damage (can be subclinical) ○ Clinical signs ■ Wt loss, anorexia, icterus, hepatoencephalopathy, coagulopathy, edema ● Depression, circling, head pressing, hyperammonemia ○ CSF, serum ● ○ Dx ■ ■ ■ ■ ■ ○ GLDH and SDH liver values GGT=cholestasis Bile acids for presence, not type of dz Liver u/s Biopsy R side ICS 12-14 Tx ■ ● Secondary photosensitization hyperammonemia= lactulose (pH change), metronidazole (reduce bact byproducts) ■ Support until liver regenerates ● Fluids, acid-base, nutrition (high carb low protein) ■ Hyperlipemia ● Correct primary dz ● Correct neg energy balance ● Exogenous insulin- suppress hormone-sensitive lipase, increase lipoprotein lipase ● Exogenous heparin- stimulate lipoprotein lipase and promote TG metabolism ○ Chronic Megalocytc Hepatopathy ■ Magalocytosis, biliary hyperplasia, fibrosis ○ Cholelithiasis ■ Icterus, fever, colic ■ Increase bile acids, globulins ○ Tyzzer’s Dz ■ Clostridium piliforme ■ Acute necrotizing hepatitis, high mortality ○ Theiler’s Dz ■ 4-10wk reaction to equine biologics ■ Acute hepatic necrosis ○ Chronic active hepatitis ■ Tx corticosteroids, Abx Eq GI Sx 1 ○ colic=pain (symptom, not sign) ■ Stretch, tension, inflammation, infarction ■ Ddx myositis, laminitis, ataxia ○ Anatomy ■ Ileocecal fold ○ Gastric ulcers ■ Adult signs= off feed, foal sign= colic, bruxism ○ Gastric impaction ■ Risk factors sugar beet pulp persimmon seeds, dental dz ○ SI strangulating lesion ■ Epiploic foramen entrapment (L to R, cribbing) ■ pedunculated lipoma on mesenteric pedicle (older horses) ■ Intussusception (-cipiens receives) ■ Hernia ● adults=acquired, short loop, irreducible ○ SI non-strangulating lesion ■ ■ ■ ● ● ● Ileal impaction ● Coastal bermuda grass hay, tapeworms ascarid impaction (parascaris equorum in foals <6mo) proximal enteritis ● Hella nasogastric reflux, may need Sx if big pain Eq GI Sx 2 ○ Large colon tympany and impaction most common colic ○ Impactions can be managed if caught quick, but need Sx for pain ○ Focal obstructions always need Sx ○ Large colon displacement or volvulus ■ Volvulus needs Sx ASAP ○ Bowel rupture big risk ■ Be gentle ■ Gas, impaction, or both ○ Rectal tears will get you sued ■ Careful with expensive horses ■ Low-grade tears heal fine, bad ones may result in euthanasia Eq GI Sx 3 ○ Pain is #1 reason to go to Sx ○ Exploratory laparotomy is best method to ID lesions ■ But not all can be fixed ○ Gentle tissue handling of bowel is key ○ Resectioning depends on length and severity of damage ○ Most common post-op issues ■ Recurrent pain/colic ■ Incision infection/drainage ■ Pain and ileus are reasons to go back in ○ SI lesions typically do worse than LI lesions ■ If survive to discharge, good odds ○ Laparoscopy is fancy, but expensive. Needs training and many people to use Swine clinical approach ○ Pathogen presence does not mean disease necessarily ○ Separate By: ■ -Age ● diff receptors with age=diff dz/severity ● pH drops post-weaning>fewer bugs ■ Anatomical location ● -ileocecocolic junction as the border SI/LI ● LI dz=watery stool, high vol ● SI dz=undigested feed, fat, some water in stool ○ Ileal lesion=protein loss ○ Colic lesion=water loss ○ Duodenal lesion=basic stools ● Jejunum ○ Rotavirus=mature enterocytes ■ Mild blunting ○ Coronavirus=immature enterocytes ■ Severe villus blunting ○ Coccidia= lamina propria under crypt cells ■ ■ ■ Focal ○ E coli (F18/K88) ■ Functional dz (hypersecretory) ■ Shiga toxin (edema dz, leaky vessels) ● Brain swelling, neuro signs ○ Lawsonia=physical dz ■ Ileum dz ■ PPE=young, proliferation ■ PHE=adult, pipestream blood (mucosal sloughing) mechanism of Dz ● Malabsorption ○ degree of villus blunting=degree of dz ○ physical damage can be seen on histo ○ Results in metabolic acidosis ● Hypersecretory ○ altered phys (electrolytes, etc) ○ increased water in the lumen (functional change) ○ E. coli ■ Fimbriae ■ Toxin ○ Clostridium ■ Dificile=LI ■ Perf A,C=SI, blood/acute death (nephrotoxin C) LI environmental bugs ● Salmonella ○ Toxin, colitis (button ulcers) ○ Oral Abx ● Roundworms ○ Liver milk spot scarring ● Whipworms in the colon ○ fenbendazole