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Medicine Exam

Medicine Exam

by c.a.childs9, Mar. 2015

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3rd eyelid resection	-Good sedation is needed -prepare skin and conjunctiva with dilute betadine solution -Local block, topical anesthetic, topical phenylephrine -Use hemostat to crush well below the mass -Cut with scissors to protect cornea -Palpate for any remaining cartilage of 3rd eyelid, if exposed resect depper and remove -Let heal by 2nd intention -Look for prolapsed fat -Submit for histopath
Sarcoid	-Most common equine skin tumor -2nd most common equine periocular skin tumor -More frequent in young horses -Can be one or multiple sites, under skin or on surface -Often diagnosed by appearance -Biopsy can exacerbate situation -With surgical excision only, more than 80% recurrence --need adjunctive therapy (chemotherapy, cryotherapy, phototherapy, vaccine) -Enucleation is not a cure
Corneal anatomy	-Tear film (mucins, lipids, aqueous layers) -Epithelium: 8-10 cell layers thick --stratified non-keratinized squamous cells -Stroma: 90% of corneal volume, 75-80% water and 20-25% collagen and proteins -Descemet’s membrane: basement membrane of endothelium --produced continuously throughout life, thickness increases with age -Endothelium: monolayer of hexagonal cells, cell density is inversely proportional to age
Normal cornea	-Avascular, transparent, light-refracting surface -Equine cornea is 1mm thick -sensory nerves in anterior 1/3 of stroma and epithelium --causes superficial tumors to be more painful than deep stromal ulcers
Corneal Wound healing	-Starts within hours -Centripetal epithelial migration -increased epithelial thickness, from 8-15 cells -Wound edges retract via apoptosis -Epithelial cells adhere to basement membrane or anterior stroma -Complete re-epithelialization in 5-7 days -Vessels bud in 3-5 days, migrate 1-2mm per day -Epithelial basement membrane is complete in 6 weeks -Scar remodeling for 3-6 months
Clinical signs of corneal ulcer	-Blepharospasm (look at lash angle) -Blepharitis -Epiphora -Chemosis -Conjunctival hyperemia -Foal corneal edema -Miosis
Describing a corneal ulcer	-Size and shape -Location on cornea -Color of lesion --infiltrate, edema, plaque -Vessels --branching, brush border, location -Depth --superficial, deep, descemetocele, perforation -Texture --melting, gritty, dry, bulging, smooth
Diagnostics for eye ulcerations	-Fluorescein stain -Rose Bengal stain -Cytology -Culture
Corneal staining	-Moisten fluorescein strip with saline, touch to conjunctiva --do not touch to cornea -Cobalt blue light can show intensity of stain uptake -Corneal epithelium disruption is easily shown with stain --exposed hydrophilic stroma absorbs stain
Staining eye ulcerations	-Fluorescein stain 1st, look for ulcer -Rose Bengal stain 2nd --rose Bengal stain indicates instability of tear film, mucin tear layer blocks rose Bengal stain -Indicates risk for fungal colonization or invasion, keratoconjunctivitis sicca, or viral keratitis -Rose Bengal stains exposed epithelial cells, mucous, and stroma
Culture for eye ulcerations	-Culture before stain or topical anesthetic -Auriculopalpebral block with or without sedation and sterile topical anesthetic -Touch edge and center of ulcer for culture -DO NOT touch eyelids! -Aerobic with sensitivity and fungal culture -Culture tip dry or wet
Cytology for eye ulceration	-Auriculopalpebral block, sedation, topical anesthetic -Scrape edge and base of the ulcer, need deep sample for fungal cytology -Use back of scalpel blade, spatula, or brush -Take 2-4 samples on 2 slides, dry and stain -Look for epithelial cells, inflammatory cells, bacteria, fungal hyphae, vegetative material, mineral crystals, number of bacteria
Treatment of simple superficial uncomplicated corneal ulcer	-Treat underlying cause -Prevent or control infection --broad-spectrum antibiotic --antifungal -Treat uveitis -No topical steroids or topical NSAIDs --can cause melting or infection -Recheck in 1-2 days -If not healed in 2 weeks, consider indolent ulcer
Treatment for simple superficial uncomplicated ulcer	-Treat underlying cause -prevent or control infections --broad spectrum antibiotic: Neopolybac --antifungal: Itraconazole/DMSO -Treat uveitis --topical atropine (only one dose, need to be careful about Colic) --Systemic NSAIDs (banamine, Bute, equioxx) -NO topical steroids or topical NSAIDS --can cause melting ulcer or infection -Recheck in 1-2 days -If not healed in 2 weeks. Consider indolent ulcer
Indolent Ulcer	-Slow healing corneal ulceration, lasts more than 2 weeks -Non-healing ulcer -Edema and loose epithelium -Anterior stroma is abnormal, inhibits adhesion complexes --epithelium does not adhere to stroma --fluorescein diffuses under loose epithelial edge -Often there is decreased corneal sensitivity
Debridement of Indolent Ulcer	-Need to rule out infection before debriding! -Only debride with superficial ulcers, if there is any divot do not debride -Culture and cytology -Rule out mechanical cause -Sedate, block, and give topical anesthetic -Use sterile cotton tip to get all loose tissue off, push cells off --rotate cotton tip, remove all loose cells --If corneal tissue can be removed with Q-tip, cells should not be there -Treat ulcer after debridement -Recheck every few days, wait 10-14 days to repeat debrdement
Keratotomy	-Treatment for superficial, non-healing, non-infected ulcers -Treat underlying cause if one can be identified --identify infection with culture and sensitivity -Initially Use sterile, dry cotton tip for debridement, wait 10-14 days --If not healed, do keratotomy to promote epithelial adhesion to stroma (roughen stroma) -Use caution if eye is positive for Rose Bengal stain -Can do grid, punctate, or diamond tipped burr keratotomy
Grid keratotomy	-Roughens cornea, gives epithelial cells something to attach to -Need to rule out infection first! Culture and cytology -Do not do if there is any cellular infiltrate -ONLY do on superficial ulcers! If there is a divot, do not do! -Sedate animal, use nerve block, twitch, and local anesthetic -Dilute betadine corneal prep -Debride loose epithelial cells with dry sterile cotton swab -Use 22-25g needle and sterile gloves to create grid --checkerboard pattern across entire ulcer, from healthy epithelium to healthy epithelium -Use enough pressure to make a mark but not too much to go through cornea -Treat ulcer -Recheck in a few days -Wait 10-14 days before repeating
Complications of Grid keratotomy	-Can put infection deeper into the eye -Can puncture the eye if animal moves due to improper anesthesia
Diamond Tipped Burr	-Removes loose epithelial cells and roughens stroma -Need to rule out infection first (culture and cytology) --if there is cellular infiltrate, do not use burr! -ONLY for superficial ulcers -Debride cornea with sterile cotton tip first -Use sterile tip of burr to pulish ulcer surface and edges -Treat ulcer -Recheck in a few days -Wait 10-14 days to repeat -Results in less scar tissue after healing -No chance of puncturing the eye!
Complicated Ulcers	-Stromal loss -Melting ulcer (keratomalacia) --proteases from infection, PMNs, epithelium/stroma -Cellular infiltrate, PMNs migrate faster than vessels and epithelium -Laceration -Foreign body -Infection --bacterial: pseudomonas, staphylococcus, streptococcus --fungal: aspergillus, fusarium -Iris prolapse
Treating a complicated ulcer	1. Antibiotic: based on culture and sensitivity, cytology 2. Antifungal 3. Anticollagenase, decreases Matrix metalloproteinases --serum, EDTA, Mucomyst, systemic doxycycline 4. Atropine to relieve ciliary spasm and stabilize blood aqueous barrier 5. Anti-inflammatory (systemic) --banamine is best, least amount needed to help uveitis and pain --monitor for right dorsal colitis and nephrotoxicity
Complications of Ulcers	-Fungal ulcerative keratitis -Iris prolapse
Fungal Ulcerative Keratitis	-Variable appearance -Early form may not stain with fluorescein --do not put horses on steroids just because they are painful and no stained ulcer -Can rapidly progress to a melting ulcer -Can progress to deep stromal abscess -Surgery is best option to decrease fungus, remove fungal burden
Iris Prolapse	-Dyscoric pupil (abnormal shape), darker pigment to iris, shallow anterior chamber -More than 15mm has poor prognosis -Crossing limbus has poor prognosis -Acute has better prognosis than chronic -Traumatic has better prognosis than ulcerative -Do Seidel’s test for leaking aqueous -Surgery is best treatment
Seidel’s Test	-Test for deep stromal ulcers -Iris prolapse -Shallow anterior chamber -Need sedation, AP block, topical anesthetic -Look for leakage of aqueous humor and a green stream
Sub-palpebral lavage system	-Recommended for all complicated ulcers and horses that are difficult to treat with simple ulcers -Place lavage system in dorsal or ventral conjunctival fornix -Poorly placed sub-palpebral lavage may cause more issues for patient
Sub-palpebral lavage placement	-Good sedation -Topical anesthetic -Dilute betadine prep of eyelids and cornea -Local nerve block, frontal nerve -Twitch -Sterile gloved finger is placed into fornix at site of lavage -Put finger along side of the needle to protect the eye -Push needle through conjunctiva and skin, pull tubing through until footplate is seeded in the fornix -Suture to skin, braid mane, and feed through braids and tape near withers
Protective hood on horses	-Use in conjunction with sub-palpebral lavage system -Use hood to protect against self-trauma -Limits visual inspection -Provides warm moist environment for bacterial or fungal growth
Atypical corneal ulcers	-Eosinophilic keratitis (keratoconjunctivitis) -Clacific band keratopathy -Viral keratitis
Non-ulcerative corneal disease	-Immune-mediated keratitis -Stromal abscess -Keratoconjunctivitis sicca
Eosinophilic Keratitis	-Caseous discharge and focal corneal edema -Moderate to severe blepharospasm before ulceration -Corneal ulcers are in periphery, will see raised vascular plaques -Often minimal discomfort -Diagnose with corneal or conjunctival cytology, will see eosinophils --only need 1-2 eosinophils to diagnose -Treatment: topical steroids if there is no ulcer --systemic steroids and zyrtec --ivermectin -Slow healing, can take many weeks to months -Seasonality in mid-atlantic region (June-August) -Also occurs in cats
Calcific band Keratopathy	-Complication of chronic inflammation or chronic topical steroids -Eye is painful -Focal corneal edema -Will see white bands in interpalpebral cornea -Indolent ulcer due to poor epithelium migration and adherence -Microfractures of epithelium may cause faint stain uptake -Minerals auto-fluoresce -Treat with superficial keratectomy or burr debridement, topical Ca++ chelators, NSAIDs, bandage contact lens
Herpes viral Keratitis	-EHV-2 in foals and adults -Blepharospasm and epiphora -Cornea often looks clear without magnification -May see superficial ulcers or superficial erosions -Multifocal punctate or dendritic pattern of opacification -May have corneal edema and neovascularization -Need to rule out fungal keratitis -Diagnose via PCR for EHV-2 (not reliable, really a diagnosis of exclusion) -treat with topical antiviral and treat simple ulcer -May give topical NSAIDs, NO steroids -Common in cats, rare in dogs
Non-ulcerative keratitis	-No fluorescein stain uptake -Corneal neovascularization -May see blepharospasm
Immune-mediated keratitis	-Chronic, non-ulcerative keratitis -Non-infectious -Responds to anti-inflammatories -Non-painful, corneal opacity in one or both eyes -Focal corneal edema and branching vessels, infiltrate may be seen at the end fo the vessels, negative stain -Uveitis is usually not present -Superficial stromal, mid-stromal, or endothelial
Stromal abscesses	-Acute onset! May or may not have history of an ulcer -Yellow-white opacities in the stroma -Photophobia, epiphora, blepharospasm, very painful! -Will see diffuse corneal edema, yellow-white stromal opacity, deep vascularization --vascular response is proportional in severity to depth and diration of the lesion -Hypopion and fibrin will be present in anterior chamber in severe cases -No stain uptake -DDx: anterior uveitis, immune-mediated keratitis -Occurs mostly in large animal species, rare in small animals
Formation of a stromal abscess	-Stroma is inoculated with infectious agent through defect in epithelium --defect can be due to puncture, ulcer, laceration, foreign body -Epithelial cells migrate over defect, deal infection in stroma --Epithelium heals over infectious agent -Fluorescein negative -Infection is almost always fungal, hyphae can get deep into stroma --penetrate descemet’s membrane and causes uveitis to get worse
Medical Treatment of Stromal Abscesses	-Healing occurs via vascularization --vessel growth is slowed by fungal infection, vessels do not always go deep enough -Antifungal, Antibiotic, Atropine, and Anti-inflammatory are needed for proper treatment
Surgical treatment for Stromal Abscess	-Need to do when abscess is not responding to medical therapy -Abscess progresses or persists even with medical therapy -Severe pain, vision-thretening uveitis -Severe uveitis, endophthalmitis that compromises vision and globe -Race between resolution of abscess/healing and vision loss from uveitis -Do surgery under general anesthesia --shorter duration of therapy results in faster recovery --healing occurs quickly when abscess is removed -Good outcome -May have scar if there is graft rejection
Penetrating keratoplasty	-Use when abscess involves most of stromal thickness -Need full thickness donor graft -Also need conjunctival graft -75% or more of patients are visual post-operative -Larger size results in increased complication rate
Posterior lamellar keratoplasty	-Do for abscess that only involves posterior stroma -Partial thickness graft -May or may not need conjunctival graft -90% of patients are visual post-operatively
Deep lamellar Endothelial keratoplasty	-Done for peripheral abscess involving posterior stroma -Partial thickness graft -90% of patients are visual post-operatively -Approach is through limbus
Stromal abscess treatment where Sx is not an option	-Stromal anti-fungal injections, inject right into stroma -Need standing sedation or short anesthesia -High magnification and good light are essential
Keratoconjunctivitis Sicca	-“Dry eye” -Very uncommon in the horse -Blepharospasm, minimal to no epiphora, increased discharge -Will see a corneal ulceration and vascularization, may see pigmentation -Diagnose with schirmer tear test, less than 10mm wetting within 1 minute --normal is 25mm or more -Treatment with lacrostimulants, lubricants, partial tarsorraphy parotid duct transposition
Overview of Ulcers	-Fluorescein stain every abnormal eye and every painful eye -Cytology helps direct immediate therapy -Debride with sterile cotton tip if not healed in 2 weeks -DO NOT grid an infected ulcer -Complicated ulcers need early referral -Treatment: antifungal, antibiotic, atropine, anticollagenase, anti-inflammatories
Birth Transition	-Changes in respiration, metabolism and endocrine system mark switch from in-utero to birth
Vital birth transition	-Cardiovascular responsiveness -Systemic blood pressure changes --transition from fetal circulation -Establish respiration -CNS responsiveness
Breathing at Birth	-Fetal Breathing --fetus only breathes during REM sleep -Need to stimulate sustained rhythmic respiration --Catecholamine surge at birth, induces substances important for breathing (substance P) --Removal of the placenta --cooling, change in temperature --tactile stimulation --increasing CO2
Apnea at birth	-Birth asphyxia -Maternal drugs -CNS injury -Septicemia -Muscular or neurological disease -Obstructing congenital malformations -Other mechanical obstruction
Neonate not breathing at birth	-Monitor heart rate --birth bradycardia is normal --increase in HR is important --persistent bradycardia is bad news -Birth arrhythmias are common --if perfusion is OK, monitor --if poor perfusion or non perfusion, resuscitate
Preparation for resuscitation of Neonate	-Anticipate! Have plan in place -high risk situations -50% of neonates requiring birth resuscitation are unexpected -Need to always be prepared!
EXIT procedure	-Ex-utero Intrapartum Treatment -Treatment of the fetus during birth while fetus is still partially in utero -Intubate fetus in-utero -Resuscitation during parturition -Oxygen therapy in the mare, fetal ECG -Intubate foal if nose is available -Use capnograph -Expect poor lung perfusion initially -Redirect blood away from the placenta, decrease the effect of drugs given to the dam on the fetus -Cannot be done in all cases, but if it can it takes a lot of pressure off of parturition and foal
Benefits of EXIT procedure	-Gives time to correct dystocia -Can assess fetal viability -Rescue foals during dystocia -Increase successful referral radius
Elements of neonate resuscitation	-Initial assessment and APGAR score -Clear airway -Tactile stimulation, rubbing -Thermal management -Free flow oxygen -Positive pressure ventilation -Chest compressions -Medication
Initial assessment of neonatal foal	-Rapid assessment, check when looking at vaginal positioning -Check relative pulse rate and strength -Check apical pulse as soon as the chest clears -Expect initial bradycardia --Heart rate should rapidly increase -May hear transient arrhythmias
APGAR score for foals	-Heart rate: --absent --less than 60 bpm, irregular --more than 60 and regular -Respiratory rate: --absent --irregular --regular -Muscle tone: --limp, lateral --some flexion --active sternal -Reflex nasal stimulation or ear tickle: --no response --grimace, weak ear flick --sneeze/cough, ear flick or head shake
Clearing neonatal airway	-During dystocia, clear as soon as nose is visible --may ventilate while foal is still in birth canal -Clear meconium via suctioning --only if neonate is not vigorous --can induce apnea and bradycardia --can collapse lungs, induce hypoxia
Tactile stimulation of foals	-Rub chest while drying -clean out nose -Evaluate response while stimulating
Thermal management of Neonates	-dry neonate with towels -Move to warm area -If not in shock, use radiant heat, hot water bottles, or warm air
Respiratory support for neonates	-Free-flow oxygen --intranasal oxygen --flow-by oxygen -Mouth-to-nose ventilation -Intubation
Mouth-to-nose ventilation in neonates	-Can be done if foal does not breathe spontaneously
Ventilation of the neonate	-Self-inflating bag with O2 reservoir --compressed bad that recoils and refills with air --series of 1-way valves that allow appropriate flow -No spontaneous ventilation: --establish functional residual capacity --give prolonged inspiration phase, 1st breath lasts 5 seconds --use appropriate tidal volume -Hyperventilate patient 40 breaths per minute --unless patient requires CPR --avoid more than mild hyperventilation -If there is early asphyxia, give 30 second ventilation to increase HR -If late asphyxia, indicates myocardium is failing --need to d chest compressions
Cardiovascular support for the Neonate	-Assessment -Non-perfusing rhythm is most often bradycardia -Chest compression should be done BEFORE the heart stops --start compressions when heart is not perfusing -If heart is not perfusing after 30 seconds of chest compressions, use drugs
Efficacy of chest compressions and cardiac output in neonates	-Feeling the central arterial pulse is not effective! Cannot get to carotid, aorta, or femoral artery -Monitor pupil size -Measure end-tidal CO2
Medication reversal for neonatal foals	-Epinephrine and vasopressin for vascular support -Alpha-2 agonist reversal if needed --atipamazole, yohimbine --tolazoline causes changes and bleeding in the lungs, do not give -Flumazenil for diazepam/midazolam reversal -Naloxone for opiate reversal -Ventilation for inhalant reversal
Intratracheal drug administration in neonates	-Epinephrine -Atropine -Lidocaine -Naloxone
Intraosseous route for drugs and fluids in neonates	-Easy and rapid vascular access --especially in kids, lambs and cria --small, young beasts -Need practice in larger neonates -More reliable drug delivery -Need special needle in foal and calf -Difficult to stabilize patient for procedure -ONLY ONE HOLE PER BONE -Tibia is easiest placement, has medial flat area without muscular attachments
Meconium	-Formed when fetus swallows amniotic fluid -Formed from intestinal secretions, amniotic fluid, cellular debris, and other debris -Appears during 1st trimester -Accumulates throughout the fetal period -Bile acids excreted by beginning of 2nd trimester
Meconium and Bilirubin	-Concentration of bilirubin in meconium, 50x serum concentration -Due to intestinal absorption of the bilirubin -Dark color of meconium is due to bilirubin pigments -If meconium is retained, color becomes the same as “milk feces” --bilirubin pigments are absorbed and excreted in urine
In-utero meconium passage	-Associated with fetal distress? -Can occur as early as 2nd trimester -Late-term meconium passage can occur --fetal maturation of GI innervation --defecation is controlled by parasympathetic stimulation --vagal stimulation with cord or head compression in-utero
Fetal Diarrhea	-In-utero meconium passage -Animal is born passing profuse, liquid meconium -Resolves within 48 hours of birth -Associated with intrauterine stress --hypoxia/asphyxia --FIRS/sepsis -Manifestation of fetal enteritis?
Causes for Meconium impactions	-Increased incidence in colts due to narrow pelvic canal -Excessive meconium formation (due to longer gestation?) -Impaired GI function --asphyxia, sepsis -Meconium retention --premature or postmature fetus --prolonged recumbency --dopamine
Signs of meconium impaction	-Straining to defecate, arched back -Frequent nursing but not effective nursing --will see dried milk on head of neonate -Persistent colic --rolling on back, kicking at abdomen, frantic tail swish -Abdominal distention -Umbilicus may re-open, bleed, or drip urine -Variable amount of meconium in individual foals -Easy to miss passage of meconium
Urination vs. Defectaion in neonates	-Urination: legs apart -Defecation: legs together
Physical Exam of a foal with Meconium impaction	-Digital rectal exam --will see edema of rectal mucosa -Enema can be diagnostic -Deep abdominal palpation --meconium is distinct in the caudal abdomen, above the bladder --may be in anterior abdomen, between the ribs -Do abdominal ultrasound
DDx for meconium impactions	-Ruptured blader -Necrotizing enterocolitis -Intussusception -Intestinal volvulus -Rectal perforation -Colonic atresia -Lethal white Syndrome
Enema as treatment for meconium impaction	-Soapy water gravity enema --may cause rectal irritation and persistent tenesmus -Lubricant enema -Dioctyl sodium suldosuccinate enema (DSS) -Glycerine enema -Retention enema --4% acetyl cysteine --rectal distention stimulates motility --can add barium for osmotic effect -Buscopan: anti-cholinergic, decreases spasms of GI tract
Oral laxatives as treatment for Meconium impactions	-Colostrum -Mineral oil -Milk of magnesia -DSS -Castor oil
Supportive care for Meconium impactions	-Close attention to adequate passive transfer --decrease risk for sepsis -May give plasma transfusion -If impaction is prolonged, give IV fluids with dextrose
Meconium retention	-Neonatal gastroenteropathy --dysmotility --meconium retention -Animal is not passing meconium, no abdominal pain or distention, and retains enema fluid -Can last 4-8 days or as long as 30 days
Rib fractures during parturition	-Not rare -Usually occur 2-4cm above costochondral junction -Involve 4-12 ribs in a straight line -Any rib or set of ribs can fracture --most frequently anterior chest ribs, ribs 2-8 -Over the heart is common location -May feel “click” on palpation --palpate all ribs in newborn foals! -Can auscultate click associated with heartbeat due to fracture -Easily confirmed on radiographs and ultrasound
Hemorrhage due to rub fracture during parturition	-Primary bleeding from intercostal arteries -Most often diffuse chest wall/subpleural/hemothorax -May be extensive -May not be evident externally -Lung contusions lead to hemothroax -Lacerations of myocardium can cause cardiac tamponate or arrhythmias -Trauma to other structures can occur due to sharp rib ends --diaphragm
Clinical signs of rib fracture in foals	-Variable signs -Pain, anemia, cardiac arrhythmias -Tachycardia, tachypnea -Positional pain --on examination --when down -Weak, minimally responsive foal -Anemia and pale Mucus membranes
Umbilical Bleeding	-Can be major source of bleeding in neonates -External bleeding or internal bleeding -Internal umbilical artery rupture -Commonly occurs in calves, rare in foals -May form large hematomas if bleeding is contained within fascia -Often clinically inapparent -If in umbilical artery, animal may pass bright read urine without hours of birth
Umbilical artery bleeding	-Artery pulls back into umbilical stump -Ineffective stop of bleeding iatrogenic -Ineffective umbilical clamp or umbilical tape -Leaking blood can travel along fascial planes --body wall hematoma or internal hematoma -Blood may flow through urachus if there is hematoma in bladder or urachus -Animal may pass bright red urine within hours of birth -Occasional urinary obstruction -Body wall hematomas and secondary edema -Some foals will have extensive bleeding that can lead to hemorrhagic shock --most do not bleed extensively -May have signs of urachitis, persistent straining to urinate -Icteric or mildly anemic foal
Diagnosis of umbilical artery bleeding	-Careful abdominal palpation! -Sleeping or weak neonate -Palpation can be as accurate as ultrasound
Patent urachus	-Most often seen in 3-5 day old foals --see when umbilical scab falls off -May see wet or constant leak at urachal stump -Can treat via benign neglect -Other treatment: --antimicrobials -DO NOT SUTURE
Urachitis	-Urachal disease: --infection, hematoma, delayed atrophy -Signs: straining to urinate after normal urination or repeat posturing -Usually no consequences -Tx: benign neglect or phenazopyridine if straining a lot --try to use for as short a period as possible
colitis	-Inflammation of the colon
Typhlitis	-Inflammation of the cecum
Enteritis	-Inflammation of the small intestine
Onset of colitis and diagnosis	-Surgical lesions have acute onset --strangulation --entrapment -Enteritis and colitis have more gradual onset
Colitis signs that indicate inflammatory disease	-Fever -Inappetence -Dull, depressed -Hyperemic mucus membranes -Injected sclera -Tachycardia -Hypovolemia
Clinical pathologic signs of endotoxemia in colitis cases	-Abnormal leukogram --leukopenia (specifically neutropenia), indicates salmonella and other toxins, due to neutrophil margination and diapedesis --Leukocytosis -Electrolyte abnormalities --hypochloremia --hyponatremia --may or may not see hypokalemia -Hyperlactatemia, related to poor perfusion
Ancillary diagnostics for enteritis colic cases	-Check for reflux via nasogastric intubation (be sure to have a siphon that works!) -Ultrasonography --thickened bowel --fluid distention -Abdominocentesis -Exploratory celiotomy --not the most ideal ancillary diagnostic, but can be done -Need to identify causative organism --fecal culture --fecal PCR --toxin identification --Serologic titer
Treatment for Enteritis and colic	-Supportive care is KEY -Address hemodynamic instability --fluid therapy --correct electrolyte imbalances --colloid support -Cardiovascular monitoring --lactate, arterial line, jugular refill, pulse rate and quality, central venous pressure line, CRT -Endotoxemia -Intestinal protectants or probiotics -Antimicrobial therapy
Treatment of Endotoxemia	-Polymixin B: --neutralizes circulating endotoxin, binds to lipid A --need to use caution in horses that have hypovolemia or azotemia -Flunixin meglumine/ Banamine (NSAIDs) --inhibits inflammatory mediators -Hyper-immunized plasma (J5) -Pentoxifylline
Intestinal protectants and probiotics	-Bio sponge --binds clostridial exotoxins ex vivo --reduces diarrhea in horses with large intestine disease -Bismuth subsalicylate -Saccharomyces boulardii --probiotic in clinical trials
Antibicrobial therapy for enteritis	-Potomac horse fever (Oxytetracycline) -Clostridia (metronidazole) --should have antimicrobial administration in history --need a confirmed diagnosis -Controversial to use antibiotics in salmonella and idiopathic colitis -If there is neutropenia (less than 1,000), worry about bacterial translocation and sepsis
Important questions to ask in a colic case	-History -Medications -Describe the pain, what is happening -How long -Eating/drinking -Manure and urination
Causes of Colitis	-NSAID use (right dorsal colitis) -Potomac horse fever -Salmonella -Clostridium -Coronavirus -Parasites (strongyles) -Idiopathic -Anti-microbial associated diarrhea
Monitoring for a horse with endotoxemia	-TPR -PCV, TS -lactate -Central venous pressure -Blood pressure -Progression of endotoxemia --mucus membrane color, scleral injection -Comfort level -GI motility, volume of diarrhea, urine production
Client communication Essentials	-Empathy! -What does the client want? -What do you think is wrong -What do you think needs to be done -Prognosis -Cost
Abdominocentesis Procedure	-Clip and aseptically prepare ventral abdomen -Insert needle slightly right of midline -18g needle -Teat cannula -EDTA tube (purple top) -Serum tube (red top) -Sterile gloves -Normal nucleated cell count is less than 5,000 cells/uL -Normal total protein is less than 2 g/dL
Colostrum Shortage	-Current shortage in dairy colostrum -Dairy cows do not produce high-quality colostrum -Want to decrease the amount of bacteria in colostrum, bacteria get in the way of IgG availability -Can pasteurize to get rid of bacteria, but difficult to pasteurize colostrum -Can acidify colostrum, make pH 4-5 --may cause clumping of milk, need to control temperature
Ideal Colostrum Characteristics	-Quality: 50g/dL minimum -Quantity: 4L -Total: 200g minimum
Bacteria causing GI disease in calves	-E. Coli -Coronavirus -Clostridium perfringens -Salmonella -Rotavirus (not very intense diarrhea)
E. coli K99	-Most common E. coli strain in dairy cows -Named for method of attachment -Kills dairy cows within 3 days of life -Very effective vaccine exists (First Defense) --give within 12 hours of life --acts locally to prevent attachment of E. coli K99
Respiratory disease in Calves	-BRSV -IBR -PI3 -Coronavirus (usually enteric, can cause pneumonia) -Leptospira -Mannheimia haemolytica -Mycoplasma -Pasteurella multocida -Inforce 3 vaccine
Inforce 3 vaccine	-Modified live virus -Bovine rhinotracheitis -Parainfluenza 3 -Bovine respiratory syncytial virus -intranasal vaccine
Newborn calf vaccines	-First defense (E. coli K99) --local to intestine -InForce 3 (BRSV, IBR, PI3) --intranasal
2 main camps of calf vaccination	1. modified live early: --boosts lymphocytes, cell-mediated immunity response --give day 8-15 2.Modified Live late: --colostrum is gone --humoral response --give day 36-43
Weaned calf vaccination schedule	-Inforce 3 intranasal vaccine -Can be given multiple times -Give whenever something stressful is going to happen, gives immune system boost
Bovi-Shield Gold FP 5 L5 HB	-Bovine rhinotracheitis virus -Parainfluenza 3 -Bovine respiratory syncytial virus -Leptospira --Canicola, grippotyphosa, hardjo, icterhemorrhagiae, Pomona --killed vaccine, needs booster! -Modified live vaccine for viruses, does not need booster -Do not give to pregnant heifers or cows if they have not been previously vaccinated! --causes abortions -Give 1 month before breeding
Clostridial diseases in Cows	-Clostridium chauvoei: black leg -Clostridium haemolyticum: red water -Clostridium novyi: black’s disease -Clostridium perfringens C and D: Enterotoxemia, overeating disease, pulpy kidney disease -Clostridium septicum: malignant edema -Clostridium sordellii: gas gangrene
Ultrabac 8	-Clostridium vaccine -Subcutaneous administration under the skin --5ml dose
Growing heifer vaccination schedule	-Heifers more than 4 months of age --Bovi-shield gold (needs yearly booster) --Ultrabac 8 (needs yearly booster) -Need to give yearly booster for Bovi-Shield --can cause abortions if given to cow that has not seen virus before
Breeding Heifer vaccination schedule	-Bovi-shield and Ultrabac one month before breeding -NEED to give before breeding! Can cause abortions if given during pregnancy to animal that has not been exposed to vaccine
Mammary gland disease	-Common in dry cows, right after dry-off --teat sphincter does not stay closed, allows ascending infection -Common right before parturition, before start of milking colostrum -Gram- infection: E. coli
J5 E. coli vaccine	-Initially developed from a salmonella vaccine, has same LPS -Subcutaneous injection at 7 and 8 months gestation
Scourguard vaccine	-Bovine rotavirus and coronavirus killed virus -Clostridium perfringens C and E. coli -Helps prevent diarrhea in calves of vaccinated dames due to rotavirus, coronavirus, E. coli, and clostridium perfringens -IM injection -Prevents endotoxemia in cows, which helps calf
Spirovac vaccine	-Leptospirosis vaccine for cattle -Canicola, Grippothyphosa, Hardjo, Icterhemorrhagiae, Pomona -Give subcutaneously -Need to booster every year
Important points of bovine vaccination	-Do not vaccinate pregnant cow with modified life vaccine she has not seen before! -Do not administer more than 7 gram- vaccines at one time --too many toxins can create endotoxemia -Avoid vaccinating fresh cows -Follow all label directions -Modified live vaccines need only one injection -Killed vaccines generally need a booster
Foundation vaccines in Cows	-Give to young animals and build on -respiratory viruses: --IBR, BVDV type I and II, BRSV -Leptospira -Clostridium -E. coli J5 bacterin
Components to evaluate on a dairy farm	-Cow records -Reproduction -Milk quality and milking parlor -Facilities -Transition cow health -Feet and lameness -Calves and heifers -Finances -Production -Rations and feeding
DHI testing and records	-Monthly evaluation of individual lactating cows -DHI technician collects on-farm data --animal identification, calvings, breedings, pregnancy checks, dry-offs, milk weights -DHI technician collects milk samples --somatic cell count --milk components
Culling	-Departure of a cow from the herd --sale, slaughter, salvage, death -Major cost to operation -Annual cull rate: (# sold + # died)/ average cows in herd -Average cows in herd: 0.93* # of fresh cows -Goal is for cull rate to be less than 30% -Sold cows generate income for produced -Dead cows do not involve any income recovery for producer
Data analysis on a dairy farm	-Identify at-risk populations --analysis of udder infection dynamics using individual cow somatic cell count
Milking routine goals on dairy	-Pre-dip contact time: more than 30 seconds -Stimulation time: 90-180 seconds -Mean teat-end peak flow vacuum: 10-12 inches Hg
Dairy farm bedding	-Sand is the new thing --keeps cows dry and clean, most comfortable -Shavings -Composted manure solids -Mattress -Nothing
Dairy farm bunk space and lying space	-Want 27-30” per lactating cow in the bunk --Want all cows to be able to eat all of the time -Lactating cows need 100 square feet -Far-off dry cows need 80 square feet -Close-up dry cows need 120 square feet -Maternity cows need 140-200 square feet
Management of Transition cows	-Prevention is more important than treatment -Screen cows daily -Do a PE on cows identified during screening -treat cows based on herd protocols --define disease and specific treatments --need to know doses, frequency, routes, duration, and withhold times -MONITOR!
Important aspects of evaluating a livestock operation	-Know farm before making suggestions --talk to produced, workers, farm manager, etc. -Analyze current and historic methods -Watch and pay attention -Follow up
Chronic Colic DDx	-Equine gastric ulcer syndrome (EGUS) -IBD/lymphoma -Sand enteritis -Right dorsal colitis -Peritonitis -Abscess/bastard strangles -Enterolith -Adhesions -Parasitism -“Wierdomas” -Idiopathic (at least 50% of chronic colic cases)
Chronic colic overview	-Exact etiology is not found in more than 50% of cases -Often no treatable -Expensive workup -No diagnosis -Prognosis is hard to determine -Usually results in a dissatisfied client
Equine Gastric Ulcer Syndrome (EGUS)	-Gastric ulcers are very common in horses -93% of racehorses have gastric ulcers -60% of other performance horses -57% of foals -50% of horses have no clinical signs at all
Clinical signs of EGUS	-Mild, chronic colic -Bruxism (especially in foals) -Weight loss -Poor performance -inappetence (eats hay, but not grain) -No clinical signs is a common presentation
Pathophysiology of EGUS	-Horses secrete acid 24 hours per day -In wild, eat 18 hours a day --in stalls eat 3 hours per day -Risk factors: --stress --shipping --exercise --high grain diets
EGUS diagnosis	-Endoscopy via 3m scope --expensive and not always available -Fecal occult blood is NOT an effective diagnostic tool --GI tract is too long, blood will not be occult in feces --tests exist but are not sensitive or specific enough, do not use! -Therapeutic trial can be helpful for diagnosis --give ant-acid medication and see if it works --placebo effect on owner
Location of Equine ulcer formation	-Form in squamous portion of stomach -Along margo plicatus -Can result in squamous hyperplasia -May see islands of squamous epithelium with bleeding ulcers -Pyloric ulcers are harder to treat
EGUS treatment	-Proton pump inhibitors --Gastrogard (FDA approved): omeprazole paste -H2-receptor antagonists --Cimetidine (almost useless) --ranitidine (does not work as well as gastrogard) -Antacids (not effective) -Sucralfate (not effective) --patches ulcers, acts as band-aid -Environmental changes
Gastrogard	-FDA approved treatment for EGUS -Paste formulation -Proton pump inhibitor -Very effective, but costly ($50 per day) -Specially formulated t protect active drug from low pH of the stomach -Compounded omeprazole is cheap, but not effective because omeprazole is destroyed by gastric acid before it can have an effect -Can give ¼ tube per day
EGUS prognosis	-Excellent, if treated appropriately -Can be prophylactically prevented with Ulcergard omeprazole paste --1/4 dose of gastrogard
IBD/Lymphoma in horses	-4 main types: --granulomatous enteritis --Multi-systemic eosinophilic epitheliotrophic disease --Lymphocytic plasmacytic enterocolitis --Idiopathic eosinophilic enterocolitis
IBD/Lymphoma diagnosis	-Rectal biopsy (easy, not very sensitive) -Open biopsy (expensive!) -Treat presumptively based on ultrasound findings and clinical signs
IBD/Lymphoma treatment	-Corticosteroids --palliative -Generally poor response to treatment -Prognosis is poor
Sand Enteritis Clinical Signs	-Mild colic -Weight loss -Diarrhea -hypoproteinemia -Any combination of the above
Sand enteritis diagnosis	-Sand test: put manure in rectal sleeve, fill with water, and see if sand settles into fingers -Radiographs -History of animal being stabled in sandy area
Sand Enteritis treatment	-Oral or nasogastric psyllium --1-2 lbs per day --gooey, sticks to sand -Stop access to sand! Feed animal in raised feeder, move pasture
Right dorsal colitis clinical signs	-Hypoproteinemia -May or may not have edema, weight loss, colic -Rarely diarrhea -bad disease
Right dorsal colitis pathophysiology	-Caused by idiosyncratic reaction to NSAIDs --not dose-dependent -results in thick, edematous, granulating right dorsal colon mucosa -Diagnose via history of NSAID use and very low protein -Can confirm diagnosis with ultrasound, but not 100% sensitive --especially in mild cases
Right dorsal colitis treatment and prognosis	-Stop NSAID use! -Low bulk diet, complete feed and no hay -Misoprostol, sucralfate, vegetable oil -Resection? Hard to do, have to take out a rib -Prognosis is guarded, only some cases recover -May have some stricture at the right dorsal colon, may need colic surgery --if stricture continues, may result in scar tissue
Peritonitis in horses	-Cause of chronic colic -Clinical signs: fever, colic, depression, diarrhea --high fibrinogen -Diagnose via abdominocentesis and ultrasound -Treat with broad-spectrum antibiotics -Prognosis depends on cause, better if it is due to primary cause --Actinobacillus is common cause
Bastard strangles/abscesses	-Cause of chronic colic in horses -Animal will probably have a fever, high fibrinogen (over 1,000 mg/dL) -Usually history of S. equi equi exposure -Diagnose via CBC and fibrinogen -Can use ultrasound for diagnosis, may be able to see abscess directly -Abdominocentesis can be helpful for diagnosis, may see some degree of peritonitis -Strep M titer will be very high with bastard strangles
Treatment of bastard strangles	-long-term antimicrobials --IM penicillin --Rifampin can be added for penetration -Surgical drainage as last resort -Prognosis is variable -May result in chronic colic due to adhesions
Enteroliths	-Cause of chronic colic --causes periodic colic, often severe -Much more common on west coast (due to alfalfa?) -Diagnose via radiographs, exploratory celiotomy -Excellent prognosis with removal
“Wierdomas” or other causes of chronic colic	-Foreign body -Recurrent nephrosplenic entrapment -tumor -Non-GI cause of colic --pheochromocytoma --pneumonia or pleuritis --ventricular tachycardia --rabies (usually not very chronic)
Diagnostic plan for chronic colic cases	-EGUS: gastroscopy -IBD/Lymphoma: ultrasound, rectal biopsy -Sand enteritis: sand test, radiographs -Right dorsal colitis: check protein, history of NSAIDs, and ultrasound -Peritonitis: abdominocentesis, ultrasound -Abscess/bastard strangles: ultrasound, Strep EM titer, abdominocentesis -Enterolith: radiograph, surgery -Adhesions: history of colic surgery, peritonitis -Parasitism: fecal, maybe
DDx for “feed out of the nose”	-Neurologic dysphagia --guttural pouch disease --any other cause of neurologic disease (EPM!!) -Obstructive dysphagia --esophageal obstruction --“choke” (grain, pellets, alfalfa cubes, carrot) --old horses with bad teeth that eat quickly -Usually obvious which one it is based on clinical exam --neuro cases are dull, have other neurologic signs --“choke” horses are gagged, neck is stretched out -Pass a tube if you are not sure! --if tube does not pass to stomach, know it is choke
Treatment of Choke	-Treat immediately: --sedate, pass nasogastric tube, lavage --can be traumatic and have greater likelihood of aspiration pneumonia -Wait and see: --only pass tube if needed for diagnosis --sedate mildly, give 12-24 hours for resolution --may need to make multiple visits, horse can become dehydrated if wait too long
Choke sequelae	-Aspiration pneumonia --common, can be fatal --give prophylactic antibiotics -Esophageal stricture: causes repeated episodes of choke --feed wet, sloppy feed for 3-4 months, usually resolves on own -Esophageal Rupture: --usually fatal and untreatable, especially if rupture occurs in thoracic esophagus --be gentle with tube!
Prevention of Choke	-Avoid feed that increases risk of choke -Correct dental problems -Slow feed intake --put rocks in bucket of feed --scatter feed on floor so horse has to nibble, no gulping
Neurologic exam of horses	-normal or abnormal? --if abnormal, what is the neuroanatomical diagnosis? -Possible differentials? Diagnostic plan? Therapeutic plan?
Unilateral Vestibular disease in horses	-balance loss --drifts, leans, falls, rolls towards affected side --recumbent on affected side -Head and neck tilt/turn towards affected side -Nystagmus in acute phase (first 24-48 hours) -Stabismus (ventral strabismus on side with lesion)
Peripheral vestibular disease	-CN VIII, affected outside of CNS --within petrous temporal bone -More common than central vestibular disease -Normal mental state -CN VII possibly involved, no other CN involvement -No weakness or proprioceptive deficits --“scrambles” to correct, usually catches before falls --may have some vertigo, may fall down -head/neck tilt towards affected side -Horizontal nystagmus with fast phase away from affected side (don’t trust the nystagmus!)
Central vestibular disease	-Vestibular components within CNS are affected --CN VIII nuclei, vestibular pathways --brainstem, cerebellum involvement, multiple CNs involved -May have abnormal mental state -Weakness, proprioceptive deficits -Head/neck tilt towards affected side -Nystagmus can occur in any direction and change direction
Peripheral vs. vestibular disease	-Important to know the difference, different DDx list -will do different diagnostic tests -Prognosis is better for peripheral vestibular disease
Peripheral vestibular disease DDx	-Temporohyoid osteoarthropathy --may also have otitis media-interna -head trauma and petrous temporal bone fracture -Polyneuritis equi
Central vestibular disease DDx	-Equine Protozoal Myeloencephalitis (EPM) -head trauma --basisphenoid/basioccipital bone fracture -Neoplasia (lymphoma) -Aberrant parasite migration -Bacterial or viral infection
Temporohyoid Osteoarthropathy	-Unique equine disease -Caused by fusion of stylohyoid bone to petrous temporal bone --articular joint becomes arthritic -Signs occur after pathologic fracture of petrous temporal bone -Can be related to otitis media-interna -Signs of peripheral vestibular disease -ipsilateral facial nerve deficits, difficulty eating, depression -Dx based on clinical signs, guttural pouch endoscopy, and skull imaging (CT or radiographs) --endoscopy will show bone proliferation of stylohyoid bone --radiograph will show pathologic remodeling of joint, bony proliferation leads to fused joint, fracture occurs when joint is moved --CT is best diagnostic tool
Polyneuritis equi	-Neuritis of cauda equina -Acute form presents as initial hyperesthesia of the head, perineum -Insidious form presents with slow, progressive paralysis of the tail, bladder, rectum, anus -May have cranial nerve involvement -Lesions are granulomatous inflammation of nerve roots -Undetermined etiology, immune-mediated disease? -Supportive care as treatment --dexamethasone, azathioprine -Poor prognosis
Important aspects of vestibular disease in horses	-Peripheral disease is more common than central disease -Need to be convinced that other intracranial signs are present to diagnose central vestibular disease -Most common cause of peripheral disease is temporohyoid osteopathy --easy to rule in/out, endoscopy of guttural pouches --if normal, consider other diseases and diagnostic tests
Neuromuscular disease in horses	-Signs can be focal or diffuse -Focal: --lameness or gait deficit, focal muscle atrophy --equine protozoal myeloencephalitis --peripheral nerve damage due to trauma or neoplasia -Diffuse: --generalized weakness, difficulty supporting weight, base-narrow stance, muscle tremors, and excessive recumbency --Equine motor neuron disease --botulism
Botulism in horses	-Diffuse neuromuscular disease -Weak tongue tone, animal cannot eat or drink normally --chews for a very long time
Diagnostic plan for diffuse neuromuscular disease in horses	-Tongue test, grain test --if positive, continue to specific botulism treatment and testing -Serum vitamin E -Fundic exam -Biopsy of sacrocaudalis dorsalis medialis muscle or spinal accessory nerve
Equine Motor neuron Disease	-Diffuse neuromuscular disease -Similar to ALS in people -Caused by vitamin E deficiency -Adult onset, no ataxia -only affects lower motor neurons -Easier for animal to walk than to stand still -Usually occurs when horse has little to no access to pasture and poor quality hay for prolonged period of time (more than 17 months) -Vitamin E deficiency leads to increased CNS oxidative stress, leads to increased permeability of blood
Clinical signs of Equine Motor neuron Disease	-Weight loss -Trembling, cramped under stance -reluctance to stand still -Elevated tail head -Short/choppy stride -Low head/neck carriage -Prolonged or frequent recumbency -Diagnose via serum vitamin E levels and muscle biopsy --spinal accessory nerve biopsy (CN XI) --fundic exam, expect to see lipofuscin deposits on retina -Prognosis is poor for return to normal function --can stop progression, but may not return to normal -DDx: botulism
Headshaking	-Unknown cause -Age of onset 7-9 years -Geldings and thoroughbreds are over-represented -Seasonal in over 50% of cases --usually spring, summer, fall -Often exercise-induced, worse under saddle or only shows up under saddle
Head shaking grading system	1. intermittent, mild clinical signs --facial muscle twitching, rideable 2. Moderate clinical signs --can define conditions under which shakes occur or develop --rideable with some difficulty 3. Rideable, but unpleasant to ride and difficult to control 4. Unrideable, uncontrollable 5. Dangerous with bizarre behavior patterns
Proposed causes of headshaking	-Ears: mites, otitis media/interna -Eyes: corpora nigra cysts -Teeth: periapical osteitis -Guttural pouch: mycosis, temporohyoid osteoarthropathy -Nasal/paranasal: allergic rhinitis, sinusitis, progressive ethmoidal hematoma, trombicula autumnalis larval infestation -Neurogenic: vasomotor rhinitis, cranial nerve dysfunction (trigeminal neuralgia), photic headshaking due to optic-trigeminal summation, infraorbital neuritis, Equine protozoal myelitis -Other: cranial nerve injury, maxillary osteoma, partial asphyxia
Trigeminal nerve neuroanatomical location DDx	-Damage from sinus cyst or sinus surgery -Infraorbital neuritis or neuropathy -Vasomotor rhinitis or allergies
Headshaking diagnostic plan	-Ophthalmologic exam -Oral exam -Aural exam via endoscopy -Radiographs of paranasal sinuses and head -Endoscopy of nasal passages, pharynx, guttural pouches -Infraorbital nerve blocks -Therapeutic trials
Therapeutic trials for headshaking	-Nasal masks/nose net -Change lighting or environment where animal is ridden --contact lenses, goggles -Bilateral infraorbital analgesia --be careful! May result in hyperesthesia of the face -Bilateral posterior ethmoidal nerve anesthesia -Medication trials
Equine Metabolic Syndrome (EMS)	-“Peripheral Cushing’s” -“Insulin resistance” -Overweight horses -Common in Morgans, Peruvian Pasos, Paso Finos, Spanish Mustang, Warmblood, Rocky Mountain Horses -Horses age 5-15 years (younger horses)
Equine Metabolic Syndrome (EMS) Clinical signs	-Obesity and fat deposits --cresty neck, gluteals, sheath, udders -Chronic laminitis, may be sub-clinical -Insulin Resistance -Possibly Infertility in mares
EMS contributing factors	-Chronic Over-feeding -Limited physical activity -Enhanced metabolic efficiency
EMS Pathophysiology	-Fat: storage organ to endocrine organ -Adipocytes produce excessive levels of endogenous glucocorticoids --inhibits action of insulin at central and peripheral tissues -Animal develops glucose intolerance -Affected horses have increased insulin secretion, but action of insulin is inhibited -Increased 11-betahydroxysteroid dehydrogenase 1 activity
Laminitis and Equine Metabolic Syndrome (EMS)	-Nitric oxide production decreases in animals with EMS -results in vasoconstriction -Impairs ability of the vessels to respond to vascular changes --vessels cannot respond when needed -Horse has “smoldering” laminitis
EMS diagnosis	-History -Physical exam --regional adipocyte deposition --High body condition score --crest neck score of more than 3 --radiographs of feet (hard to convince owner to take radiographs when horse is sound -Lab tests --single glucose and insulin concentrations --IV glucose tolerance test (only done in research setting) -Oral glucose test (dynamic test)
EMS diagnostic testing results	-Glucose will be high-normal -hasting hyperinsulinemia --more than 20 uU per ml --need to do with 6 hour food withhold -Fasting oral glucose test in field --0.15 ml/kg light karo syrup PO --measure insulin 1-1.5 hours after administration --more than 60 uU/ml is positive for EMS -Do not sample during a laminitic episode, stress will give false increase -Sample after 6 hour period of feed withhold between 8-10am
EMS treatment	-Diet! Reduce obesity -Feed low glycemic index foods --Eliminate pasture time --Forage diet with vitamin and mineral supplementation --be sure to test hay/pasture before allowing animal to eat it -Put animal on dry lot -Soak hay to get rid of sugars, have to also supplement with vitamins -More exercise -Anti-oxidants -Decrease cool season grasses (C3), increase warm season grasses (C4) --bermuda grass, bluestem, switch, Gramma, native prairie grass species -Graze animal when grass is less “stressed,” overnight -If animal is insulin resistant, feed commercial low-NSC feed -Beet pulp or soy hull based feeds -Feed multiple small meals
Levothyroxine Sodium	-Treatment for EMS -“Safe” treatment -Induces weight loss and insulin sensitivity -48 mg/day PO for 3-6 months --give for a finite period of time then wean off --wean off over a month
Metformin	-Treatment for EMS -Really an anti-diabetic drug -Increases insulin sensitivity at the post-receptor level -Controls post-prandial insulin spikes -Decreases carbohydrate load within the gut -No long-term safety studies -30 mg/kg every 8-12 hours PO --give 1 hour before feeding
PPID vs. EMS	-Older horses vs. horses less than 15 years old -Regional adiposity in both -Laminitis in both -Hyperinsulinemia sometimes present vs. hyperinsulinemia present -Hirsutism vs. no hirsutism -PU/PD vs. no PU/PD -Skeletal muscle atrophy vs. no atrophy -Failure to shed winter coat vs. no failure -ACTH increased vs. ACTH normal -Abnormal dex suppression test vs. normal dex suppression test
Pituitary pars intermedia Dysfunction (PPID)	-Hypertrophy/hyperplasia od pars intermedia of the pituitary gland -Pituitary micro and macroadenomas are common -Increased expression of pars intermedia POMC-derived peptides (ACTH) -Gland is functional, produces increased hormones -Usually occurs in older horses, 18-23 years old -“Cushing’s disease” -Hirsutism is most frequent clinical sign -Posterior pituitary/neurohypophysis stores and secretes hormones made in hypothalamus -Anterior pituitary/adenohypophysis --made of pars distalis, pars intermedia, and pars tuberalis
PPID clinical signs	-Hirsutism is most frequent -Chronic laminitis, solar abscesses -Weight loss with fat distributed around ribcage --abnormal fat distribution -Increased infection -Poor wound healing -Muscle wasting, weight loss -Hyperhidrosis -PU/PD -Seizures, blindness
PPID pathogenesis	-Loss of hypothalamic control of dopamine inhibition --dopamine neuron degeneration? --oxidative stress and protein misfolding? --parkinson’s like disease? -Pituitary hyperplasia, hypertrophy, and microadenoma --excessive production of ACTH and other PMOC derived peptides (MSH, beta endorphins, CLIP) --Insensitive to glucocorticoid negative feedback -In horses is ALWAYS pituitary based, not adrenal based -Elevated ACTH and other peptides is associated with adrenal hyperplasia --increased cortisol and androgen production -Pituitary adenoma leads to compression of hypothalamus, posterior pituitary lobe, and optic chiasm
Hematologic changes associated with PPID	-Hyperglycemia, hyperinsulinemia --due to insulin resistance? -Elevated endogenous ACTH -Loss of cortisol level circadian rhythm -Anemia, neutrophilia, and lymphopenia are rare -Do not measure cortisol levels to make diagnosis
PPID diagnosis	-Many tests available but no good test -Poor sensitivity, poor specificity -Safety of tests? -results vary by the time of year --increased in the fall, need to use fall-specific reference range and do not compare to the spring value
PPID diagnosis via ACTH serum levels	-Baseline ACTH level: --ponies: more than 27 pg/ml --horses: more than 35 pg/ml -Need special handling of samples -Results can be falsely elevated with stress and pain -Seasonality plays a role --increased values in the fall -Regional values? -Use purple top blood collection tube with EDTA
PPID diagnosis via Dex suppression test	-no longer the “gold standard” -Use caution in horses with recurrent laminitis --may cause laminitis in susceptible horses -Draw baseline cortisol, give dex, test 20 hours post cortisol --normal: cortisol will be less than 1 ug/ml --PPID: more than 1 ug/ml -Increased values in the fall -Low sensitivity
PPID diagnosis via Thyrotropin Releasing hormone test	-TRH stimulation test -draw baseline blood, Give TRH, draw post- test and look at ACTH levels -In PPID cases, ACTH levels increase by more than 50% -TRH can be difficult to get -Can be combined with dex suppression test -Not commercially available
PPID diagnosis via Domperidone stimulation test	-Blocks peripheral dopamine D2 receptors -Marketed for use in horses, wide margin of safety -Does not cross BBB -Give domperidone paste at 8am, run ACTH levels at 0 and 8 hours -More than 2x increase indicates PPID -Seasonal effect is unknown -ACTH stimulation test may be better?
PPID diagnosis via physical exam	-Hirsutism will be present, 86% accurate for diagnosis -May not see in early PPID -Better than all other tests! -Ideally pair with other tests, also test to see if medication is working
Pergolide	-Treatment for PPID
PPID Prognosis	-Lifelong condition, no current cure -Effective treatment is possible with medication and management changes -Prognosis is guarded to fair --based on response to treatment and development of complications
Johne’s Disease	-Chronic bacterial infection -Mycobacterium avium subspecies paratuberculosis (MAP) -Affects the intestinal tract --can lead to disseminated infection of the body -Affects cattle, deer, bison, sheep, goats, camelids -Long incubation period, 2-10 years
Signs of Johne’s Infection	-95% of infected cattle show no signs at all -Clinical signs in animals present in animals over 2 years old
Clinical signs of Johne’s Disease in cows	-Weight loss despite normal appetite -Decreased milk production -Diarrhea (may be intermittent) --loose, then progresses to pipe-stream -Sub-mandibular edema/bottle jaw due to hypoproteinemia -Lethargy -Emaciation, VERY thin cows -Animal starts to go into negative energy balance -Usually individual animals are culled before advanced disease is present -On herd level, may see one animal with chronic diarrhea and then another several months later
Clinical signs of Johne’s disease in small ruminants	-Emaciation -Hypoproteinemia causing bottle jaw -No diarrhea!
Stages of Johne’s disease infection	-stage 1: calf infected in early neonatal period --infected via oral ingestion of manure with MAP -Stage 2: eclipse phase --animal shows no clinical signs and MAP is unable to be detected --no antibody production, no immune response, no way to know animal is infected -Stage 3: starts to shed organism --can detect organism with PCR or ELISA -Stage 4: clinical stage --rare that an animal makes it to stage 4, usually removed or culled first
Stages if Johne’s Infection	1. Invasion phase (stage 1): calves --intestinal invasion of M-cells --can also affect yearling heifers if immunocompromised 2. Eclipse phase (stage 2): 2-10 years --shedding organism, but not able to be detected 3. Asymptomatic phase (stage 3): 2+ years --positive fecal test for MAP --may be 1-9 years until animal is clinical --serology becomes positive with increased organism numbers 4. Clinical phase (stage 4): heavy shedder
Johne’s Iceberg	-Only 1% of affected animals will show clinical signs fo weight loss and diarrhea -3-5% of animals are in shedding phase -25% of animals are in eclipse phase -60% of animals are infected but not detectable!
Sources of Johne’s disease Infection	-In-utero -Peri-natal period --most likely time of infection --heavily infected cows shed MAP into colostrum -Environment: --fecal contamination of feed and water --manger sweepings --infected Manure spread on crops can result in infection if fed to animals (put to silage! Not grazing crops!)
Johne’s disease diagnostic tests	-Serology: antibody-based test --AGID --ELISA -Fecal culture --solid media (gold standard) --liquid media -Fecal RT-PCR -Histopathology
AGID test for Johne’s disease	-For cattle with clinical signs -High specificity (95%) -Sensitivity varies based on stage of disease --high in clinical cows --low in asymptomatic cows -Reliable test for individual cows that are clinical suspects -Not reliable as a screening tool, not effective for finding non-clinical cows
ELISA test for Johne’s disease	-Can be done on serum or milk -Great screening test -On serum, sensitivity is 25-45% (not great, especially for non-clinical cows) --specificity is 95-99% -Positive test indicates animal is likely to culture positive on fecal -Negative test does not mean animal is not infected --animal could be negative, could also be infected but not able to be detected by ELISA -Used as herd screening tool, followed by fecal culture of ELISA-positive animals (follow up with fecal culture) -Rapid turnaround time -Low cost -Lots of samples can be processed on the same day -Specificity is not 100%, may identify negative cattle as positive -Sensitivity is poor on sub-clinical cows
Milk ELISA for Johne’s disease	-Special ELISA kits -Sensitivity and specificity are similar to serum ELISA -More convenient sampling -“Target testing” is easier, can check at specific life stages -Can take bulk tank samples --bulk tank samples become very dilute, no way to know which cow specifically is positive -Specificity is not 100%, may identify negative cattle as positive -Sensitivity is poor on sub-clinical cows
Fecal culture for Johne’s disease	-“Gold standard” johne’s testing -high sensitivity and high specificity -Usually positive 1 year before clinical signs develop -Can quantify number of contagious untis, can identify super-shedders -Expensive, costs $20-25 per sample -Sample collection process is involved, have to go into rectum for sample -Incubation time is 12-16 weeks, slow turn-around -Need specific lab, trustworthy lab -Can use as screening tool on pooled samples from 5-10 cows --spilt group if needed -Can be used to confirm ELISA positive animals before culling -Liquid media is faster than solid media, reduced incubation period --correlation between time it takes to show up positive and amount of MAP in sample -Some small ruminant strains do not grow in liquid media -Try to quantify shedding by comparing with Herrold’s Egg yolk media
Herrold’s Egg yolk media	-Testing for Johne’s disease -Allows quantification of shedding -informs culling of high-shedders -White dots indicate MAP colonies
Fecal RT-PCR for johne’s disease	-Commercial kit, identified specific MAP DNA segments -Can be done on individual samples or pooled fecal samples -High specificity, 100% -High sensitivity, can detect very low shedders -rapid turnaround, 203 days -Quantification of the amount of MAP in the sample -Can be used for small ruminants, camelids, bison -Expensive, $15-25 per sample -Need precise technical skills
Histopathology for Johne’s disease	-Can only do on clinical cases -Rarely used to confirm cases -Will see “corrugated cardboard” intestine -Samples obtained during exploratory laparotomy or at necropsy --usually not done on alive animals! -Intestinal tissues and adjacent ileocecal lymph nodes -Need acid-fast staining with Ziehl-Neelsen stain -Sensitivity is poor in animals in stage I and II of infection
Single animal testing of Johne’s disease	-Done to determine an animal’s infective status before introduction into a new herd --challenging! Animals in stage I and II are basically impossible to detect! --should look at history of herd -test 30 animals from native herd, perform composite environment samples on native herd -Fecal RT-PCR positive indicates positive -Fecal culture positive indicates positive -Serology should always be followed by fecal culture or RT-PCR --ELISA or AGID -Histopathology of ileum/ileocecal lymph nodes
Herd diagnosis of Johne’s disease	-Individual ELISA on serum or mil as a screening tool --identified MAP within the herd --Confirm ELISA-positive cows with fecal culture -1 animal with positive culture indicates 3 infected animals within the herd -Bulk tank ELISA can be done --not as sensitive as individual samples if prevalence is low within the herd -Pooled fecal samples can be helpful --sensitivity depends on shedding level --possible false negative on infected animals that are not yet shedding -Composite environmental manure samples are great for herd infection detection --3-4 manure samples from high-traffic areas
Johne’s Passive Shedding Phenomenon	-“pass through shedding” -Positive fecal culture followed by several negative cultures from same cow -Result of passive excretion of MAP after consumption of contaminated feed materials -Can impact PCR testing, will not affect culture --PCR tests for genetic material, not actual organism -Can be more than 50% of positive cultures within a herd -Cultures are usually “low positive” -Need to focus on detection of super-shedders
Johne’s Super-Shedders	-Low shedders: 1-10 cfy/4 tubes, 5-50 cfu/g -Moderate shedders: 11-100 cfu/4 tubes, 55-550 cfu/g -Heavy shedders: more than 100 cfu/4 tubes, more than 550 cfu/g -Super shedders: more than 2,000 cfu/4 tubes, more than 10,000 cfu/g -Want to detect and cull super shedders
Johne’s vaccination	-Must be approved by the state veterinarian -Herd has to be infected -vaccinate calves less than 35 days old -Decreases shedding but does not get rid of the organism -Need special ear tattoo: JD VAC -Vaccinate SQ into brisket
Disease management in swine herds	-How do you know if there is a problem? --lots of animals --cannot really do physical exams --observation alone may not be enough -What do you do about the problem? -Diagnosing a problem --production records --Serology --Pathogen identification
Swine production records	-Good method for identifying and diagnosing problems -Readily available measures of performance -provide monitor of herd health -Examine regularly to identify problems -Can establish target values --system specific -Can establish intervention levels and initiate action if parameter is exceded
Common production record benchmarks in swine production	-Death loss: --pre-weaning mortality should be less than 12% --nursery room mortality less than 2% (if piglet makes it to weaning age, it should make it to market) --finish floor mortality less than 2% -Farrowing room performance: --total born: 12 (alive: 11, dead:1) --stillborn: 0.5 --mummies: 0.5 --Weaned: 10 -Pigs weaned per sow per year: more than 22 -Finishing performance: --165 days to market --2.3 lbs average daily gain --2.8 feed efficiency ratio
Serology in swine herds	-Regulatory -Diagnostic --monitoring, need to take acute and convalescent titers --outbreak situations
Diagnostics used in a swine herd disease outbreak	-Isolation or culture -Immunohistochemistry -FA -PCR
Preventing disease in swine	-Biosecurity: keep disease out of facility --shower-in --barn-specific clothing and footwear -All in/All out management --fill rooms with animals of 1 age, empty all at the same time --Age and site segregation -Vaccinate and acclimatize --most biosecurity measures fail at acclimatization due to bottom line pressure to cut corners based on finances
Treating Swine	-Can treat sick animals or the whole herd -Sick vs. going to be sick -Mass medication: --water (sick animals tend to go off-feed, but do not go off-water as fast) --feed --need to know dose (grams of drug per kilo of pig), pounds to treat (number of animals * average weight)
Mass medication of Pigs	-Need to know how much feed or water is consumed by each animal each day --Determines volume in which to dilute the drug -Feed: 4% of body weight per day -water: 1 gallon/100 lbs body weight per day --8% of body weight
Porcine Reproductive and Respiratory Syndrome (PRRS)	-Arterivirus -Enveloped, positive stranded RNA virus -Related to equine arterivirus -Replicates in macrophages, highly host restricted --does not spread to other species -Asymptomatic, persistent infections -Highly infections, fewer than 10 virus particles are needed to spread -Not highly contagious, need animal to animal contact to spread -Causes acute reproductive failure/abortion at 3-4 months gestation -Post-weaning respiratory disease
Economic impact of PRRS	-Single most economically devastating health problem facing swine industry! -Causes acute reproductive failure at 3-5 months gestation (abortion) -Post-weaning respiratory disease --piglets do poorly after birth --affects all age groups within production system
PRRS effects on suckling pigs	-Respiratory distress -Delayed development -Depression -Palpebral edema, conjunctivitis -Mummified, dead animals -Weak piglets -Up to 80% mortality
PRRS effects on post-weaners	-Respiratory distress -Secondary viral and bacterial infections -Decreased growth rate -Sneezing, conjunctivitis -Respiratory distress
PRRS effects on sows	-INappetance -Lethargy -Fever for 1-7 days -Abortion in last trimester
PRRS progression	-Initial phase (1-3 weeks) --inappetence, lethargy, depression, pyrexia --virus is spreading rapidly through other phases of production --Respiratory distress in piglets, rapid abdominal breathing --born dead, increased numbers of stillborn/mummy piglets -Climax phase (8-12 weeks) --Sows have premature farrowings, increased stillborn and increased mummies --Piglets are weak, increased pre-weaning mortality --post-weanling piglets have respiratory signs, increased secondary infections, mortality can approach 10%+ -Final phase (1 year or more) --Reproductive performance returns to almost normal --occasional sporadic flare-ups of reproductive failure --respiratory disease persists in post-weanlings -Reoccurrence -Clinical picture is variable, most deaths come from secondary infections
PRRS reoccurrence	-RNA virus, is a persistent infection in asymptomatic animals -High rates of mutation results in more than 100 strains of the virus -Immunity is not always cross-protective between strains -Continued introduction of animals can be a problem -Disease can spread to surrounding area --aerosol, ducks, rodents, mosquitoes, humans -Humans can carry virus in upper respiratory tract!
Diagnosing PRRS	-Serology: bleed a sample of the herd --30 animals insure 95% confidence of finding 10% prevalence --sample different aged animals depending on clinical picture --ELISA is most common -Virus identification --IHC, FA --virus isolation --PCR
ELISA for PRRS	-Most common assay -Titers are not maintained post exposure -Titer greater than 2.0: very recently exposed -Titer greater than 1.5: recently exposed -Titer 0.4-1.5: hard to interpret, distant previous exposure? Vaccine titer
PRRS Immunology	-Initial fever in first week -IgG levels rise and viremia occur around week 2 -CMI rises around week 4 -SN rises around week 5.5
Diagnosing PRRS virus ID	-ICH/FA: tissue sample of lung, spleen, tonsil, lymph nodes --fast and relatively inexpensive -Virus isolation: sera or tissue sample --takes 10-14 days, slightly more expensive -PCR: serum --usually less than 7 days, but most expensive
Controling PRRS	-Vaccinate sow herd regularly -Acclimate breeding stock -Closed herd -All-in/All-out nurseries -Treat secondary infections
Vaccination for PRRS	-Vaccinate sow herd regularly -Vaccine control is somewhat limited -Modified live virus: --vaccinate entire population housed in the same air space --current form of vaccine is pathogenic in late gestation -Killed vaccine: --can be used in gilt acclimatization or following exposure to field strains --Safe, but not sure if it is effective
Acclimatization of breeding stock to control PRRS	-Isolate animals when they arrive for 60-90 days -Test, then vaccinate -Expose to local strains -Re-test before introducing to the herd
Closing the herd to control PRRS	-let infection run its course -Do not introduce any new livestock -internal multiplier --gilts are now used for replacement instead of going to market, reduces income
Porcine Circovirus Associated Disease PCVAD	-AKA Post-weaning multi-systemic wasting syndrome (PWMS),
PCVAD epidemiology	-Poorly understood -First recognized in 1991 in western Canada -World-wide -Exposure to PCV2 may not be sufficient to cause disease --95% of animals are also infected with PRRS, mycoplasma, and SIV
PCVAD Clinical Presentation	-Pigs 5-18 weeks of age -Anorexia -Rapid weight loss -Unthrifty pigs -Skin discoloration and crusting -Respiratory signs -Diarrhea -Wasting -Death loss up to 40%
PCVAD Pathology	-Animal is emaciated with stomach ulcers -Severe inflammation or degeneration of lung, kidney, liver, lymphoid tissue -Lymphoid depletion -Granulomatous inflammation on lymphoid or other tissues -Confirm diagnosis by presence of PCV2 antigen in affected lymphoid tissue
PCVAD treatment and control	-Treat secondary pathogens --Pasteurella multocida --S. suis --Salmonella -Maintain biosecurity -Good production practices --limit cross-fostering --do not re-use needles --strict all-in/all-out --Hygiene and sanitation -Vaccinate?
Controlling PRRS in the farrowing room	-None for acute PRRS -NSAIDs to reduce fever (minimal benefit) -B-vitamins to stimulate appetite (minimal benefit) -Antibiotics to treat opportunistic bacterial infections -Prevention is primary means of control -Vaccination in the face of an outbreak?
Controlling PRRS in the nursery	-Want to know what is causing death loss --neurologic? (strep suis) --Pneumonia? (Pasteurella) --Chronic wasting (H. parasuis) -Do necropsy for further information --submit tissues based on findings --identify secondary bacterial invaders -Inject clinically ill animals with penicillin for 3-5 days IM -Medicate feed or water
Veterinary Feed Directive	-Prescription written to feed mill -Allows medicated feed to be mixed and delivered to the farm -Requires valid veterinary-client-patient relationship
Camelid restraint	-Needed! Just do it -Physical restraint -Chemical restraint --xylazine --butorphanol --tend to be more like ruminants than like horses
Lab value differences in camelids	-WBC: 8,000-21400/ul -RBCs are elliptical, small, non-nucleated -PCV of 27-45% is normal -Creatinine 1.4-3.2 mg/dL --should be closer to 1 -Higher than normal Na and Cl when compared to other species --Na: 148-158 --Cl: 102-120 -Glucose: 74-154 and often higher
Treating Camelids	-Challenge -Mostly a ruminant, oral medications are useless --unless a cria -More susceptible to aminoglycoside toxicity, avoid aminoglycoside or gentamycin
Congenital abnormalities in Camelids	-More common in camelids than in other animals -Cardiac: VSD, Complex defects -Ophthalmic: cataracts, Atresia of nasolacrimal duct at nasal puncta -Urogenital -Factor VIII deficiency clotting disorder -Musculoskeletal defects: angular limb deformity, umbilical hernia, polydactylism, vertebral malformation -Always look for a congenital defect!
Choanal atresia in Camelids	-Partition between nasal passage and nasopharynx does not regress/breakdown -Prevents air passage from nose to trachea -Evident at birth, will see open-mouthed breathing --cannot nurse -Surgical outcome is not that great -Genetic defect? Euthanasia is recommended
Diagnosing Choanal atresia in camelids	-Clinical signs: mouth breathing, not nursing -Try to pass feeding tube into nose -Infuse contrast media and take radiograph, look for contrast agent collecting in nasal passage -Euthanize animal!
Reproductive issues with camelids	-Adhesions --sequela to trauma --mucometra or pyometra if adhesion heals closed --can result in predisposition to infection -Sensitive to manipulation or trauma of reproductive tract -Uterine torsion -Treatment is difficult
Uterine torsion in Camelids	-Most common cause of dystocia in camelids -Usually clockwise --cria is usually in left horn -First option is to sedate and roll -Second option is celiotomy --usually also includes caesarian section -Present in late gestation or at term -Signs can be subtle -Use lots of lube! -Usually pre-cervical, vaginal exam is not helpful
Nerurologic diseases in Camelids	-p. tenuis -polioencephalomalacia -listeriosis
GI diseases in camelids	-Viral: coronavirus (most common), rotavirus -BVD: will be seropositive
Coronavirus in Camelids	-Most common viral cause of diarrhea -Causes outbreaks -Common in young animals -Crias and adults are affected -Treatment is supportive care
Bacterial diarrhea in Camelids	-Clostridium perfringens --C, D, A --vaccination is recommended -Salmonella (rare, does not cause severe disease) -Johnes disease --testing used in other species is not helpful in camelids --diagnostic challenge
BVD in camelids	-Bovine viral diarrhea virus -Lots of similarities in cattle -Acute infections can cause young animals to be sick -Can result in abortions, congenital anomalies, or persistently infected/silent shedder crias -No vaccine yet
Protozoal diseases causing diarrhea in camelids	-Coccidia --E. alpacae, E. lamae, E. punoensis --E. macusaniensis -Cryptosporidium -Giardia
Coccidia E. macusaniensis in Camelids	-VERY large --diagnostic tests for small coccidian cannot identify, needs more dense solution for fecal flotation -Often missed as a cause of illness -Very pathogenic in adults -Ponazuril has some efficacy
Nutritional muscular dystrophy in Camelids	-Selenium deficiency (white muscle disease) -Will see stiff, lame, recumbent camelids -Almost always taken care of in diet, not seen often -Will have increased CPK, AST, and decreased Se -Treat by giving selenium
Rickets in Camelids	-Vitamin D deficiency -Hypophosphatemic rickets -Occurs in nursing crias, growing animals --cria born in the fall, low colostrum levels, low levels of sunlight, higher elevations -Will be lame, stiff, ill thrift, angular limb deformities --metaphyseal flaring on radiographs -Treat by giving vitamin D --injectable form SQ --can be toxic, do not overdose!
Juvenile Llama Immunodeficiency Syndrome (JLIDS)	-Unknown etiology -Clinical signs: wasting, recurrent infections -Low IgG -Anemia due to mycoplasma haemolama -Diagnose with lymph node biopsy -Can do vaccine challenge -B-cell defect? -Has decreased in recent years, but is still present -No treatment
Lymphosarcoma in Camelids	-Most common neoplasm -Can occur at any age -Clinical signs: weight loss, lymphadenopathy
Mycoplasma haemolama	-Previously Eperythrozoonosis -RBC parasite -Fairly common -Black dots in RBCs -Found in healthy animals and sick animals --unknown role in causing sickness -Red flag for immunodeficiency -Tx: oxytetracycline --will clear parasitemia, but will not clear carrier state
Heat stress in camelids	-Camelids are not well-suited for heat --mountain animals -Often fatal! Very serious! -heat sets off a whole inflammatory cascade, cannot just cool to treat -Tx: lower body temp --clip hair --put in air conditioning --anti-inflammatories to counter effects of inflammatory cascade --supportive care (good bedding, physical therapy, swimming) -Prevention is key!
Clinical signs of heat stress in Camelids	-Elevated temperature (104-108) -Depression -Recumbency -Neurologic signs -Open mouth breathing -Scrotal edema, ventral edema -Edema -Needs to occur in hot season -Can be due to additional stress or exertion
Preventing heat stroke in Camelids	-Shear in summer -Give shade! -Plenty of water
Camelid metabolism	-Blood glucose is higher than ruminants --low concentration of circulating insulin --slow glucose clearance --partial insulin resistance -Susceptible to stress hyperglycemia -Cannot increase glucose clearance to match increased glucose mobilization during times of stress --leads to persistent or extreme hyperglycemia
Metabolic disease in Crias	-Stress causes hyperglycemia, leads to osmotic diuresis -Hyponatremia and dehydration -Neurologic disease and death -As soon as animal becomes glucosuric, be aware! Leads to downward spiral!
Metabolic disease in Adult camelids	-Anorexia leads to hepatic lipidosis and death -Hyperlipemia is common during stress events --causes fatty liver -Usually secondary to a primary problem
Neonatal disease in Camelids	-Usually have good success treating neonatal disease -Crias are a lot like foals, get all of the same problems -Failure of passive transfer has different numbers --need higher levels of IgG, should be more than 1,000 mg/dL -Treat with colostrum PO if less than 24 horus, plasma IV if more than 24 hours --can also give plasma intraperitoneally
Herd health in Camelids	-Vaccines --clostridium C+D --tetanus --rabies --WNV? -Deworming (P. tenuis specifically) --ivermectin SQ every 4 weeks --doramectin? -Nail trimming -Weigh -Check BCS -Castrate
Castration of Camelids	-Not done until 18-24 months old --If earlier, more prone to arthritis -Can do standing or under general anesthesia
Principles of Vaccination	-Based on: --risk of disease --consequence of disease --Effectiveness of the product/vaccine --Adverse reactions --Cost
Expectations of Clients when Vaccinating horses	-Good management practices -Primary series prior to exposure -Each animal is not the same, may need different vaccines -Understand that Vaccination minimizes infection but does not prevent infection -Protection is not immediate -Need to stick to recommended intervals -Herd technique -Never complete protection -Adverse reactions are possible
Infectious Disease Control	-Reduce exposure -Minimize factors that decrease resistance --corticosteroid usage -Occurrence of disease increases with: --increased population density --sales, track activities, breeding --Movement of animals
External factors increasing risk of infectious disease incidence	-Stress -Overcrowding -Parasitism -Poor nutrition -Inadequate sanitation -Contaminated water supply -Lack of pet control -Lack of biosecurity
Vaccine labeling	-Prevent infection -Prevent disease -Aid in prevention of disease -Aid in control of disease
Adverse vaccine reactions	-Local muscle soreness or swelling (most common) -Transient, self-limiting fever, anorexia, lethargy -Systemic reaction --Urticaria --purpura hemorrhagica --anaphylaxis
Horse Vaccine administration	-All vaccines are IM unless otherwise noted -Neck, pectorals, semimembranosus muscle injection -Some vaccines are intranasal
Vaccine storage and handling	-Keep in recommended temperature range -Keep thermometer in fridge to know if temp is maintained -Color change may occur during storage -Protect from UV light -May need to reconstitute --only reconstitute as much as needed at any given time, do not save! -Botulism is 1st vaccine to freeze
Vaccination in foals	-May have interference due to passive transfer --maternal antibodies interfere with vaccination -Difference between foals from a vaccinated mare and unvaccinated mares -Primary booster 3 shot series --Botulism, 3 shots all 1 month apart --All others 1st and 2nd shot 1 month apart, 3rd shot within the 1st year of life
Vaccination of pregnant mares	-Pre-foaling vaccines 4-6 weeks before parturition -Need to use vaccines that provide colostral antibodies --intranasal vaccines are usually ineffective -Herpesvirus vaccine is specific for pregnant mares --specific form that prevents abortion
Core vaccines in horses	-Tetanus -Eastern Equine Encephalitis -Western Equine Encephalitis -West Nile Virus -Rabies -(Botulism in PA) -Other core vaccines vary by area
Tetanus vaccine for horses	-Adults: 2 dose initial series, 1 month apart -Annual revaccination -Booster vaccine when there is a penetrating injury if previous vaccine was given more than 6 months ago
Eastern and Western Equine Encephalitis	-Vaccinate before spring (vector seasion) -Adults: 2 dose initial series -Annual revaccination
West Nile Virus Vaccine	-Adults: Initial 2-3 dose series --depends on vaccine -Annual or biannual revaccination --may need to give more often, depending on brand of vaccine
Rabies vaccine in horses	-Adults: single primary dose -Foals: 2 dose initial series, 1 month apart -Annual revaccination -Can do rabies antibody testing, but rarely done
Risk-based Vaccines in horses	-Botulism -Equine herpesvirus -Equine Influenza -Potomac Horse Fever -Strangles -Venezuelan Equine Encephalitis (not recommended) -Rotavirus (breeding farm vaccine, give to pregnant mares to protect foals) -Equine Viral Arteritis
Botulism vaccine in horses	-Initial 3-dose series, 1 month apart for all ages -Give to ALL horses -Botulism B is in soil -Botulism C and D in carcasses
Equine herpesvirus vaccine	-Rhinopneumonitis -NO available vaccine labeled for neurologic form of disease!! -Adult, non-breeding horses: --initial 3 dose series, 1st and 2nd one month apart, 3rd within a year --annual revaccination --6-month interval revaccination in horses less than 5 years old, horses in contact with pregnant mares, or performance show horses (high risk) -Pregnant mares: specific vaccines --Give at 3, 5, 7, 9 months of gestation
Equine Influenza Vaccine	-3 initial doses of series are recommended -Use recent strain to vaccinate -All vaccines on market have protection for 6 months -Clad 1 vs. Clad 2
Strangles vaccine	-Streptococcus equi equi -Vaccination is recommended on farms with persistent problems, or animals with high risk of exposure -Vaccination or exposure to natural infection can result in Purpura hemorrhagica -Do not vaccinate in face of an outbreak! -Killed vaccine is not recommended, associated with increased inhection site reactions --does not prevent disease
Strangles Intranasal vaccine	-Modified live vaccine -High level of immunity against experimental challenge -Accurate delivery is needed! -Small number of cases have residual vaccine virulence --slow growing abscess in lymphoid tissues -Need careful handling of vaccine, do not let clients give vaccine!
General Concepts of Evidence-based de-worming	-Aim to kill larval stages, not adults --larval stages do the most damage -Previous techniques/tactics have been incorrect and created resistance issues -All worms will eventually become resistant, it is just a matter of when -Get clients involved with deworming -No new classes of drugs are being developed, need to care for the ones we have!
Parasite Control Goals	-Minimize risk of parasitic disease -Control parasite egg shedding -Maintain efficacious drugs -Try to avoid further resistance development
Parasites in Adult horses	-Large strongyles (Strongylus vulgaris) --causes blood clot at cranial mesenteric artery, cuts off blood supply to small intestine -Small strongyles (Cyathostomins) -Tapeworms -Pinworms
Parasites in young horses	-Ascarids (roundworms -Large strongyles (Strongylus vulgaris) -Small strongyles (Cyathostomins) -Tapeworms -Pinworms
Worm egg reappearance period	-Interval between treatment and return of eggs to pre-treatment levels -Benzimidazoles (fenbendazole, oxibendazole): 4 weeks -Pyrimidines: --Pyrantel tartate, daily wormer (Strongid C) --Pyrantel pamoate: 4 weeks -Macrocyclic Lactones: --Ivermectin: 6-8 weeks --Moxidectin: 10-12 weeks
Historical De-worming Methods	-Interval deworming -Bi-monthly interval with rotating anthelmintic classes -Treatment based on observation of fecal egg counts rising 8 weeks after treatment with benzimidazole -All methods selected for resistance!
De-wormer resistance	-Benzimidazoles: --Fenbendazole (panacur): resistance at lower levels --Oxibendazole (Anthelcide): Widespread resistance -Pyrimidines: --Pyrantel tartate (Daily Strongid C): Some populations are resistant --Pyrantel pamoate (Strongid paste): Some populations resistant -Macrocyclic Lactones: --Ivermectin (Zimectrin): Decreased Egg reappearance period --Moxidectin (Quest): Decreased Egg reappearance period
Refugia	-Stages of parasites in the horse not affected by anti-parasitic treatment -Encysted cyathostomins (when non-larvaicidal treatments are used) -Free living parasite stages on pasture -Parasites in animals that are not treated -Do not want to get rid of refugia! Adds important genetic diversity, provides continued susceptibility
Seasonality of DE-worming	-No larval development less than 42 degrees or more than 100 degrees --will not die, but will not develop further -Larvae cannot survive temperatures more than 90 -L3 (infective) stage can survive freezing well -“Killing frost” is a myth! -In south, winter is transmission season --hot summers prevent transmission -In north, transmission occurs year-round --winter pastures can still be infective due to L3 surviving freezing -Stabling for long periods on dry lots can stop cycle
Evidence-based DE-worming	-Show anthelmintic efficacy, use anthelmintic that works! -Identify heavy parasite shedders -Use the biology of the parasites to design the timing of the anthelmintics
Showing Anthelmintic Efficacy	-Part of evidence-based deworming -Performed separately on each individual farm -Efficacy or resistance is identified via Fecal Egg Count Reduction Test (FECRT) -Do on horses more than 5 years old -Need representative sample, at least 6-10 horses per farm per drug
Fecal Egg Count Reduction Test (FECRT)	1. Collect sample and do McMasters Fecal egg counts 2. Give de-wormer and weight tape animals 3. Animals with more than 200 Egg reappearance period Will get tested again 10-14 days after deworming 4. Reduction calculation: (Mean pretreatment – mean postreatment)/ Mean pretreatment *100
Cutoff values for Strongyle FECRT	-Benzimidazoles (Fenbendazole, oxibendazole): --more than 95% reduction = susceptible --90-95% reduction = suspect resistance --less than 90% reduction = resistant population -Pyrimidines (pyrantel): --More than 90% reduction = susceptible --85-90% reduction = suspect resistance --less than 85% reduction = resistant population -Macrocyclic Lactones (Ivermectin, Moxidectin): --More than 98% reduction = susceptible --95-98% reduction = suspect resistance --less than 95% reduction = resistant population, but re-check because here is no known resistance yet
Heavy parasite shedding horses	-Need to be identified with FECRT -More than 80% of parasite load in the field is from 20% of the horses -Genetically determined -Test all mature horses in field after appropriate egg reappearance period + 1 month -Low shedders: less than 200 eggs per gram -Moderate shedders: 200-500 eggs per gram -Heavy shedders: more than 500 eggs per gram
Use biology of the parasites to design timing of anthelmintic administration	-Use seasonal patterns of transmission -Evidence-based timing of treatment applications -Implement de-worming schedule for individual horses
High Shedder de-worming protocol	-March: Quest plus (Moxidectin + praziquantal) -July: Ivermectin -October: Equimaxx/Zimectrin gold -January: Pyrantel Pamoate (if effective on farm)
Low shedder de-worming protocol	-April: Quest plus -October: Ivermectin --Needs to be 6 months after moxidectin administration -Need to be careful, can do if all other animals are on similar program --difficult if other animals are highly infected or resistant
Local Known Dewormer Resistance	-Single dose fenbendazole is ineffective at reducing strongyle egg counts -Oxibendazole (Anthelcide) is better than fenbendazole, but still poor -Single dose of Pyrantel pamoate has widely varying efficacy, depending on farm -Ivermectin and Moxidectin have good efficacy
Parascaris Equorum Treatment	-Foals should not be treated before 60-70 days of life --prepatent period -S. Westeri is rare and usually not pathogenic
Adult Horse De-worming schedule	-If 5 years or less, treat as high shedder --de-worm at least 4x per year -If over 5 years, deworm according to fecal egg counts --less than 200 eggs per gram, do not need to deworm, recheck egg count before next deworming to confirm “low-shedder” (still treat 2x per year with ivermectin and moxidectin) -More than 200 eggs per gram, deworm with effective medication for specific farm
Pregnant mare de-worming schedule	-Do not deworm during first 60 days of gestation -Use targeted deworming for remainder of gestation --2x per year minimum -Deworm all mares with Ivermectin 1 month before parturition -Moxidectin (Quest) is not labeled for use in pregnant mares
Foal De-worming schedule	-Do not de-worm during first 60 days of life -Deworm between 60 and 70 days of life --double dose of fenbendazole for 5 days in a row, may be substituted with 1 10mg/kg dose of fenbendazole -At 4 months of age give Ivermectin -At 6 months of age give Pyrantel pamoate -At 8 months of age give Ivermectin and Praziquantel -NEVER use Moxidectin (Quest) in foals
Important points of De-worming	-Do not treat whole herd at once -Treat high shedders more than low shedders -treat according to egg reappearance periods -Do not use products that are resistant -Consider transmission period -Resistance will happen! Just try not to speed it up
Principles of Vaccination	-Based on: --risk of disease --consequence of disease --Effectiveness of the product/vaccine --Adverse reactions --Cost
Expectations of Clients when Vaccinating horses	-Good management practices -Primary series prior to exposure -Each animal is not the same, may need different vaccines -Understand that Vaccination minimizes infection but does not prevent infection -Protection is not immediate -Need to stick to recommended intervals -Herd technique -Never complete protection -Adverse reactions are possible
Infectious Disease Control	-Reduce exposure -Minimize factors that decrease resistance --corticosteroid usage -Occurrence of disease increases with: --increased population density --sales, track activities, breeding --Movement of animals External factors increasing risk of infectious disease incidence	-Stress -Overcrowding -Parasitism -Poor nutrition -Inadequate sanitation -Contaminated water supply -Lack of pet control -Lack of biosecurity Vaccine labeling
Vaccination in foals	-May have interference due to passive transfer --maternal antibodies interfere with vaccination -Difference between foals from a vaccinated mare and unvaccinated mares -Primary booster 3 shot series --Botulism, 3 shots all 1 month apart --All others 1st and 2nd shot 1 month apart, 3rd shot within the 1st year of life
Vaccination of pregnant mares	-Pre-foaling vaccines 4-6 weeks before parturition -Need to use vaccines that provide colostral antibodies --intranasal vaccines are usually ineffective -Herpesvirus vaccine is specific for pregnant mares --specific form that prevents abortion
Core vaccines in horses	-Tetanus -Eastern Equine Encephalitis -Western Equine Encephalitis -West Nile Virus -Rabies -(Botulism in PA) -Other core vaccines vary by area
Tetanus vaccine for horses	-Adults: 2 dose initial series, 1 month apart -Annual revaccination -Booster vaccine when there is a penetrating injury if previous vaccine was given more than 6 months ago
Eastern and Western Equine Encephalitis	-Vaccinate before spring (vector seasion) -Adults: 2 dose initial series -Annual revaccination
West Nile Virus Vaccine	-Adults: Initial 2-3 dose series --depends on vaccine -Annual or biannual revaccination --may need to give more often, depending on brand of vaccine
Rabies vaccine in horses	-Adults: single primary dose -Foals: 2 dose initial series, 1 month apart -Annual revaccination -Can do rabies antibody testing, but rarely done
Risk-based Vaccines in horses	-Botulism -Equine herpesvirus -Equine Influenza -Potomac Horse Fever -Strangles -Venezuelan Equine Encephalitis (not recommended) -Rotavirus (breeding farm vaccine, give to pregnant mares to protect foals) -Equine Viral Arteritis
Botulism vaccine in horses	-Initial 3-dose series, 1 month apart for all ages -Give to ALL horses -Botulism B is in soil -Botulism C and D in carcasses
Equine herpesvirus vaccine	-Rhinopneumonitis -NO available vaccine labeled for neurologic form of disease!! -Adult, non-breeding horses: --initial 3 dose series, 1st and 2nd one month apart, 3rd within a year --annual revaccination --6-month interval revaccination in horses less than 5 years old, horses in contact with pregnant mares, or performance show horses (high risk) -Pregnant mares: specific vaccines --Give at 3, 5, 7, 9 months of gestation
Equine Influenza Vaccine	-3 initial doses of series are recommended -Use recent strain to vaccinate -All vaccines on market have protection for 6 months -Clad 1 vs. Clad 2
Strangles vaccine	-Streptococcus equi equi -Vaccination is recommended on farms with persistent problems, or animals with high risk of exposure -Vaccination or exposure to natural infection can result in Purpura hemorrhagica -Do not vaccinate in face of an outbreak! -Killed vaccine is not recommended, associated with increased inhection site reactions --does not prevent disease
Strangles Intranasal vaccine	-Modified live vaccine -High level of immunity against experimental challenge -Accurate delivery is needed! -Small number of cases have residual vaccine virulence --slow growing abscess in lymphoid tissues -Need careful handling of vaccine, do not let clients give vaccine!
General Concepts of Evidence-based de-worming	-Aim to kill larval stages, not adults --larval stages do the most damage -Previous techniques/tactics have been incorrect and created resistance issues -All worms will eventually become resistant, it is just a matter of when -Get clients involved with deworming -No new classes of drugs are being developed, need to care for the ones we have!
Parasite Control Goals	-Minimize risk of parasitic disease -Control parasite egg shedding -Maintain efficacious drugs -Try to avoid further resistance development
Parasites in Adult horses	-Large strongyles (Strongylus vulgaris) --causes blood clot at cranial mesenteric artery, cuts off blood supply to small intestine -Small strongyles (Cyathostomins) -Tapeworms -Pinworms
Parasites in young horses	-Ascarids (roundworms -Large strongyles (Strongylus vulgaris) -Small strongyles (Cyathostomins) -Tapeworms -Pinworms
Worm egg reappearance period	-Interval between treatment and return of eggs to pre-treatment levels -Benzimidazoles (fenbendazole, oxibendazole): 4 weeks -Pyrimidines: --Pyrantel tartate, daily wormer (Strongid C) --Pyrantel pamoate: 4 weeks -Macrocyclic Lactones: --Ivermectin: 6-8 weeks --Moxidectin: 10-12 weeks
Historical De-worming Methods	-Interval deworming -Bi-monthly interval with rotating anthelmintic classes -Treatment based on observation of fecal egg counts rising 8 weeks after treatment with benzimidazole -All methods selected for resistance!
De-wormer resistance	-Benzimidazoles: --Fenbendazole (panacur): resistance at lower levels --Oxibendazole (Anthelcide): Widespread resistance -Pyrimidines: --Pyrantel tartate (Daily Strongid C): Some populations are resistant --Pyrantel pamoate (Strongid paste): Some populations resistant -Macrocyclic Lactones: --Ivermectin (Zimectrin): Decreased Egg reappearance period --Moxidectin (Quest): Decreased Egg reappearance period
Refugia	-Stages of parasites in the horse not affected by anti-parasitic treatment -Encysted cyathostomins (when non-larvaicidal treatments are used) -Free living parasite stages on pasture -Parasites in animals that are not treated -Do not want to get rid of refugia! Adds important genetic diversity, provides continued susceptibility
Seasonality of DE-worming	-No larval development less than 42 degrees or more than 100 degrees --will not die, but will not develop further -Larvae cannot survive temperatures more than 90 -L3 (infective) stage can survive freezing well -“Killing frost” is a myth! -In south, winter is transmission season --hot summers prevent transmission -In north, transmission occurs year-round --winter pastures can still be infective due to L3 surviving freezing -Stabling for long periods on dry lots can stop cycle
Evidence-based DE-worming	-Show anthelmintic efficacy, use anthelmintic that works! -Identify heavy parasite shedders -Use the biology of the parasites to design the timing of the anthelmintics
Showing Anthelmintic Efficacy	-Part of evidence-based deworming -Performed separately on each individual farm -Efficacy or resistance is identified via Fecal Egg Count Reduction Test (FECRT) -Do on horses more than 5 years old -Need representative sample, at least 6-10 horses per farm per drug
Fecal Egg Count Reduction Test (FECRT)	1. Collect sample and do McMasters Fecal egg counts 2. Give de-wormer and weight tape animals 3. Animals with more than 200 Egg reappearance period Will get tested again 10-14 days after deworming 4. Reduction calculation: (Mean pretreatment – mean postreatment)/ Mean pretreatment *100
Cutoff values for Strongyle FECRT	-Benzimidazoles (Fenbendazole, oxibendazole): --more than 95% reduction = susceptible --90-95% reduction = suspect resistance --less than 90% reduction = resistant population -Pyrimidines (pyrantel): --More than 90% reduction = susceptible --85-90% reduction = suspect resistance --less than 85% reduction = resistant population -Macrocyclic Lactones (Ivermectin, Moxidectin): --More than 98% reduction = susceptible --95-98% reduction = suspect resistance --less than 95% reduction = resistant population, but re-check because here is no known resistance yet
Heavy parasite shedding horses	-Need to be identified with FECRT -More than 80% of parasite load in the field is from 20% of the horses -Genetically determined -Test all mature horses in field after appropriate egg reappearance period + 1 month -Low shedders: less than 200 eggs per gram -Moderate shedders: 200-500 eggs per gram -Heavy shedders: more than 500 eggs per gram
Use biology of the parasites to design timing of anthelmintic administration	-Use seasonal patterns of transmission -Evidence-based timing of treatment applications -Implement de-worming schedule for individual horses
High Shedder de-worming protocol	-March: Quest plus (Moxidectin + praziquantal) -July: Ivermectin -October: Equimaxx/Zimectrin gold -January: Pyrantel Pamoate (if effective on farm)
Low shedder de-worming protocol	-April: Quest plus -October: Ivermectin --Needs to be 6 months after moxidectin administration -Need to be careful, can do if all other animals are on similar program --difficult if other animals are highly infected or resistant
Local Known Dewormer Resistance	-Single dose fenbendazole is ineffective at reducing strongyle egg counts -Oxibendazole (Anthelcide) is better than fenbendazole, but still poor -Single dose of Pyrantel pamoate has widely varying efficacy, depending on farm -Ivermectin and Moxidectin have good efficacy
Parascaris Equorum Treatment	-Foals should not be treated before 60-70 days of life --prepatent period -S. Westeri is rare and usually not pathogenic
Adult Horse De-worming schedule	-If 5 years or less, treat as high shedder --de-worm at least 4x per year -If over 5 years, deworm according to fecal egg counts --less than 200 eggs per gram, do not need to deworm, recheck egg count before next deworming to confirm “low-shedder” (still treat 2x per year with ivermectin and moxidectin) -More than 200 eggs per gram, deworm with effective medication for specific farm
Pregnant mare de-worming schedule	-Do not deworm during first 60 days of gestation -Use targeted deworming for remainder of gestation --2x per year minimum -Deworm all mares with Ivermectin 1 month before parturition -Moxidectin (Quest) is not labeled for use in pregnant mares
Foal De-worming schedule	-Do not de-worm during first 60 days of life -Deworm between 60 and 70 days of life --double dose of fenbendazole for 5 days in a row, may be substituted with 1 10mg/kg dose of fenbendazole -At 4 months of age give Ivermectin -At 6 months of age give Pyrantel pamoate -At 8 months of age give Ivermectin and Praziquantel -NEVER use Moxidectin (Quest) in foals
Important points of De-worming	-Do not treat whole herd at once -Treat high shedders more than low shedders -treat according to egg reappearance periods -Do not use products that are resistant -Consider transmission period -Resistance will happen! Just try not to speed it up
History of Equine Nutrition	-Horses designed for: --roaming long distances, 25 miles per day --eating many small meals, grazing 18 hours per day --flight instead of fight -Small stomach and streamlined digestive system
Considerations for Equine feeding program	-Body condition score -Age -Feeding class based on work level, reproduction, lactation -Metabolic issues, dentition, other special considerations
How much to feed a horse	-1.5-3% of body weight per day -Consider body condition score, work level, reproduction status, etc. -Can feed between 50-100% hay per day -Never feed less than 1% body weight in forage per day -More than 50% grain is less than ideal --NEVER feed a horse grain alone! --If given the chance, a horse will eat grain forever and will DIE (colitis contributes to laminitis)
Balanced nutrition for a horse	-Hay -Grain -Salt -Water -Select quality roughage, minimum 1% body weight per day -Select balanced concentrate and feed at recommended level based on tag instructions
Minerals important in Equine nutrition	-Quality commercial diet at correct rates -Make sure salt is always available --red salt blocks do not provide many useful minerals -Ca:P ratio is important --between 1:1 and 2:1 --Alfalfa is high in Ca --Wheat bran is very high in P, can lead to secondary PTH
Estimating weight in a horse	-Use tape: --heart girth --length from point of shoulder to curvature of rear -Girth X girth x length / 330 = weight in lbs -For weanling, divide by 280 -For yearling, divide by 301
Body Condition Score	-Measurement of fat deposition, based on location of fat pads -Scale 1-9 --1: poor/emaciated --2: very thin --3: Thin --4: moderately thin --5: moderate --6: moderately fleshy --7: fleshy --8: fat --9: extremely fat -Fat areas: --along neck --along withers --crease down the back --tailhead --ribs --behind the shoulder --flank --Inner buttocks
Body Condition Score 1	-Poor! -Emaciated -Backbone, spinous processes, ribs, tailhead, tuber coxae, tuper ischia project prominently -No fat anywhere -Horse cannot get any thinner -Usually only seen in neglect situations
Body Condition Score 2	-Very thin animal -Backbone is prominent -Ribs, tailhead, pelvic bones stand out -Bone structures of the withers, neck, and shoulders are faintly visible
Body Condition Score 3	-Thin animal -Spinous processes stand out, fat covers to midpoint -Slight fat cover over ribs -Tailhead is prominent but individual vertebrae cannot be seen -Tuber coxae are visible, but rounded -Pins cannot be seen
Body Condition Score 4	-Moderately thin -Negative crease down the back, backbone is still sticking up but can’t see individual vertebrae -Outline of ribs can just be seen -Fat can be felt around tailhead -Tuber coxae cannot be seen
Body condition score 5	-Threshold level of body condition -Back is level -Ribs cannot be seen, but can be easily felt -Fat around tailhead is slightly spongy -Withers look rounded -Shoulder and neck blend smoothly into the body
Body Condition Score 6	-Moderate to fleshy animal -May have a slight crease down the back -Fat around the tailhead feels soft -Fat over ribs feels spongy -Ribs can still be felt -Fat is being deposited along sides of withers, behind shoulders and along sides of the neck
Body Condition Score 7	-Fleshy animal -May have a crease down the side of the neck -Ribs can still be felt, but noticeable fat between the ribs -Fat exists along sides of the withers, behind shoulders, and along sides of the neck
Body Condition Score 8	-Fat animal -Crease down the back -Ribs cannot be felt -Fat is evident along the sides of the withers -Space behind shoulders is filled in -Fat around tailhead is soft
Body Condition Score 9	-Obese, extremely fat animal -Crease down the back is very obvious -Bulging fat around tailhead, withers, shoulders, and neck -Fat is bulging between rear legs
Work levels and calorie requirements	-Light: 1-3 hours per week --40% walk, 50% trot, 10% canter --western pleasure horse, trail riding, non-competitive animal -Moderate: 3-5 hours per week --30% walk, 55% trot, 10% canter, 5% low jumping or cutting --ranch work, roping, cutting, jumping -Heavy/Very heavy: 4-5 hours or more per week --20% walk, 50% trot, 15% canter, 15% gallop, jumping, etc. --race training, polo, eventing
Broodmare energy requirements	-Ideal BCS is 5-7 -Allows animal to cycle earlier in the year -Fewer cycles per conception -Higher pregnancy rate -Maintains pregnancy better -Spends fewer days at the breeding farm
Energy requirements based on exercise level	-Maintenance: 16,500 kcal/day -Moderate exercise: 23,000 kcal/day -Heavy exercise: 27,000 kcal/day -Weaning to 6 months: 15,500 kcal/day -Broodmare in late gestation: 21,000 kcal/day -Early lactation: 32,000 kcal/day
Information on feed bags	-Tends to omit calorie count! -Also omits carbohydrate -Need to check company website or call company directly -Crude protein is not totally important -Crute fat is good way to add calories to a diet -Feeding rates are important --make sure animal is getting the nutrients it needs into body consistently every day
Portion size for Equine Nutrition	-Make sure feeding rates provide a balanced diet -5 lbs grain /meal maximum -Horse does not care about % in product, responds to grams of nutrient he eats
Feed management tips for horses	-Feed by weight, not by volume --weight full feed scoop -Do not feed more than 0.5% body weight in grain per meal --5lbs grain per meal max in 1000lb horse -Feed minimum of 1% body weight in hay -Avoid irregular feeding schedule -Make gradual changes in feeding program
Diagnosis of Nutritional problems in horses	-History is very important! -How many animals are affected? -If there is more than one animal affected, is there a common factor? -If only one animal is affected, what is unique about that animal?
Factors affecting Nutritional needs of a horse	-Age: growing horses show deficits or excess quickly --geriatrics have special needs -Activity level: strenuous exercise increases energy/protein/electrolyte requirements --equine athletes are more likely to be over-supplemented -Physiological status: --pregnant? Lactating? Sick? -Environment: --stalls, turnout --recent changes or unusual weather --competition from herd-mates
Feeding history for a horse	-Document type and amount of grain, hay, and supplements -Get manufacturer and label info, when purchased -Ask about source of hay and when last purchased -Make sure salt is available
Water for horses	-Availability -Accessibility -Contaminants
When bad lot of grain is suspected	-Take samples using gloves or scoop for analysis -Contact diagnostic lab before sending sample --discuss analyses needed -Contact manufacturer with lot# and other label information --Ask if there have been other reports of problems with batch
When bad hay is suspected	-Examine hay carefully -Take samples of weeks and foreign materials in hay -Take samples from at least 10 bales, use hay corer if possible -Contact laboratory to discuss analysis -Consider how hay is fed --from feeders and bags contamination is not likely --from ground, may have contamination
Common problematic mineral excesses in equine nutrition	-Vitamin A -Vitamin D -Phosphorus -Iron -Copper -Selenium -Chromium -Magnesium
Physical exam for horse with nutritional imbalance	-Check teeth for points, hooks, missing teeth, malocclusion -Check hooves for ring -Blood chemistry for CBC and fibrinogen --serum chemistry analysis to rule out renal and hepatic dysfunction
Blood chemistry for nutritional imbalances in horses	-levels of Calcium, Sodium, Potassium, Iron, and Magnesium do not reflect dietary intake --not diagnostic -Copper, selenium, zinc may reveal gross excess or deficits -Heavy metals (lead, arsenic) will reveal toxic intakes
Post-mortem tissue analysis for equine nutritional imbalance	-Gastric contents: can reveal toxic plants, blister beetles, toxins that cause sudden death -Liver: vitamin A, copper, and zinc concentrations can indicate excesses or deficits -Kidney: toxins, heavy metals can accumulate with low-grade chronic exposure -Body fat: fat soluble toxins may accumulate
Common Nutritional Problems in Horses	-Weight loss -Developmental orthopedic disease -Recurrent rhabdomyolysis -Colic -Enteroliths -Laminitis -Anemia
Weight loss in horses	-Non nutritional DDx: --disease (renal, hepatic, diarrhea, infection) --not just old age -Nutritional DDx: --inadequate feed --Dentition --intestinal parasitism --Sand ingestion --Malabsorption (IBD, lymphoma) --Heavy metal toxicity
Anemia in horses	-Non-nutritional DDx: --chronic disease --primary disease process -Nutritional DDx: --copper deficit --Vitamin B deficit --Iron excess --Iron deficit (rare) -Blood ferritin or Iron binding tests diagnose iron status, do not reflect intake
Developmental Orthopedic disease in horses	-Non-nutritional DDx: --genetics, conformation --trauma --lack of exercise -Nutritional DDx: --energy or carbohydrate excess --Ca P imbalance --Copper, Zinc, Selenium excess or deficit --Magnesium excess or deficit, not well established -NOT a protein problem!!
Recurrent Rhabdomyolysis	-“Tying up” -Non-nutritional DDx: --Polysaccharide storage myopathy, can often be controlled with diet --Over-exertion or warm-up failure --Stress? -Nutritional DDx: --excess carbohydrate intake --electrolyte imbalances --Vitamin E or Selenium deficit
Enteroliths	-Ingestion of foreign objects -Alkalinizing feeds --western alfalfa fed as sole source of nutrition Laminitis DDx	-Non-nutritional DDx: --metabolic --Mechanical trauma --Colitis/GI disease associated with but not caused by endotoxemia -Nutritional DDx: --Obesity? --Equine Metabolic Syndrome --Grain or soluble carbohydrate overload --Spring/fall grass
Therapeutic Nutrition	-Reduces clinical signs of disease -Enhances wound healing -Improves immune competence -Increases survival rates
Feeding a Clinically Ill horse	-Estimate nutritional needs --take into account disease and injury alterations -Decide mode of food administration --oral, nasogastric, IV --type of feed or nutrient source -Monitor feed intake and body weight/BCS -Most hospitalized or injured horses do not need more than maintenance rations --good quality hay free choice --concentrates formulated for life stage, reduced amounts --Free choice water and salt
Prolonged fasts in horses	-Should be avoided -More than 3 days in adults -More than 24 hours in neonates
Conditions requiring special nutrition	-Severe sepsis or trauma -Previously malnourished or starved animal -Post-abdominal surgery -Renal failure -Hepatic failure
Nutrition for horses with Severe Sepsis, Trauma, or burns	-14-16% protein -6-10% fat -Added B-vitamins -Vitamin C -Fluid balance is critical
Dietary management of horses with renal failure	-Limit Ca, 0.4-0.6% --limit alfalfa hay -Protein only 8-10% -Phosphorous 0.2-0.4% -Grass hays, fats, and fat soluble vitamin supplements are recommended -Avoid legumes, beet pulp, and brans
Dietary management of horses with Hepatic failure	-Limit protein, especially feeds with high tryptophan if hepatoencephalopathy is a problem -Limit fat to less than 5% -Increase soluble carbohydrates (corn) and B-vitamins -Grass hays, corn/barley/molasses concentrates are recommended -B-vitamins are helpful -Vitamin C cupplements are helpful -Avoid soybean meal, wheat bran, and oats
Re-feeding Syndrome in horses	-Electrolyte imbalances due to starvation -Hypophosphatemia -Need to monitor electrolytes during re-feeding -Can result in death within 3-7 days of re-feeding an emaciated horse -Due to high carbohydrate diets --causes insulin release, hypophosphatemia, hypomagnesemia --cardiac, respiratory, and renal failure -Feed more proteins than carbohydrates --do not give any grain! High in carbohydrates -Start feeding slowly
Mechanisms of Weight loss in horses	-Anorexia -Increased nutrient demands -Protein-calorie malnutrition --“acrocerosis”
Anorexia in horses	-Usually secondary to primary disease -Loss of appetite -Can result in fast weight loss -Dysphagia may be occurring --unable to hold onto food, unable to masticate appropriately or effectively -Decreased nutrient intake -Can go unnoticed
Increased Nutrient demands in Horses	-Physiological conditions --cold weather, exercise, pregnancy, lactation -Pathologic Processes --sepsis, trauma, parasitism, burns, neoplasia -Nutrient demands change based on activity level, age, physiologic processes
Nutrient demands in horses	-Maintenance -Growth -Pregnancy -Lactation -Exercise
Increased nutrient demands based on procedure or illness	-10% elective surgery -20% fractures -30-60% with severe infection or sepsis -40% with peritonitis -50-110% with major burns
Pathophysiology of increased nutrient demands	-Stress, increased sympathetic nervous system stimulation, and increased epinephrine release contribute to increased nutritional demands -Net effect is inefficient metabolic activity and increased nutrient requirements
Pathology causing nutrient loss	-Burns -Peritonitis -Pleuritis -Granulomatous bowel disease
Mechanisms of weight loss in horses	-Anorexia -Increased nutrient demands -Protein-calorie malnutrition --“agrocerosis” -Macronutrient deficiencies -Parasitism
Protein-calorie malnutrition in horses	-Inadequate quantity of feed --under feeding --competition for feed with other horses --dental disease -Inadequate feed quality -Malabsorption -Malassimilation
Macronutrient deficiencies in horses	-Deficiency of macronutrients --Copper --Cobalt (Vitamin B12) --Vitamin A -Rare in horses -More of an issue in ruminants -Cannot process feed efficiently -Results in bleached coat in winter
Parasitism and weight loss in horses	-Parasites result in increased nutrient requirements --loss of body fluids --inflammation --organ or vascular damage -Protein-calorie malnutrition --competition for nutrients --malassimilation and malabsorption --Anorexia -Macronutrient deficiencies
Taking a history for weight loss in horses	-Look for additional clinical signs -What EXACTLY is the animal eating? --inspect feed, grain bag and hay -Herd dynamics and pecking order are important -Deworming history -Toxic substances in environment -Need to do more than just a physical exam
Physical exam for a horse with weight loss	-Look for signs of concurrent disease --dental abnormalities, diarrhea, pyrexia, dysphagia, melena, icterus, dyspnea, tachycardia -Make sure patient is able to prehend, masticate, and swallow food normally -Weight animal and BCS -Rectal exam --melanoma, internal abscesses
Clinical approach to Weight Loss	1. Adequate intake --poor quality food --dentition --Malabsorptive or malassimilation disorder --excessive nutritional need (primary disease) 2. Inadequate intake --under feeding --competition --dysphagia, inability to eat or masticate (primary disease) --Anorexia (primary disease)
Diagnostics for Weight loss	-CBC/Chemistry -Urinalysis -Fecal float for parasites and sand -Rectal exam -Function test --oral glucose absorption test --D-xylose absorption test --direct bilirubin serum concentrations -Body cavity search/ultrasound
Treatment for weight loss in horses	-Address any primary disease present -Address diet insufficiencies present -Address macronutrient requirements
Quick Nutrition benchmarks for horses	-Feed 1-2% body weight in total feed -No more than 50% of feed should be concentrates -Minimum of 1% body weight is forage -Weigh forages! Alfalfa weighs more than grass!
Glucose absorption test	-Assess glucose absorption from the gut -Measure blood glucose at regular intervals after a meal or nasogastric administration of glucose -Normal absorption has distinctive spike at 120 minutes after feeding
Heart Murmurs	-Physiological flow murmurs and murmurs associated with cardiac pathology are common -Determine significance of murmur with auscultation
Heart Murmur Characteristics	-Intensity (1-6) -Timing (systolic, diastolic, continuous) -Duration (early, mid, late, holo, pan) -Quality (soft, blowing, coarse, raspy, musical) -Shape (band-shaped, crescendo, decrescendo, crescendo-decrescendo) -Location, point of maximal intensity -Radiation (cranial, caudal, dorsal, ventral, or specific valve area
Common Heart Murmur characteristics in Horses	-Grade is usually 1-3/6, may change with exercise -Early, mid, or late systolic --holosystolic --early to late diastolic --usually not holodiastolic -Crescendo-decrescendo or blowing when systolic -Blowing and decrescendo when diastolic, due to laminar flow -Systolic point of maximal intensity can be in all valve areas, especially aortic valve and pulmonic valve areas -Diastolic point of maximal intensity is usually aortic or pulmonic valve area -Murmur can usually be localized
Common systolic murmurs in horses	1. Mitral regurgitation --maximal intensity in mitral valve or aortic valve area -ANY loud systolic murmur on the left should be mitral regurgitation until proven otherwise 2. Tricuspid regurgitation --maximal intensity over tricuspid valve, loud on right side 3. Ventral septal defect --point of maximal intensity in tricuspid valve area or pulmonic vlave area
Mitral valve prolapse in horses	-Valve leaflet bulges back into left atrium during contraction --deflects jet of mitral regurgitation -maximal intensity over mitral valve area or aortic valve -Systolic crescendo, mid to late murmur -Usually 2-6/6 -Often varies in intensity with different loading conditions --hypovolemia or sedation will change murmur -Usually mid to late systolic, occasionally holosystolic -Usually crescendo, may be honking or coarse -Radiates dorsally and cranial or caudal
Pansystolic murmur	-Murmur from beginning of S1 to end of S2 -Cannot hear any heart sounds -Indicates cardiac pathology
Mitral regurgitation murmur in horses	-Usually grade 3-6/6 -Holosystolic or pansystolic -Coarse, band-shaped -Radiates dorsally and cranial or caudal -With more severe mitral regurgitation, murmur radiates dorsally up lung field to mid or dorsal thorax -On ultrasound will see thickened mitral valve with enlarged volume loaded left atrium and ventricle --Rounded left ventricle apex and left atrium appendage
Ruptured mitral chordae tendinae	-“Honking” murmur, “musical” murmur -Maximal intensity over mitral valve to aortic valve area -Murmur is usually grade 3-6/6 -Holosystolic or pansystolic murmur -Radiates dorsally and cranial or caudal --more severe murmur radiates dorsally up lung field to mid or dorsal thorax -Ruptured chordae tendinae will flip into left atrium
Summary of Mitral regurgitation in horses	-Degenerative change -Usually incidental finding on routine exam -Usually normal performance life and life expectancy -Can be acquired at any age -Degenerative or inflammatory etiology --vlavulitis or endocarditis -Ruptured chordae tendinae is associated with acute onset of poor performance or congestive heart failure (left sided) --can also be incidental finding -Atrial fibrillation is common with left atrial enlargement
Congestive heart failure in horses	-Right sided CHF is most common --venous distention, jugular pulses, ventral edema -Overt left sided CHF is uncommon --foamy nasal discharge, coughing, elevated RR, labored breathing -Atrial fibrillation and tachycardia are usually present, unless condition is acute --HR is usually elevated, more than 60 beats per minute
Echocardiographic findings in horses with mitral regurgitation and CHF	-Large left atrial diameter -Pulmonary artery diameter is larger than aortic root diameter --indicates pulmonary artery hypertension and low cardiac output
Grading severity of valvular regurgitation with Doppler	-Insignificant (1+): jet is just behind valve leaflets -Mild (2+): Jet occupies less than 1/3 of receiving chamber -Moderate (3+): Jet occupies more than 1/3 but less than 2/3 of receiving chamber -Severe (4+): Jet occupies more than 2/3 of receiving chamber
Estimating chronicity of mitral regurgitation	-Acute: --large jet area with minimal left atrial or left ventricular enlargement --round, turgid left atrium with minimal left atrial enlargement --interarterial septum bulges towards right atrium -Chronic: --jet area is appropriate for degree of chamber enlargement --left atrium is enlarged but does not appear round and turgid
Determining significance of Mitral regurgitation on performance and life expectancy	-Evaluate for pulmonary hypertension! --if pulmonary artery diameter is more than aortic root diameter, grave prognosis --horse is not safe! Sudden death may occur -Evaluate for evidence of elevated left atrial pressures --round, turgid left atrium --interarterial septum bulging towards right atrium --distended pulmonary veins
How to approach a patient with Mitral Regurgitation	-Determine etiology -Assess severity -Re-exam annually, unless mild -Monitor HR and rhythm on regular basis in horses with moderate to severe regurgitation -Do exercise ECG tests -Manage complications of advanced disease
Prognosis for horses with CHF and mitral regurgitation	-Grave without treatment for CHF --death in days to weeks -Guarded with treatment of CHF --positive inotrope (digoxin), diuretics (furosemide), afterload reducers (ACE inhibitors) -If horses respond to therapy, will live 2-6 months -NOT SAFE for athletic use, unless pulmonary hypertension resolves!
Arrhythmia vs. murmur	-Arrhythmia = electrical activity --need ECG to diagnose -Murmur = change in blood flow --need echocardiogram to diagnose
Arrhythmia classification	-Supraventricular (atrial) vs. Ventricular -Normal sinus rhythm ECG is base-apex lead setup --normally has biphed p-wave, notched --T-wave can be any conformation
Supraventricular arrhythmias	-Benign, physiologic: due to changes in vagal tone --sinus tachycardia --sinus arrhythmia --2nd degree AV block, common arrhythmia in horses -Pathologic: --atrial fibrillation --supraventricular premature depolarizations --complete (3rd degree) heart block --other
AV nodal block	-2nd degree AV block -“Dropped beat” -Regularly irregular rhythm -Pause in rhythm is equal to twice the normal diastolic interval --beat is just missed, next beat occurs on time -S4 is heard during the pause -ECG shows normal “on time” p-wave that does not have a corresponding QRS complex
AV block electrophysiology	-Electrical activity is blocked at the AV node --Type I: due to high vagal tone --Type II: diseases AV node, usually fibrosis -Can differentiate between type I and type II with tests --Exercise test: eliminates vagal tone, type I block will go away --vagolytic drugs: atropine, glycopyrrolate --ECG findings -No treatment for type I -Treat type II with anti-inflammatories/corticosteroids or a pacemaker --horse is not considered safe to ride
3rd degree AV block	-P-waves are not conducted -Heart pumps via ventricular escape complexes
1st degree AV block	-Prolonged P waves
Supraventricular premature depolarizations	-Atrial and junctional premature depolarizations --APC, SPC, SPD, PAC -ON Auscultation underlying rhythm is interrupted by early heart beats -Can be difficult to differentiate from VPCs on auscultation
ECG for “classic” supraventricular premature complex	-Early P’ wave followed by normal QRS complex -P’ wave often has different morphology compared to sinus P wave(not always) -P-R interval is normal --can be variable beat to beat, but within the normal range
ECG for Supraventricular premature complex with aberrant conduction	-P’ wave often has different morphology from sinus P wave -Early P’ wave followed by slightly wide or tall QRS complex
ECG for non-conducted supraventricular premature complex	-Very early P’ wave, not followed by QRS -Ventricles are still refractory to depolarization --P-wave occurs too early and is non-conductive, ventricle has not repolarized yet -Must differentiate from 2nd degree AV block
Clinical significance of Supraventricular premature complexes	-At rest: unlikely to cause clinical signs -Exercise: need exercising ECG to know if SPC at rest persist during exercise --may affect performance if occur frequently during high intensity exercise -Under anesthesia: SPC are suppressed -Increased numbers of SPCs may increase risk of atrial fibrillation or sinus ventricular tachycardia --more than 24 in 24 hours
Supraventricular premature complex treatment	-Tailor treatment to clinical situation -treat if: --associated with clinical signs and poor performance --history of tachyarrhythmia --history of atrial fibrillation --for resale, even benign arrhythmias may affect resale value -Treat underlying cause
Atrial Fibrillation	-Most common arrhythmia affecting performance in equine athletes -Need to be able to recognize and treat atrial fibrillation -Can be idiopathic in horses or secondary to heart disease -Large atria and high vagal tone predisposes animals to lone atrial fibrillation (idiopathic) -no underlying detectable heart disease is a common finding -IN cattle, secondary GI disease or other metabolic disturbances (sick animal) --usually resolves when underlying disease resolves -Uncommon in other large animal species --usually due to underlying heart disease or severe metabolic disturbances
Auscultation of Atrial Fibrillation	-Irregularly irregular rhythm --need to listen for a long period of time -Absence of S4 -Variable intensity of heart sounds -Normal HR at rest, unless animal is sick -Elevated HR may occur --severe heart disease (CHF) --systemic disease in cattle --draft horses --It is rare that a horse will have elevated HR without some underlying condition
ECG for atrial fibrillation	-Irregular rhythm -No P-waves -F-waves present (fibrillation waves) --can be fine or coarse, may not be obvious at low amplitude -Normal QRS complexes
Diagnostic workup of Atrial fibrillation	-Rule out underlying heart disease, GI disease, or metabolic disease -Confirm auscultation with ECG -Echocardiogram -Electrolytes or complete chemistry if indicated -Cardiac troponin I --may not be helpful for horses with lone Atrial fibrillation
Treatment of Atrial Fibrillation	-Pharmacologic cardioversion --quinidine is main option -Electrical cardioversion --transvenous electrical cardioversion (TVEC) --transcutaneous is ineffective unless combined with quinidine and is not currently used -No treatment --horses are not at risk of stroke if in atrial fibrillation --should treat underlying disease, but do not need to treat atrial fibrillation
Factors determining treatment of Atrial Fibrillation in horses	-Length of time in atrial fibrillation --less than 2 days --less than 2 weeks --more than 2 weeks --unknown -Athletic job, cannot successfully compete with atrial fibrillation -Presence of underlying heart disease --conversion is contraindicated with CHF, do not treat! -Previous treatments -Resale prospect
Atrial fibrillation treatment timeframes	-Less than 2 days: anti-inflammatory --wait to see if horse spontaneously converts --only really occurs with athletes -Less than 2 weeks: Quinidine gluconate or quinidine sulfate, TVEC --may respond to IV or nasogastric quinidine --easier to convert if less than 2 weeks -More than 2 weeks: Quinidine sulfate, TVEC -Unknown time period: Quinidine sulfate or TVEC --long-term time period, need to give nasogastric quinidine sulfate
Quinidine gluconate	-Treatment for atrial fibrillation -IV formulation -0.5-2.2 mg/kg bolus, every 10 minutes to effect -Do not exceed 12 mg/kg IV total dose -Total treatment time is 2 hours
Quinidine sulfate	-Treatment for long-term atrial fibrillation -Nasogastric tube administration --very irritating to oral mucosa -22 mg/kg every 2 hours until converted, toxic, or plasma quinidine concentration is 3-5 ug/ml -Once in therapeutic range, continue every 6 hours until converted, toxic, or owner withdraws consent -Begin digoxin 0.011 mg/kg PO 2x daily on day 2
Adverse reactions to Atrial fibrillation treatment	-Depression, inappetance, flatulence, mild hypotension, tachycardia, paraphimosis -Idiosyncratic reactions: --laminitis, colic, ventricular arrhythmias, diarrhea, sudden death -Toxic effects: --seizures, ataxia, sudden death, nasal congestion leading to upper airway obstruction -Monitor quinidine concentration to avoid toxic reactions! --strict monitoring to decrease adverse reactions TVEC	-Treatment for atrial fibrillation -Good option, but not always the best choice for all owners or horses -Pass 2 sterile catheters into right atria and left pulmonary artery -Confirm catheter placement with ultrasound, pressure traces, and radiographs -Give general anesthesia -Series of shocks timed to ECG to avoid inducing ventricular fibrillation -High risk of reversion in first few hours post-treatment
Quinidine vs. TVEC for atrial fibrillation	-TVEC does not have an advantage over quinidine in terms of prognosis for maintaining normal sinus rhythm post conversion --reversion risk is higher in immediate post-conversion period --no long-term advantage to either one -Quinidine has short-term advantage -Can use TVEC if there has been a previously failed quinidine attempt -TVEC is better for --chronic or unknown duration of atrial fibrillation --underlying atrial enlargement --concurrent ventricular arrhythmias -Consider risk of GA and jugular vein thrombosis
Quinidine conversion Prognosis	-No underlying heart disease: --less than 4 months of atrial fibrillation, 90% conversion with 25% recurrence within 1 year --more than 4 months, 80% conversion with 60% recurrence -Underlying heart disease: --80% conversion and nearly 100% recurrence -TVEC has similar prognosis, increased risk of immediate recurrence of atrial fibrillation compared to quinidine
Atrial fibrillation Post-conversion treatment	-Anti-inflammatories -ACE inhibitors, may prevent re-occurrence --benazepril has best data --quinapril has some supportive data for use
Atrial fibrillation in cattle	-Rarely treated, only if it is a very valuable cow -Most casers resolve once GI disease resolves, treat underlying cause -Quinidine sulfate is not effective due to the rumen -Quinidine gluconate can be used -Digoxin can be used for rate control -Persistent atrial fibrillation will affect milk production -Supraventricular premature complexes are more common than atrial fibrillation in sick cattle
Ventricular Premature Complex physical exam findings	-Often no clinical signs, incidental finding -Poor performance if frequent, or occurs during high intensity exercise -Drop in milk production in frequent in cattle
Ventricular tachycardia physical exam findings	-Dull, agitated animal -Marked exercise intolerance -Collapse, history of collapse -Colic -Weak peripheral pulses and pulse deficits -Jugular venous distention and pulsations -Sudden death, nothing found on necropsy -May present like a colic --if HR is more than 100, start to think about VT --if HR is more than 200, very convincing for VT! -May result in aortic fistula
Cardiac auscultation of ventricular premature complexes	-Regularly irregular rhythm -Regular rhythm with occasional early beat -Occasional couplets or triplets -Intensity of premature beat may be increased --“bruit de cannon”
Cardiac auscultation of ventricular tachycardia	-Rapid, regular rhythm if uniform -Rapid irregularly irregular rhythm if multiform
ECG for ventricular premature complexes	-QRS complexes are not normal at all -Not associated with P-wave before it --p-wave still exists and is regular, normal P-P interval
ECG for ventricular tachycardia	-If sustained, can look normal -Not atrial fibrillation, rhythm is regular -R on T, premature complex occurs on top of T complex, on P-wave of previous beat --very dangerous, can lead to ventricular fibrillation
Malignant ventricular arrhythmias	-Multiform ventricular tachycardia -Ventricular flutter (“death is coming”) -Torsades des pointes
Ventricular tachycardia vs. atrial fibrillation	-VT has slower rate, regular rhythm with regularly spaced beats -Atrial fibrillation is irregularly irregular rhythm Summay of ECG findings for ventricular premature complexes and ventricular tachycardia	-P-waves are present and regular --may be difficult to find, P-waves may be buried in other complexes --increase in paper speed to 50mm/sec -VPCs look different from sinus QRS --variation depends on where ectopic beat is coming from within the ventricle -Sustained uniform VT is a regular rhythm --need high degree of clinical suspicion to make diagnosis of VT vs. sinus tachycardia in certain clinical situations (like a colic) --use calipers to differentiate VT from rapid atrial fibrillation, look for regular vs. irregular rhythm -Increase paper speed to 50 mm/sec if needed
Cardiac causes of VPC and VT	-Aortic regurgitation -Myocarditis -Myocardial fibrosis
Aortocardiac fistula Non-cardiac causes of VPCs and VT	-Electrolytes and acid base balance --need to address underlying imbalances or causes -Endotoxemia and sepsis -Myocardial toxins -Hypoxia and hypoxemia -Severe hemorrhage -Anesthetics or other drugs -Autonomic imbalance -Pain
Additional diagnostics for VPC/VT in sick animals	-Electrolytes -Acid/base status -Fibrinogen -Cardiac troponin I --can be consequence of severe tachycardia --peaks in 12 hours, half life is 12-24 hours -Echocardiogram -Electrocardiogram (ECG) -Toxicology tests -Analgesic trial
Additional diagnostics for VPC/VT in healthy animals	-Echocardiogram -ECG --24 hour holter, exercising ECG -Other tests on case-by-case basis
When to treat VPC and VT with antiarrhythmic drugs	-Other abnormalities have been corrected and arrhythmia persists -Arrhythmia is causing clinical signs --poor performance, colic -Sustained ventricular tachycardia with HR more than 120 beats per minute --more likely to progress to heart failure --more likely to be unable to maintain cardiac output -If ventricular rhythm is the type that is more likely to degenerate to ventricular fibrillation --R on T --multiform VT --wide VT, sine wave or Torsades 1st line anti-arrhythmic drugs	-Lidocaine --readily available, inexpensive --narrow therapeutic range, if give too much the animal will seizure! -Quinidine (proarrhythmogenic) --same drug as treatment for atrial fibrillation, same adverse risks
Anti-arrhythmic drugs	-Lidocaine -Quinidine -Magnesium sulfate (causes hypotension if given too quickly) -Sotalol (proarrhythmogenic) -Phenytoin -Procainamide (proarrhythmogenic) -Propafenone (proarrhythmogenic)
Most common Nosocomial Infections in Vet Hospitals	-Salmonella -MRSA
Zoonotic Infections in Veterinary hospitals	-Cryptosporidium -MRSA -Salmonella -Cutaneous dermatophytes/ringworm
Species associated with infections introduced to vet hospitals	-Horses -Cows -Dogs
Other factors associated with infections in vet hospitals	-Increase in caseload -Concern was greater 10 years ago, laxed -Greater true risk than merely increased concern or awareness -Vulnerability increases as we treat more critically ill animals
Hospital Biosecurity	-Disease agents are introduced to hospitals and dealt with on a daily bases --exclusion is not an option -Biosecurity = any strategy, efforts, or planning designed to protect human, animal, and environmental health against biological threats -Infection control = biosecurity Surveillance for biosecurity	-Collect and summarize contagious disease diagnoses -Compile results of cultures or tests --test patient and environment -Ideally conduct activities at predetermined intervals -Actively collect samples
Treating hospital as a biosecurity “patient”	-Decrease likelihood of exposing patients to infectious agents --optimize hygiene --decrease direct and indirect contact among patients --manage patient housing and movement -Maximize participation -Optimize efficiency -Avoid cross-contact
Treatment for biosecurity concern patients	-Isolation -barrier nursing -Cleaning and disinfection -Change procedures?
Risk factors leading to increased likelihood of hospital infection	-Failure of healthcare workers to wash hands between patients and before procedures -Failure of visitors to wash hands before and after a hospital visit -Prolonged hospital stay (hard to know cause and effect) -Weakened immune system -Poor nutrition -Overuse of antibiotics
Common procedures leading to increased risk of Hospital infection	-Catheterization of the bladder -Surgery and dressing of surgical wounds -Respiratory procedures that require intubation -IV procedures to deliver nutrition or medication -Dialysis
Preventing Hospital infections	-Clean hands is not enough alone -Need clean hands touching clean equipment in clean environments NBC ptotocol for diarrhea in neonatal calves	-Infectious until proven otherwise, most likely cryptosporidium -Submit feces for acid-fast stain --results reported immediately to biosecurity -PPE must include mask, cap, tyvek coveralls -No contact with non-isolated ruminants or camelids -WASH HANDS!
Protocol for rabies suspect animal	-Put up barriers -Clearly label patient as rabies suspect -All samples must be labeled -Restrict personnel contact to a minimum -Sign-up sheet so all contacts are immediately identifiable -Provide mandatory PPE --disposable gowns, coveralls, gloves, boots, full face shields -No ante-mortem testing is available! -If euthanized, handle carcass appropriately --inform pathologist and ensure samples are submitted -Leave stall overnight before cleaning, wear PPE when cleaning stall
Protocol for Confirmed Rabies patient	-Contact authorities -Contact all potentially exposed personnel -Determine each individual’s contacts with affected animal -Discuss CDC guidelines for what is an exposure --contact with saliva, CSF, neural tissue via mucus membranes or compromised skin -Discuss benefits and risks of post-exposure prophylaxis -Rabies post-exposure prophylaxis is a medical urgency, NOT an emergency!
MRSA infection	-Important cause of hospital-associated infection in human medicine -Relatively uncommon infection in vet hospitals -Catheter related, incisional, device-related infection is possible -No active surveillance at NBC but protocols are in place for handling patients confirmed positive
Anatomy of the eye	-Cornea -Anterior chamber -Iris/pupul -Ciliary body -Lens -Vitral chamber -Retina -Optic nerve -mechanics in the front focus the image onto the retina
Patient history for ophthalmologic exam	-Signalment -Primary complaint --vision deficits, color changes, comfort changes, duration -Concurrent disease --cushing’s, systemic infection, immune-mediated conditions -Previous treatments --eye medications, other medications, surgeries
Location for ophthalmologic exam	-Dark, quiet stall -Turn eye into the darkest corner -Cover head if possible -Early in the AM and late PM
Observation during ophthalmologic exam	-Look from front, side, and rear for facial symmetry -Lash angle -Globe size and position, globe movement -Head tilt -Skull symmetry -Nasal discharge -Blinking -Pupil position -Stabismus -Periorbital swelling, masses, depressions -Epiphora, blephrospasm -Ocular discharge
Palpation during ocular exam	-Orbital rim palpation --with gloved finger go underneath eyelid -Retropulse globe --check to make sure both eyes retropulse equally -Globe firmness and position
Reflex testing for ophthalmologic exam	-Menace response -Dazzle reflex -Pupillary light reflex -Palpebral reflex
Menace response	-Motion of hand towards eye should cause a blink response --may also cause withdrawl of head or 3rd eyelid protrusion -Tests CN II, VII, retina, and visual cortex --lack of menace may indicate pathology -Minimize airflow -Approach each eye lateral, medial, and central -Learned response, foals less than 4 weeks may not respond -Crude vision test, can be legally blind and still have menace response --does not mean vision is excellent if present
Dazzle reflex	-Direct bright light into the eye, patient should partially close lids or retract globe -Subcortical reflex -Tests retina, rostral colliculus, supraoptic nuclei of hypothalamus, CN II, VII, and orbicularis oculi muscle -Important response when determining if vision is possible -May not be present with bad ulcers, cataracts, or glaucoma -Presence indicates at least some retinal cells are working
Pupillary light reflex	-Bright light directed towards fundus causes pupillary constriction in the eye --consensual response in opposite eye -Tests function of retina, CN II, midbrain, and CN III -Do test in bright and dim light -Be sure to check for consensual response, swing light or have weak light on opposite side -Consensual response is important for when posterior segment of affected eye cannot be visualized
Palpebral reflex	-Touch periocular skin, expect blinking -Tests facial nerve paralysis via CN VII and looks for periorbital swelling -If not intact, may see 3rd eyelid protrusion
Vision testing	-Maze -Obstacle course --uneven trotting poles -Cotton ball tracking -Cover one eye, then other
Problems with eyelids	-Blepharoedema -Blepharitis -Blepharospasm (blinking) -Ptosis (drooping) -Epiphora and discharge -Margin defects or lacerations -Neoplasia -Alopecia -Poor conformation (entropion, ectropion) -Distichiasis (lashes growing from within meibomian glands) -Trichiasis (lashes angled towards eye)
Problems with Conjunctiva	-Hyperemia -Chemosis -Bruising -Hemorrhage -Follicles -Symblepharon -Foreign bodies -Neoplasia
Problems with Limbus	-Pigmentation -Dermoid -Vessel in-growth
3rd eyelid exam	-Look at edge, palpebral surface, and bulbar surface -Retropulse globe to look at palpebral surface -Use anesthesia and allis tissue forceps to look at bulbar surface -May have neoplasia, laceration, or orbital fat prolapse
Orbit and globe exam	-Check around orbital rim with gloved finger -Retropulse globe -Check globe firmness and position
Anterior segment of the eye	-Tear film should be smooth and moist -Cornea should be clear, no scars, smooth, no vessels or cellular infiltrate -Limbus: check for pigment and vessels, dermoid, change to curvature -Iridocorneal angle: check width and meshwork -Anterior chamber should be clear, check for haziness and debris -Iris: look at color, contour, vessles, and ppm -Pupil: check size, shape, and response to light -Corpora nigra: check texture, size, and look for cysts
Tear film	-Assess smoothness: --specular reflections can be used to determine smoothness --bright, crisp reflections = good tear film --disrupted, dull reflection = poor tear film -Lacrimal lake: tear pool between lower eyelid margin and cornea
Corneal assessment	-Most eye pathology is in the cornea! -Examine from limbus to limbus -Normal: clear, avascular, non-pigmented, convex -Abnormal: --focal haziness, diffuse haziness --blood vessels present, infiltrate, pigment, crystalline --ulceration (superficial, stromal, loose epithelium) --Foreign bodies, sequestrum, discharge, dermoid -Examine thickness --increased thickness: edema, melting, neoplasia, plaque --decreased thickness: stromal ulcer, stromal facet
Slit beam examination	-Look at corneal thickness -Anterior chamber depth and clarity -Surface of the iris -Location of cataracts in the lens
Anterior chamber examination	-Normal: transparent -Check clarity of aqueous humor --flare indicates increased protein --fibrin may see inflammatory clots and strands --Hyphema = RBCs --Hypopyon = WBCs --keratic precipitates may be inflammatory cells or endothelium -Look for foreign bodies, cysts, tumors, parasites -Examine depth with slit beam and magnification --increased depth: lens instability, aphakia, resorbing cataracts --decreased depth: intumescent cataract, iris bombe -Check iridocorneal angle
Iris examination	-Normal: variable color, textured surface, persistent pupillary membranes, pupil shape -Check for diffuse or focal change in color --darkening can indicate inflammatory process or neoplasia -Check texture: --thinning: atrophy of iris muscle --thickening: inflammation or neoplasia -Contour should be checked for iridodonesis (quivering of the iris) or iris bombe (iris bulging forward) -Persistent pupillary membranes, iris collarette, lens collarette can be congenital -Iris coloboma -Anterior synechia: strands from iris to cornea -Posterior synechia: strands from iris to lens
Pupil examination	-miotic: congenital microphthalmia, horner’s syndrome, anterior uveitis, posterior synechia -Mydriatic: iris atrophy, glaucoma, coloboma, retinal disease, optic nerve disease, atropine use -Look for lens luxation, anterior or posterior synechia, iris neoplasia, trauma, iris atrophy
Corpora nigra examination	-Normally is textured -Abnormal: --mass (textured, enlarged) --cyst (smooth, enlarged) --ERU (smooth, small)
Posterior segment assessment	-Dilate with tropicamide, not atropine -Check lens clarity, look for cataracts, nuclear sclerosis, or displacement -Vitreous humor should be checked for clarity, cells, blood, and color -Check retina for vessels, scars, bleeding -Check tapetum and non-tapetal surface -Look at optic nerve head, assess color, shape, and size
Lens examination	-Normal: transparent, just behind the pupil -Use direct illumination and retroillumination for assessment
Abnormal lens position	-Lens subluxation will have aphakic crescent -Anterior lens luxation will have abnormal pupil shape, glaucoma, lens will be in anterior chamber --will see aphakic crescent -Posterior lens luxation: lens is sitting in vitreous --optic nerve will look small --does not usually result in glaucoma
Focal opacity in lens	-Retroilluminate lens -If issue with anterior lens, eye and opacity move in same direction --Y suture is right-side up -If issue with posterior lens, eye and opacity move in opposite directions --Y suture is upside down -If issue is in center/nucleus, eye moves but opacity stays in the center
Superficial irregularities of the Lens	-Pigment -Persistent pupillary membranes -Cysts -Corpora adhesions -Capsular lacerations due to penetrating injury
Issues with Lens transparency	-Nuclear sclerosis: retro-illuminates with clear fundic exam, patient is visual -Nuclear cataract: center of lens is opaque on retroillumination, central fundus obstruction -Incipient cataract: small opacity, does not affect fundic view or patient vision -Immature cataract: larger opacity, partly affects fundic view, patient has some vision -Mature cataract: completely opaque lens, view of fundus is obstructed, vision is obstructed -Hypermature cataract: wrinkles in lens capsule, lens opacity starts to clear, will see small optic nerve on fundic exam, far-sighted vision
Vitreous examination and problems	-Normal: transparent, behind the lens -Use direct illumination and retroillumination for exam -Degenerative changes: --asteroid yalosis: crystalline opacities suspended or shifting --Vitreal floaters: faint opacities floating -Examine surrounding structures --retinal or uveal hemorrhage --optic nerve or uveal neoplasia --parasites --foreign body --retinal detachment --uveitis --cysts
Distant Direct Ophthalmoscopy	-Observe tapetal reflex and look for silhouette opacities --cornea, anterior chamber, lens, vitreous
Direct Ophthalmoscopy	-Start with distant direct exam, set at 0 diopter lens -Move in toward patient’s eye, keep tapetal reflex until 2-3cm from patient’s eye --Closer to eye gives wider angle of view -Use right eye to examine patient right eye, left eye to examine patient left eye -Focus on optic nerve first, then look at quadrants of the retina -If out of focus, move closer to or further from eye -If unable to move, use positive and negative movement to refocus
Indirect Ophthalmoscopy	-Hold lens at arm’s length, hold upper eyelid open -Focal light source at temple (Finhoff transilluminator, head lamp, direct ophthalmoscope light) -Look for tapetal reflex -Keep light, lens, and eye in a lone
Direct vs. Indirect Ophthalmoscopy	-Direct: --real image --greater magnification --greater image distortion --Need to piece together smaller images to get whole picture -Indirect: --inverted and reversed image --larger field of view --safer working distance --less image distortion
Components of normal equine fundus	-Stars of winslow in tapetal area -Retinal vessels -Non-tapetal area -Optic nerve head in non-tapetal area -6 o’clock notch
Normal tapetal color variants	-Green-yellow is most common -Atapetal: albinotic/subalbinotic --choroidal vessels show
Components of Fundic Exam	-Optic nerve head: --shape, color, size -Retinal vessels: --number, size -Tapetum --reflectivity --pigmentation --depigmentation --hemorrhages
Important components of Ophthalmologic exam to record	-Comfort level -Light reflexes -Eyelid changes -Corneal abnormalities -Anterior chamber qualities -Pupil size -Iris abnormalities -Lens abnormalities -Retina and optic nerve -Record things that are NORMAL also!
Standards for ophthalmologic exam and descriptions	-Indicate if patient was dilated for exam -Note normal AND abnormal -Use clock hours to describe location -Can use limbal, axial, paralimbal, peripheral, dorsal, ventral, nasal (medial), temporal (lateral) -Describe color, shape, depth, size -Cataracts: --location (capsular, cortical, nuclear, anterior, posterior) --shape (punctate, floriform, elliptic, web-like) --extent: focal, multifocal, diffuse, % of lens affected --stage of progression: immature, mature, hypermature
Diseases of the Eyelids	-Entropion -Eyelid laceration -Neoplasia
Entropion	-Rolling inward of the eyelid -Most common in foals on lower lid -Often secondary to enophthalmos due to dehydration, systemic illness, poor muscle tone, weak tarsal plate -Clinical signs: epiphora, blepharospasm, corneal ulcer, reflex uveitis -Treatment: temporary tacking, procaine penicillin injection, contact lens placement
Temporary tacking as treatment for entropion	-Need sedation and local block -Place vertical mattress sutures or staples -Over-correct -Be sure to treat ulcer also
Eyelid laceration	-Examine eyelid and orbit for trauma -Repair eyelid margin and function -DO NOT cut off the pedicle! -Give tetanus prophylaxis -Poor repair can lead to catastrophic ulceration -Non-healing ulcer can result --look for suture after repair --chronic rubbing may cause damage to stroma --treat as indolent ulcer (keratotomy)
Eyelid laceration repair	-Need good sedation -Clip and prep with dilute betadine solution --do not scrub with alcohol! -Local block and Auriculopalpebral nerve block -Need light and magnification -Remove foreign material, freshen edges until they bleed -2 layer closure is preferred -Start with figure-8 suture -Close tarsal-muscle layer, do not go through conjunctiva -Close skin with suture tags away from eye -Feel inside of repair for suture -Check eyelid margin apposition -Topical and systemic antibiotics
Auriculopalpebral nerve block	-Blocks motor aspect of CN VII (facial nerve) --orbicularis oculi of upper eyelid -Lidocaine or mepivacane --1-2ml over nerve with 25g 5/8 inch needle -Temporal ridge, lateral orbital fossa, base of the ear -Lasts 1-2 hours -Apply ointment after exam to keep eye lubricated
Eyelid sensory nerve blocks	-Block sensory innervation via CN V (trigeminal) -Lidocaine or mepivacaine --1-2ml over nerve, 25g 5/8 inch needle -Frontal, lacrimal, zygomatic, and infratrochlear areas -Helpful for sub-palpebral lavage placement, lid laceration repairs, TE resection
Squamous cell carcinoma in horse eyes	-Most common eyelid tumor -Common in gray horses, horses with pink eyelid margins --excess UV exposure, sun and altitude -Common locations: eyelid margin, lateral limbus, 3rd eyelid
Eyelid Squamous cell carcinoma treatment	-Wide surgical excision, try to preserve as much vision and eyelid function as possible -Treat early -Adjunctive therapy: --cryotherapy, 5-fluorouracil, mitomycin, photodynamic therapy, beta-irradiation, cisplatin, imiquimod -UV protective fly mask for life
3rd eyelid Squamous cell carcinoma	-Examine palpebral and bulbar surface of 3rd eyelid -Digital palpation of mass and orbital rim -Standing resection is best option if hemostats can get well below ventral edge of the mass --if not, resection under general anesthesia is best -If tumor is invading medial canthus or orbit, prognosis is guarded or poor -Recheck every 6 months after growth
3rd eyelid resection	-Good sedation is needed -prepare skin and conjunctiva with dilute betadine solution -Local block, topical anesthetic, topical phenylephrine -Use hemostat to crush well below the mass -Cut with scissors to protect cornea -Palpate for any remaining cartilage of 3rd eyelid, if exposed resect depper and remove -Let heal by 2nd intention -Look for prolapsed fat -Submit for histopath
Sarcoid	-Most common equine skin tumor -2nd most common equine periocular skin tumor -More frequent in young horses -Can be one or multiple sites, under skin or on surface -Often diagnosed by appearance -Biopsy can exacerbate situation -With surgical excision only, more than 80% recurrence --need adjunctive therapy (chemotherapy, cryotherapy, phototherapy, vaccine) -Enucleation is not a cure
Corneal anatomy	-Tear film (mucins, lipids, aqueous layers) -Epithelium: 8-10 cell layers thick --stratified non-keratinized squamous cells -Stroma: 90% of corneal volume, 75-80% water and 20-25% collagen and proteins -Descemet’s membrane: basement membrane of endothelium --produced continuously throughout life, thickness increases with age -Endothelium: monolayer of hexagonal cells, cell density is inversely proportional to age
Normal cornea	-Avascular, transparent, light-refracting surface -Equine cornea is 1mm thick -sensory nerves in anterior 1/3 of stroma and epithelium --causes superficial tumors to be more painful than deep stromal ulcers
Corneal Wound healing	-Starts within hours -Centripetal epithelial migration -increased epithelial thickness, from 8-15 cells -Wound edges retract via apoptosis -Epithelial cells adhere to basement membrane or anterior stroma -Complete re-epithelialization in 5-7 days -Vessels bud in 3-5 days, migrate 1-2mm per day -Epithelial basement membrane is complete in 6 weeks -Scar remodeling for 3-6 months
Clinical signs of corneal ulcer	-Blepharospasm (look at lash angle) -Blepharitis -Epiphora -Chemosis -Conjunctival hyperemia -Foal corneal edema -Miosis
Describing a corneal ulcer	-Size and shape -Location on cornea -Color of lesion --infiltrate, edema, plaque -Vessels --branching, brush border, location -Depth --superficial, deep, descemetocele, perforation -Texture --melting, gritty, dry, bulging, smooth
Diagnostics for eye ulcerations	-Fluorescein stain -Rose Bengal stain -Cytology -Culture
Corneal staining	-Moisten fluorescein strip with saline, touch to conjunctiva --do not touch to cornea -Cobalt blue light can show intensity of stain uptake -Corneal epithelium disruption is easily shown with stain --exposed hydrophilic stroma absorbs stain
Staining eye ulcerations	-Fluorescein stain 1st, look for ulcer -Rose Bengal stain 2nd --rose Bengal stain indicates instability of tear film, mucin tear layer blocks rose Bengal stain -Indicates risk for fungal colonization or invasion, keratoconjunctivitis sicca, or viral keratitis -Rose Bengal stains exposed epithelial cells, mucous, and stroma
Culture for eye ulcerations	-Culture before stain or topical anesthetic -Auriculopalpebral block with or without sedation and sterile topical anesthetic -Touch edge and center of ulcer for culture -DO NOT touch eyelids! -Aerobic with sensitivity and fungal culture -Culture tip dry or wet
Cytology for eye ulceration	-Auriculopalpebral block, sedation, topical anesthetic -Scrape edge and base of the ulcer, need deep sample for fungal cytology -Use back of scalpel blade, spatula, or brush -Take 2-4 samples on 2 slides, dry and stain -Look for epithelial cells, inflammatory cells, bacteria, fungal hyphae, vegetative material, mineral crystals, number of bacteria
Treatment of simple superficial uncomplicated corneal ulcer	-Treat underlying cause -Prevent or control infection --broad-spectrum antibiotic --antifungal -Treat uveitis -No topical steroids or topical NSAIDs --can cause melting or infection -Recheck in 1-2 days -If not healed in 2 weeks, consider indolent ulcer
Treatment for simple superficial uncomplicated ulcer	-Treat underlying cause -prevent or control infections --broad spectrum antibiotic: Neopolybac --antifungal: Itraconazole/DMSO -Treat uveitis --topical atropine (only one dose, need to be careful about Colic) --Systemic NSAIDs (banamine, Bute, equioxx) -NO topical steroids or topical NSAIDS --can cause melting ulcer or infection -Recheck in 1-2 days -If not healed in 2 weeks. Consider indolent ulcer
Indolent Ulcer	-Slow healing corneal ulceration, lasts more than 2 weeks -Non-healing ulcer -Edema and loose epithelium -Anterior stroma is abnormal, inhibits adhesion complexes --epithelium does not adhere to stroma --fluorescein diffuses under loose epithelial edge -Often there is decreased corneal sensitivity
Debridement of Indolent Ulcer	-Need to rule out infection before debriding! -Only debride with superficial ulcers, if there is any divot do not debride -Culture and cytology -Rule out mechanical cause -Sedate, block, and give topical anesthetic -Use sterile cotton tip to get all loose tissue off, push cells off --rotate cotton tip, remove all loose cells --If corneal tissue can be removed with Q-tip, cells should not be there -Treat ulcer after debridement -Recheck every few days, wait 10-14 days to repeat debrdement
Keratotomy	-Treatment for superficial, non-healing, non-infected ulcers -Treat underlying cause if one can be identified --identify infection with culture and sensitivity -Initially Use sterile, dry cotton tip for debridement, wait 10-14 days --If not healed, do keratotomy to promote epithelial adhesion to stroma (roughen stroma) -Use caution if eye is positive for Rose Bengal stain -Can do grid, punctate, or diamond tipped burr keratotomy
Grid keratotomy	-Roughens cornea, gives epithelial cells something to attach to -Need to rule out infection first! Culture and cytology -Do not do if there is any cellular infiltrate -ONLY do on superficial ulcers! If there is a divot, do not do! -Sedate animal, use nerve block, twitch, and local anesthetic -Dilute betadine corneal prep -Debride loose epithelial cells with dry sterile cotton swab -Use 22-25g needle and sterile gloves to create grid --checkerboard pattern across entire ulcer, from healthy epithelium to healthy epithelium -Use enough pressure to make a mark but not too much to go through cornea -Treat ulcer -Recheck in a few days -Wait 10-14 days before repeating
Complications of Grid keratotomy	-Can put infection deeper into the eye -Can puncture the eye if animal moves due to improper anesthesia
Diamond Tipped Burr	-Removes loose epithelial cells and roughens stroma -Need to rule out infection first (culture and cytology) --if there is cellular infiltrate, do not use burr! -ONLY for superficial ulcers -Debride cornea with sterile cotton tip first -Use sterile tip of burr to pulish ulcer surface and edges -Treat ulcer -Recheck in a few days -Wait 10-14 days to repeat -Results in less scar tissue after healing -No chance of puncturing the eye!
Complicated Ulcers	-Stromal loss -Melting ulcer (keratomalacia) --proteases from infection, PMNs, epithelium/stroma -Cellular infiltrate, PMNs migrate faster than vessels and epithelium -Laceration -Foreign body -Infection --bacterial: pseudomonas, staphylococcus, streptococcus --fungal: aspergillus, fusarium -Iris prolapse
Treating a complicated ulcer	1. Antibiotic: based on culture and sensitivity, cytology 2. Antifungal 3. Anticollagenase, decreases Matrix metalloproteinases --serum, EDTA, Mucomyst, systemic doxycycline 4. Atropine to relieve ciliary spasm and stabilize blood aqueous barrier 5. Anti-inflammatory (systemic) --banamine is best, least amount needed to help uveitis and pain --monitor for right dorsal colitis and nephrotoxicity
Complications of Ulcers	-Fungal ulcerative keratitis -Iris prolapse
Fungal Ulcerative Keratitis	-Variable appearance -Early form may not stain with fluorescein --do not put horses on steroids just because they are painful and no stained ulcer -Can rapidly progress to a melting ulcer -Can progress to deep stromal abscess -Surgery is best option to decrease fungus, remove fungal burden
Iris Prolapse	-Dyscoric pupil (abnormal shape), darker pigment to iris, shallow anterior chamber -More than 15mm has poor prognosis -Crossing limbus has poor prognosis -Acute has better prognosis than chronic -Traumatic has better prognosis than ulcerative -Do Seidel’s test for leaking aqueous -Surgery is best treatment
Seidel’s Test	-Test for deep stromal ulcers -Iris prolapse -Shallow anterior chamber -Need sedation, AP block, topical anesthetic -Look for leakage of aqueous humor and a green stream
Sub-palpebral lavage system	-Recommended for all complicated ulcers and horses that are difficult to treat with simple ulcers -Place lavage system in dorsal or ventral conjunctival fornix -Poorly placed sub-palpebral lavage may cause more issues for patient
Sub-palpebral lavage placement	-Good sedation -Topical anesthetic -Dilute betadine prep of eyelids and cornea -Local nerve block, frontal nerve -Twitch -Sterile gloved finger is placed into fornix at site of lavage -Put finger along side of the needle to protect the eye -Push needle through conjunctiva and skin, pull tubing through until footplate is seeded in the fornix -Suture to skin, braid mane, and feed through braids and tape near withers
Protective hood on horses	-Use in conjunction with sub-palpebral lavage system -Use hood to protect against self-trauma -Limits visual inspection -Provides warm moist environment for bacterial or fungal growth
Atypical corneal ulcers	-Eosinophilic keratitis (keratoconjunctivitis) -Clacific band keratopathy -Viral keratitis
Non-ulcerative corneal disease	-Immune-mediated keratitis -Stromal abscess -Keratoconjunctivitis sicca
Eosinophilic Keratitis	-Caseous discharge and focal corneal edema -Moderate to severe blepharospasm before ulceration -Corneal ulcers are in periphery, will see raised vascular plaques -Often minimal discomfort -Diagnose with corneal or conjunctival cytology, will see eosinophils --only need 1-2 eosinophils to diagnose -Treatment: topical steroids if there is no ulcer --systemic steroids and zyrtec --ivermectin -Slow healing, can take many weeks to months -Seasonality in mid-atlantic region (June-August) -Also occurs in cats
Calcific band Keratopathy	-Complication of chronic inflammation or chronic topical steroids -Eye is painful -Focal corneal edema -Will see white bands in interpalpebral cornea -Indolent ulcer due to poor epithelium migration and adherence -Microfractures of epithelium may cause faint stain uptake -Minerals auto-fluoresce -Treat with superficial keratectomy or burr debridement, topical Ca++ chelators, NSAIDs, bandage contact lens
Herpes viral Keratitis	-EHV-2 in foals and adults -Blepharospasm and epiphora -Cornea often looks clear without magnification -May see superficial ulcers or superficial erosions -Multifocal punctate or dendritic pattern of opacification -May have corneal edema and neovascularization -Need to rule out fungal keratitis -Diagnose via PCR for EHV-2 (not reliable, really a diagnosis of exclusion) -treat with topical antiviral and treat simple ulcer -May give topical NSAIDs, NO steroids -Common in cats, rare in dogs
Non-ulcerative keratitis	-No fluorescein stain uptake -Corneal neovascularization -May see blepharospasm
Immune-mediated keratitis	-Chronic, non-ulcerative keratitis -Non-infectious -Responds to anti-inflammatories -Non-painful, corneal opacity in one or both eyes -Focal corneal edema and branching vessels, infiltrate may be seen at the end fo the vessels, negative stain -Uveitis is usually not present -Superficial stromal, mid-stromal, or endothelial
Stromal abscesses	-Acute onset! May or may not have history of an ulcer -Yellow-white opacities in the stroma -Photophobia, epiphora, blepharospasm, very painful! -Will see diffuse corneal edema, yellow-white stromal opacity, deep vascularization --vascular response is proportional in severity to depth and diration of the lesion -Hypopion and fibrin will be present in anterior chamber in severe cases -No stain uptake -DDx: anterior uveitis, immune-mediated keratitis -Occurs mostly in large animal species, rare in small animals
Formation of a stromal abscess	-Stroma is inoculated with infectious agent through defect in epithelium --defect can be due to puncture, ulcer, laceration, foreign body -Epithelial cells migrate over defect, deal infection in stroma --Epithelium heals over infectious agent -Fluorescein negative -Infection is almost always fungal, hyphae can get deep into stroma --penetrate descemet’s membrane and causes uveitis to get worse
Medical Treatment of Stromal Abscesses	-Healing occurs via vascularization --vessel growth is slowed by fungal infection, vessels do not always go deep enough -Antifungal, Antibiotic, Atropine, and Anti-inflammatory are needed for proper treatment Surgical treatment for Stromal Abscess	-Need to do when abscess is not responding to medical therapy -Abscess progresses or persists even with medical therapy -Severe pain, vision-thretening uveitis -Severe uveitis, endophthalmitis that compromises vision and globe -Race between resolution of abscess/healing and vision loss from uveitis -Do surgery under general anesthesia --shorter duration of therapy results in faster recovery --healing occurs quickly when abscess is removed -Good outcome -May have scar if there is graft rejection
Penetrating keratoplasty	-Use when abscess involves most of stromal thickness -Need full thickness donor graft -Also need conjunctival graft -75% or more of patients are visual post-operative -Larger size results in increased complication rate
Posterior lamellar keratoplasty	-Do for abscess that only involves posterior stroma -Partial thickness graft -May or may not need conjunctival graft -90% of patients are visual post-operatively
Deep lamellar Endothelial keratoplasty	-Done for peripheral abscess involving posterior stroma -Partial thickness graft -90% of patients are visual post-operatively -Approach is through limbus
Stromal abscess treatment where Sx is not an option	-Stromal anti-fungal injections, inject right into stroma -Need standing sedation or short anesthesia -High magnification and good light are essential
Keratoconjunctivitis Sicca	-“Dry eye” -Very uncommon in the horse -Blepharospasm, minimal to no epiphora, increased discharge -Will see a corneal ulceration and vascularization, may see pigmentation -Diagnose with schirmer tear test, less than 10mm wetting within 1 minute --normal is 25mm or more -Treatment with lacrostimulants, lubricants, partial tarsorraphy parotid duct transposition
Overview of Ulcers	-Fluorescein stain every abnormal eye and every painful eye -Cytology helps direct immediate therapy -Debride with sterile cotton tip if not healed in 2 weeks -DO NOT grid an infected ulcer -Complicated ulcers need early referral -Treatment: antifungal, antibiotic, atropine, anticollagenase, anti-inflammatories
Colostrum Shortage	-Current shortage in dairy colostrum -Dairy cows do not produce high-quality colostrum -Want to decrease the amount of bacteria in colostrum, bacteria get in the way of IgG availability -Can pasteurize to get rid of bacteria, but difficult to pasteurize colostrum -Can acidify colostrum, make pH 4-5 --may cause clumping of milk, need to control temperature
Ideal Colostrum Characteristics	-Quality: 50g/dL minimum -Quantity: 4L -Total: 200g minimum
Bacteria causing GI disease in calves	-E. Coli -Coronavirus -Clostridium perfringens -Salmonella -Rotavirus (not very intense diarrhea)
E. coli K99	-Most common E. coli strain in dairy cows -Named for method of attachment -Kills dairy cows within 3 days of life -Very effective vaccine exists (First Defense) --give within 12 hours of life --acts locally to prevent attachment of E. coli K99
Respiratory disease in Calves	-BRSV -IBR -PI3 -Coronavirus (usually enteric, can cause pneumonia) -Leptospira -Mannheimia haemolytica -Mycoplasma -Pasteurella multocida -Inforce 3 vaccine
Inforce 3 vaccine	-Modified live virus -Bovine rhinotracheitis -Parainfluenza 3 -Bovine respiratory syncytial virus -intranasal vaccine
Newborn calf vaccines	-First defense (E. coli K99) --local to intestine -InForce 3 (BRSV, IBR, PI3) --intranasal
2 main camps of calf vaccination	1. modified live early: --boosts lymphocytes, cell-mediated immunity response --give day 8-15 2.Modified Live late: --colostrum is gone --humoral response --give day 36-43
Weaned calf vaccination schedule	-Inforce 3 intranasal vaccine -Can be given multiple times -Give whenever something stressful is going to happen, gives immune system boost
Bovi-Shield Gold FP 5 L5 HB	-Bovine rhinotracheitis virus -Parainfluenza 3 -Bovine respiratory syncytial virus -Leptospira --Canicola, grippotyphosa, hardjo, icterhemorrhagiae, Pomona --killed vaccine, needs booster! -Modified live vaccine for viruses, does not need booster -Do not give to pregnant heifers or cows if they have not been previously vaccinated! --causes abortions -Give 1 month before breeding
Clostridial diseases in Cows	-Clostridium chauvoei: black leg -Clostridium haemolyticum: red water -Clostridium novyi: black’s disease -Clostridium perfringens C and D: Enterotoxemia, overeating disease, pulpy kidney disease -Clostridium septicum: malignant edema -Clostridium sordellii: gas gangrene
Ultrabac 8	-Clostridium vaccine -Subcutaneous administration under the skin --5ml dose
Growing heifer vaccination schedule	-Heifers more than 4 months of age --Bovi-shield gold (needs yearly booster) --Ultrabac 8 (needs yearly booster) -Need to give yearly booster for Bovi-Shield --can cause abortions if given to cow that has not seen virus before
Breeding Heifer vaccination schedule	-Bovi-shield and Ultrabac one month before breeding -NEED to give before breeding! Can cause abortions if given during pregnancy to animal that has not been exposed to vaccine
Mammary gland disease	-Common in dry cows, right after dry-off --teat sphincter does not stay closed, allows ascending infection -Common right before parturition, before start of milking colostrum -Gram- infection: E. coli
J5 E. coli vaccine	-Initially developed from a salmonella vaccine, has same LPS -Subcutaneous injection at 7 and 8 months gestation
Scourguard vaccine	-Bovine rotavirus and coronavirus killed virus -Clostridium perfringens C and E. coli -Helps prevent diarrhea in calves of vaccinated dames due to rotavirus, coronavirus, E. coli, and clostridium perfringens -IM injection -Prevents endotoxemia in cows, which helps calf
Spirovac vaccine	-Leptospirosis vaccine for cattle -Canicola, Grippothyphosa, Hardjo, Icterhemorrhagiae, Pomona -Give subcutaneously -Need to booster every year
Important points of bovine vaccination	-Do not vaccinate pregnant cow with modified life vaccine she has not seen before! -Do not administer more than 7 gram- vaccines at one time --too many toxins can create endotoxemia -Avoid vaccinating fresh cows -Follow all label directions -Modified live vaccines need only one injection -Killed vaccines generally need a booster
Foundation vaccines in Cows	-Give to young animals and build on -respiratory viruses: --IBR, BVDV type I and II, BRSV -Leptospira -Clostridium -E. coli J5 bacterin
Components to evaluate on a dairy farm	-Cow records -Reproduction -Milk quality and milking parlor -Facilities -Transition cow health -Feet and lameness -Calves and heifers -Finances -Production -Rations and feeding
DHI testing and records	-Monthly evaluation of individual lactating cows -DHI technician collects on-farm data --animal identification, calvings, breedings, pregnancy checks, dry-offs, milk weights -DHI technician collects milk samples --somatic cell count --milk components
Culling	-Departure of a cow from the herd --sale, slaughter, salvage, death -Major cost to operation -Annual cull rate: (# sold + # died)/ average cows in herd -Average cows in herd: 0.93* # of fresh cows -Goal is for cull rate to be less than 30% -Sold cows generate income for produced -Dead cows do not involve any income recovery for producer
Data analysis on a dairy farm	-Identify at-risk populations --analysis of udder infection dynamics using individual cow somatic cell count
Milking routine goals on dairy	-Pre-dip contact time: more than 30 seconds -Stimulation time: 90-180 seconds -Mean teat-end peak flow vacuum: 10-12 inches Hg
Dairy farm bedding	-Sand is the new thing --keeps cows dry and clean, most comfortable -Shavings -Composted manure solids -Mattress -Nothing
Dairy farm bunk space and lying space	-Want 27-30” per lactating cow in the bunk --Want all cows to be able to eat all of the time -Lactating cows need 100 square feet -Far-off dry cows need 80 square feet -Close-up dry cows need 120 square feet -Maternity cows need 140-200 square feet
Management of Transition cows	-Prevention is more important than treatment -Screen cows daily -Do a PE on cows identified during screening -treat cows based on herd protocols --define disease and specific treatments --need to know doses, frequency, routes, duration, and withhold times -MONITOR!
Important aspects of evaluating a livestock operation	-Know farm before making suggestions --talk to produced, workers, farm manager, etc. -Analyze current and historic methods -Watch and pay attention -Follow up
Chronic Colic DDx	-Equine gastric ulcer syndrome (EGUS) -IBD/lymphoma -Sand enteritis -Right dorsal colitis -Peritonitis -Abscess/bastard strangles -Enterolith -Adhesions -Parasitism -“Wierdomas” -Idiopathic (at least 50% of chronic colic cases)
Chronic colic overview	-Exact etiology is not found in more than 50% of cases -Often no treatable -Expensive workup -No diagnosis -Prognosis is hard to determine -Usually results in a dissatisfied client
Equine Gastric Ulcer Syndrome (EGUS)	-Gastric ulcers are very common in horses -93% of racehorses have gastric ulcers -60% of other performance horses -57% of foals -50% of horses have no clinical signs at all
Clinical signs of EGUS	-Mild, chronic colic -Bruxism (especially in foals) -Weight loss -Poor performance -inappetence (eats hay, but not grain) -No clinical signs is a common presentation
Pathophysiology of EGUS	-Horses secrete acid 24 hours per day -In wild, eat 18 hours a day --in stalls eat 3 hours per day -Risk factors: --stress --shipping --exercise --high grain diets
EGUS diagnosis	-Endoscopy via 3m scope --expensive and not always available -Fecal occult blood is NOT an effective diagnostic tool --GI tract is too long, blood will not be occult in feces --tests exist but are not sensitive or specific enough, do not use! -Therapeutic trial can be helpful for diagnosis --give ant-acid medication and see if it works --placebo effect on owner
Location of Equine ulcer formation	-Form in squamous portion of stomach -Along margo plicatus -Can result in squamous hyperplasia -May see islands of squamous epithelium with bleeding ulcers -Pyloric ulcers are harder to treat
EGUS treatment	-Proton pump inhibitors --Gastrogard (FDA approved): omeprazole paste -H2-receptor antagonists --Cimetidine (almost useless) --ranitidine (does not work as well as gastrogard) -Antacids (not effective) -Sucralfate (not effective) --patches ulcers, acts as band-aid -Environmental changes
Gastrogard	-FDA approved treatment for EGUS -Paste formulation -Proton pump inhibitor -Very effective, but costly ($50 per day) -Specially formulated t protect active drug from low pH of the stomach -Compounded omeprazole is cheap, but not effective because omeprazole is destroyed by gastric acid before it can have an effect -Can give ¼ tube per day
EGUS prognosis	-Excellent, if treated appropriately -Can be prophylactically prevented with Ulcergard omeprazole paste --1/4 dose of gastrogard
IBD/Lymphoma in horses	-4 main types: --granulomatous enteritis --Multi-systemic eosinophilic epitheliotrophic disease --Lymphocytic plasmacytic enterocolitis --Idiopathic eosinophilic enterocolitis
IBD/Lymphoma diagnosis	-Rectal biopsy (easy, not very sensitive) -Open biopsy (expensive!) -Treat presumptively based on ultrasound findings and clinical signs
IBD/Lymphoma treatment	-Corticosteroids --palliative -Generally poor response to treatment -Prognosis is poor
Sand Enteritis Clinical Signs	-Mild colic -Weight loss -Diarrhea -hypoproteinemia -Any combination of the above
Sand enteritis diagnosis	-Sand test: put manure in rectal sleeve, fill with water, and see if sand settles into fingers -Radiographs -History of animal being stabled in sandy area
Sand Enteritis treatment	-Oral or nasogastric psyllium --1-2 lbs per day --gooey, sticks to sand -Stop access to sand! Feed animal in raised feeder, move pasture
Right dorsal colitis clinical signs	-Hypoproteinemia -May or may not have edema, weight loss, colic -Rarely diarrhea -bad disease
Right dorsal colitis pathophysiology	-Caused by idiosyncratic reaction to NSAIDs --not dose-dependent -results in thick, edematous, granulating right dorsal colon mucosa -Diagnose via history of NSAID use and very low protein -Can confirm diagnosis with ultrasound, but not 100% sensitive --especially in mild cases
Right dorsal colitis treatment and prognosis	-Stop NSAID use! -Low bulk diet, complete feed and no hay -Misoprostol, sucralfate, vegetable oil -Resection? Hard to do, have to take out a rib -Prognosis is guarded, only some cases recover -May have some stricture at the right dorsal colon, may need colic surgery --if stricture continues, may result in scar tissue
Peritonitis in horses	-Cause of chronic colic -Clinical signs: fever, colic, depression, diarrhea --high fibrinogen -Diagnose via abdominocentesis and ultrasound -Treat with broad-spectrum antibiotics -Prognosis depends on cause, better if it is due to primary cause --Actinobacillus is common cause
Bastard strangles/abscesses	-Cause of chronic colic in horses -Animal will probably have a fever, high fibrinogen (over 1,000 mg/dL) -Usually history of S. equi equi exposure -Diagnose via CBC and fibrinogen -Can use ultrasound for diagnosis, may be able to see abscess directly -Abdominocentesis can be helpful for diagnosis, may see some degree of peritonitis -Strep M titer will be very high with bastard strangles
Treatment of bastard strangles	-long-term antimicrobials --IM penicillin --Rifampin can be added for penetration -Surgical drainage as last resort -Prognosis is variable -May result in chronic colic due to adhesions
Enteroliths	-Cause of chronic colic --causes periodic colic, often severe -Much more common on west coast (due to alfalfa?) -Diagnose via radiographs, exploratory celiotomy -Excellent prognosis with removal “Wierdomas” or other causes of chronic colic	-Foreign body -Recurrent nephrosplenic entrapment -tumor -Non-GI cause of colic --pheochromocytoma --pneumonia or pleuritis --ventricular tachycardia --rabies (usually not very chronic)
Diagnostic plan for chronic colic cases	-EGUS: gastroscopy -IBD/Lymphoma: ultrasound, rectal biopsy -Sand enteritis: sand test, radiographs -Right dorsal colitis: check protein, history of NSAIDs, and ultrasound -Peritonitis: abdominocentesis, ultrasound -Abscess/bastard strangles: ultrasound, Strep EM titer, abdominocentesis -Enterolith: radiograph, surgery -Adhesions: history of colic surgery, peritonitis -Parasitism: fecal, maybe
DDx for “feed out of the nose”	-Neurologic dysphagia --guttural pouch disease --any other cause of neurologic disease (EPM!!) -Obstructive dysphagia --esophageal obstruction --“choke” (grain, pellets, alfalfa cubes, carrot) --old horses with bad teeth that eat quickly -Usually obvious which one it is based on clinical exam --neuro cases are dull, have other neurologic signs --“choke” horses are gagged, neck is stretched out -Pass a tube if you are not sure! --if tube does not pass to stomach, know it is choke Treatment of Choke	-Treat immediately: --sedate, pass nasogastric tube, lavage --can be traumatic and have greater likelihood of aspiration pneumonia -Wait and see: --only pass tube if needed for diagnosis --sedate mildly, give 12-24 hours for resolution --may need to make multiple visits, horse can become dehydrated if wait too long
Choke sequelae	-Aspiration pneumonia --common, can be fatal --give prophylactic antibiotics -Esophageal stricture: causes repeated episodes of choke --feed wet, sloppy feed for 3-4 months, usually resolves on own -Esophageal Rupture: --usually fatal and untreatable, especially if rupture occurs in thoracic esophagus --be gentle with tube!
Prevention of Choke	-Avoid feed that increases risk of choke -Correct dental problems -Slow feed intake --put rocks in bucket of feed --scatter feed on floor so horse has to nibble, no gulping
Equine Metabolic Syndrome (EMS)	-“Peripheral Cushing’s” -“Insulin resistance” -Overweight horses -Common in Morgans, Peruvian Pasos, Paso Finos, Spanish Mustang, Warmblood, Rocky Mountain Horses -Horses age 5-15 years (younger horses)
Equine Metabolic Syndrome (EMS) Clinical signs	-Obesity and fat deposits --cresty neck, gluteals, sheath, udders -Chronic laminitis, may be sub-clinical -Insulin Resistance -Possibly Infertility in mares
EMS contributing factors	-Chronic Over-feeding -Limited physical activity -Enhanced metabolic efficiency
EMS Pathophysiology	-Fat: storage organ to endocrine organ -Adipocytes produce excessive levels of endogenous glucocorticoids --inhibits action of insulin at central and peripheral tissues -Animal develops glucose intolerance -Affected horses have increased insulin secretion, but action of insulin is inhibited -Increased 11-betahydroxysteroid dehydrogenase 1 activity
Laminitis and Equine Metabolic Syndrome (EMS)	-Nitric oxide production decreases in animals with EMS -results in vasoconstriction -Impairs ability of the vessels to respond to vascular changes --vessels cannot respond when needed -Horse has “smoldering” laminitis
EMS diagnosis	-History -Physical exam --regional adipocyte deposition --High body condition score --crest neck score of more than 3 --radiographs of feet (hard to convince owner to take radiographs when horse is sound -Lab tests --single glucose and insulin concentrations --IV glucose tolerance test (only done in research setting) -Oral glucose test (dynamic test)
EMS diagnostic testing results	-Glucose will be high-normal -hasting hyperinsulinemia --more than 20 uU per ml --need to do with 6 hour food withhold -Fasting oral glucose test in field --0.15 ml/kg light karo syrup PO --measure insulin 1-1.5 hours after administration --more than 60 uU/ml is positive for EMS -Do not sample during a laminitic episode, stress will give false increase -Sample after 6 hour period of feed withhold between 8-10am
EMS treatment	-Diet! Reduce obesity -Feed low glycemic index foods --Eliminate pasture time --Forage diet with vitamin and mineral supplementation --be sure to test hay/pasture before allowing animal to eat it -Put animal on dry lot -Soak hay to get rid of sugars, have to also supplement with vitamins -More exercise -Anti-oxidants -Decrease cool season grasses (C3), increase warm season grasses (C4) --bermuda grass, bluestem, switch, Gramma, native prairie grass species -Graze animal when grass is less “stressed,” overnight -If animal is insulin resistant, feed commercial low-NSC feed -Beet pulp or soy hull based feeds -Feed multiple small meals
Levothyroxine Sodium	-Treatment for EMS -“Safe” treatment -Induces weight loss and insulin sensitivity -48 mg/day PO for 3-6 months --give for a finite period of time then wean off --wean off over a month
Metformin	-Treatment for EMS -Really an anti-diabetic drug -Increases insulin sensitivity at the post-receptor level -Controls post-prandial insulin spikes -Decreases carbohydrate load within the gut -No long-term safety studies -30 mg/kg every 8-12 hours PO --give 1 hour before feeding
PPID vs. EMS	-Older horses vs. horses less than 15 years old -Regional adiposity in both -Laminitis in both -Hyperinsulinemia sometimes present vs. hyperinsulinemia present -Hirsutism vs. no hirsutism -PU/PD vs. no PU/PD -Skeletal muscle atrophy vs. no atrophy -Failure to shed winter coat vs. no failure -ACTH increased vs. ACTH normal -Abnormal dex suppression test vs. normal dex suppression test
Pituitary pars intermedia Dysfunction (PPID)	-Hypertrophy/hyperplasia od pars intermedia of the pituitary gland -Pituitary micro and macroadenomas are common -Increased expression of pars intermedia POMC-derived peptides (ACTH) -Gland is functional, produces increased hormones -Usually occurs in older horses, 18-23 years old -“Cushing’s disease” -Hirsutism is most frequent clinical sign -Posterior pituitary/neurohypophysis stores and secretes hormones made in hypothalamus -Anterior pituitary/adenohypophysis --made of pars distalis, pars intermedia, and pars tuberalis
PPID clinical signs	-Hirsutism is most frequent -Chronic laminitis, solar abscesses -Weight loss with fat distributed around ribcage --abnormal fat distribution -Increased infection -Poor wound healing -Muscle wasting, weight loss -Hyperhidrosis -PU/PD -Seizures, blindness
PPID pathogenesis	-Loss of hypothalamic control of dopamine inhibition --dopamine neuron degeneration? --oxidative stress and protein misfolding? --parkinson’s like disease? -Pituitary hyperplasia, hypertrophy, and microadenoma --excessive production of ACTH and other PMOC derived peptides (MSH, beta endorphins, CLIP) --Insensitive to glucocorticoid negative feedback -In horses is ALWAYS pituitary based, not adrenal based -Elevated ACTH and other peptides is associated with adrenal hyperplasia --increased cortisol and androgen production -Pituitary adenoma leads to compression of hypothalamus, posterior pituitary lobe, and optic chiasm
Hematologic changes associated with PPID	-Hyperglycemia, hyperinsulinemia --due to insulin resistance? -Elevated endogenous ACTH -Loss of cortisol level circadian rhythm -Anemia, neutrophilia, and lymphopenia are rare -Do not measure cortisol levels to make diagnosis
PPID diagnosis	-Many tests available but no good test -Poor sensitivity, poor specificity -Safety of tests? -results vary by the time of year --increased in the fall, need to use fall-specific reference range and do not compare to the spring value
PPID diagnosis via ACTH serum levels	-Baseline ACTH level: --ponies: more than 27 pg/ml --horses: more than 35 pg/ml -Need special handling of samples -Results can be falsely elevated with stress and pain -Seasonality plays a role --increased values in the fall -Regional values? -Use purple top blood collection tube with EDTA
PPID diagnosis via Dex suppression test	-no longer the “gold standard” -Use caution in horses with recurrent laminitis --may cause laminitis in susceptible horses -Draw baseline cortisol, give dex, test 20 hours post cortisol --normal: cortisol will be less than 1 ug/ml --PPID: more than 1 ug/ml -Increased values in the fall -Low sensitivity
PPID diagnosis via Thyrotropin Releasing hormone test	-TRH stimulation test -draw baseline blood, Give TRH, draw post- test and look at ACTH levels -In PPID cases, ACTH levels increase by more than 50% -TRH can be difficult to get -Can be combined with dex suppression test -Not commercially available
PPID diagnosis via Domperidone stimulation test	-Blocks peripheral dopamine D2 receptors -Marketed for use in horses, wide margin of safety -Does not cross BBB -Give domperidone paste at 8am, run ACTH levels at 0 and 8 hours -More than 2x increase indicates PPID -Seasonal effect is unknown -ACTH stimulation test may be better?
PPID diagnosis via physical exam	-Hirsutism will be present, 86% accurate for diagnosis -May not see in early PPID -Better than all other tests! -Ideally pair with other tests, also test to see if medication is working
Pergolide	-Treatment for PPID
PPID Prognosis	-Lifelong condition, no current cure -Effective treatment is possible with medication and management changes -Prognosis is guarded to fair --based on response to treatment and development of complications
Johne’s Disease	-Chronic bacterial infection -Mycobacterium avium subspecies paratuberculosis (MAP) -Affects the intestinal tract --can lead to disseminated infection of the body -Affects cattle, deer, bison, sheep, goats, camelids -Long incubation period, 2-10 years
Signs of Johne’s Infection	-95% of infected cattle show no signs at all -Clinical signs in animals present in animals over 2 years old
Clinical signs of Johne’s Disease in cows	-Weight loss despite normal appetite -Decreased milk production -Diarrhea (may be intermittent) --loose, then progresses to pipe-stream -Sub-mandibular edema/bottle jaw due to hypoproteinemia -Lethargy -Emaciation, VERY thin cows -Animal starts to go into negative energy balance -Usually individual animals are culled before advanced disease is present -On herd level, may see one animal with chronic diarrhea and then another several months later
Clinical signs of Johne’s disease in small ruminants	-Emaciation -Hypoproteinemia causing bottle jaw -No diarrhea!
Stages of Johne’s disease infection	-stage 1: calf infected in early neonatal period --infected via oral ingestion of manure with MAP -Stage 2: eclipse phase --animal shows no clinical signs and MAP is unable to be detected --no antibody production, no immune response, no way to know animal is infected -Stage 3: starts to shed organism --can detect organism with PCR or ELISA -Stage 4: clinical stage --rare that an animal makes it to stage 4, usually removed or culled first
Stages if Johne’s Infection	1. Invasion phase (stage 1): calves --intestinal invasion of M-cells --can also affect yearling heifers if immunocompromised 2. Eclipse phase (stage 2): 2-10 years --shedding organism, but not able to be detected 3. Asymptomatic phase (stage 3): 2+ years --positive fecal test for MAP --may be 1-9 years until animal is clinical --serology becomes positive with increased organism numbers 4. Clinical phase (stage 4): heavy shedder
Johne’s Iceberg	-Only 1% of affected animals will show clinical signs fo weight loss and diarrhea -3-5% of animals are in shedding phase -25% of animals are in eclipse phase -60% of animals are infected but not detectable!
Sources of Johne’s disease Infection	-In-utero -Peri-natal period --most likely time of infection --heavily infected cows shed MAP into colostrum -Environment: --fecal contamination of feed and water --manger sweepings --infected Manure spread on crops can result in infection if fed to animals (put to silage! Not grazing crops!)
Johne’s disease diagnostic tests	-Serology: antibody-based test --AGID --ELISA -Fecal culture --solid media (gold standard) --liquid media -Fecal RT-PCR -Histopathology
AGID test for Johne’s disease	-For cattle with clinical signs -High specificity (95%) -Sensitivity varies based on stage of disease --high in clinical cows --low in asymptomatic cows -Reliable test for individual cows that are clinical suspects -Not reliable as a screening tool, not effective for finding non-clinical cows
ELISA test for Johne’s disease	-Can be done on serum or milk -Great screening test -On serum, sensitivity is 25-45% (not great, especially for non-clinical cows) --specificity is 95-99% -Positive test indicates animal is likely to culture positive on fecal -Negative test does not mean animal is not infected --animal could be negative, could also be infected but not able to be detected by ELISA -Used as herd screening tool, followed by fecal culture of ELISA-positive animals (follow up with fecal culture) -Rapid turnaround time -Low cost -Lots of samples can be processed on the same day -Specificity is not 100%, may identify negative cattle as positive -Sensitivity is poor on sub-clinical cows
Milk ELISA for Johne’s disease	-Special ELISA kits -Sensitivity and specificity are similar to serum ELISA -More convenient sampling -“Target testing” is easier, can check at specific life stages -Can take bulk tank samples --bulk tank samples become very dilute, no way to know which cow specifically is positive -Specificity is not 100%, may identify negative cattle as positive -Sensitivity is poor on sub-clinical cows
Fecal culture for Johne’s disease	-“Gold standard” johne’s testing -high sensitivity and high specificity -Usually positive 1 year before clinical signs develop -Can quantify number of contagious untis, can identify super-shedders -Expensive, costs $20-25 per sample -Sample collection process is involved, have to go into rectum for sample -Incubation time is 12-16 weeks, slow turn-around -Need specific lab, trustworthy lab -Can use as screening tool on pooled samples from 5-10 cows --spilt group if needed -Can be used to confirm ELISA positive animals before culling -Liquid media is faster than solid media, reduced incubation period --correlation between time it takes to show up positive and amount of MAP in sample -Some small ruminant strains do not grow in liquid media -Try to quantify shedding by comparing with Herrold’s Egg yolk media
Herrold’s Egg yolk media	-Testing for Johne’s disease -Allows quantification of shedding -informs culling of high-shedders -White dots indicate MAP colonies
Fecal RT-PCR for johne’s disease	-Commercial kit, identified specific MAP DNA segments -Can be done on individual samples or pooled fecal samples -High specificity, 100% -High sensitivity, can detect very low shedders -rapid turnaround, 203 days -Quantification of the amount of MAP in the sample -Can be used for small ruminants, camelids, bison -Expensive, $15-25 per sample -Need precise technical skills
Histopathology for Johne’s disease	-Can only do on clinical cases -Rarely used to confirm cases -Will see “corrugated cardboard” intestine -Samples obtained during exploratory laparotomy or at necropsy --usually not done on alive animals! -Intestinal tissues and adjacent ileocecal lymph nodes -Need acid-fast staining with Ziehl-Neelsen stain -Sensitivity is poor in animals in stage I and II of infection
Single animal testing of Johne’s disease	-Done to determine an animal’s infective status before introduction into a new herd --challenging! Animals in stage I and II are basically impossible to detect! --should look at history of herd -test 30 animals from native herd, perform composite environment samples on native herd -Fecal RT-PCR positive indicates positive -Fecal culture positive indicates positive -Serology should always be followed by fecal culture or RT-PCR --ELISA or AGID -Histopathology of ileum/ileocecal lymph nodes
Herd diagnosis of Johne’s disease	-Individual ELISA on serum or mil as a screening tool --identified MAP within the herd --Confirm ELISA-positive cows with fecal culture -1 animal with positive culture indicates 3 infected animals within the herd -Bulk tank ELISA can be done --not as sensitive as individual samples if prevalence is low within the herd -Pooled fecal samples can be helpful --sensitivity depends on shedding level --possible false negative on infected animals that are not yet shedding -Composite environmental manure samples are great for herd infection detection --3-4 manure samples from high-traffic areas
Johne’s Passive Shedding Phenomenon	-“pass through shedding” -Positive fecal culture followed by several negative cultures from same cow -Result of passive excretion of MAP after consumption of contaminated feed materials -Can impact PCR testing, will not affect culture --PCR tests for genetic material, not actual organism -Can be more than 50% of positive cultures within a herd -Cultures are usually “low positive” -Need to focus on detection of super-shedders
Johne’s Super-Shedders	-Low shedders: 1-10 cfy/4 tubes, 5-50 cfu/g -Moderate shedders: 11-100 cfu/4 tubes, 55-550 cfu/g -Heavy shedders: more than 100 cfu/4 tubes, more than 550 cfu/g -Super shedders: more than 2,000 cfu/4 tubes, more than 10,000 cfu/g -Want to detect and cull super shedders
Johne’s vaccination	-Must be approved by the state veterinarian -Herd has to be infected -vaccinate calves less than 35 days old -Decreases shedding but does not get rid of the organism -Need special ear tattoo: JD VAC -Vaccinate SQ into brisket
Camelid restraint	-Needed! Just do it -Physical restraint -Chemical restraint --xylazine --butorphanol --tend to be more like ruminants than like horses
Lab value differences in camelids	-WBC: 8,000-21400/ul -RBCs are elliptical, small, non-nucleated -PCV of 27-45% is normal -Creatinine 1.4-3.2 mg/dL --should be closer to 1 -Higher than normal Na and Cl when compared to other species --Na: 148-158 --Cl: 102-120 -Glucose: 74-154 and often higher
Treating Camelids	-Challenge -Mostly a ruminant, oral medications are useless --unless a cria -More susceptible to aminoglycoside toxicity, avoid aminoglycoside or gentamycin
Congenital abnormalities in Camelids	-More common in camelids than in other animals -Cardiac: VSD, Complex defects -Ophthalmic: cataracts, Atresia of nasolacrimal duct at nasal puncta -Urogenital -Factor VIII deficiency clotting disorder -Musculoskeletal defects: angular limb deformity, umbilical hernia, polydactylism, vertebral malformation -Always look for a congenital defect!
Choanal atresia in Camelids	-Partition between nasal passage and nasopharynx does not regress/breakdown -Prevents air passage from nose to trachea -Evident at birth, will see open-mouthed breathing --cannot nurse -Surgical outcome is not that great -Genetic defect? Euthanasia is recommended
Diagnosing Choanal atresia in camelids	-Clinical signs: mouth breathing, not nursing -Try to pass feeding tube into nose -Infuse contrast media and take radiograph, look for contrast agent collecting in nasal passage -Euthanize animal!
Reproductive issues with camelids	-Adhesions --sequela to trauma --mucometra or pyometra if adhesion heals closed --can result in predisposition to infection -Sensitive to manipulation or trauma of reproductive tract -Uterine torsion -Treatment is difficult
Uterine torsion in Camelids	-Most common cause of dystocia in camelids -Usually clockwise --cria is usually in left horn -First option is to sedate and roll -Second option is celiotomy --usually also includes caesarian section -Present in late gestation or at term -Signs can be subtle -Use lots of lube! -Usually pre-cervical, vaginal exam is not helpful
Nerurologic diseases in Camelids	-p. tenuis -polioencephalomalacia -listeriosis
GI diseases in camelids	-Viral: coronavirus (most common), rotavirus -BVD: will be seropositive
Coronavirus in Camelids	-Most common viral cause of diarrhea -Causes outbreaks -Common in young animals -Crias and adults are affected -Treatment is supportive care
Bacterial diarrhea in Camelids	-Clostridium perfringens --C, D, A --vaccination is recommended -Salmonella (rare, does not cause severe disease) -Johnes disease --testing used in other species is not helpful in camelids --diagnostic challenge
BVD in camelids	-Bovine viral diarrhea virus -Lots of similarities in cattle -Acute infections can cause young animals to be sick -Can result in abortions, congenital anomalies, or persistently infected/silent shedder crias -No vaccine yet
Protozoal diseases causing diarrhea in camelids	-Coccidia --E. alpacae, E. lamae, E. punoensis --E. macusaniensis -Cryptosporidium -Giardia
Coccidia E. macusaniensis in Camelids	-VERY large --diagnostic tests for small coccidian cannot identify, needs more dense solution for fecal flotation -Often missed as a cause of illness -Very pathogenic in adults -Ponazuril has some efficacy
Nutritional muscular dystrophy in Camelids	-Selenium deficiency (white muscle disease) -Will see stiff, lame, recumbent camelids -Almost always taken care of in diet, not seen often -Will have increased CPK, AST, and decreased Se -Treat by giving selenium
Rickets in Camelids	-Vitamin D deficiency -Hypophosphatemic rickets -Occurs in nursing crias, growing animals --cria born in the fall, low colostrum levels, low levels of sunlight, higher elevations -Will be lame, stiff, ill thrift, angular limb deformities --metaphyseal flaring on radiographs -Treat by giving vitamin D --injectable form SQ --can be toxic, do not overdose!
Juvenile Llama Immunodeficiency Syndrome (JLIDS)	-Unknown etiology -Clinical signs: wasting, recurrent infections -Low IgG -Anemia due to mycoplasma haemolama -Diagnose with lymph node biopsy -Can do vaccine challenge -B-cell defect? -Has decreased in recent years, but is still present -No treatment
Lymphosarcoma in Camelids	-Most common neoplasm -Can occur at any age -Clinical signs: weight loss, lymphadenopathy
Mycoplasma haemolama	-Previously Eperythrozoonosis -RBC parasite -Fairly common -Black dots in RBCs -Found in healthy animals and sick animals --unknown role in causing sickness -Red flag for immunodeficiency -Tx: oxytetracycline --will clear parasitemia, but will not clear carrier state
Heat stress in camelids	-Camelids are not well-suited for heat --mountain animals -Often fatal! Very serious! -heat sets off a whole inflammatory cascade, cannot just cool to treat -Tx: lower body temp --clip hair --put in air conditioning --anti-inflammatories to counter effects of inflammatory cascade --supportive care (good bedding, physical therapy, swimming) -Prevention is key!
Clinical signs of heat stress in Camelids	-Elevated temperature (104-108) -Depression -Recumbency -Neurologic signs -Open mouth breathing -Scrotal edema, ventral edema -Edema -Needs to occur in hot season -Can be due to additional stress or exertion
Preventing heat stroke in Camelids	-Shear in summer -Give shade! -Plenty of water
Camelid metabolism	-Blood glucose is higher than ruminants --low concentration of circulating insulin --slow glucose clearance --partial insulin resistance -Susceptible to stress hyperglycemia -Cannot increase glucose clearance to match increased glucose mobilization during times of stress --leads to persistent or extreme hyperglycemia
Metabolic disease in Crias	-Stress causes hyperglycemia, leads to osmotic diuresis -Hyponatremia and dehydration -Neurologic disease and death -As soon as animal becomes glucosuric, be aware! Leads to downward spiral!
Metabolic disease in Adult camelids	-Anorexia leads to hepatic lipidosis and death -Hyperlipemia is common during stress events --causes fatty liver -Usually secondary to a primary problem
Neonatal disease in Camelids	-Usually have good success treating neonatal disease -Crias are a lot like foals, get all of the same problems -Failure of passive transfer has different numbers --need higher levels of IgG, should be more than 1,000 mg/dL -Treat with colostrum PO if less than 24 horus, plasma IV if more than 24 hours --can also give plasma intraperitoneally
Herd health in Camelids	-Vaccines --clostridium C+D --tetanus --rabies --WNV? -Deworming (P. tenuis specifically) --ivermectin SQ every 4 weeks --doramectin? -Nail trimming -Weigh -Check BCS -Castrate
Castration of Camelids	-Not done until 18-24 months old --If earlier, more prone to arthritis -Can do standing or under general anesthesia