Horses Flashcards

Question

Equine degenerative myelopathy (EDM)/equine motor neuron disease (EMND)

Answer 1

Classic case: Northeast U.S. Lack of access to fresh green forage EDM: (aka neuroaxonal dystrophy) Signalment: 6- to 12-month-old foals Familial in Appaloosa, Standardbred, and Paso Fino Possibly familial in Norwegian Fjord, Arabian, Quarter horse, Welsh pony, and Haflinger Signs: Insidious onset Slowly progressive ataxia Hypometria Weakness Poor thoracolaryngeal reflex ("slap test") Poor cutaneous trunci reflex EMND: Signalment: Adult onset (peak of 16 y) Quarter horses, Thoroughbreds, and similar Signs: Standing with all four limbs close together ("elephant on a ball" stance) Progressive weakness Increased recumbency NO ataxia Muscle and weight loss Trembling Low head carriage Unable to lock stifles Weight-shifting Hypometria Dx: Etiology: Both are likely a result of vitamin E deficiency Low serum vitamin E concentration: Not specific, but suggestive EDM: Diagnosis based on history, clinical signs, serum vitamin E, and response to therapy EMND: Sacrocaudalis dorsalis medialis muscle and spinal accessory nerve biopsies Electromyography (EMG) Necropsy Rx: Vitamin E supplementation Prevention: Adequate access to vitamin E-rich forage Pearls: Prognosis: Guarded; treatment helps, but not curative EDM: Strong evidence for a familial predisposing component EMND: Affected horses move better than they stand

Answer 2

Classic case: Usually adult horses Single horse or epizootic Acute onset ataxia or recumbency Urinary incontinence Ascending paralysis Stabilize after 24 h +/- Stupor or cranial neuropathies Other horses in herd: Distal limb edema in pregnant mares Scrotal edema in stallions Abortions Respiratory infections Fever Dx: Etiology: Equine herpesvirus 1 (EHV-1): Typically the D752 strain causes neurologic disease and N752 strain causes non-neurologic disease Strain-specific disease is not always clear cut and crossover does occur Diagnosis based on a combination of clinical suspicion and clinical testing (below) PCR (on nasopharyngeal swab, buffy coat) CSF from lumbar puncture: Xanthochromia (yellow-tinged) Elevated protein Usually no increase in cell count Fourfold rise in EHV-1 serum titer over 2 wks (not practical in acute cases) Rx: Glucocorticoids for up to 3 d Nursing care: Urinary bladder catheterization Safe environment Segregation and isolation of affected animals for 21-28 d after clinical signs and new cases stop Anti-virals (Valacyclovir) and heparin are used on a case-by-case basis Prevention: Vaccination may decrease respiratory signs and abortion but does NOT prevent infection nor prevent neurologic disease Isolate new arrivals for 2-3 wks Pearls: Prognosis: Good for horses that can walk well Guarded to poor for recumbent horses

Answer 3

Classic case: Signalment: Newborn up to 1 wk of age Thoroughbreds are over-represented +/- History of premature placental separation or dystocia Typical scenario: First: Normal newborn for mins to hrs Then: Loses interest in nursing, inability to suckle (dysphagia) Lethargic, stuporous, comatose Aimlessly wandering Central blindness Opisthotonus Seizures Hypotonia Abnormal vocalization (hence the nickname "barkers") Typically afebrile in cases without concurrent sepsis or meningitis Dx: Etiology: Thought to be due to unrecognized in utero or peripartum hypoxia, neuronal hypoxia, oxidative stress, or upregulation of the fetal inflammatory response Diagnosis based on exclusion of sepsis, premature birth, trauma, or meningitis CSF may be xanthochromic Rx: Anticonvulsants 24 h nursing care Antibiotics due to risk of sepsis and/or hospitalization Pearls: Prognosis: Up to 80% survivial and good quality of life if not septic Previously referred to as neonatal maladjustment syndrome Madigan squeeze: New technique that shows great promise! Affected foals are squeezed to mimic the birth canal transition. Check out this video, courtesy of Performance Equine Vets

Answer 4

Classic case: Head tilt (ipsilateral) exacerbated when blindfolded Nystagmus (fast phase opposite lesion) Ipsilateral ventral strabismus when head is raised Ataxia: Staggering Truncal swaying Leaning or falling toward side of lesion Drifting sideways during ambulation Examiner unable to predict where feet will land during ambulation Lifts only one foot at a time Hypometria Violent thrashing Rolling Wide base stance and gait Circling (toward affected side) If central disease (brainstem): Nystagmus may be in any direction, but vertical nystagmus is only seen with central disease Somnolence Weakness Hemiparesis (ipsilateral) If peripheral disease (anywhere the vestibular nerve passes from the skull to the inner ear): Typically horizontal nystagmus with fast phase away from lesion; may be rotary or angular, but never vertical Facial nerve paralysis may be concurrent in some cases of peripheral disease (otitis, guttural pouch disease, temporohyoid osteoarthropathy, trauma) due to close anatomic proximity of facial and vestibular nerves Bilateral disease will cause wide swaying movements of the head Dx: Multiple etiologies: Central: Head trauma EPM Migrating parasites Neoplasia Peripheral: Temporohyoid osteoarthropathy Suppurative otitis media/interna Guttural pouch disorders Idiopathic Skull radiography, CT, MRI Upper airway, guttural pouch endoscopy CSF analysis if central Culture and sensitivity of CSF or exudates +/- Brainstem auditory evoked response Rx: Treat infections aggressively with antibiotics or antifungals (at least 2-4 wks) Treat for head trauma if indicated (see Equine Neuro Part 1) Ceratohyoidectomy for temporohyoid osteoarthropathy Pearls: Prognosis: Depends on underlying cause Fair to good with otitis interna/media Chronic cases don't do as well May have residual head tilt Head trauma is guarded, depending on extent of injury The most common causes are temporohyoid osteoarthropathy and head trauma Paradoxical vestibular syndrome occurs in central lesions that involve specific areas of the cerebellum, resulting in a head tilt and circling away from side of lesion

Answer 5

Classic case: (aka cauda equina neuritis) Any breed or age (except young foals or aged horses) Urinary incontinence and fecal impaction Urine scald Tail head rubbing (see broken tail head hairs) Analgesia and areflexia of tail, anus, perineum, rectum, and penis (but not prepuce) Cranial neuropathies (head tilt, facial nerve paralysis, tongue paralysis) Impotence in stallions +/- Recent history of vaccination or respiratory illness Dx: Etiology: Likely autoimmune Can measure circulating antibodies to P2-myelin protein via ELISA (many false positives) Highly based on clinical suspicion - presence of cauda equina +/- cranial nerve involvement CSF: Xanthochromia Mononuclear pleocytosis Elevated protein May be normal in some cases Electromyography (EMG) Rx: Nursing care Frequent bowel and bladder evacuation Pearls: Prognosis: Poor for functional recovery

Answer 6

Classic case: Usually neonatal or weanling foals; sometimes adults Hyperesthesia (tactile and auditory) Stiff, extended neck Muscle tremors Somnolence Concurrent omphalitis, ophthalmitis in neonates Lack of suckling reflex in neonates +/- Fever If brain involvement (meningoencephalitis): Seizures Central blindness Wandering Head pressing Star gazing Abnormal vocalization Dx: Bacteria: Most commonly ... Actinobacillus equuli Rhodococcus equi Streptococcus equi equi CSF: Neutrophilic pleocytosis (acute): May not occur in neonates or foals if neutropenic from sepsis Monocytic pleocytosis (chronic) Increased protein Negative glucose (can use urine strip to test) Blood and CSF culture Rx: Antimicrobial therapy: Based on culture and sensitivity Treat for 2-6 wks Notes on the blood brain barrier (BBB): Meningitis compromises the BBB which allows penetration of most antibiotics early on However, should always try to start with antibiotics that penetrate the BBB as it will heal before treatment is complete NSAIDs +/- Plasma for neonates Pearls: Prognosis: Guarded to poor (25% survival in foals) Failure of passive transfer is a huge risk factor in neonates

Answer 7

Classic case: Sudden behavoir changes Agitation Aggression Progressive paralysis Rapid respirations +/- Rolling (often misinterpreted as colic) Dx: Etiology: Lyssavirus in family Rhabdoviridae Fresh brain tissue sent to a designated laboratory: Medulla oblongata Cerebellum Immunofluorescent microscopy diagnoses 98-100% of cases Viral isolation via mouse innoculation or tissue culture if immunofluorescent microscopy results are inconclusive Rx: No treatment, always fatal Prevention: Vaccination Pearls: Common reserviors/vectors are cats, dogs, skunks, raccoons, foxes, and bats Zoonotic risk with fatal outcomes

Answer 8

Classic case: Ataxia Uveitis Cranial nerve deficits Lethargy Poor tongue tone Tremors of the muzzle Spinal pain Inappetence, weight loss Blank staring Spooking Muscle atrophy Occasionally: Lameness Peripheral neuropathy Seizures Cardiac arrhythmias Dx: Etiology: Borrelia burgdorferi sensu stricto CSF-to-serum ratio using Lyme multiplex (detects 3 different antibodies) Serology: C6 ELISA antibody test is most often used Serology alone (positive or negative) is not diagnostic (may indicate infection or exposure) Prevention: Vaccination is controversial Rx: Doxycycline or minocycline Pearls: Prognosis: Poor, even with aggressive therapy Life cycle: Vector: Ixodes spp. ticks Tick host: Odocoileus virginianus (whitetail deer) B. burgdorferi reservoir hosts: Small mammals (esp. Peromyscus leucopus , the white-footed mouse), birds, reptiles Many horses in the mid-Atlantic region have been exposed and most do not show clinical signs

Answer 9

Classic case: Eastern equine (EEE) and Western equine encephalomyelitides (WEE): (5-14 d incubation) Fever, depression Altered mentation Hypersensitivity Visual impairment Head droop Dysphagia Ataxia Paresis or paralysis Seizures Lateral recumbency with paddling +/- pruritus Rapid progression, especially EEE Venezuelan equine encephalomyelitis (VEE) May be asymptomatic or mild Similar neurologic signs as EEE and WEE Tachycardia Diarrhea Colic Sudden death Dx: Etiology: Alphaviruses are arboviruses (ARthropod-BOrne viruses) in the Togaviridae family EEEV: Reservoir hosts: Primarily passerines (perching songbirds), +/- rodents Horses are dead-end hosts The Culiseta melanura mosquito is the vector WEEV: Reservoir hosts: Passerines +/- blacktail jackrabbits Horses are dead-end hosts The Culex tarsalis mosquito is the primary vector VEEV: Reservoir hosts: Wild rodents Horses are important amplifiers for epidemic VEE Many species of mosquitos can be vectors, but also blackflies, mites, and ticks Serology: IgM antibody-capture ELISA (EEE, WEE) 4-fold titer elevation in plaque reduction neutralization (PRN) or high titer in an unvaccinated horse Vaccination may complicate serology results Viral isolation: Can only be done during the early febrile stage for antemortem diagnosis Brain tissue (EEE) Pancreatic tissue (VEE) Immunohistochemistry or PCR (EEE) Lymphopenia (EEE) Azotemia from decreased water consumption is common CSF: Neutrophilic or mononuclear pleocytosis (EEE) Rx: Supportive care: Pain control Tranquilizers and/or anticonvulsants Fluids, nutritional support Sling and hoist Broad spectrum antibiotics for bacterial infections due to injuries or pneumonia Prevention: Vaccination Mosquito repellants (permethrins) Clear weeds, feces, and stagnant water from barns, paddocks, and pastures Pearls: Mortality: EEE: 50-90%; sudden death may occur; survivors usually have residual neurologic deficits WEE: 20-50% VEE: 50-75% REPORTABLE! VEE has not been reported in the U.S. since 1971 Human disease is uncommon, but usually occurs approximately 2 wks after equine cases reported

Answer 10

Classic case: Many horses are asymptomatic Mild fever and depression Asymmetric ataxia or paresis involving one or more limbs Cranial nerve deficits (facial (CN 7) or tongue (CN 12) paralysis) Behavioral changes Hyperesthesia Hyperexcitable responses to various stimuli Coarse head and neck tremors Head droop with secondary facial edema Sudden death may occur Dx: Etiology: An arbovirus, Flavivirus , in the Flaviviridae family Lineage 1a causes WNV in North America Vector: Typically Culex pipiens in east and midwest, and C. tarsalis in western U.S. (other arthropods are possible) Reservoir hosts: Predominantly passerines, but also shorebirds, raptors, and owls Serology: Elevated IgM antibodies (IgM-capture ELISA) 4-fold PRN IgG titer elevation Vaccination may complicate serology results (for IgG, but not IgM) RT-PCR can be useful Viral isolation: Best detected in thalamus, hypothalamus, rostral colliculus, pons, medulla, spinal cord Difficult due to low viral load and short viremic period Requires biosafety level 3 containment CSF: Normal to mononuclear pleocytosis with increased protein Lymphopenia Azotemia from decreased water consumption is common Rx: Supportive care: Pain control Flunixin meglumine can help with tremors and fasciculations Tranquilizers and/or anticonvulsants Fluids, nutritional support Sling and hoist Broad-spectrum antibiotics for bacterial infections due to injuries or pneumonia Prevention: Vaccination Mosquito repellants (permethrins) Clear weeds, feces, and stagnant water from barns, paddocks, and pastures Pearls: Mortality for symptomatic horses is 35-45% First identified in U.S. in 1999 Fatal illness occurs in corvids (crows, ravens, jays) ZOONOTIC (birds to humans) but horses and humans are dead-end hosts Reportable to state vet, then US reports it to World Health Organization

Answer 11

Classic case: Fumonisin: Apathy, drowsiness Pharyngeal paralysis Central blindness Circling Ataxia Lateral recumbency Icterus Death Hemlock: Poison hemlock: Weakness Ataxia Ptyalism Colic Bradycardia Irregular respirations and respiratory failure Death Water hemlock: Ptyalism Muscle twitching of lips, ears, and nose Dilated pupils Agitation Bruxism Seizures Coma Death in less than an hour Locoweed: Depression Emaciation Ataxia Infertility and abortion Circling Heart failure Yellow star thistle: Involuntary chewing Lip twitching Tongue flicking Submerging head into deep water Mouth held open (or tightly closed) Death from dehydration/starvation due to inability to eat Dx: Fumonisin: Etiology: Mycotoxin produced by Fusarium verticillioides and F. proliferatum growing on moldy corn/maize History of moldy corn in feed Necropsy: Unilateral or asymmetric malacia (liquefactive necrosis) of cerebral white matter (leukoencephalomalacia) +/- Hepatic necrosis Hemlock: Poison hemlock: Etiology: Alkaloids produced byConium maculatum Diagnosed by history and clinical signs Water hemlock: Etiology: Cicutoxin and cicutol produced by Cicuta spp. Diagnosed by history and clinical signs Locoweed: Etiology: Certain species of Astragalus or Oxytropis spp. produce swainsonine which inhibits Golgi alpha-mannosidase II Chronic ingestion causes excess build-up of glycoproteins which damage CNS neurons (metabolic storage disease) Diagnosed by history and clinical signs Yellow star thistle: Etiology: Toxin produced by Centaurea solstitialis inhibits brain's dopamine transporter system Diagnosed by history and clinical signs Necropsy: Malacia of substantia nigra and globus pallidus (nigropallidal encephalomalacia) Rx: Fumonisin: Supportive care No effective treatment Prevent by avoiding moldy corn Hemlock: Poison hemlock: Activated charcoal Saline cathartics Atropine Gastric lavage Stimulants Tannic acid Prevention: Herbicidal treatment of plants (2,4-D plus dicamba) Water hemlock: Sedatives Prevention: Herbicidal treatment of plants (2,4-D plus dicamba) or digging up and burning plants Locoweed: No treatment Prevention via various herbicides Yellow star thistle No treatment Euthanasia Prevention: Various herbicides Pearls: Fumonisin: Horses are very sensitive to this toxin and can develop signs after chronic ingestion of only 8-10 ppm Hemlock: Poison hemlock: The hemlock moth defoliates the plant and may help in its control Water hemlock: Herbicidal treatment appears to enhance the plant's palatability before it dies off Locoweed: There are more than 300 species of Astragalus and Oxytropis in the U.S., but only 20 or so are toxic locoweeds Yellow star thistle: This is only ingested when other forage unavailable

Answer 12

Classic case: Less than 5-d-old (and definitely less than 10 d) foal Acute Hemorrhagic diarrhea Colic Severe obtundation Hypovolemic/septic shock Often rapidly fatal Dx: Etiology: C. perfringens type C (less commonly, type A) C. difficile can also be found in intestine/feces of healthy foals and adults Fecal toxin analysis PCR for C. perfringens ELISA for C. perfringens and C. difficile Fecal culture +/- blood culture Abdominal ultrasound: see necrotizing enterocolitis - thickened bowel wall with gas in the wall Necropsy: intraluminal hemorrhage and mucosal necrosis of small intestine (+/- colon) Rx: Metronidazole PO or per rectum Supportive care (applies to all these foal diarrheas): Broad-spectrum antimicrobials to decrease risk of bacterial translocation and sepsis IV fluids with electrolyte replacement Correct failure of passive transfer, if present NSAIDs Anti-endotoxemics: polymyxin B, hyperimmune plasma Intestinal adsorbents: kaolin, pectin, bismuth subsalicylate, di-tri-octahedral (DTO) smectite (Biosponge®) Nutrition: enteral feeding or parenteral nutrition +/- Lactase administration PO Prevention: Improve farm hygiene Vaccine? Pearls: Prognosis is guarded Can occur in outbreaks or sporadically

Answer 13

Classic case: Usually foals less than 1 mo old Diarrhea Lethargy, poor nursing Sepsis Progresses to hypovolemic shock - cool limbs, thready pulses, recumbent Dx: Etiology: Most often Salmonella enterica CBC shows severe neutropenia Fecal PCR or culture Rx: See supportive care guidelines under clostridiosis Pearls: ZOONOTIC Salmonella can be present in healthy horses' feces Stress can increase fecal shedding

Answer 14

Classic case: Foals less than 2 mos old Depression, anorexia Profuse, watery, malodorous diarrhea More severe in younger foals Self-limiting, usually lasts 4-7 d Dx: Fecal immunoassay kit Fecal electron microscopy Rx: See supportive care guidelines under clostridiosis Pearls: Rotavirus more common than coronavirus Rotavirus destroys enterocytes at tips of small intestinal villi, leading to malabsorption Often secondary lactase deficiency Use rotavirus vaccine in pregnant mares Highly contagious

Answer 15

Classic case: 4-6-mo-old foal Poor doer, failure to thrive, weight loss Diarrhea Pot-belly Colic Ventral abdominal subcutaneous edema Dx: Usually do both: Fecal PCR Serology - IFAT (can be hard to differentiate exposure from disease with 1-time sample) Abdominal ultrasound: thickened small intestine Bloodwork: marked hypoproteinemia Necropsy: silver stain shows characteristic intracellular bacteria in small intestinal tissue Rx: Antimicrobials: tetracyclines, erythromycin, or chloramphenicol Plasma transfusion if severely hypoproteinemic Pearls: L. intracellularis is an intracellular bacteria Does not grow in culture without permissive cell lines Lipophilic or amphoteric antimicrobials required Excellent prognosis with recovery Takes 4-8 wks for full recovery Causes a protein-losing enteropathy

Answer 16

Classic case: 4-10-d-old foal Mild diarrhea, NOT malodorous No other clinical signs Dx: Usually none Rule out other causes if necessary Rx: Usually none Apply protectant (e.g. zinc oxide or vasoline) around perineum, on hind limbs Pearls: Not actually related to mare's heat cycle because also seen in orphan foals Most likely due to changes in foal's GI flora - as foals start eating grain and hay in addition to milk, and as they perform coprophagy to inoculate their GI tracts Often concerning to owners

Horses Flashcards

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