MSK Final Review PDF

Module E1: Muscular system disorders of ruminants Clostridium spp. Gram + bacteria Infection occurs through: - Clostridium botulinum - ingestion - Clostridium perfringens - ^ toxins produced by GIT - Clostridium chauvoei/septicum/tetani - Wound Diagnosis: If alive, muscle enzyme (CK...

Module E1: Muscular system disorders of ruminants Clostridium spp. Gram + bacteria Infection occurs through: - Clostridium botulinum - ingestion - Clostridium perfringens - ^ toxins produced by GIT - Clostridium chauvoei/septicum/tetani - Wound Diagnosis: If alive, muscle enzyme (CK and AST test), impression smear Treatment - ABs, surgery Vaccine available Clostridium Chauvoei Blackleg Effects: upper leg, diaphragm, tongue, heart, neck and jaw No penetrating trauma CS: Initial hot, tight and painful muscles -> muscles are painless and cold emphysema in skin - (bubble wrap) Infected muscles are dark and dry * if localized post mortem - always significant * Clostridium septicum / novyi Malignant edema Effects: any muscle Penetrating trauma present CS: Soft doughy muscles (edema) Infected muscles are red and wet Selenium and Vitamin E deficiencies White muscle disease or nutritional muscular dystrophy Selenium - reduces free radical formation (created during cell metabolism > converts to water) Vitamin E - lipid soluble, antioxidant, bings/reduces effects of free radicals Primary cause - diet insufficiency CS: Cardiac form - acute onset, frothy or bloody discharge from pulmonary congestion, normal temp, ^ or normal HR, dyspnea Skeletal muscle form - more common, lie down and try to stand, BAR, stiffness/trembling, stiff shoulder/back/hip muscles, normal temp, myoglobinuria Smooth muscle form - Dystocia, ^ retained placentas, chronic bloats, LDA (left displaced abomasum) DIagnosis: Bloodwork - ^ CK and AST = muscle damage, ^ creatinine myoglobinuria Subclinical - test milk or blood for selenium Post mortem - liver analyzes, light muscles Treatment: Parental selenium and or Vit. E Module E2: Muscular system disorders of horses Tendon damage Soft tissue lameness Thoroughpin: swelling above caudal aspect of hock Bog Spavin: swelling in hock - no associated with lameness Wind puffs: fluid in palmar/plantar aspect of fetlock joint Bowed Tendon: strain of SDFT or DDFT Curb: inflammation/thickening of plantar tarsal ligament of the hock Tendonitis: involves tendon but not sheath Tenosynovitis: inflammation of tendon and sheath Tendon rupture: fibers rupture Cause: trauma/injury - footing, overgrown hooves, improper wraps, fatigue SDFT - mid cannon bone of front limbs DDFT- fetlock Accessory check ligament bows - show up in upper third Clinical signs: Lameness, swelling, heat Diagnosis: ultrasound - look for dark areas Treatment: Rest, cold therapy, bandage, NSAIDs, DMSO (dimethylsulfoxide) Sole Bruises Hematoma between sole and P3 due to damages blood vessel in lamina Caused by: hard/rocky footing, improper shoeing/trimming, genetics/confirmation Bruising at xs = corns^ Clinical signs: Lameness, bruising, infection Diagnosis: Hoof testers Treatment: anti-inflammatories, shoe pad Exertional Rhabdomyolysis Tying up, azoturia, monday morning disease Sporadic: (SER) Over-exercise, dietary, inadequate warm up Clinical signs: Muscle cramping, stiff after exercise Diagnosis: Clinical signs and no history, chem = ^CK and AST Treatment: Acepromazine, IV fluids, rest Chronic form: (CER) - Recurrent: Abnormal intracellular Ca regulation due to stress = disrupted muscle contractions Breeds most at risk: Thoroughbreds, standardbreds and arabians - < fit horses fed < carbs Clinical signs: Cramping, stiff pst exercise Diagnosis: Muscle biopsy with clinical signs, history present, chem = ^CK and AST - Polysaccharide Storage Myopathy (PSSM): Type 1 and 2 Type 1 - excess storage of carbs in muscles Common breeds: QH, morgan, drafts Diagnosis: genetic testing of hair or blood Clinical signs: stiff, sweating, tucked up, abnormal gait, colic Type 2 - Clinical signs: young - stiff, difficulty rising, ^ CK levels Muscle atrophy Diagnosis: muscle biopsy for abnormal glycogen storage Treatment: High fat, low starch diet - grass or hay, less sweet feeds Hyperthermia Cause: thermoregulatory process fails to remove excess heat from the body Clinical signs: produce sweating, ^ body temp. (41 C), ^ HR, RR, CRT, skin tent, colic Diagnostic: ^ PCV/TP, dec. K/Na Module F1: Nervous System Disorders of Large Animals Tetanus Clostridium tetani Clinical signs: Muscular rigidity and spasms, prolapse of third eyelid, hyperesthesia, puncture wound Diagnosis: culture and gram stain smear from sight Treatment: antitoxin, abs Prevention: vaccination Neonatal Encephalitis Inflammation of brain Cause: Virus - Bovine Herpes Virus (IBR) Bacterial - E. coli Clinical signs: Salivation, inflammation of nasal and oral mucosa, resp. Distress, opisthotonus (star gazing), Diagnosis: CSF - ^WBCs, protein Prevention: vaccinate cows Histophilus Somni Histophilosis Cause: bacteria, septicemia -> vasculitis Clinical Signs: Pre acute - found dead Acute - neurological involvement, pneumonia/pleural involvement, myocardial necrosis, synovial involvement and laryngitis ITEME form - apparent blindness, depressed Diagnosis: microscopic eval of CSF - neutrophils, bacterial culture Prevention - vaccine Listeriosis Listeria monocytogenes Zoonotic!! Cause: bacteria enters through oral mucosal abrasions and travels up cranial nerves to the brain Clinical signs: encephalitis - unilateral s=brain stem infection, unilateral facial hypoplasia, facial nerve paralysis, ataxia/circling, head tilt, abortion, septicemia, ophthalmitis Diagnosis: CSF - not definitive, PM histology Treatment: broad spectrum abs Prevention: no vaccine Transmissible Spongiform Encephalopathies (TSE) Mad cow BSE - cattle Scrapie - sheep Chronic wasting disease - cervids Normal isoform prion protein - PrPc Abnormal isoform protein - PrPsc PrPsc binds to PrPc causing it to resemble a PrPsc -> chain reaction in CNS Source of PrPsc: Genetic mutation Iatrogenic Ingestion - PrPsc -> gut lymphoid tissue -> replicate -> nerves -> brain All TSEs cause spongiform changes to the brain (holes) Bovine Spongiform Encephalopathy BSE Clinical signs - long incubation period, weight loss, neurological signs, behavior changes Diagnosis: only in CFIA lab - ELISA test on obex of brain stem Specific risk materials: must be removed from beef before used for human construction Include - skull, brain, trigeminal ganglia in brain, eyes, tonsils, spinal cord, dorsal root of ganglia in cattle > 30 months Scrapie Clinical signs: rubbing/biting at wool, weeks in between episodes - behavioral, incoordination, tremors Diagnosis: done pm - find PrPsc in brain, lymph, or spleen or biopsies from live animals - rectal or third eyelid lymphoid tissue Polioencephalomalacia Cause: sporadic in feedlot aged cattle, causes softening of grey matter in the brain -> thiamine deficiency Lead poisoning - public health concern Nitrate/sulfate poisoning Salt poisoning Clinical signs: Thiamine deficiency - sudden blindness, tremors/convulsions, hyperesthesia Lead poisoning - plants, batteries, petroleum = ataxia, blindness, hyperesthesia Nitrate/sulfate poisoning - binds to O2 = cant carry O2 Salt poisoning - tremors, blindness, head tilt, circling, convulsions Diagnosis - only for lead toxicity - heparinized blood sample Module F2: Nervous System Disorders of Horses Equine encephalomyelitis Sleeping sickness Cause: virus spread by mosquitoes = inflammation of the brain Birds are reservoir host Strains: Eastern and Western (E more severe) Zoonotic!! Clinical Signs: lethargy, fever, circling/head pressing, blindness, seizures, and permanent CNS damage Diagnosis: CBC - lymphopenia and neutropenia CSF tap - ^ total protein and WBCs Prevention: vaccine at start of mosquito season West nile virus Cause: virus spread by mosquitoes Birds are main host - crows, ravens, jays and magpies Affects the brain and spinal cord Zoonotic!! Clinical signs: may be asymptomatic, ataxia/head tilt, hypermetria, seizures, fever, bahavior changes Humans - 3-15 day incubation, may be asymptomatic, flu like symptoms Diagnosis: antibody testing to confirm exposure Prevention: vaccine Module G1: Infectious Disorders of Eyes of Large Animals Squamous Cell Carcinoma of the Eye Cancer eye Cause: Uv exposure, light pigmented animals Causes neoplasm of the eyelids, nictitating membrane and cornea Stages: Epithelial dysplasia -> carcinoma in situ -> squamous cell carcinoma Clinical signs: lesion in cornea Treatment: surgery, cryotherapy + radiation, immunotherapy, enucleation, cull Infectious bovine keratitis Pinkeye Cause: Moraxella bovis bacteria - fomites ex. dust, flies, long grass spread Clinical signs: infection, edema of conjunctiva, epiphora, blepharospasm Advanced - opacity of cornea/ulceration, purulent discharge Treatment: subconjunctival injections, eye patch, Abs Prevention: vaccine, fly tags Entropion Cause: eyelid rolls inward - cilia rubs on cornea Inherited condition of lambs -> causes ulceration of cornea Clinical signs: epiphora, corneal edema, blepharospasm Treatment: may self-correct, evert eyelid with sutures, inject penicillin Equine recurrent uveitis Moon blindness Cause: bacteria, parasites, and trauma Common in: appaloosas, paints, drafts,and warmbloods Effects: uvea - iris, ciliary body and choroid Clinical signs: stages 1 - Active: corneal edema, photophobia, blepharospasm, epiphora etc 2- Quiescent: hyperpigmentation, lens luxations, cataracts 3 - End stage: eventual blindness Diagnosis: fluorescein dye, tonometry, CBC/chem, test for leptospirosis Treatment: NSAIDS, steroids, atropine, ABs Ophthalmic Procedures: Fluorescein Dye: does not adhere to healthy surfaces - shows orange -> green/yellow if attaches to corneal stroma Method 1: place strip directly on cornea Method 2: 2-3 mL of saline + strip in syringe Ophthalmic solution application: Subpalpebral lavage (SPL): tube placed through eyelid and is attached to mane- do not aspirate Subconjunctival/Palpebral injection: treat pink eye, 4 point nerve block: Peterson eye block: