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completely dropped hock

-SDF and gastric tendons both ruptured. prognosis grave but horses will still bear weight

Liver damage vs. failure

damage: recover/regenerate as long as blood supply is in tact when lots of fibrosis--> cant regenerate damage: can be focal or diffuse. failure: can be diffuse or multifocal acute vs. chronic: 1. acute: look worse clinically but better prognosis (fever, anorectic, weight loss) chronic: irreversible when results in fibrosis and loss of blood supply **want biopsy to figure out if acute or chronic before spend time/effort on animal if cant recover

dog fetal skeletons visible

days 41-50 of gestation

horse twins

abortion at about 6 mo best thing to do is to check at 13-15 days gestation and manually crush one embryo to give other best chance at survival -or transcutaneous or transvaginal US guided twin reguction crushing has 90% success rat: other likee 20-50%

ketones

acetoacetic acid B-hydroxybutyric acid acetone

postparturient hemoglobinuria

because of hypophosphatemia decreased RBC ATP which isnt compatible with maintenance of ATP-dependent membrane pumps, and cells lyse!

Cow brucellosis

effective management: - ID infected, isolate and slaughter

Heinz body anemia in horses

phenothiazine red maple leaf methylene blue acetylphenyl hydrazine low Molybddeenum diet rye grass dieet brassica plants onions

Type I Photosensitivity

photodynamic compounds accumulate under skin right after ingestion ex: bisserula, clover, buckwheat, st. John's wort, phenothiazine (a drug)--> pheothiazine sulfoxide

lactate

metabolized by liver kidneys and skeletal m. metabolize it to a lesser extent should be under 2.5 mmol/L associated with anaerobic metabolism; predicts prognosis in GDV dogs and colic/sepsis in horse

what is an advantage to having bulls with larger testicles?

their female offspring reach sexual maturity at an earlier age

most effective way to synchronize lactating pigs

batch wean at 3-4 weeks this results in estrus 4-6 days later as long as a pig is lactating, it wont ovulate so need to stop lactation

phenothiazine

can cause Heinz Body anemia in horses

Breed of dog with chondroidal hypoplasia, large choroidal vessels, varying degrees of visual dysfunction

chondroidial hypoplasia: abnormality in the pigmentation or development of the choroid. Collies have this (aka Collie Eye Anomaly) and other dogs can get it too. other signs: 1. optic disc coloboma (little white/yellow shiny oval in retina around optic n/vessels) 2. retinal hemorrhage

Type III Photosensitivity

"hepatic photosensitivity" most common type - PS substance is phylloerytherin (derivative of chlorophyll maded by boddy) - normally excreeted in bile: then in feces. damage to biliary system prevents excretion--> to circulatory system hepatic parasites exacerbate this condition!!

P pulmonale (EKG)

- P wave is tall and slender and peaked (over 0.4 mV) - hx of chronic pulmonary disease represents R atrial enlargement

Migrating Foxtail

-Midwest -draining rectal tract not improved with abx course -uncomfortable upon palpation but still active/good appetite -ddx: anal gland impaction: resolves with abx therapy. AGASACA: not draining tracts usually. Perineal hernia: obvious on visual inspection, may improve with abx if infectious component.

Bismuth subsalicylate (Pepto-Bismol)

-can cause melena -forms bismuth sulfide in colon which is v dark

long term sling use

-muscle contracture -joint fibrosis -disuse m. atrophy

eimeria in dogs and cats

-not pathogenic in these spp dont need to tx passes thru after they eat poop 4 sporocysts or a ddistinct micropyle cap parasitic in birds, reptiles, and herbivores isospora is the coccidian thats parasitic in SA: tx with Alban (sulfamethoxine)

Lab Tests for Liver dmg

1. Liver enzymes in serum (increases): SDH, GGT, AST, LDH, ALP, OCT (ALP and GGT from bile ducts-- bile duct prolif: more of a chonic failure rather than the other hepatocellular enzymes, which are more active/acute dmg) 2. Fibrinogen (decreases): positive APP 3. Bilirubin (increases): conjugated and unconjugated. Also bilirubinuria with liver dmg. 4. Albumin (decreases in serum) 5. BUN (decreases in serum) 6. Ammonia (increases in blood) 7. Glucose (decreases in blood) 8. abnx clotting teests: factors made or stored in liver 9. dye excretion tests (IV BSP)--> BSP half time is prolonged, liver not nx fxn 10. fecal sedimentation (r/o flukes) 11. U/s (fibrosis, abscesses) 12. biopsy (percutaneously on R side)

Liver functions:

1. Metabolic (gluconeogenesis, urea cycle enzymes (where ammonia--> urea)) 2. Synthetic (fibrinogen, albumin, clotting factors) 3. Excretory (bilirubin, phylloerythrin) **excess capacity: can live with less than half of your liver

Liver Damage: causes

1. Rumenitis 2. Enteritis/enteropathy - material in Rumenitis and enteric dz: from portal circulation cleared from liver 3. Sepsis 4. Flukes 5. Abscesses (often from rumenitis) 6. Fatty liver (lactating or starving animals)

Top 9 Equine Respiratory Diseases

1. Streptococcus equi ssp. equi (Strangles) 2. EHV 9herpes) 1 and 4, Equine Rhinopneumonitis 3. Equine Influenza A 4. Exercise Inducted Pulmonary Hemorrhage (EIPH) (Bleeders) 5. RAO (Heaves) 6. Sinusitis 7. Laryngeal Hemiparesis, Recurent Laryngeal Nerve Paralysis (Roarer) 8. Rhodococcus Equi 9./ Pleuropneumonia (Shipping Fever) 10. Mimics: a. Gastro-esophageal Obstruction (Choke)

Addison's clinical signs

1. acute onset weakness/depression 2. bradycardia -wide, flat or absent p waves, wideQRS complexes or tall, spiked t waves (hyperkalemia) 3. hypovolemic shock 4. Lyte abnx: high K, low Na, low blood sugar hx of wax/wane GI signs **r/o whipworms (fecal float): can cause symptoms similar to addisons. (Seather's sugar sltn): Avermectin wont kill whipworms: milbemycin will. perenal azotemia hypercalcemia low blood glucose is possible abesence of stress leukogram and eosinophilia sodium:k ratio is 19.5 and addedsinians have ratios less than 23 negative radsd/fecal floats dx: acth stim test

Porcine Respiratory Dz

1. atrophic rhinitis 2. Influenza A 3. Mycoplasma pneumonia 4. Actinobacillus pleuropneuumoniae 5. Pasteurella 6. Verminous pneumonia (Ascaris suum) 7. PCVAD 8. Salmonella

Canine cornea histopath

1. corneal epithelium -most superficial -5-10 cells thick 2. corneal stroma -90% of corneal thickness -mostly collagen, followed by GAGs and some keratocytes 3. decemet's membrane -BM 4. corneal endothelium -innermost layer

Treatment of Liver Dz

1. remove toxic substance 2. keep animal from sublight to prevent photosens. 3. correct diet if fatty liver 4. abscesses: antimicrobials 5. vitamin B and K 6. Maintain blood glucose 7. control protein to prevent ammonia elevation

phenoxybenzamine

A non-speccific alpha agonist in pheochromocytoma given 2-3 weeks before adrrenalectomy until have nx BP to reduce risk of anesthetic cimplications if tachycadic may also use a beta blocker to avoid exacerbating the hypertension that could pccur due to unopposed stim of alpha adreneergic RR's

Ventroflexion

A sign of m. weakness most common cause: low K other causes: - myasthenia gravis -polymyopathies (toxoplasma, IM disease, hyperadrenocorticism) - neuropathies (organophosphate poisoning, thiamine deficiency, botulism) -aldosterone-secreting adrenal tumor (K deficiency) -aggressive furosemide tx (K deficiency) -thiamine deficiency (also ataxia, dilated pupils, obtundation, etc.)

Exercise Induced Pulmonary Hemorrhage (EIPH)

Aka Bleeders - signalment: athletic horses in HIGH SPEED EVENTS (racehorses, barrel racers) -or horses with previous lung damage or chronic infections MOA: we think d/t high capillary pressure from high cardiac output: cause wall failure and hemorrhage into airspace or trauma or increased blood viscosity and decreased RBC deformity=hemorrhaging of airways CS: - nearly all cases are SUBCLINICAL with no external signs - epistaxis during/right after athletic event (dont always see it) - swallowing a lot after athletic event -poor performance/slow recovery dx: -airway endoscopy (to IDD hemorrhage, should do this within 2 hours of event) -cytology of airway (BAL) within a few days of event (see RBC's/ hemosiderophages) tx: - furosemide (Lasix): diuretic a few hours before event to decrease interstitial pressure and hemorrhage. - abx to prevent secondary risk of penumonia prognosis: excellent for survival, will probably have repeat bleeding events in future

cTLI

Canine trypsinogen-like immunoreactivity test to look for EPI EPI: wt loss, hx of diarrhea, german shepherds predisposed. usually no lyte imbalances with EPI. Usually not acute presentation

EBA (Epizootic Bovine Abortion)

Caused by a delta proteobacterium in (discovered in 2005) by a tick (Ornithodoros coriaceus) causes abortion 3-4 mo after exposure **KEEP PREGNANT HEIFERS OUT OF THE FOOTHILLS UNTIL THEY ARE 6 MO PREGNANT** (calf before fatal lesion appear for fetus) Raise heifers in the foothills until breeding: can provide premonition immunity If a heifer aborts, it's then immune to EBA so the rancher should keep them. these ticks only like dry brush and wont live on irrigated pastures so keep the heifers 1-6 mo pregnant on irrigated pastures fetus (aborted): -enlarged LNs -enlarged spleen - chronic granulomatous infection no vaccine, a live bacT vax is in the works - may consider control of tick vector or prophylactic abx use

Gastro-Esophageal Obstruction

Choke May present as nasal discharge or coughing and can cause aspiration pneumonia if not treated quickly signalment: older horses w poor dental care, horses that eat rapidly, horses fed a lot of dry grain or pellets MOA: food bolus not properly chewed--. lodged in esophagus CS: - copious bilateral nasal dschg (usually green tinged at first): as obstruction continues, will be saliva only and interpreted as resp. nasal dschg -cough, gag, retch, ptyalism -colicky, anxious -anorectic -aspiration penumonia if not resolve within 6-12 hrs dx: clin signs, cant pass NG tube into stomach tx: gentle lavage with water via NG tube, lubricating agents are contraindicated (bc aspiration!!) sedation: lowers head, reduces risk of aspiration, allows NG passage esoph. relaxants: oxytocin, buscopan -abx, antiinflammatories prog: good if tx early, fair to guarded if has asp. pneumonia

most common cat anal sac infection

E. colis

Rabies

Dog cS: 1. furious stage (photophobia, hyperesthesia, excitable, irritable): can last 1-7 days in dogs. - pharyngeal and laryngeal m. spasms, dysphagia, drooling, hydrophobia seizing, coma, die later prodromal stage: dumb/paralytic stage ddx: -RMSF (no neuro signs) -Lepto (no neuro signs) distemper: a diff, but ddx rabies first to bee safe.

most common dog UTI bacteria

E. coli

what ascending infection causes repro failure in pigs?

E. coli Streptococci Staph Actinomyces Pseudomonas

systemic repro infections in pigs

Eperythrozoon suis leptospirosis interrogans parvovirus toxoplasma PRRS pseudorabies brucellosis

EHV 1 and 4

Equine Rhinopneuminitis?? at risk: horses that show or travel, especially young horses MOA: 1 and 4 are endemic in equine population - latent in individuals until stressed-- then can spread -vasculitis in CNS and associated clinical signs -neeuro signs usually acute EHV-1 can mutate to a wildtype that causes neuro signs (equine herpes myeloencephalopathy) -EHV1 CS: (worse in <5 yo horses) - fever, lethargy, anorexia, cough, mucopurulent nasal dschg, rarely secondary pneumonia -dog sitting, hindlimb ataxia, dribbling urine (multiple horses at the facility will show these signs), hypotonia of tail/anus (ddx: EPM: less likely to affect more than one horse on a farm and herpes will) - vaccinated/partially vax horses can still get it with less severe signs, source of subclinical spread - abortions in pregnant mares (rarely by EHV1 that infects fetal tissues): occur months after initial infection dx: PCR of nasal dschg tx: antiinflammatories, supportive care, antiviral drugs, sometimes abx with secondary infections prog: excellent (rarely secondary complications) prev: isolate new horses, vaccinate with mod live intranasal vax or killed IM vax. Biannual vaccine in high risk or mares in late preg to prevent abortion

Rivalata's Test

Highest negative predictive value for ruling out FIP - good to rule out FIP as best you can NPV over 90% false positives: usually in older cats or cats with lymphoma/bacT infections this test involved: 1. filling a reagent tube with distilled water--> dropping 98% acetic acid--> drop one drop of effusion 1. if drop disappears and solution is clear, Rivalata test is negative 2. if drop retains shape, stays attached to surface, or floats slowly to bottom, it's positive other tests have high PPV's but more false negatives: rtPCR: for coronaviral RNA in serum (PPV=90, NPV 47) 2. coronavirus AB detection in effusion: PPV=90, NPV 79 3. immunofluorescence for coronavirus in macrophages in effusion fluid: PPV=100, NPV=57 also: bloodwork will show an albumin/globulin rartioo below 0.8 becaus ehave totall protein high bc of globulins but low albumin but it has a low PPV-- so instead, do immunofluorescence staining for corona in macrophages in effusion fluid (highest PPV)

Type IV Photosensitivity

Idiopathic! After ingestion of some plants: like alfalfa

Swine Influenza

Influenza A Can go to humans: ZOONOTIC Pigs: High Morbidity, low mortality (100% morbidity in short time period) respiratory outbreaks in most pigs in a herd CS: high fever (over 105 F) prostration, cough, anorexia, conjunctivitis, clear oculonasal dschg -no loose stool disease associated with movement or extreme weather changes recover takes 1-2 weeks concurrent infections/poor husbandry can exacerbate this dz and cause higher mortality rates dx: necropsy (patchy cranioventral pneumonia) - fluorescent AB test - PCR (nasal swab or fluids) (**PCR is the primary means for diagnosis these days but dont always do it) tx: supportive care Prev: -vax?? (have to match strain properly tho) -closed herd -ctrl secondary infections -keep away from humans (no shows)

P mirale

L atrial enlargement - increased duration of p wave lasts 0.05 seconds

Type II Photosensitivity

Lack of enzymes needed to break down PS compound--> eliminated by urine/body fluids or accumulate in tissues (bone or teeth) ex: congenital porphyria (d/t accumulation of uroporphyrin)=pink colored bon and teeth or pink pee under UV light

Equine Sinusitis

MOA: - almost always secondary to a dental problem (teeth most commonly affected are 08-11, usually 09) CS: - chronic, unilateral mucopurulent nasal dschg (foul-smelling) - may respond to abx but return when abx are over - afebrile and BAR dx: - culture/PCR of dschg to r/o other pathogens -nasal endoscopy to ID neoplasia, masses, etc. - dental/head rads/CT to look for dental involvement especially tx: - extract afected tooth -repeat sinus lavage for up to one week (can use a bone flap to allow better lavage) - culture with appropriate abx, may need extended abx duration prog: good but tx may be intensive

photosensitization

PS: causes redness/rashes, edema of head and eyes, sloughing of skin/hide: usually affects light areas but not dark areas etc.

Atrophic Rhinitis

Pigs resp dz caused by two different organims: 1. Bordatella bronchiseptica 2. Pasteurella multocida type D (PM type A causes penumonia) can also be caused by chronic irritation d/t high Ammonia levels CS: 1. sneezing, sniffing, twisted snouts, excessive lacrimation (bc lacrimal duct is plugged bc of inflamm. or snout twisting), epistaxis (d/t dmg and erosion) Dx: 1. cut snout at second premolar and do a nasal culture for either organism - usually need both organisms to cause dz - deviation of septum, etc. Tx: tetracyclines in the feed - long-acting tetracycline injection in neonates Ctrl/prevention: all in-all out, reduce stress, clean air - vax pre-farrowing, also weanlings - vax should contain a Pasteruella toxoid (bc toxoid causes the lesions) **don't have this a lot today in production systems

Senecio spp.

Pyrrollizidine alkaloids can be in alfalfa hay: yellow flowers turn to white puggs in hay

Heaves (RAO)

Recurrent airway obstruction (used to be known as COPD) disease of mature horses (over 6-10 yo) direct cause debatable pathogenesis: inflammation of the lower airways, causing bronchospasm, excess mucus, and airway remodeling--leads to partially obstructed airways-->neutrophilic inflammation to airways/bronchospasm of the airways with exposure to dust, molds, vegetative materials, noxious gases, etc. progressive onset, thought to be related to hypersensitivity/environmental factors CS: - afebrile -tachypnea, dyspnea, respiratory noise, flared nostrils, dry cough (intermittent to severe), wheezing during respiration, especially end exhalation. - Heave line: chronically affected horses have hypertrophied external abdominal oblique m. from chronic m effort to exhale -afebrile, BAR -can be asymptomatic btwn flare-ups most commonly seen in winter in stabled horses in warm, dry climates (dusty, dirty, poor ventilation): theye allergic to hay allergens basically dx: clinical signs, cytology of bronchoalveolar lavage (increased neutrophils for definitive dx) (Cushmann's spirals may be seen: mucus plugs from lower airways) normal hose BAL shows majority of macrophages! tx: **not cured: managed** environmental modifications (reduce dust, turn to pasture, need good ventilation) - corticosteroids (Dex, pred) - bronchodilators (albuterol, ventipulmin) (inhaled or oral) - antihistamines (effectiveness unknown) - allergen testing, desensitization prog: mgmt and tx to decrease and control dz flares, but it's chronic and rarely "cured"

Citrobacter freundii

SCUD (septicemic cutaneous ulcerative disease) in turtles most commonly caused by this organism CS: -pitted scutes that slough -underlying purulent exudate -petechiae on skin -liver necrosis prev: -good husbandry tx: -chloramphenicol

Pyrrolizidine Alkaloids

Toxins in several plant species: 1. sencio (jacobaea, vulgaris, longilobus) 2. Amsinckia intermedia, 3. Crotalaria sp. 4. others Cause antimitotic effect: so get huge as they age and aren't replaced. and then fibrotic once die. so long, slow chronic effect histo in liver: - megalocytosis, fibrosis, bile duct hyperplasia spp susceptibility: 1. chicken needs 5% BW 2. horse needs 5-20% BW 3. Cattle needs 15-20% bw 4. Sheep and goats need 150-400% BW

best lab test to characterize azotemia and pre, renal or post

USG to see if kidneys can concentrate urine if normal or high, they are functioning (so its pre or post) if ddilute, kidneeys arent working: likely renal

pheochromocytoma

a benign tumor of the adrenal medulla that causes the gland to produce excess epinephrine some may be non functional of chromaffin cells many are made post-mortem: rare tumor! CS: -may be a result of a space occupation or catecholamine release -hyperteension -tachyarrhythmias -weakness -collapse -anorexia/vomiting -cough -dyspnea -PU/PD -diarrhea -weight loss -hindlimb edema, abdominal distension, epistaxis, blindness (hypertension), restlessness/anxiety, pacing, ataxia, seizures/tremors/shaking, cyanosis, adipsia dx: -PE, BP, BW, ECG, US (65-83% f the time can ID: small tho) -CT, rads may shw it (mass in like 30-60% of cases) tx: -goal: prevent/control hypertension and arrhythmias -normalize BP with an alpha agonist over a 2-3 week period (phenoxybenzaminee: alpha-1 antagonist): start low, gradually increase until you reach normotensin. also prrazosin -can use beta blockers but also use with an alpha blocker -dont premed with atropine!! sx: -IV meds to control issues with pressures: -phentolamine -sodium nitroprusside -propanalol or esmolol for arrhythmias -20-40% of the time it can invade into vena cava: not a prog indicator tho if good surgeon. may be more aggressive tho -hypotension is biggest concern prog: -50% malignant but 18 mo-2 yr survival time -22% perioperative mortality rate

hepatoencephalopathy

less dramatic in cattle than horses -

Laryngeal Hemiparesis: Recurrent Laryngeal Nerve Paralysis

aka Roarer horse resp dz signalment: thoroughbreds, warmbloods, large athletic breeds MOA: idiopathic neuropathy of LEFT recurrent laryngeal n.: causes L arytenoid a\cartilage to either partially or completely fail to abduct--> obstruction -L side is the longest equine nerve so the left is usually affected one CS: -upper resp noise with inspiration during exercise exercise intolerance/poor performance dx: enddoscopy (esp if not seadted and exercising) tx: laryngoplasty (tie back) - chronic cough, potential pneumonia risk/ prog: good. mild cases unlikely to affect performance in low-intensity events.

Strep equi ssp. equi

aka Strangles (an equine resp dz) - shed in resp secretions of infected horses: can be inhaled or ingested CS: 2 days to 2 weeks post-exposure - fever, lethargy, anorexia - mucopurulent nasal dschg (from guttural pouch empyema) - enlarged LNs of head and neck (usually submandibular): swollen nodes can abscess and are painful! may drain externally... - rarely it can disseminate to internal organs, known as bastard strangles - purpura hemorrhagica: aseptic vasculitis (severe edema, petechiae, septicemia): this is an immune reaction from repeated exposures (to either a natural infection or vax): can be fatal! - chondroids: these are solidified caseous material (small little stones) that are in guttural pouches and can persist for years/be a source of bacterial shed if not removed dx: - acute dz: PCR or bacT culture from a nasal swab, nasopharyngeal lavage fluid, guttural pouch lavage fluid - chronic dz: serology for SeM-specific ab, high titers suggest Purpura hemorrhagica or bastard strangles. may consider guttural pouch endoscopy -Aspirated LN: purulent inflammation with gram + cocci with large capsules tx: most cleared naturally! abx contraindicated bc can cause bacT to hide/prolong clearance: - penicillin/ceftiofur can be used only for complicated cases lavage gut. pouch and instill penicillin antiinflammatories supportive care -use IM pen with strep-associated pneumonia (beta-strep pneumonia) - the LN abscesses can rarely become large and strangle/block off airway: tracheotomy to maintain! -if have PP hemorhagica, treat with high doses of dexamehtasone and penicillin (bc its an immune cmopllex disrder with high numberrs of S equi antigens and antibodies prog: good for survival. can be PI's if abscesses or chondroids reemain in ZGPs and can shed bacT without CS's - GP fluid PCR or 3 neg nesal PCR's recommended to make sure a horse is no longer a carrier prev: isolate new horses/infected gorses with strict biosecurity measures vax: modified life IN vax or killed IM vax./ increases risk of Purpura hemorrhagica immune reaction tho and is contraindicated in an outbreak when is it safe to put back with other horses? -wait 30 days afterr resolution of CS, then do 3 consecutive weekly negative nasopharyngeal cultures -get rid of chondroids/PI's

complicated corneal ulcers

any of these things.... -involve corneal stroma -have some depth to them -persist over 1 weeks -infected -malacic (melting) dx: -same as uncomplicated: fluorescin stain complicated ulcers: see the stain permeates thru stroma cause: -fail to dx or treat an uncomplicated -secondary bacT infection and maybe malacia -or is now indolent tx: -prevent progression -promote healing 1. aggressive topical abx (tobramycin and triple abx NOT sufficient in these cases as for superficial ulcers: these ones need second genoration fluoro like ofloxacin or suprafloxacin or moxifloxacin etc) 2. cycloplegia: atropine 1-2x ddaily -paralyze iris and ciliary body and strengthens barrier to not allow reflex anterior uveitis 3. stop melting: anticollagenase factors: serum or tetracyclines or acetylcysteine 4. prevent self trauma (cone) 5. oral antiinflammatory therapy: notttt steroids tho 6. structural report (referral) may be needed esp. if progressed can get a desmetocoele: occupies 99% of the thickness of cornea -walls take up stain but not hydrophobic floor (donut: see pic!) : require emergency referral and surgery : conjunctival graft or corneal conjunctival transposition: prog: -fair. may take several weeks and may bee significant scarring: may affect vision

mackenzie toothbrush teechnique

best way to screen for asymptomatic ringworm cats are asymtomatic carriers sterile toothbrush to comb thru haircoat and toothbrush bristles are pushed into a DTM culture woods lamp has low sens and spec for m canis so do histopath and trichogram pcr is available but false + are common

BLV

bovine leukemia virus dx: -ELISA to detect AB's to BLV: best hypersensitivity and specificity of all tests on a herd basis -PCR can be negative in animals with low levels of ab circulating only 0-5% cows infected with BLV will get clinical signs of leukemia

Liver failure: causes

by toxins that can cause chronic liver failure such as: 1. pyrrolizidine alkaloids 2. aflatoxins or from: 3. accumulation of over 35% fat in liver (late pregnancy or early lactation) 4. environmental toxins like digoxin 5. infectious diseases - bacillary hemoglobinuria (clostrodium hemolyticum)

bird anaerobic infections

like clostridium tx: -metronidazole also can use metronidazole in birbs for trichomonas, giardia and cochlosoma

Fatty Liver Syndrome

definition; hepatic lipidosis is over 35% fat in liver MOA: mobilize excess fat in NE balance as FFA, NEEFA, and glycerol: in liver, glycerol can be used to make glucose or recombines with FFA/NEFA's to make triglycerides -insufficient oxaloacetate is available to enter Krebs cycle to excess acetyl CoA is used for ketone bodies **fatty liver develops once rate of triglyceridde formation exceeds utilization and release as VLDL gross signs: loss of mahogany color, fatty looking signalment: in fat cows with negative E balance (have extra fat when go into neg E balance: now mobilize all of it) protein-energy malnutrition, early in course pregnancy toxemia in ruminants, esp. sheep and goats w multiple fetuses hyperlipidemia in ponies some people treat w insulin to try to prevent fat mobilization

horse NSAIDs

dont use together flunixin meglumine and phenylbutazone **always give FM IV!!!! (IM can result in m. necrosis and allow clostridium spores in--> myositis and tissue necrosis--> serosanguinous exudate--> SQ emphysema. tx with wound fenestration to get O2 in there gastric ulceration

bird staphylococcal dermatitis

g- bacT tx: -amoxicillin -absorbed orally and can be given in birds' water

Bordatella avium

gram -, nonfermentative, motile, aerobic bacili "turkey rhinotracheitis" highly-infectious upper respiratory disease most common in turkeys (young birds) (under 6 wk old--older turkeys could get a dry cough) **opportunistic infections in people morbidity in young turkeys: 80-100%: mortality about 40%when . coli or newcastle ddx is present too. spread thru water, food, aerosol. direct contact. MOA: attach to cilia of pseudostratified columnar epithelial cells--> make toxins and stuff--> progress to trachea and bronchi--> dmg to tracheal cartilage (need iron to spread0 CS: - inflammation of sinuses -clear nasal dschg (esp if apply gentle pressure to nares) - a lot of mucus in trachea and tracheal collapse can cause suffocation - cough ("snicks") - dyspnea - tracheal rales/collapse of tracheal rings: tracheal cartilage can return to noraml 4-6 weeks after infection -changes in vocalization - watery/swollen eyes -swollen eyelids: pasted shut -raccoon eye: ring of exudate and pasted feathers around the eye (may also be exudate on shoulders of birds) dx: -necropsy: soft tracheas, flattening/collapsing of trachea - Culture (MacConkey agar, blood agar): B avium or B hinzii -serology tx: - abx dont usually help prev: -limited vax efficacy -may reduce severity, probably wont prevent.

Acetaminophen Cats

heinz bodies on RBC's (inclusions)-- they are denatured hemoglobin -heinz body hemolytic anemia cats do not have Glucoronyl transferase thats needed to metabolize it MOA: -acetaminophen broken down in liver--> metabolites cause oxidative dmg to RBC's--> dmg to hemoglobin causes HB's to form on RBC's. Also ,the iron part of Hgb is altered and methemoglobin forms during this oxidative dmg. Methemoglobin hangs on to O2 and won't release to tissues--> hypoxemia -possible secondary liver tox onion tox. can also cause HB anemia

myxedma

hypothyroid condition causing metabolic slowing causes increased amount of mucin and other ground substances in the dermis can be markeer for hypoT also, excessive GH--> acromegaly could be associated with this

Feline Eosinophilic Granuloma Complex

immune mediated or allergic etiology not a specific dx: still need to find underlying problemo CS: -usually on upper lip near comimssure -erythmatous, alopecic, raised edges around a pink-yellow, ulcerated surface tx: glucocorticoids

infectious keratoconjunctivitis

in sheep: -Mycoplasma and Chlamydia are most common in sheep tx: -oxytetracycline -topical twice daily -if bilateral corneal lesions, inject w/ long-acting oxytetra's -house inside if cant see

post-estrual hemorrhage in a cow

indicates that its been 12-24 hours since ovulation too late to breed! normal in cattle from endometrium. only seen post-estrus unlike other spp.

environmental protection agency

insecticides that work topically are controlled by EPA not FDA! off label use is illegal under federal law bc of this if administered orally (milbemectin, ivermectin) or applied topically with transdermal absorption (selamectin), then still FDA

IBD Diagnosis

it is most often lymphocytic-plasmacytic enterocolitis in cats -Usually want a strict diet trial first to R/o food allergy - for definitive IBD dx, need biopsy and histopathology - tx: management of IBD, not rly a cure

Pyrrolizidine alkaloid toxicity

liver findings: 1. megalocytosis 2. fibrosis 3. bile duct hyperplasia plants: ammsinckia intermmedia (aka fiddleneck, aka fireweed, aka tarweed) PAs are hepatotoxic and can cause liver lesions above, and as a result cant clear their chlorophyl products and get photosens.

vitamin K3

nephrotoxic in horses k1 can be given sq in warfarin toxicosis and plasma

cycloplegia

paralysis of the ciliary body

uncomplicated corneal ulcer

only loss of corneal epithelium ALWAYS heal in 5-7 days dx: -fluorescin stain: apply to bulbar conjunctiva or moist drop to corneal surface only binds to hydrophilic stroma, not to hydrophobic corneal epithelium causes of superficial corneal ulcers: 1.) traumatic: a. endogenous: eyelid abnormality (actopic cilia, entropion, distichia) b. exogenous: foreign body (plant material, cat claw, etc.) 2.)decreased corneal protection: -decreased tear production or quality (KCS, exposure keratitis, pigmentary keratitis) -decreased blink reflex (lagophthalmos, CN 5 or 7) tx: **goal is to prevent it from becoming a complicated ulcer 1. find and remove cause if possible 2. use broad spectrum topical abx to prevent secondary infection and promote healing 3. cycloplegia, using a topical anticholinergic like atropine to give increased comfort and decrease secondary reflex anterior uveitis 4. prevent self trauma (e-collar to prevent worsening) 5. NEVER use a topical steroid: primary cause of progression and promotion of a melting corneal ulcer prog: -should always heal in 5-7 days: if doesnt, rediagnose (indolent, infected, or preexisting condition is preventing healing)

Verminous pneumonia

pigs ascaris suum: direct life cycle - a roundworm! metastrongylus elongatus: earthworm intermediate prob with pasture pigs/niche pigs MOA: pig ingests egg with L2 larva inside--> hepatic migration (milk spots)--> thru lungs and becomes L3--> enters alveoli and gets coughed up (thumps=rapid, shallow breathing) CS: -poor doer, respiratory distress (sometimes distress can be v severe) -cn cause obstruction if severe Secondary bacT infection: sometimes put on tetracyclines when have worms to control these dx: -milk spots in liver (sub capsular white spots in liver), worms in GI - dx: can do a fecal float and see characteristic double-operculated eggs tx: **roundworm of pigs, will treat with fenbendazole!! levamisole, avermectins, pyrantel

Cytauxzoon felis

protozoan usually southern US transmitted to cats via tick bites **signet ring shape with prominent nuclear area (Pic) MOA: invades the reticuloendothelial cells of the lungs, spleen, kidneys, liver, LNs: see cranial organomegaly CS: -1-3 weeks post infection -nonregen. anemia -anemia associated heart murmur -anorexia, lethargy, icterus -pyrexia -pancytopenia (BM can be affected) -DIC can develop: thrombocytopenia -spontaneous bleeding -icterus or pallor -scleral hemorrhage tx: no effective therapy, correct dehydration -blood transfusions, -heparin to help DIC -imidocarb/antiprotozoal meds have been used with varied success -antimillarial drugs (atovaquone) with azithromycin steroids dont help, neither does doxy ddx: -IMHA, -cholangiohepatitis -FIP -mycoplasma hemofelis (both infect erythrocytes but MH is cocci, rings, rods and CF is signet rings) prog: poor to grave -mort without tx is 100%, with it's over 40% -tx isnt great so prev is best:

Amsinckia

pyrrolizidine alkalaloid contaminatee grains

phylloerytherin

red pigment: made as a degradation product of chlorophyll in herbivores -nx excreted in bile but absorbed in blood in some pathology conditions (geeldikkop) - photodynamic substance: accumulation of this in skin causes photosensitization (free radical production in skin when react to light): TypeI-IV PS reactions

Actinobacillus pleuropneumonia (APP)

sometimes referred to as just "pleuropneumonia" -pig resp dz -actinobacillus pleuropneumoniae is a g- coccobacillus -rapid onset -usually affects young pigs concurrent infections with influenza, mycoplasma, pasteurella, PRRRS are common - in continuous flow operations -inapparent carriers -peracute, acute and chronic forms exist clinical signs: -sudden onset usually, severe resp distress, death - open mouth breathing, frothy, pink oral and nasal discharge ddx: actinobacillus suis **concurrent infections with mycoplasma, pasteruella, PRRS or swine influenza are common - swine influenza is different bc all ages of pigs usually affected, and no blood-tinged oral and nasal froth **pigs fine one day, next day they're dead dx: -necropsy: fibrinous, necrotic and hemorrhagic lung lesions pleuropneumonia, usually diaphragmatic lobes are most severe. - Culture is difficult. - complement fixation serology -PCR - Multiple eliza's tx: ceftiofur, florfenicol, enrofloxacin -if an outbreak, inject all pigs with enro or one of these abx: treat all immediately bc exotoxins made by APP can cause death in hours (once clin signs, success of tx is v decreased): dont wait for water or fed abx to take effect ctrl: vax not v effective (takes mult. doses and need right serotype) ddx: influenza, but influenza affects all ages, and doesnt cause blood tinged froth from mouth and nose

dog humeral fracture

spica spint immobilize femur or humorous while waiting for surgery

brachyspira pilosicoli

spirochaetal colitis in swine swine dysentery

two most common organisms in middle ear infections

staphylococcus and pseudomonas

Cutaneous Drug Reaction

toxic epidermal necrolysis, (cutaneous ulceration w mixed inflammation of dermis and epidermis and coagulative necrosis) fluids and lytes can be lost extensively w this can be prone to secondary bacT infection after this guarded prognosis tx: hospitalization w supportive care, testing (removal of suspected inciting cause)

Rhodococcus equi

- gram +, facultative intracellular coccobacillus (used to be known as corynebacterium equi) causes suppurrative, pyogranulomatous pneumonia signalment: most in 2-6 month old foals!! (materrnal ab protection before then, resistant afteer) -MOA: lives in soil, can survive for years-- farms could have endemic dz. Inhaled early in life: has a slow insidious onset! invaddes alveolar macrophages and replicates--> pyogranulomatous pneumonia and pulmonary abscessation. can also cause ulceerative colitis, mesenteric lymphadenitis--> diarrhea/colic -significant morbidity and mortality CS: foals or weanlings mostly (1-6 mo): gradual onset of disease can cause really bad pulmonary lesions before sickness is seen clinically - pyogranulomatous bronchopneumonia - intermittent fever - cough, tachypnea, increased effort (flaring nostrils and abdominal tucking on inspiration) - abnormal auscultation (wheezes/crackles) -rarely nasal dschg - lethargy, anorexia, poor weight gain - **R equi can disseminate and cause other issues (septic arthritis, osteomyelitis, non-septic jt effusion, uveitis, internal abscesses, IM diseases, GI upset, intervertebral abscesses-->neuro disease) and even an abdominal abscess. - hyperfibrinogenemia and neutrophilic leukocytosis on bloodwork Dx: - Transtracheal wash (intracellular rods) and culture - abscesses on thoracic U/S or radiography w/ clinical signs (alveollar patteern with multifocal nodular cavitary lesions) tx: - prolonged (4-10 wk) abx with rifampin with a macrolide like azithromycin or erythromycin - NSAID's, cool temp, IN O@ supp, hydration help prog: fair to good unless severe infection prev: if have endemic dz on farm, tx foals with R. equi hyperimmune plasma at birth and 1 month old **pic: pulmonary abscess in caudodorsal lung field of 4 mo foal with weight loss, fever, tachypnea

Hepatic lipidosis

1. eliminate NE balance 2. Insulin 3. IV glucose drip 4. IM glucocorticoids 5. oral propylene glycol or glycerol **most important: encourage animal to eat

Fatty liver: clin signs

1. ketonuria 2. elevated FFA's 3. low Ca++ 4. Decreased glucose 5. decreased insulin 6. metabolic acidosis (maybe) 7. elevated liver enzymes 8. neutrophilia

parvo

shed for 7-10 days once infected -puppies less than 1 y/o transmission: thru contact with infected feces and fomites, resilient in environment, resistance to disinfection MOA: replicates in crypt epithelium of the gut and causes epithelial necrosis and hemorrhagic diarrhea can affect young puppies' hearts--> myocarditis maternal a's from mom's vaccination can protect the babies from this

sporotrichosis

sporothrix zoonotic in soil CS: can cause cutaneous, pulmonary, disseminated. esp in cats: high risk to vets -usually cutaneous (small painless bump) -disseminated symptoms depend on where -rom rose thorns, can get it - lungs, bb, joints, CNS, etc. immune suppressed people more likely to get it S. brasiliensis cn be from cat bites

Milk Fever

MOA: -insufficient calcium, usually within first 24 hours after calving (or 2-3 days later): bc huge need for Ca for colostrum! -low ca; reduced smooth m tone and cxn of GI/CV system, reduced m tone of uterus (retained placenta, etc.), reduced sphincter tone (leakage of milk--> lets bacT in--> mastitis -see low ca-->reduced appeetite--> ketosis and abomasal displacement stages: i: unnoticed: loss of appetite, nervous, weak, shuffle hind legs ii: lies down, head in flank or stretched, moderate depression, coordination issues when walking, m trembling, constipation, tachycardia III: cow lays flat, unable to stand, severely depressed, loss of consciousness-->coma--> death CS: -downed cow -dry muzzle -staring eyes -cold ears, cold legs -hypothermia -tachycardia -mild to moderate distention of L lateral abdomen -lack of rumen cxns tx: - IV calcium gluconate but Ca is cardiotoxic, so if bradycardia occurs once yoou've began administration to treat tachycardia then stop giving until HR returns to normal, then complete the admin while listening at a slower rate. need to give Ca solutions slowly over 20-30 mins bc cardiotoxic oral or SQ ca wont be fast enough to treat a recumbent cow. continuing admin of Ca to a bradyC cow without waiting for HR to regulate can be fatal.

Equine Pleuropneumonia

Shipping Fever risk factors: - recent transport (especially over 6 hours, with bad ventilation and not many rest stops and tied head inside trailer. CS (within 24 hours of travel, usually): - severe fevers (over 104) -lethargy, anorexia, depression, dyspnea, tachypnea -Auscultation of decreased lung sounds ventrally - nasal dschg, mildd cough - reluctant to move bc pleural pain from fluid accumulation dx: - thoracic US with hx and CS that fir Tx: supportive care (IV fluids, antiinflammatories, abx, supplemental O2) - thoracocentesis and indwelling chest tubes prog: fair to guarded (dep on severity)

Pregnancy toxemia

v. severe manifestation of fatty liver dz multiple fetuses or one taking up a lot of energy usually sheep, maybe goats twinning in goats, but usually 3 or more can occur in cattle poor prognosis once occurs, best to prevent w weight control and proper diets **during neg E balance, body cant make enough oxaloacetate to feed into the citric acid cycle: so, get mobilization of fat and subsequeent production of ketones tx: 1. c section or induction of abortion 2. oral E: ex: 30 ml propylene glycol BID 3. IV glucose cont. drip 4. Calcium if low 5. rumen transfaunation to encourage to eat 6. insulin sometimes to decrease peripheral fat mobilization 7. good nutrition

otodectes cyanosis

ear mite cats tx: -Milbemycin (Milbemite) 1x (topical, may need to be repeated once) -ivermectin (Acarexx otic sltn): 1x , may repeat 1x (oral ivermectin not approved for ear mites) -selamectin (revolution) and moxidectin (advantage multi) are approved to control them but better for preventative. topically btwn shoulders Thiabendazole (in tresderm) effective vs yeast and mites if used over 10 days

Equine Influenza A

horse resp dz an orthomyxovirus endemic in horse population, outbreaks in horses that travel, esp young and racehorses MOA: inhaled aerosolized virus from respiratoy secretions CS: -fever, lethargy, anorexia - dry cough -mucoid nasal dschg - rareely secondary penumonia -vaccinated horses can still get it, less CS so subC carriers dx: nasal swab PCR nasophayngeal swab fo virus isolation tx: antiinflammatories, supportive care, rare abx except secondary penumonia prog: excellent prev: isolate new horses, mod live or killed IM vax biannual vax in high risk horses

Liver Failure: Clinical Signs

occurs when over 1/2 of the liveer capacity is lost or bypassed (shunts) - manifested by clinical signs that relate to functions... 1. loss of normal growth and weight 2. depressed mentation (yawns, lethargy), progressed to encephalopathy 3. icterus 4. photosensitization (herbivores) 5. tenesmus/diarrhea in cattle 6. loss of clotting

Mycoplasma hyopneumoniae

pig resp dz "enzootic pneumonia" MOA: bacT attach to mucociliary apparatus and prevent function: makes lungs much more susceptible to other bacT infections pigs: most common cause of chronic pneumonia - chronic, non-productive cough - low mortality - secondary bacT infefction: complicates dx: plum-colored (pale) cranioventral pneumonia - culture: not done bc hard (need special media, easily overgrown with other organisms) - PCR -Fluorescent Ab test on lung transmission: primarily from sow to piglet tx: - lincomycin in feed -CTC in water -fluoroquinolone injection prev: (mgmt): - vaccinate weanlings vaccines used widely in US air quality, temp and ventilation need to be addressed too myco's dont have cell walls so tx with penicillin isnt effective

Pasteurella multocida

pig resp pathogen (PM type D causes atopic rhinitis with bordatella bronchiseptica, PM type A causes pneumonia) most common bacT isolate in pig lungs: doesnt cause issues on its own opportunistic! (with mycoplasma, influenza, actinobacillus, stress) CS: 1. moist, productive cough 2. dyspnea 3. some die dx: necropsy: suppurative cranioventral bronchopenumonia may look like APP lesions: culture can help differentiate tx: all abx ctrl: look for underlying dz, medicate feed and water (tetracyclines) pic looks like mycoplasma pneumonia.. need confirmation with lab tests

knemidocoptes mutans

scaly leg mite turkeys and chickens CS: -honeycomb crusts on legs (white/grey powdery debris) -legs may become thick/distorted dx: -skin scraping or exam under a crust microscopically looking for thee mites -male and female mites look a lot different: female on left (round w short legs and no suckers) vs male on left (longer legs and suckers on long stalks tx: -ivermectin


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