Food Ani. Med- Small Ruminant Diseases 1

wilsbach's version from 2016-01-20 01:49

intro (all Dz lists are just to get an idea and feel for it, each section gone over later)

Question Answer
What does DAMNIT-V stand for again?Degenerative, Anomalous, Metabolic, Neoplastic, Inflammatory, Traumatic, Vascular
GI dz--> 2 dz which cause mouth lesions?ORF, blue tongue.
GI dz--> 2 that are GI toxins?Rhododendron toxicity, flurosis
GI dz--> Anatomically related dzs? (3- one we care about)(bloat, ruminitis), abomasal emptying defect
Differential diagnoses you must keep in mind for small rumi dzsE. Coli, eimeria, lamb dysentery, Haemorrhagic enterotoxemia, Johnne's dz, copper deficiency
Respiratory Dzs for small rumi (10, 4 we care about)Enzootic nasal tumor, oestrus ovis, OPP, CAE, ((blue tongue, Mycoplasma (Contagious Caprine Pleuropneumonia), Jaagsiekte virus (Ovine progressive adenomatosis), Verminous pneumonia, toxoplasma, Tracheitis laryngitis)
5 skin dzs of small rumisORF, mastitis, mycoplasma, CLA, ectoparasites
repro--> diseases (4, 2 we care about)Brucella, pregnancy toxemia, (toxoplasma, enzootic abortion)
repro--> non-disease (infectious) causes of problems/ comlicationscastration, dystocia, Estrus synchronization, infertility, chlamydia
Neuro dzs (8, 4 we care about )Cu deficiency, listeria, PEM (polioencephalomalacia), scrapie, (botulism, tetanus, electrolyte imbalances, CAE)
5 possible kidney dzsleptospirosis, Cu tox, urine obstruction, urolithiasis, pizzle rot
musculoskele dz--> 10, 4 we care aboutCLA, Spider lamb Dz, foot and mouth, foot rot, (CAE, mycoplasma, Erysipelothix rhusiopathiae, Electrolyte imbalances, flurosis, Vit E/Se deficiency)
4 cardiovascular dzsMonensin toxicity, Ionophore toxicity, Vit E/Se deficiency, Blue tongue
3 hemolymphatic dzs (1 we care about)Thymoma, (lymphoma, copper tox)
3 hepatobiliary dzsHepatic lipidosis, preg tox, liver fluke

GI part 1

Question Answer
wut disORF
WHO can get Orf?Young AND adult sheep and goats, other species, AND HUMANS TOO
which GI dz is zoonotic?Orf
What is the seasonality of orf? What can affect this?If they (S+G) are PASTURED, it is more common in late summer. However if they are feedlotters, it is more common in winter (basically, when are a ton of them all together?)
mode of transmission of Orf?Direct contact, fomites
what is the agent which causes Orf, and what is another name for it?Parapoxvirus (Contagious Ecthyma)
who is more predisposed to Orf- sheep or goats?GOATS more prone
what are 3 major predisposing factors to getting ORF?Being a goat, being an orphan (moving mommy to mommy), or if there is a long lambing/kidding season (bc babies have no immunity, they pick it up and spread it, and then a longer season means more of this)
What are the clinical signs of Orf like? (where are lesions etc)Mouth lesions on lips, gums and tongue, Udder lesions where infected babies have been nursing, Limb lesions on coronary bands and between toes, occasionally on legs.
describe Orf lesionsSwelling --> crusting --> bleeding and painful
how do you dx orf?CS + PCR
how do you treat Orf?you can give Antibiotics for secondary infections, otherwise just "tincture of time" (ie: wait till it goes away)
does Orf have a vx?yes
When do you give Vx for orf? what is the protocol?give it only on farms where it is endemic. You give the live vx for 1mo old lambs and 2-3mo later you booster. This vx has Good efficacy except in highly virulent strains. There is also a Autogenous vaccines
would you prefer to vx or allow small rumis to get natural immunity to orf?Natural immunity is fair, vx immunity is better. (colostral immunity also poor)
after you vx for orf what should you do?isolate them till scab heals bc it is a live vx so it's contagious!
what is the carrier of blue tongue?culicoides midge
who can get blue tongue? (who is MOST likely to?)sheep, goats, cattle, deer
what is the seasonality of bluetongue like?Long viremia in cattle and concentration in midge mouth parts make it possible for Bluetongue to occur year round :(
mode of transmission of blue tongue?transmitted by culicoides midge, fomites, or semen
what is the causative agent of blue tongue?Bluetongue virus is the type-species of the genus Orbivirus in the family Reoviridae
what is the pathogenesis of damage/lesions caused by the blue tongue agent?(orbivirus of reoviridae) Causes vascular endothelial damage, altering capillary permeability, leading to edema, congestion, inflammation, hemorrhage, and necrosis
What are the clinical signs of blue tongue? (what is seen most often?)*Pulmonary edema and tachypnea(see these the most), Fever developing apprx 1 – 6 weeks of incubation, Severe swelling and cyanosis of the tongue (Blue Tongue) in some sheep, Edema of face and submandibular region, Congestion of oral, nasal, and ophthalmic cavities, Serous nasal discharge progressing to a mucopurulent discharge, Decreased caloric intake, due to sore, swollen, congested muzzle (sore mouth affect), Lameness, due to inflammation in hoof coronet, depression
what are the three types of presentations of blue tongue, and which is most common(1) Most cases very mild, self limiting disease (2) Peracute type= death in 7-9 days from asphyxia, pulmonary edema (3) Chronic type= death in 5 weeks from secondary bacterial diseases (especially Pasteurella)
what are Pathologic lesions highly suggestive of blue tongue?Range from petechia to large hemorrhages at base of pulmonary artery and in papillary muscles
how do you dx bluetongue? WHEN do you see a serologic response?Serologic techniques for detection of BTV antibody include: Agar gel immunodiffusion (AGID) and competitive ELISA. Will take 7-14 days to detect a response.
is natural immunity of blue tongue good?Immunity generally lifelong after a field infection
how do you tx blue tongue?supportive tx only
does blue tongue have a vx?yes- Live attenuated vaccine and inactivated vaccines are available
what kinda vx are there for bluetongue? how effective are they? how must you be careful? live attenuated or inactivated vxs available. Good efficacy to reduce but not eliminate prevalence, and vx are type-specific. DO NOT use in preg stock, and practice basic biosecurity
who is affected by Rhododendron Toxicity?sheep and goats
What is the seasonality of rhododendron tox like?Evergreen, so when other greens are in short supply they are available...also more accessible after being pruned
causative agent of rhododendron tox?Gryanotoxin
what is the pathophysiology/ causative agent of rhododendron tox?Gryanotoxin –> Cardio-active steroids and cardiac glycosides: Na+/K+ ATPase inhibition, increased intra-cellular Ca2+ leaving excitable cells depolarized (so, hyperexcitable cell, eventually it runs out of energy and then it gives out)
which part of the rhododendron is toxic?all of it, but ESP the leaves
what is a lethal dose for rhododendron tox? How quickly do you see CS?Lethal dose is 1g/kg and cs within 6 hours of ingestion
What are the clinical signs of rhododendron tox?Gryanotoxins effect leading to myocardial excitation, and later bradycardia with ventricular tachycardia/fibrillation and heart block (bc hyperexcitable uses all ATP and then cell can't function when it's all gone). You will also see Salivation and perspiration, Later, paralysis of limbs and eventually diaphragm. You will see HYPERKALEMIA (bc Na+/K+ ATPase inhibition), Abdominal distress, and vomiting. Also Anorexia, and inactivity
how do you dx rhododendron tox?hx and GI content
Why do you give activated charcoal when there is tox, such as in rhododendron tox? What are the DOWNSIDES to using activated charcoal?Charcoal binds reversibly to most toxins...which is great for getting rid of them, BUT if defecation is slow it may release toxin further down GI tract only resulting in absorption of toxin later when not expected. (look for dark poop or add mineral oil to see when the charcoal and what its bound to has passed through system)
how do you treat rhododendron tox? If caught early induce vomiting then give vegetable oil to coat the rumen. Sedate the animal for the first day to ease distress. Give activated charcoal for the first day, Fluid therapy for electrolyte support and Respiratory support may be necessary. Atropine if patient falls into severe bradycardia. Isoproterenol or sodium channel blockers like quinidine might have to be used to treat heart block
if the patient falls into a severe bradycardia/ they get heart block, what drugs would you use to tx? (what dz am i talking about?)(rhododendron tox) use atropine for bradycardia, and use Isoproterenol or sodium channel blockers like quinidine to tx heart block

GI part 2

Question Answer
who gets fluorosis?anyone can- it's just having too much fluoride (Cows, Sheep and Goats, Pigs and Poultry)
what are some situations where animals can be exposed to high levels of fluoride, resulting in fluorosis? (4)(1) Soil levels are high: Fertilizer application/naturally occurring (2) Feed (>1%) or water levels are high (3) exposure to rodenticides (can contain fluoride) (4) Large doses of sodium fluoride containing anthelmintics
how do LOW levels of fluoride affect the body? HIGH levels?Low levels of fluoride are good, decrease solubility of enamel= protection. High levels of fluoride are bad, enamel becomes dense and brittle
how does fluorosis affect pregnancy?If occurs during pregnancy can affect developing bone and teeth
how does fluorosis affect electrolyte balance?Systemically, aper the influx of fluoride, calcium and magnesium levels decline rapidly
what are predisposing factors for fluorosis?Animals with long production lives have greater chance for exposure (so cow more at risk than a sheep, for instance). Location/Area is also a big factor
clinical signs of ACUTE fluorosis? (being exposed to a whole bunch of fluoride all at once)Gastroenteritis, salivation, restlessness, sweating, anorexia, muscle weakness, stiffness, dyspnea, ventricular tachycardia, convulsions --> depression and death
clinical signs of CHRONIC fluorosis?(chronic more commonly seen) Unthrifty animals with skeletal and dental abnormalities: Reduced feed/water intake with poor weight gain and milk production due to dental lesions and impaired mastication (it's painful), Mottled, chalky, pitted and stained enamel, and uneven excessive wear on teeth. Skeletal abnormalities due to increased bone resorption and remodeling (osteomalacia, osteoporosis, osteofluorosis) (--> Hip lameness, stiff limbs, painful gait, abnormal hoof growth, and exostosis). Later stages of the syndrome, severely affected animals may move on their knees because of spurring and bridging of joints
which bones are more likely to be affected by fluorosis?Metabolically active/growing bones of young animals are more severely affected
why does fluorosis lead to anemia and hypothyroidism?due to reduced T3 +T4 levels + reduced serum calcium concentrations
4 things you can do to dx fluorosis? (what gives a final/definitive dx?)(1) look at History of exposure with clinical symptoms (2) Measurement of urine or serum calcium and magnesium levels (fluoride causes these electrolytes to drop steeply) (3) Measurements showing Increased fluorine levels in blood and urine (4) Fluorine assay can lead to a final diagnosis
3 common post-mortem findings for fluorosis?(1) Mottling of tooth enamel (2) Deposition of fluorine on the periosteal surface of long bones (3) Radiographs for detecting osteomalacia and osteoporosis
So obviously you want to remove the source of fluorine causing the fluorosis.... what can you do otherwise to tx ACUTE fluorosis? chronic?ACUTE: IV calcium gluconate and magnesium hydroxide or milk orally to minimize fluoride absorption. CHRONIC: once chronic, treatment not effective and the teeth can never return to normal
how much fluoride should be in feeds?<1%
what protocol can you use to help prevent fluorosis?Supplement with calcium carbonate, aluminum salts, magnesium to reduce absorption or enhance excretion of fluoride. (And obv dont give feeds with over 1% fluoride)
what kinda sheep are these, and what GI thing are they genetically prone to having?Suffolk sheep, abomasal emptying defect
WHO gets abomasal emptying defect?adult suffolk sheep most predisposed
what is seasonality of abomasal emptying defect like?Can be Winter months associated with lambing and feeding concentrates, or can just happen sporadically at any time
mode of transmission of abomasal emptying defect?Unproven heritability
pathophysiology of abomasal emptying defect?Suspected dysautonomia linked to potential neurotoxic agent
what are the clinical signs of abomasal emptying defect?Partial to total anorexia, leading to progressive weight loss and emaciation is the main sign. There will be a Palpable, firm abomasum in advanced cases. Will be Ruminal tympany, pear shaped abdominal distention, due to dilation of abomasum
(FYI) what side is the abomasum on again?RIGHT SIDE (remember rumens all up on that left side yo)
what are clinical signs of abomasal emptying defect?Changes in ruminal contraction frequency (increased or decreased), Tachycardia, mild abdominal pain, dullness, atrial fibrillation. Signs could be observable for a few days, or develop over months
how do you dx abomasal emptying defect?Usually just at post mortem (PM), look at hx and signalment too
tx for abomasal emptying defect?Palliative, surgical
Protocol for prevention of abomasal emptying defect?cull affected animals (unproven heritability)

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