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What plasma total magnesium (tMg) level indicates hypomagnesemia requiring treatment (as per Page 16)?

Less than 0.5 mg/dL (0.2 mmol/L).

What plasma total calcium (tCa) level indicates hypocalcemia requiring treatment?

Less than 8 mg/dL (2.0 mmol/L).

What post-mortem vitreous humor Mg concentration is associated with magnesium depletion?

Less than 1.8 mg/dL (0.75 mmol/L).

What is the recommended initial treatment for hypomagnesemia and hypocalcemia in ruminants?

Magnesium and calcium given slowly via IV, followed by subcutaneous and oral magnesium.

Why must stimulation be minimized during treatment?

Stimulation can trigger fatal convulsions.

What follow-up administration route should be used after IV treatment?

Subcutaneous and oral magnesium supplementation.

What preventive measure should be used during risk periods for at-risk animals?

Daily oral magnesium oxide.

What clinical signs are associated with low magnesium levels in CSF?

Hyperexcitability, muscular spasms, convulsions, respiratory distress, collapse, and death.

What is magnesium loss related to lactation?

Magnesium is lost in milk.

Which animals are at risk due to lush green pasture, and what is the underlying issue?

Lactating animals grazing on lush green pasture; lush grass is low in magnesium and can lead to metabolic alkalosis, decreasing ionized calcium and magnesium.

When are clinical signs of hypomagnesemia rare?

They are rare until concurrent hypocalcemia.

What are the typical external signs of bluetongue infection in sheep?

Muzzle edema with edema of lips, nose, face, submandibular area and eyelids (± ears), and mucopurulent nasal discharge.

Which animals on lush pasture are at highest risk for hypomagnesemic tetany?

Lactating animals.

What congenital defects can bluetongue infection in pregnant dams cause in fetuses?

Hydrancephaly or porencephaly causing ataxic and blind lambs.

Which sheep breeds are mentioned as affected by bluetongue?

Fine-wool and mutton breeds.

What are common signs of bluetongue related to the mouth, nasal passages, and skin/wool?

Listless, reluctant to move; congestion of mouth, nose, nasal cavities, conjunctiva, and coronary bands; lameness and depression; dermatitis with abnormal wool growth.

What laboratory methods can identify bluetongue virus isolates?

Virus isolation from blood of febrile animals; PCR to ID a specific isolate.

Which serology tests are used for bluetongue?

Competitive ELISA or agar gel immunodiffusion (AGID).

What are classic necropsy findings in bluetongue?

Petechia, ecchymoses, or hemorrhages in walls of the pulmonary artery; focal necrosis of the papillary muscle of the left ventricle.

What is the pathophysiology of bluetongue?

Viral vascular endothelial damage with changes to capillary permeability, intravascular coagulation, edema, congestion, hemorrhage, inflammation, and necrosis.

What is the vaccination strategy for bluetongue in endemic regions?

Vaccinate; there is no cross-protection between serotypes.

What is the vaccination strategy in nonendemic regions during outbreaks?

Use serotype-specific inactivated vaccines; also use insecticides to control Culicoides spp. vectors.

What are the Bluetongue ‘pearls’ about distribution and vector involvement?

Worldwide distribution mimics the distribution of Culicoides biting midges; the virus causes vascular endothelial damage leading to edema, congestion, hemorrhage, inflammation, and necrosis, and affects cattle and wild ruminants (less commonly).

What is one of the classic external signs of scrapie observed near the tailhead?

Hair loss adjacent to tailhead.

What herd surveillance method is mentioned for detecting antibodies to scrapie at the bulk level?

Bulk tank milk test for antibodies.

What is the purpose of serology of dams with affected lambs in scrapie management?

To test dams for antibodies indicating exposure or infection.

What breeding practice before breeding season is suggested to enhance natural immunity against scrapie?

Mix lambs recovered from infection with breeding stock before breeding season.

Should recovered scrapie lambs be bred?

No, DO NOT breed recovered lambs.

Is there an effective vaccine for scrapie?

No, there is no effective vaccine.

What is the global distribution status of scrapie?

Worldwide distribution.

What fetal infection outcome can occur if the fetus is infected early in pregnancy?

Abortion or widespread distribution of the virus in fetal tissues.

What is true about surviving scrapie lambs and virus shedding?

Surviving lambs are persistently viremic and shed virus in excretions/secretions, including semen.

Is the BVDV vaccine effective against scrapie?

No, BVDV vaccine is not effective.

Which sheep breeds are more predisposed to scrapie?

Black-faced breeds.

What is an early sign of scrapie related to gait?

Progressive ataxia with bunny-hopping gait in pelvic limbs, then high-stepping gait in thoracic limbs.

What are some neurological signs of scrapie besides gait changes?

Fine head tremors (especially ears).

What behavioral signs may occur in scrapie (stare/ aggression)?

Vacant, fixed stare or sudden aggression.

What is a hallmark cutaneous sign of scrapie?

Cutaneous hypersensitivity; scratching the back may cause head throwing and licking the air or nibbling lower limbs.

What tissue is examined at necropsy to diagnose scrapie?

Brain.

Which tissues are used for IHC testing in scrapie, and which is more sensitive?

IHC on eyelid or rectal mucosa; rectal biopsy is easier and more sensitive.

What surveillance program governs scrapie control in the US and what happens to positives?

USDA/APHIS scrapie slaughter surveillance; positives traced to herd, herd quarantined and tested.

What does the US Scrapie Eradication Program require for breeding sheep leaving their origin?

Individual and premises identification for all breeding sheep leaving their original premises.

What is the PrP change in scrapie and where does it deposit?

Abnormal prion protein (PrPSc) converts PrP to PrPSc and deposits as amyloid plaques in lymphoreticular and nervous tissue.

Does scrapie affect humans?

Does NOT affect humans.

What is the incubation period for scrapie?

2–5 years.

What is the goat-related geographic note for scrapie?

Worldwide distribution except Australia and New Zealand; rare but possible in goats.

When is scrapie transmitted in relation to lambing tasks?

Transmitted during lambing (not in utero).

Bluetongue: what is a classic sign mentioned in this page?

Cyanotic tongue.

What are the classic clinical features of Border disease in lambs (the 'hairy shaker lambs')?

Hairy, low birth-weight lambs; dams often barren with abortions of mummified or macerated fetuses; lambs may have hairy coats and other signs related to CNS involvement.

What maternal reproductive issues are associated with Border disease?

Increased number of barren dams with abortions of mummified or macerated fetuses.

What lamb characteristics are typical for Border disease besides hairiness?

Hairy, low birth-weight lambs; darkly pigmented wool; shortened bones with decreased crown-rump length and limb measurements; tremors of the trunk and pelvic limbs.

What is the etiological agent group responsible for Border disease?

A pestivirus (family Flaviviridae) with seven known genotypes; related to classical swine fever and bovine viral diarrhea virus (BVDV).

When should Border disease testing be performed for accurate results and why?

Do testing before colostral intake because maternal antibodies can interfere with test results.

What diagnostic methods are used to detect Border disease infections?

Virus isolation, PCR, fluorescent antibody (FA), and immunohistochemistry (IHC) on affected tissues or blood.

What histopathologic finding is considered pathognomonic for Border disease?

CNS lesions with myelin deficiency and increased interfascicular glial cells with intracellular accumulation of myelin-like lipid droplets.

What is the prognosis for Border disease in affected lambs?

Poor survival rate.

Is there an effective treatment for Border disease?

No specific treatment is available; management focuses on prevention and control of infection.

Where is Border disease seen geographically and across which species?

Seen worldwide in sheep and goats; also reported in cattle, deer, and camelids according to notes.

What plants are associated with thiamine deficiency leading to polioencephalomalacia (PEM) in lambs?

Kochia scoparia and Lambsquarter (Chenopodium spp.).

Besides thiaminase-containing plants, what other factors can cause PEM in small ruminants?

Water deprivation, sodium toxicosis, and lead poisoning.

What is the pathognomonic CNS pathology seen in PEM?

Laminar cerebrocortical necrosis with autofluorescent lesions.

What is the recommended thiamine treatment regimen for PEM?

First dose given slowly via IV, then intramuscular injections for 3–5 days; improvement may be seen within 24 hours; complete recovery may be limited if the disease is advanced; dexamethasone may help reduce cerebral edema.

What preventive measures are advised to minimize PEM risk related to thiamine deficiency?

Thiamine supplementation; calculate total sulfur intake on a dry-matter basis to avoid excess; provide sufficient roughage during outbreaks to maintain rumen microbes and prevent ruminal acidosis.

Why is thiamine measurement sometimes challenging in PEM cases?

Most laboratories are not capable of accurate thiamine measurement; diagnosis often relies on response to thiamine and clinical/pathological findings.

What is the described pathophysiology of PEM in the notes (Pearls)?

Abnormal cerebral energy metabolism leading to increased intracellular sodium and water, resulting in cerebral edema and cerebral necrosis.

What are the clinical signs of complete urethral obstruction in male ruminants?

Tenesmus, tail swishing, colic, weight-shifting, +/- bloat, rectal prolapse, inappetence, depression.

What signs suggest urethral or bladder rupture in urinary obstruction?

Abdominal swelling, preputial swelling, necrosis of ventral abdominal skin with a pseudourethral development.

How is urolithiasis typically diagnosed (dx)?

Usually obvious from history and clinical signs; may see a urolith in the urethral process.

Which uroliths are radiopaque and which are radiolucent on radiographs?

Calcium carbonate and calcium oxalate calculi are radiopaque; struvite stones are radiolucent.

What ultrasound finding indicates uroperitoneum due to rupture?

Large volume of hypoechoic (fluid) in the abdomen.

What does abdominocentesis show in uroperitoneum?

Abdominal fluid creatinine is about 2X that of peripheral blood.

What electrolyte and acid-base abnormalities are commonly seen with obstruction-related urolithiasis?

Low sodium and chloride; high phosphate; metabolic alkalosis.

What is the preferred treatment for an obstructed but non-ruptured bladder?

Tube cystotomy.

Do calculi ever expel spontaneously in this condition?

Yes, calculi are expelled spontaneously over time in some cases.

What management may be used for early, mild, or partial obstruction?

Antispasmodics and tranquilizers to relax the sigmoid flexure of the penis.

What is the recommended action if the blockage is at the urethral process?

Amputate the urethral process.

What surgical procedure bypasses uroliths and serves as a salvage option?

Perineal urethrostomy.

What is a common long-term complication after a perineal urethrostomy?

Urethral stricture (stricture formation).

What should be done if there is ruptured urethra or bladder with uroperitoneum?

Drain uroperitoneum slowly via teat cannula or trocar.

What IV fluid therapy is used to correct electrolyte abnormalities and dehydration?

IV normal saline.

What is the purpose of a salvage perineal urethrostomy?

To bypass the obstruction; often followed by culling within 3–4 months.

Can the bladder usually be repaired surgically in these cases?

Cannot usually repair the bladder; it may heal on its own.

How long are animals usually kept before culling after salvage procedures?

Usually culled within 3–4 months.

What are strategies to prevent struvite uroliths?

Increase chloride excretion with sodium chloride in the diet; reduce urine pH with ammonium chloride; maintain calcium:phosphorus ratio around 2:1.

How can struvite stones be prevented by dietary chloride manipulation?

Add sodium chloride to the ration to increase water intake and chloride excretion.

How can urine pH be decreased to prevent struvite stones?

Add ammonium chloride to the ration to lower urine pH.

What calcium to phosphorus ratio is recommended to prevent struvite stones?

Calcium:phosphorus ratio of 2:1.

What dietary factors predispose to urolith formation, particularly struvite?

High-grain diets with a Ca:P ratio near 1:1 and diets high in magnesium predispose.

Where are urethroliths most likely to cause problems?

Most often at the sigmoid flexure and the urethral process.

Which type of urolith is most common to cause problems in this context?

Urethroliths (urethral calculi) are the most common.

What determines the type of urolith that forms?

Diet determines the stone type.

What are struvite stones composed of?

Magnesium-ammonium-phosphate.

Which stone type is associated with grazing on silica-rich soil?

Silica stones.

What stone type is due to high-calcium diets?

Calcium stones.

What are the classic signs of acute copper toxicity in sheep?

GI pain, diarrhea, anorexia, dehydration, shock.

What are the typical signs of chronic copper toxicity in sheep?

No signs until an acute hemolytic crisis; depression, lethargy, weakness, recumbency; rumen stasis, anorexia, thirst, dyspnea.

What necropsy findings are characteristic of acute copper toxicity in goats?

Blue-green ingesta; gun metal-colored kidneys; enlarged spleen; increased fecal or liver copper concentrations.

How is chronic copper toxicity diagnosed?

Increased blood and liver copper concentrations; molybdenum levels may also be measured.

What is the prognosis and initial management for acute copper toxicity?

Prognosis is poor; rarely successful. If acute, administer GI sedatives and treat shock as needed.

What drug chelation therapy enhances copper excretion in copper toxicity?

Penicillamine.