Small Ruminants Flashcards
Orf - Contagious Ecthyma
Classic case:
Usually young or newly introduced animals
Lesions:
Painful papules
Vesicles/pustules
Crusts at mucocutaneous junction of lips
Additional locations:
Around erupting incisor teeth +/- buccal mucosa, causing anorexia
Coronary bands, causing lameness
+/- Perineum, eyes, ears
Also may see:
Weight loss due to poor appetite
Gangrenous mastitis in ewes
Dx:
Etiology: parapox virus (related to pseudocowpox and bovine papillary stomatitis virus)
History and exam usually sufficient
PCR or electron microscopy
Rx:
Typical course is 1-4 wks
Usually heals without scars
Isolate or cull affected animals and vaccinate the rest
Antibiotics - topical or parenteral for secondary infections
Supportive care if not eating
+/- Larvicides/repellants to prevent larval screw worm myiasis
High resistance to reinfection after recovery
Pearls:
Zoonotic! Very contagious by direct contact with affected animals OR live vaccine - wear gloves
Vaccination is effective during outbreak, but don’t vaccinate on orf-free farms because vaccine can cause disease
More severe in goats than sheep, but less common in goats
Clostridial diseases(enterotoxemias,tetanus)
Classic case:
Enterotoxemia type C (a.k.a. “bloody scours”)
Bloody diarrhea in kids and lambs
Anorexia, lethargy, GI pain
Seizures, opisthotonus, ataxia
Peracute death without premonitory signs
Enterotoxemia type D (a.k.a. “pulpy kidney” & “overeating disease”)
Largest, fastest-growing lambs (less commonly kids)
Anorexia, lethargy, GI pain
Seizures, opisthotonus, ataxia
Peracute death without premonitory signs
Tetanus
History of wound 10-14 d prior
Stiffness - often starting in masseter muscles (“lockjaw”)
Generalized stiffness (“sawhorse stance”)
Tachypnea, tachycardia, sweating
Hyper-reflexive
Normal consciousness
Respiratory paralysis leads to death
Dx:
Etiologies:
Enterotoxemia: Clostridium perfringens
Type C: Beta toxin causes severe intestinal damage
Type D: Epsilon toxin
Tetanus: C. tetani neurotoxin
Enterotoxemias:
Smears of GI contents: large numbers of gram+, rod-shaped bacteria
Necropsy: hemorrhagic, ulcerative enteritis
Type D (pulpy kidney): rapid post-mortem renal autolysis
Toxin identification: ELISA or PCR on intestinal fluid
Chloroform (1 drop/ml) helps stabilize toxin in sample
Tetanus
Gram+ bacteria seen in smear from wound
Toxin analysis rarely done
Rx: Vaccinate annually with “CD&T” ~ 1 mo before parturition after initial 2-dose series when young
Enterotoxemia type C
Rx rarely successful
Hyperimmune sera and oral antibodies: probably more helpful for at-risk herd-mates
Prevent: good udder hygiene, vaccinate
Enterotoxemia type D
Prevent: minimize rapid feed changes, vaccinate
Tetanus: rarely done, try supportive care
Pearls:
C. perfringens normally present in small numbers in GI tract
Enterotoxemia type C due to drinking too much milk/indigestion
Enterotoxemia type D also due to overeating
More common in sheep than goats
Most common in lambs
Tetanus:
Sporulates in anaerobic, necrotic tissue and produces neurotoxin
Neurotoxin causes spasmodic, tonic muscle contractions
Gastrointestinal parasitism
Classic case:
Weight loss, diarrhea
Anemia with pale mucous membranes
“Bottle jaw” (submandibular edema)
Generalized weakness
Poor coat or decreased milk production
“Wool break”
+/- Death
Dx:
Etiologies
Eimeria spp.: Host-specific coccidian
Telodorsagia (formerly Ostertagia) circumcincta
Trichostrongylus spp.
Haemonchus contortus: “barber pole worm”
Fecal egg count (FEC): eggs per gram of feces
NOT very sensitive!
Perform pre- and post-treatment
Dx of coccidiosis: need >20,000 oocysts/g feces
Necropsy: ID parasites and count worms
Teladorsagia spp.: Increased plasma pepsinogen levels
PCV and/or FAMACHA score:
Sensitive indicator of anemia (from H. contortus)
Compare inferior palpebral conjunctiva with FAMACHA card to score anemia on scale of 1-5 (normal to very anemic)
Rx:
Only treat affected animals to help slow anthelmintic resistance!!
Use “targeted selected treatment”
Use FEC or FAMACHA score to determine need
Strategically time Rx based on knowledge about season and parasite life cycle
Anthelmintics:
Routes of administration: drench, bolus, injection, pour-on or topical, and in feed/water
e.g.: benzamidazoles, probenzamidazoles, imidazothiazoles, macrocyclic lactones
Eimeria spp./coccidiosis:
Rx of affected sheep is ineffective once coccidiosis is diagnosed
Reduce severity with toltrazuril, diclazuril, or sulfaquinoxaline; pasture rotation
Prevent: minimize stress (shipping, ration changes, crowding, severe weather, lambing pens, intensive grazing areas, feedlots)
Prophylactic coccidiostats for 28 d after lambs introduced to new environment
e.g.: monensin, lasalocid
Sheep:
See a “periparturient rise” in egg count due to decreased immunity
Treat pregnant ewes in last month before lambing
Prevention:
Rotational grazing (alternate pastures with cows, horses)
Don’t overgraze or overcrowd pastures
Maintain a good plane of nutrition
Pearls: All inhabit small intestine/abomasum
Fecal-oral transmission:
Eggs shed in feces
Mature into 3rd stage larvae
Ingested by host
Tissue migration
Mature in GI tract to pass eggs into feces
T. circumcincta and Trichostrongylus spp.:
More common in cooler winter/rainfall climates
Enteritis/decreased nutrient absorption
H. contortus:
Most common in tropical or subtropical climates
Does not cause diarrhea alone; causes anemia
Caseous Lymphadenitis
Classic case:
Peripheral lymph node abscesses
Esp. submandibular, parotid, prescapular, prefemoral
Once draining: odorless, creamy (goats) to caseous (sheep) purulent discharge
Heal with a scar
Recurrence common
Internal infection: weight loss, “poor doer” a.k.a. “thin ewe syndrome”
Specific clinical signs based on the organ system affected
Dx:
Etiology: Corynebacterium pseudotuberculosis, a gram+, facultative, intracellular bacterium
Culture abscess material
Internal lesions: ultrasonography, radiography, aspirate
Serology: synergistic hemolysin inhibition titer
Interpretation tricky because often positive due to ubiquitous nature of disease
Can repeat titer to see if rising in 2-4 wks
Rx:
Culling is most practical for commercial operations
If valuable animal:
ISOLATE!
Lance, drain, lavage with iodine solution
Surgical excision
Formalin injection of lesions
NOT okay in animals intended for food
Forbidden by FDA
Antibiotics in extra-label manner: systemic or intralesional
Penicillin & rifampin, tulathromycin
Likely to recur even if treated
Pearls:
Zoonotic! Highly contagious!
C. pseudotuberculosis enters through breaks in skin or mucous membranes
Worldwide, causes significant economic impact
External more common in goats, internal in sheep
Susceptible to bleach and chlorhexidine
Very resilient: can reside in organic debris for long periods
Prevention:
Strict biosecurity
Don’t contaminate environment: collect purulent abscess material & lavage fluid
Careful use of fomites (clippers & dipping tank solutions)
Vaccinate if endemic: reduces incidence, does NOT prevent
Fly control
Pneumonia
Classic case:Coughing, dyspnea, nasal discharge, weight loss,and…
Ovine progressive pneumonia (OPP) and maedi-visna (M-V): progressive wasting, respiratory distress
Sheep greater than 4 yrs old
+/- Indurative mastitis
+/- Neuro signs
Ovine pulmonary adenocarcinoma (OPA):
Respiratory distress, crackles t/o lung fields
Copious serous nasal discharge
Caprine arthritis encephalitis (CAE):
Mostly arthritis and neuro signs
+/- Indurative mastitis with respiratory signs
Chronic enzootic pneumonia: high morbidity, low mortality
Bacterial: thicker nasal discharge
Lungworms: coughing, tachypnea, +/- respiratory distress
Dx:
Etiologies:
Lambs and kids:
Usually viral: PI-3, adenovirus, respiratory syncytial virus; secondary bacterial also possible
Adults:
Viral: retroviruses
Sheep: OPP, M-V, OPA - Jaagsiekte sheep retrovirus
Goats: CAE
Bacterial
Mannheimia haemolytica, Pasteurella multocida(these are also normal flora of upper respiratory tract)
+/-Chlamydia pneumoniae, Salmonellaspp.
Mycoplasmaspp. (chronic enzootic pneumonia)
Corynebacterium pseudotuberculosis(caseous lymphadenitis)
Parasitic:
Dictyocaulus filaria(bronchi),Muellerius capillaris(alveoli and lung parenchyma - worse in goats than sheep), orProtostrongylus rufescens(bronchi)
Affects margins of diaphragmatic lung lobes
Rarely clinical
Parainfluenza-3 (PI-3): virus isolation on nasal swab or serology (2 titers, 2-4 wks apart)
OPP, M-V, CAE:
Ultrasonography of lungs
Agar gel immunodiffusion or ELISA
Necropsy (lungs heavy and don’t collapse)
PCR, virus isolation
OPA
Ultrasound lungs
Wheelbarrow test: pathognomonic for OPA
Clear frothy fluid flows from nostrils when hind end of sheep lifted
Necropsy
Bacterial: culture tracheal wash/lung material
Chronic enzootic pneumonia: necropsy, can be challenging to diagnose
Parasitic:
1st stage larvae seen on fecal float or in bronchoalveolar lavage fluid
Baermann technique may be better than fecal float
Rx:
Viral: supportive care, antibiotics for secondary infections
OPP, M-V, CAE, and OPA: none
Serology twice a year for OPP, M-V, and CAE and cull positive animals
Bacterial: antibiotics, supportive care, improve ventilation
Chronic enzootic pneumonia: maybe long-acting oxytetracycline (off-label)
Parasitic: anthelmintics +/- vaccine
Pearls:
M. haemolytica and P. multocidaare also normal flora of upper respiratory tract
D. filariaandP. rufescensaffect bronchi
M. capillarisaffects alveoli and lung parenchyma - worse in goats than sheep
Parasitic usually affects margins of diaphragmatic lung lobes and is rarely clinical
Caprine Arthritis Encephalitis (CAE)
Classic case:
Adults: progressive polysynovitis/arthritis
Swollen joints (esp. carpus)
Lameness
Weight loss, poor hair coat
Indurative mastitis (“hard udder”), agalactia
Dyspnea due to interstitial pneumonia
Kids 2-4 mos old: encephalomyelitis
Weakness, ataxia
Placing deficits in pelvic limbs
Hypertonia, hyper-reflexia
May progress to para- or tetraparesis or paralysis
Dx:
Etiology: Enveloped, single-stranded RNA lentivirus (family Retroviridae), very similar to ovine progressive pneumonia virus and Maedi-Visna
Serology for herd control programs:
Agar gel immunodiffusion (AGID) - more specific
ELISA - more sensitive
Definitive: biopsy or necropsy shows characteristic lymphoproliferation with degenerative mononuclear cell infiltration
Virus isolation or PCR
Rx: None
Supportive care:
Deep bedding, good quality feed
NSAIDs, regular foot trimming
Prevent:
Isolate kids at birth & feed heat-treated colostrum, pasteurized milk
Serology of herd biannually
Separate seropositive & seronegative animals
Eventually cull seropositive animals
Pearls:
Widespread in dairy goats, 65% prevalence in US herds
Only 20% of infected goats ever show clinical signs
Most goats infected at early age via colostrum or milk
Clinical signs develop much later
Horizontal transmission within herd possible
Pregnancy toxemia
Classic case:
Late-gestation pregnancy (last 1-3 wks)
Dam is over- or under-conditioned
Likely multiple fetuses
Partial anorexia, depression
Bruxism
Aimless pacing, muscle tremors, opisthotonus
Blindness, ataxia, recumbency, coma, death
Dx:
Ketosis: increased serum beta-hydroxybutyric acid (BHB), increased urine ketones
+/- Hypoglycemia, hypocalcemia
+/- Increased nonesterified fatty acids
Necropsy: hepatic lipidosis, adrenal enlargement
Increased BHB in aqueous humor, CSF
Rx:
Mild cases: Enteral/oral therapy
Propylene glycol
+/- Calcium, potassium
+/- Induce parturition with steroids
Severe cases:
Maybe euthanasia
Check fetal viability via ultrasound
If alive and within 3 days of due date, perform C-section
If dead, induce parturition with steroids
IV therapy: dextrose, insulin, calcium, flunixin meglumine
+/- Oral potassium
Prevention:
Assess body condition score (BCS) at breeding and mid-gestation pregnancy check
Takes 6 wks to raise BCS by 1 point
Improve feeding management:
Adequate space
Sort animals by BCS
Ration formulation
Forage analysis
Feed grain in final 6 wks
Do NOT enter last 6 wks pregnancy with BCS less than 2.5
Herd screening of ~20% of flock
Serum BHB levels should be 1.7 mmol/L high risk)
Ionophores MAY help late-gestation ewes improve feed efficiency
e.g, Monensin
Do not use in goats
Pearls:
Pregnancy toxemia develops when there is inadequate nutrition in late gestation in the face of increased metabolizable energy requirements
Mobilized fat stores + increased liver gluconeogenesis passes glucose to fetus
Can overwhelm liver leading to hepatic lipidosis & ketosis
Prognosis is good if ambulatory with mild clinical signs
Prognosis is guarded to poor if recumbent or comatose
Urolithiasis
Classic case:
Partial urethral obstruction:
Dribbling urine
Hematuria, stranguria
Mineral crystals on hair around urethral orifice
Complete urethral obstruction:
Tenesmus, tail swishing
Colic, weight-shifting
+/- Bloat, rectal prolapse, inappetence, depression
Urethral/bladder rupture
Abdominal swelling
Preputial swelling
Necrosis of ventral abdominal skin with “pseudourethral” development
Dx:
Usually obvious based on history/clinical signs, exam
May see urolith in urethral process
Abdominal ultrasound/palpation: enlarged urinary bladder unless ruptured
Abdominal radiographs: calcium carbonate and calcium oxalate calculi are radiopaque (but struvite are radiolucent)
Ruptured bladder:
Abdominal ballottement of fluid wave
Ultrasound: large volume of hypoechoic fluid in abdomen
Abdominocentesis: creatinine of abdominal fluid is 2X that of peripheral blood
Bloodwork: low sodium/choride, high phosphate, metabolic alkalosis
Rx:
If obstructed, not ruptured:
Preferred Rx = tube cystotomy
Calculi are expelled spontaneously over time
If early/mild/partial:
Try antispasmodics/tranquilizers to relax sigmoid flexure of penis
If blockage at urethral process: amputate
Perineal urethrostomy to bypass urolith
Common long-term complication: stricture
If ruptured urethra or bladder:
Drain uroperitoneum slowly via teat cannula or trocar
IV normal saline: correct electrolyte abnormalities, dehydration, acid-base imbalance
Perineal urethrostomy as salvage procedure
Cannot usually repair bladder; may heal on its own
Usually cull within 3-4 mos
Prevention:
Struvite:
Increase chloride excretion by adding sodium chloride to ration (increases water intake to dilute urine and increases chloride excretion)
Decrease urine pH: ammonium chloride in ration
Feed calcium:phosphorus ratio of 2:1
Calcium stones: decrease calcium in feed
Pearls:
Common problem, esp. in males because of long urethra with sigmoid flexure
High-grain diets with a ~1:1 calcium:phosphorus ratio or diets high in magnesium predispose
Most often at sigmoid flexure and urethral process
Urethroliths are most common type of urolith to cause problems
Type that forms is based on diet
Struvite (magnesium-ammonium-phosphate) stones: due to lots of grain with low calcium:phosphorus ratio
Silica stones: associated with grazing on silica-rich soil
Calcium stones: due to high-calcium diets
Copper Toxicity in sheep
Classic case:
Acute:
GI pain, diarrhea, anorexia, dehydration, shock
Chronic (more common! ): no signs until ACUTE hemolytic crisis
Depression, lethargy, weakness, recumbency
Rumen statis, anorexia, thirst, dyspnea
Pale mucous membranes, hemoglobinuria, and jaundice
Photosensitization
If animal survives, renal failure
Dx:
Acute: at necropsy
Blue-green ingesta
“Gun metal”-colored kidneys, enlarged spleen
Increased fecal or liver copper concentrations
Chronic:
Increased blood and liver copper concentrations
Also measure molybdenum levels
Rx:
Rarely successful; prognosis poor
If acute:
GI sedative and Rx for shock may help
Penicillamine: enhances copper excretion
Vitamin C: antioxidant for erythrocyte damage
Ammonium tetrathiomolybdate: decreases liver copper absorption and increases liver copper excretion (has 10-day withdrawal)
Molybdenum: top-dress pastures, supplement feed
Zinc acetate, sodium thiosulfate: feed supplements that both help decrease copper absorption
Pearls:
Worldwide problem
Sheep uniquely sensitive
Excessive copper ingestion for long periods leads to copper build-up in liver then STRESS causes sudden release and acute hemolytic crisis
Stress = transporation, handling, pregnancy, lactation, deteriorating plane of nutrition, weather conditions, strenuous exercise
Sheep have increased liver enzymes for weeks before acute crisis
Factors that affect copper metabolism:
Low molybdenum in diet leads to excess copper retention
Low sulfur, zinc, calcium in diet
Subterranean clover leads to excess copper retention
Plants such as Heliotropium europaeum or Senecio spp. contain hepatotoxic alkaloids which lead to liver disease, leading to release of copper into blood stream and hemolysis
Always check feed labels and use correct feed for sheep!
Polled Intersex Syndrome (PIS)
Classic case:
Most common in western European breeds: e.g., Toggenburg, Saanen, and Alpine
Usually look male (male phenotype), but are genetically female (female genotype), with testes (or ovotestes) and dysfunctional penis
Enlarged clitoris in a doe-like animal or decreased anogenital distance in a more masculine-appearing animal is typical
Polled homozygotic males have decreased fertility
Should not breed polled bucks!
Dx: Thorough exam
Rx: Cull, do NOT breed
Pearls:
Polledness is an autosomal dominant trait in males and females
Intersexism is a recessive trait seen only in polled females
Intersex goats are:
Homozygous for polled trait
Genetically female with male traits (e.g., developed testes)
Most are NOT true hemaphrodites (e.g. those that have true testes and ovarian structures)
PIS is very rare in cattle and sheep
Freemartinism occurs in 20% of opposite-sex sheep twins (arteriovenous anastomoses between their placentas lead to masculinization of the female twin)
Pizzle rot - a.k.a. enzootic posthitis and vulvitis, enzootic balanoposthitis
Classic case:
Males: especially castrated males!
Mild: preputial swelling
Severe: preputial swelling plus straining to urinate
Scabs and ulcers around preputial orifice
Urine accumulation in prepuce
Fatal if urinary blockage due to chronic scarring
Females:
Swelling, redness of vulva and clitoris
Scabs and ulcers of vulva, vestibule, and caudal vagina with yellow exudate
Dx:
Etiology: Corynebacterium renale - a gram+, diphtheroid bacterium that hydrolyzes urea
Clinical signs
Culture
Rx:
Isolate animal
Feed low-protein diet
Clip and clean around prepuce
Make sure urethra is patent
Watch for urination
Pass catheter past scarring
Antibiotics: penicillin or cephalosporin
Pearls:
High-protein diet leads to increased urea in urine causing increased ammonia produced by C. renale which causes penile/urethral irritation
Predisposing factors:
Dirt caked in hair around prepuce
Preputial hairs too short or long - alters urine flow away from urethral orifice
Seasonal incidence associated with high-protein feed intake
Polioencephalomalacia (PEM)
Classic case: Sporadic or outbreaks
Acute:
Cortical blindness (normal PLR and absent menace response) initially, followed by …
Recumbency, tonic-clonic seizures, coma
Subacute:
Anorexia, facial twitching, elevated head
Stands apart from group
Cortical blindness, dorsomedial strabismus
Ataxia, hypermetria
Head-pressing, opisthotonus, bruxism
Rarely progresses to recumbency and seizures
Dx:
2 main etiologies:
Abnormal thiamine status: thiamine normally made by rumen microbes
Any alteration in ruminal microbial activity can lead to decreased thiamine production +/- thiamine destruction
Some plants contain thiaminases (e.g., bracken fern)
Thiamine deficiency leads to decreased energy availability to the brain/impaired glucose metabolism
High sulfur intake:
Dietary: high molasses-urea diet, corn or sugar cane byproducts
High sulfur in water
Certain plants:
Alfalfa
Canada thistle (Cirsium arvense)
Kockia (Koccia scoparia)
Lambsquarter (Chenopodium spp.)
Other causes: water deprivation, sodium toxicosis, lead poisoning
Clinical syndrome is suspicious
Measure thiamine (most labs not capable)
Calculate total sulfur intake on a dry-matter basis
Necropsy: laminar cerebrocortical necrosis and autofluorescent lesions
Rx: same regardless of cause
Thiamine: first dose slow IV, then IM for 3-5 d
Improvement seen within 24 h (may not have complete recovery if advanced disease)
+/- Dexamethasone to decrease cerebral edema
Prevention:
Thiamine supplementation might help
Calculate total sulfur in diet/water and make sure not too high
Provide sufficient roughage during outbreaks to maintain happy rumen microbes/prevent ruminal acidosis
Pearls:
Pathophysiology:
Abnormal cerebral energy metabolism leads to …
Increased intracellular sodium and water leading to …
Cerebral edema, which leads to …
Cerebral necrosis
Seen worldwide in sheep, goats, cattle, deer, camelids
More common in younger animals on high-grain diets
Border disease
Classic case: “Hairy shaker lambs”
Dams:
Increased number of barren dams
Abortion of mummified or macerated fetus
Lambs:
Lambs more often than kids
Hairy, low birth-weight lambs
+/- Darkly pigmented wool
+/- Shortened bones:
Decreased crown-rump length
Decreased tibial and radial length
Decreased longitudinal axis of the cranium
+/- Muscle tremors of the trunk and pelvic limbs - worse when walking/running
Poor survival rate
Dx:
Etiology: 7 known genotypes of a certain pestivirus (Flaviviridae), related to classical swine fever and bovine viral diarrhea virus (BVDV)
Blood of affected lambs: virus isolation, PCR, fluorescent antibody, immunohistochemistry (IHC)
Do BEFORE colostral intake because maternal antibodies mess up test results
Necropsy:
Histopathology of CNS lesions pathognomonic:
Myelin deficiency
Increased interfascicular glial cells with intracellular accumulation of myelin-like lipid droplets
Viral immunocytochemical staining
Rx: None
Prevention/control:
Bulk tank milk test for antibodies
Serology of dams with affected lambs
Mix lambs recovered from infection with breeding stock BEFORE breeding season to enhance natural immunity
Do NOT breed recovered lambs
NO effective vaccine
Pearls: Worldwide distribution
Fetus infected EARLY in pregnancy leads to abortion or widespread distribution in fetal tissues
Surviving lambs are persistently viremic: virus present in excretions and secretions, including semen
BVDV vaccine NOT effective
Scrapie
Classic case: More common in black-faced breeds (genetically predisposed)
Progressive weight loss with good appetite
Pruritus
Progressive ataxia:
First bunny-hopping gait in pelvic limbs
Then high-stepping gait in thoracic limbs
Fine head tremors (esp. ears)
Vacant, fixed stare or sudden aggression
Cutaneous hypersensitivity
If you scratch the back, sheep will throw head back and lick the air or compulsively nibble lower limbs
Always fatal
Dx:
Etiology: Scrapie is a transmissible spongiform encephalopathy (TSE) caused by an abnormal prion protein, related to bovine spongiform encephalopathy and chronic wasting disease of deer and elk
Necropsy: brain IHC
3rd eyelid or rectal mucosal biopsy for IHC
Rectal biopsy is easier and more sensitive
Rx: None
Control:
USDA/APHIS scrapie slaughter surveillance program:
Brains and lymphoid tissue of black-faced sheep and those with clinical signs of scrapie at slaughter are:
Tested by IHC
Positives traced back to herd
Herd quarantined and tested
US mandatory Scrapie Eradication Program:
Individual and premises identification required for all breeding sheep leaving their original premises
Pearls:
In susceptible sheep, abnormal protein called PrPSC (found in all TSE) changes normal cellular prion protein (PrPC) to the abnormal PrPSC
PrPSC deposited as an amyloid plaque in lymphoreticular and nervous tissue leading to neuro signs
Transmitted during lambing (not in utero) and there is a 2-5 yr incubation period
Worldwide except Australia and New Zealand
Rare, but possible, in goats
Does NOT affect humans
Bluetongue
Classic case:
Cyanotic tongue
Fever (105°-107.5°F [40.5°-42°C])
Serous to mucopurulent nasal discharge
Edema of lips, nose, face, submandibular area, eyelids, +/- ears
Reluctance to eat
Congenital defects:
Infection of pregnant dams produces fetuses with hydrancephaly or porencephaly causing ataxic and blind lambs
Fine-wool and mutton breeds of sheep
Listless, reluctant to move
Worse in young lambs (30% mortality)
Congestion of mouth, nose, nasal cavities, conjunctiva, and coronary bands
Lameness and depression
Dermatitis with abnormal wool growth
Dx:
Etiology: There are at least 24 serotypes of the bluetongue virus (genus Orbivirus in the family Reoviridae)
Virus isolation from blood of febrile animals
PCR to ID specific isolate
Serology: competitive ELISA or agar gel immunodiffusion (AGID)
Classic necropsy findings:
Petechia, ecchymoses, or hemorrhages in walls of pulmonary artery
Focal necrosis of the papillary muscle of the left ventricle
Rx:
Supportive care: encourage eating, NSAIDs, deep bedding
Prevention:
Vaccinate in endemic regions
NO cross-protection between serotypes
In nonendemic regions:
Use serotype-specific inactivated vaccines during outbreaks
Use insecticides to control vectors (Culicoidesspp.)
Pearls:
Worldwide distribution mimics vector (Culicoidesbiting midges) distribution
Virus causes vascular endothelial damage:
Changes to capillary permeability
Subsequent intravascular coagulation
Edema, congestion, hemorrhage, inflammation, necrosis
Clinical signs in cattle are similar but rare
Also affects wild ruminants
