FA Med Exam 3

obesity, BCS, flooring, envronmental conditions (moisture, friction, mud), nutrition

• 4 (2 dew claws + 2 claws)
• MT 2, 3, 4, 5

Hoof (keratin); corium (dermal soft tissue); third phalanx (bone P3)

• sole: 4mm/month
• wall: 5-6mm/month, ~75mm normally

Cu, Zn, biotin

• front: medial
• rear: lateral
• More weight on the front half

• dorsal: dorsal metatarsal a. -> axial proper digital a. -> terminal arch
• plantar: terminal arch & marginal a.

• At heel, corium is impregnated with fat, fibrous and elastic tissue
• Increases circulation by pushing blood out of foot

• Vascular connections in the corium
• There are smooth muscles at arterial end; if they constrict -> increased blood flow thru dermis
• This is important for temp regulation, laminitis and systemic toxins (paralysis of smooth muscles and opening of AVAs aka shunting)

• Bier block: inject 2% lidocaine (~20 cc for adult) in vein below the tourniquet
• Dorsal common digital vein (dorsum)
• Lateral digital vein (near dewclaws)

• axially: footrot
• abaxially: vertical fissure aka sand crack

The area of the coffin joint flexor pouch, navicular bone + bursa, DDF tendon + sheath

• connect P1-P1 proximally
• connect P2-P3 distally
• Preserve the proximal during claw amputation

• Forelimb: Common digital extensor
• Hindlimb: Long digital extensor
• Extensor sheaths extend to mid P2

• 6-8 cm proximal to proximal sesamoid bones to just above coronary band
• Usually entered during digit amputation
• Signs of infection: swelling up leg from the digit; very lame!

colostrum!

tuber coxae

tuber ischium

• Backward rotation of P3 -> pinch corium between P3 and sole
• Heel erosion also makes this worse

• Restore normal shape
• Improve gait
• Decrease lameness
• Do once a year at end of lactation

• 0. Wear gloves
• 1. shorten toe using visual approach by starting at point where wall starts to point medially
• 2. draw line to heel
• 3. pare sole and trim wall as needed, stop when reach soft sole
• 4. Keep nippers parallel to sole surface so don’t gauge sole or wall

• FMDV
• BVD
• Malignant catarrhal fever
• Salmonella can occasionally cause dry gangrene of extremities from fetlock distally in calves (also tail, ears) (Salmonella dublin); more commonly in young calves see polyarthritis
• VSV
• Bluetongue virus

• Caused by F. necrophorum (suppurative necrosis from leukocidal exotoxin) and Prevotella melaninogenica (tissue invasion via proteases including collagenases). T. pyogenes facilitates anaerobe growth
• CS are seen in interdigital space; fetid, foul, anaerobic odor; severe lameness
• Resistant strains cause “super foot rot” or “super foul”

• Caused by F. nerophorum and Dichelobacter nodosus (obligate anaerobe that has proteases)
• Considered to be a highly contagious disease!
• Many strains (~20) so vaccination is difficult!
• Milder forms are called “foot scald” or “benign foot rot”

Trauma can help initiate infection, e.g. maceration of skin from constant wet, feces, urine, mud etc.

• Systemic or local abx will allow rapid (2-3 d) recovery except if bone/joint involvement
• Local wound debridement
• If deep structures involved wrap them (coffin joint/ tendon sheath/ navicular bursa/ bone) = poor prognosis

• Isolate
• Reduce environmental contamination
• Keep high traffic areas clean, dry, no sharp stones, stubble
• Fence off low wet areas
• Use Fusobacterium vaccines with management improvements
• Footbaths, if practical (two baths 10' long x 6" deep, change q150-300 cow passages)

• Regular foot trimming
• Footbaths 1x/wk
• Isolate/cull
• Check herd additions
• Vaccination (complete boosters at least 4 weeks before anticipated exposure)
• Avoid confinement in wet, muddy areas

• aka heel horn erosions aka slurry heel
• Organism colonizes the epidermis, but does not extend into dermis (in comparison to footrot)
• Has a gray, fetid, serous exudate
• Lameness but less severe than footrot
• Associated with poor hygiene

• Vaccination of cattle with D. nodusus vaccines is not successful
• Improve farm hygiene

• Clean, debride
• Tetracyclines/Nuflor/Beta lactams

• Does not usually cause lameness
• Sequelae to chronic non-papillomatous interdigital dermatitis
• Interdigital epidermal D. nodosus infection in cattle looks like a "V" diagonally across heel
• Can lead to sole ulcers, sole abscesses, white line disease, complete heel loss

• Clean environment
• Footbaths
• Stalls of sufficient length so cattle can stand up without back feet in gutter

• Contagious, superficial dermatitis of cattle
• Usually just above heels on rear feet
• Sometimes front feet, dorsal area of interdigital space
• More lame than expect!
• Can be erosive or proliferative

• Suspect spirochete: Treponema
• Multifactorial: environment, host, management
• Rough, wet, unsanitary flooring, accumulation of feces/urine
• Transmission between cattle and fomites: inadequately disinfected hoof-trimming instruments, livestock trailers, and farm equipment

• Disinfect hoof trimming equipment (knives, hoof testers, etc.)
• Footbaths with lincomycin or oxytetracycline, copper sulfate, or zinc sulfate
• More effective in low prevalence (<10%); if high prevalence us individual topical first to reduce prevalence
• Stall, corral, and alley hygiene
• Want cow to spend 10 - 14 hr/day resting in clean dry area; no overcrowding
• Closed herd

• Full-thickness 4-6 mm punch
• See plaque of eroded acanthotic epidermis with parakeratotic papillomatous proliferation profusely colonized by spirochete-dominant bacterial flora
• Invasion of stratum spinosum by spirochetes
• Infiltration of neutrophils, plasma cells, lymphocytes, and eosinophils in dermis

• Topical abx (2-4 L ag sprayer)
• Oxytetracycline
• 25g Terramycin-343/L water
• Incorporate oxytet powder in footwraps
• Lincomycin
• 8g Lincomix/L deionized or distilled water
• Repeat q45-60 d
• Systemic abx like PPG or ceftiofur

• Abaxial wall (typically on lateral hind claws) grows beneath P3, displaces sole dorsally
• Twisted, corkscrew appearance
• Usually bilateral; older than 3 yr
• Bony abnormalities because P3 abnormally narrow and long

• Tx: claw trimming q3 mos, although cannot reverse process
• Prevention: do not keep progeny from affected animals (maybe heritable)

• Overgrowth & overlapping claws assoc w/chronic laminitis
• Hard to distinguish from slipper foot
• Therapeutic trimming to treat

• Both claws long, overgrown, like slippers
• Long claw with a flat dorsal wal
• Assoc w/chronic laminitis
• Tx by trimming to restore normal foot shape

• Circumscribed zone of hemorrhage/necrosis at the sole-bulb junction of weight bearing digits
• Incidence increase with high concentrates and protein
• Danger if infection spreads!! e.g. to navicular bursa, deep flexor tendon sheath, and coffin joint
• Tx is hoof trimming or wood block normal digit (and make sure to check the other leg!) + systemic abx (don't use chemical cautery)

Flexor tuberosity causes excess compression of corium and leads to hemorrhage on caudal plantar aspect of P3

• Subclinical laminitis -> softer sole horn -> more vulnerable to trauma
• Ischemic necrosis of corium -> discolored, poor-quality horn with hemorrhage -> keratogenic layer subsequently has impaired activity -> further local hemorrhage and necrosis
• So if you ever see yellowed or bleeding keratin, subclinical laminitis (maybe from diet) is possible

• Disintegration of the sole-wall junction (from soft horn) -> penetration with debris
• Trapped pus spreads under sole/wall -> horn separated from keratogenic layer by pus -> pus discharges at coronary band; may penetrate navicular bursa, coffin joint
• Spread of infection to navicular bursa -> heel swelling, worsening lameness, and if infection spreads -> poor px

• Systemic abx if advanced, wrap claws separately
• Prevent by catching subclinical laminitis; minimize wet, unhygienic conditions; trim claws regularly; foot baths with astringents; removal of rough, coarse road ways

• Lesion starts as fine fissures across perioplic corium and coronary band -> corium below the fissure gets damaged -> extension of fissure distally to bearing surface on hoof wall
• Natural resolution is rare!

• Trauma, dehydration, laminitis, trace element deficiency
• Cu and Zn can affect skin and hair when deficient because both are essential for production and growth of good-quality claw horn
• Maybe anatomy since P3 extensor process underlies area where see some sand cracks

• Most = no treatment
• If infected, pare out, flush, bandage
• Antibiotics if deep/active infection
• Maintain adequate trace element status in animals

• aka horizontal grooves and fissures
• Groove in hoof wall; parallels coronary band
• Indicates nutritional stress or sudden nutritional change
• E.g. weaning (“weaning” groove), transportation, market, dehorning, vaccination

• Remove distal section if thimble to reduce movement during locomotion
• Prevention = reduce stress

• Bier block (consider limb perfusion)
• Clean with water/saline jet
• If horn attached, clean all around without removing wall (protects germinal layers)
• Abx (topical or systemic)
• Wood block & wrap

• Pus between sensitive laminae and sole
• CS are severe pain, 3-legged lame, ddx is a fracture
• Complicated sole abscesses is associated with swelling above coronary band

• Epidermal and dermal tissues show 4x normal thickness
• Tissue proliferates, can become infected or necrosed which causes lameness
• May spread to vital structures
• Stretches distal interphalangeal (cruciate) ligament

• Sx to remove, avoid cruciate ligaments
• Topical abx + wire claws together, wrap
• May be heritable, don't breed

• Rapidly fermentable feed
• -> rumenal lactic acidosis
• -> rumen bacteria die off
• -> endotoxins released
• -> tissue swelling causes shunting away from corium
• -> corium cells die and hoof horn cells stop making horn

• Systemic toxemias in metritis, mastitis causing elevations in histamine
• Rapid weight gains
• Small claw size (mechanical stresses on claw)
• Grain overload
• SARA (sub acute rumen acidosis) - most common cause in cattle - so change food gradually

• > 10% cows over 4 yrs have abnormal claw growth
• >10% culling rate for “feet and legs” excluding infectious foot diseases
• >50% of all lameness <60 days post calving (higher [] food at calving)
• >25% of any lactation group with sole hemorrhage

• Reduced feed intake and rumenation
• Mild diarrhea & foamy feces
• Undigested grain in manure
• Hoof/lameness issues usually 3-6 months later
• Reduced milk fat: <3% because low pH suppresses fiber digestion and end products of fiber digestion used for milk fat

• Monitor rumen pH (puncture site on left side, at top of the patella about 15 to 20 cm behind the last rib; clip and prep site using a standard three scrub surgical prep)
• 4-8 hrs after TMR, or 2-4 hrs after concentrate
• Test the highest risk cows (i.e., within 60 days of calving), ~12 per group

• Normal: >5.8
• Marginal: 5.6-5.8
• Abnormal: < 5.5
• SARA present if 3 or more have pH < 5.5

• Avoid overmixing or overprocessing TMR
• Avoid excessive intake of CHOs
• Avoid inadequate buffering (make sure there is adequate cud chewing!)
• Avoid inadequate ruminal adaptation

• House 1st calf heifers separately.
• Allow heifers time (8 wk ideal) to adjust to post-calving environment
• If mixing cows and heifers, move heifers in groups of 4 to 5 (stick together)

• Seizures
• Tetanus
• Spastic paresis
• Inherited periodic spasticity
• Myopathic disorders:
• Malignant hyperthermia
• Caprine myotonia congenita

• Denervation
• Botulism
• Electrolyte imbalances (hypoK from Predef and hypoCa)

• Increased CK, AST, LDH
• Caused by infection, toxins, nutrition, ischemia, anesthesia compartment syndrome hypoperfusion

• Increases if muscle injury, ~2-4 hrs half-life
• Strenuous exercise = hundreds
• Fatiguing exercise = low thousands (< 5000 IU/L)
• Recumbency levels = typically < 3000 IU/L
• Rhabdomyolysis = typically in the high 10s, 100s of thousands (lab needs to dilute sample)

• High: skeletal, cardiac muscle, liver, RBCs;
• Increases more slowly than CK; peaks 12 to 24 hrs after injury and is more stable than CK so the t1/2 is measured in days
• If increased CK + AST = recent active myonecrosis
• If CK persistently elevated = muscle damage ongoing
• If reduced CK & elevated AST = muscle damage not ongoing

• aka elso heel
• seen in beef calves 2wks-7months of age and Pygmy goats
• CS are straight hocks (can’t flex hock) from continuous gastrocnemius tension
• Can be uni- or bilateral

Hyperactivity of gamma efferents

• Can try tibial neurectomy or gastrocnemius tenectomy
• Better to just castrate!

• Episodic involuntary spasms affecting rear limbs, epaxial thoracolumbar muscles in dairy cattle
• CS of crampiness, stretches, periodic spasticity, muscle trembling and backward extension of rear limbs after rising

• Possibly a disorder of myotactic reflex or postural reflex mechanisms
• Often associated with musculoskeletal pain (sore foot; other lameness)

• Treat any underlying lameness
• Banamine, phenylbutazone (remember withdrawl), other NSAIDS

• Autosomal dominant with incomplete penetrance from mutation in skeletal muscle Cl-channel
• See signs by 6 weeks
• Clinical signs are stiffness after rest, marked general rigidity after visual, tactile, or auditory stimulation, and are nonprogressive
• Diagnosis is by EMG

• Usually rapidly fatal
• Infectious, not contagious
• CS of Fever, tachypnea, tachycardia, anorexia, depression, lameness with swelling, pain, and crepitus at site of infection (from anaerobic gas production)
• Cl. septicum causes malignant edema
• Cl. chauvoei causes blackleg (if you're a chauvinist, you look at legs)
• Cl. novyi (Type B) causes black disease (infectious necrotic hepatitis)
• Cl. sordellii
• Cl. perfringens

• Cl. novyi Type A
• Cl. tetani
• Cl. hemolyticum

• Clinical signs
• Fluid aspirates for culture and FA

• Found ubiquitously in the environment, feces, GI tract
• Portal of entry = alimentary tract mucosa where spores become latent in liver & muscle tissue -> disease if tissue devitalized providing anaerobic environment (e.g. liver biopsy or liver flukes) OR external wound contamination

• Act locally and systemically to create widespread organ dysfunction
• α - lecithinase
• β - deoxyribonuclease
• γ - hyaluronidase
• δ - hemolysin

• Putrefaction with legs extended stiffly
• Frothy, bloody discharge from the anus and nostrils
• Foul odor (rancid butter) and congested lungs (edema)
• Swelling, crepitus in affected muscles

• Abx, fasciotomy, supportive care
• Drug of choice is high dose IV K- or Na-penicillin or could use PPG (less expensive)
• In outbreaks vaccinate or revaccinate herd

• Vaccinate young stock
• If < 6 mos of age when they get initial series (i.e., primary and booster), booster again prior to one year
• Revaccinate annually

• Vaccinate
• Remove carcasses (or all spores infect soil)

• Find cysts in heart, esophagus and skeletal muscle (incidental at necropsy)
• 2 host cycle where definitive host is carnivores and intermediate host is a ruminant
• In cattle: S. cruzi (dog), S. hirsuta (cat), S. hominis (primates)

• Amprolium or ionophore antibiotics before the 2nd stage of parasitemia
• To control, prevent gross contamination of feed with feces!

• A phenolic pigment that binds protein and iron
• Unbound or free gossypol is toxic
• Clinical signs are ill thrift, weakness, decreased milk production, lack of spermatogenesis in bulls, death from liver (more with Pima var.)and heart failure
• Naturally acts as an insecticide

• Monogastrics, young calves <4mos should not > 100ppm = 0.01%
• Mature ruminants tolerate 20 g of gossypol/hd/d = 5–6# cottonseed/hd/d
• Rule of thumb: Don’t feed >7# cottonseed/hd/d

• Mechanism: lipid-soluble complexes with cations to facilitate transport across lipid membranes
• Use: growth promotants and coccidiostat and to prevent ketosis
• Toxicity: causes rhabdomyolysis and cardiomyopathy. CS of anorexia, pica, diarrhea, hind limb ataxia, dyspnea, weakness, tachypnea
• Necropsy: myocardial necrosis; pulmonary edema; pleural and peritoneal effusions; bloody pericardial effusion

• Monovalent: monensin (Na+), salinomycin and narasin (K+)
• Divalent: lasalocid (Ca++ and Mg++)

• aka compartment syndrome
• Decreased perfusion to down muscles causes mild elevations in CK from recumbency (probably <3000), unless there is actual muscle cell necrosis

• Txt: fix underlying cause, fluid therapy, NSAIDs, nursing care, good footing and bedding, flotation
• Prevent: Careful positioning, draw down front leg forward, support upper limb, light anesthesia, IVF, positive inotropes

• Myodegeneration of cardiac & skeletal muscle
• Young, rapid growing calves, lambs, kids
• Selenium-deficient diets of dams in gestation

Correct Se and VitE deficiencies, esp Se def

• Selenoproteins: glutathione peroxidases, deiodinase [converts T4 to T3], selenoprotein-P
• VitE:
• If antioxidant mechanisms overwhelmed, see membrane damage -> increased Ca -> damage to mitochondria -> impaired energy metabolism -> muscle hypercontraction, cell necrosis, hyalinization

• Young animals born in confinement and turned out early spring to exercise
• Yearling cattle housed all winter, fed high grain diet with high moisture content and then suddenly turned out in the spring

• Chem: AST, CK, LDH
• CK: very high 10’s, 100’s of 1000s
• U/A: myoglobinuria often in yearlings
• Blood Se (in ppm): 0.01-0.04 (deficient, should supplement), 0.05-0.06 (marginal, supplement often beneficial), >0.07 (normal). Can also measure blood Se by measuring RBC glutathione peroxidase
• Liver selenium: normal = 0.25-0.5 ppm in cattle

• Cardiac (acute-peracute): myocardial decompensation; tachypnea; resp distress; frothy nasal discharge; sudden death in <24 hrs usually 2-4 mos of age
• Skeletal (slower onset): weakness, stiffness, recumbency, difficulty rising; stands briefly; lays down; swollen, firm, painful muscles; dysphagia; weak suckle if tongue affected
• Cardiac form affects LV and septum in calves; both ventricles in lambs

Bands of coagulation necrosis, fibrosis and calcification esp seen in WMD

• Cardiac involvement: tx rarely attempted
• Skeletal muscle involvement: responds better but still guarded prognosis. Expect improvement in 3-5 days to stand or walk, but complications of pneumonia
• Give Se: 0.055-0.067 mg/kg SC or IM (BO-SE, MU-SE)
• Give VitE: Injectable (300 IU/ml as d-alpha-tocopherol, lasts ~ 3 weeks), oral (Emcelle, give daily)
• Supportive therapy: abx, monitor fluid and electrolyte status

• Inject Se at birth (do not use Bo-Se in pregnant ewes, nor Mu-Se in third trimester theoretically)
• Supplement with slow release oral formula once monthly (will often regurg)
• Monitor herd q60-90 days, unless supplementing can monitor q6-12months

• Active growth plants that are high in linolenic acid (PUFAs have hydroperoxides that make toxic free radicals)
• Acid soils, soil from volcanic rock, soil with high sulfur content are def in Se (blocks Se uptake by plants & absorption in GI tract)
• Legumes accumulate less Se than grasses
• Extended storage of grain has decreased Vit E
• Calves fed milk replacers with fish oil, linseed oil, soybean or corn oil (all have increased PUFAs)

• Exercise intolerance, collapse with exercise
• See elevated CK and can clinically look like WMD
• Autosomal recessive inheritance
• Diagnosis based on muscle biopsy and staining for phosphorylase on frozen sections, as well as presence of normal vitamin E/Se status

• congenital myopathy for double muscling in Belgian Blue, Piedmontese, South Devon
• Increase in muscle Type 2B & reduced Type 1 and 2A
• Dystocia and oral anomalies (tongue hypertrophy) are common

• Major component of sling for thorax between forelimbs
• May occur with WMD

• Peroneus tertius: distal femur to proximal metatarsal bone
• Associated with trauma/struggling
• Hock extended while stifle flexed
• Tx: rest/support; ruptures in muscle belly more likely to recover than tendon/ or origin/insertion

• Obturator, gracilis, pectineus muscles are ruptured
• Caused at parturition or poor footing
• Flotation or deep bedding with good footing to treat
• Prognosis guarded

• Rupture at muscle-tendon junction common
• Happens after lumbosacral epidural with lidocaine
• See hock flexed while stifle extended
• Treat with Thomas splint
• Prognosis is poor

• Synovial cells: A=phagocytic; B=secretory (make hyaluronic acid)
• Synovial fluid: plasma ultrafiltrate; should not clot
• Cell composition: mononuclear cells ~ 90% of the total, MPN leukocytes ~10%, protein ~ 1.5 g/dL (but variable)
• Viscosity: normal 2 cm stretch between two fingers (reduced viscosity from dilution, synovitis, or hyaluronic acid degradation)

• To see if synovial fluid normal
• 3 drops into 3 mL of 2% acetic acid (EDTA may interfere)
• Shake gently
• Normal = a tight, ropey clot
• Abnormal = loose clot w/particles floating

• Use RTT tube for culture
• Use RTT & EDTA tube for cell count & general cytologic exam
• Use Na-fluoride tube for glucose (to prevent bacteria from eating all the glucose)

Very turbid, makes a clot, 50K-100K WBCs (90-95%), >4g/dL protein, flakes in mucin clot test

• Total nucleated cell count >25,000/ul OR PMN count > 20,000/ul or >80% polymorphonuclear cells
• AND TP>4.5 g/dL

• Foreign body (puncture)
• Hematogenous
• Calf with umbilical infection, septicemia
• Extension of cellulitis from adjacent structure (eg. severe footrot)

• T. pyogenes is most common adult bovine, also Strep, Staph
• Don't culture - waste of money
• Use indirect evidence like cell counts, gram stain, protein, ultrasound appearance

• CS: Reluctance to bear weight, stiffness, joint effusion
• Scleral injection, uveitis, hypopion, petechiae also if septic
• Dx: PE, rads, synovial fluid cytology and culture, CBC, blood culture

Physeal involvement not typical in mycoplasma polyarthritis

• Lytic lesions (in physes too)
• Physeal involvement not typical in mycoplasma polyarthritis
• Radiographic changes in bone delayed up to 14-21 days after infection

umbilicus, intestine (enteritis), pneumonia

high quality colostrum (FPT increases risk of sepsis)

• Most common: enterics (E. coli; Salmonella)
• Also Mycoplasma, will see concurrent otitis media, conjunctivitis, pneumonia
• Less commonly Strep, Staph, T. pyogenes (older calves more likely)

• Joint lavage/arthrotomy
• Long term broad spectrum antibiotics
• If mycoplasma use chloraphenicol, macrolides, tetracyclines NOT beta lactams
• Prognosis:favorable (early aggressive therapy) and guarded (multiple joints affected, delayed therapy)

• Age: cattle 6-18 months
• CS: effusion of lateral femorotibial joint, absence of joint laxity, less lame than septic arthritis
• Dx: synovial fluid has high cellularity and TP but no bacteria and minimal/no neutrophil toxicity (beware - septic joints often don't see bacteria either). Radiographs show ±subchondral bone cysts (lateral tibial plateau; femoral condyles)
• Txt: box stall rest, intra-articular steroids, parenteral and intra-articular antibiotics, joint lavage, arthrotomy/arthroscopy and surgical curettage, placement of egress and ingress drains.
• Px: regardless of txt, 2/3 return to productivity

• Chronic cellulitis of epidermis and subcutis over lateral hock following repeated trauma, which causes a bursa to form on lateral aspect of hock
• Signifies there's a housing or environmental problem because she can't aly down without banging herself all up
• Can become infected and require drainage and antibiotics

• Formation of a SC bursa over carpus that rarely involves carpal joint
• Txt: sterile drain & wrap, can inject 10-20 cc renographin (makes scar tissue) & pressure wrap x 2 weeks with q5 d bandage changes, can insert drains (less cosmetic; not for show animals), or can sx remove

• Septic bursitis of hock or bursa under SDF tendon ±osteomyelitis of calcaneus
• Txt: drain via lateral incision followed by curetting/drain placement + antibiotics
• Superficial flexor tendon should not be involved unless severe necrotic changes present
• Px: guarded with osteomyelitis

• Diseases: mastitis, reproductive disease, respiratory disease, keratoconjunctivitis, otitis media
• CS: facial and vestibular nerve deficits with bilateral or unilateral ear droop, ptosis, epiphora, head tilt and recumbency
• Transmission: calves fed mycoplasma-contaminated colostrum or milk

• Etiology: Mycoplasma mycoides ssp. mycoides (large colony type)
• Pathophys: Stress -> shedding from chronic carriers, goat ear mites (Psoroptes cuniculi and Raillietia spp) may be a reservoir for M. mycoides ssp. mycoides
• CS: Adults have fever, mastitis, pleuropneumonia and arthritis
• CS: Kids have arthritis, septicemia, meningitis for 1-3 days then become BAR
• Typical scenario: polyarthritis and pneumonia in kids concurrently with mastitis in does
• Dx: PCR joint fluid (don't culture)
• Txt: don't tx! Will cause chronic shedder, and no abx work very well
• Px: Highest morbidity and mortality in young stock
• Prevention: Isolate & perform milk cultures on herd additions; if doe dry at purchase, maintain isolation until culture at kidding and @ 2 and 4 weeks fresh or swab and culture ear wax (in dry does); if outbreak, heat treat colostrum

• Lentivirus
• Targets monocytes and macrophages which localize in synovium, MG, CNS, lung (non-neutralizing antibodies produced and immune complexes cause chronic inflammation)

• Primarily colostrum and milk
• Also in utero/ horizontal
• Virus-infected cells in estrual mucus, preputial swabs, lochia post kidding, semen aspirated from tail of epididymis
• So important to segregating infected/noninfected herdmates!

• Leukoencephalomyelitis:
• 2-6 mos kids
• Rear leg paresis or paralysis
• Eat normally, alert, afebrile
• Discomfort secondary to urine retention
• Polysynovitis-arthritis:
• Mostly in mature adults >2-3 years
• Insidious onset
• Carpus commonly affected
• Chronic joint enlargement & weight loss
• “Hard Bags”: mammary gland involvement
• Decreased milk production; hungry kids; firm udder; milk looks normal
• “Hard Lungs”: chronic interstitial viral pneumonia results in progressive respiratory distress/weight loss with or without evidence of polysynovitis/arthritis
• Similar to ovine progressive pneumonia (OPPV) virus

• Joint fluid analysis:
• Normal or increased volume
• Brown-to-red tinged
• Decreased protein
• Increased cells (1000 to 20,000 cells/ul with 90% mononuclear cells
• Contrasts with neutrophil increase typical of bacterial joint infection
• CSF (on kids with leukoencephalomyelitis):
• Increased CSF mononuclear cells
• Official USDA tests:
• AGID test using OPPV as antigen
• Competitive ELISA (cELISA) – more sensitive
• Test for maternal CAEV antibodies in kids up to 4 mos

• Tx: none, keep pet goats comfortable with NSAIDs, glucosamine, nursing care
• Prevention:
• Block transmission by contaminated milk or colostrum (use duct tape)
• Isolate seropositive goats
• Serologically monitor herd
• Heat treat colostrum (too high = D), thoroughly mix! and watch temps!

• Parturition, dystocia
• Riding injury during breeding/heat
• Predisposing factors like relaxation of pelvic ligaments (relaxin hormone)

• CS: subluxation = mild ataxia, rear limb weakness; luxation = severe posterior paresis, recumbency
• Txt: rest, good footing, analgesics, NSAIDs, flotation therapy

• Dystocia with sciatic (or ‘obturator’) paralysis
• Slipping/falling due to weakness
• Electrolyte weakness leads to struggle to get up -> splits
• Neonates that are forcefully extracted if posterior presentation
• Cranial dorsal is most common!
• Caudal ventral is possible, determine by palpating femoral head per rectum through obturator foramen

• 1) Limb is circumducted with maximal abduction (disperses blood/fluid)
• 2) Attach a pulley and apply traction caudally while attempting to rotate the hock outward to forces femoral head medially back into acetabulum
• 3) Apply hobbles and rest for at least 24 hours
• Px: Younger animals, <12 hours duration, still standing, <400 kg, cranial luxation all correlated with better px

• Cause: Arthrogryposis, lupin ingestion by dam
• Tx: choose cases carefully; conservative = splinting, support bandages, NSAIDs, toe extension shoes; invasive = sx to cut SDF / DDF tendons

• Primary: if Cu in diet < minimum requirements (4-10 ppm in cattle, 5 ppm in sheep).
• Young animals/fetus more susceptible than adult
• Cattle more susceptible than sheep
• Secondary: reduced availability of Cu due to high dietary Mo, S, Ca, Zn, Fe
• Therefore keep Cu:Mo ratio more than 2:1, but 5:1 ideal for sheep and 6-10:1 ideal in grazing cattle

• Enzootic ataxia/swayback, ill thrift, decreased immunity, anemia, reproductive inefficiency
• Osteoporosis secondary to depressed osteoblastic activity -> spontaneous fractures and widened growth plates/metaphysis
• Lysyl oxidase synthesizes collagen in connective tissue to mineralize bone; also aortic rupture reported in Cu deficient pigs
• Achromotrichia because tyrosinase (Cu-dependent) converts L-tyrosine to melanin so you see diluted coat color
• Diarrhea results from villous atrophy

• Liver better than serum (serum decreases only when liver is depleted, and serum is slow to rise post supplementation)
• Liver biopsy (or from necropsy) best! Ongoing basis
• Sample at least 5 animals (want 25-100 ppm)
• Before or after biopsy administer _______?
• Ceruloplasmin is an acute phase protein, so serum Cu can be falsely elevated with inflammation

• Some injectable forms (inj site abscesses) so oral supplementation preferred
• Intraruminal boluses, top dressing of pastures, and or via addition of copper to salt mixes or a total mixed ration
• Control competing dietary factors! Dietary Mo, S, Zn, Ca, Fe
• Mineral mixes containing copper sulfate 0.25 – 0.5% in sheep, 0.2% in cattle

• Age: 5-12 mos old; variable lameness
• Etiology: overloading poorly formed metaphyseal bone and subsequent loss of structural integrity, microfracture, pain, and callus formation
• CS: Enlarged, abnormal shaped distal physes (widened irregular physes; lipping)
• Dx: CS, rads
• Tx: Evaluate/adjust trace element status, pay attention to Cu, Zn, Ca, Ph

• Osteochondrosis: abnormal physeal or epiphyseal cartilage growth
• Osteochondrosis dissecans (OCD): a portion of articular cartilage splits off in an area of dysplastic subarticular cartilage and forms a flap
• Caused by: rapid growth, nutrition, genetics, copper deficiency
• CS: Joint effusion, mild to moderate lameness. Commonly in stifle, hock, shoulder
• Dx: Rads, CBC, joint taps (aseptic)
• Txt: Evaluate nutrition, correct macro/micronutrient deficiencies, rest

• Animals: young, rapidly growing animals
• Etiology: P or VitD deficiency, inadequate exposure to direct sunlight, Ca def and excess dietary P causing nutritional secondary hyperparathyroidism; Mg, Zn, Mn, VitA deficiency
• CS: bowlegged, stiffness, reluctance to move, lameness, joint enlargement, arching of the back, enlarged costochondral junctions
• Dx: Thin cortices, bowing long bones, enlarged and widened physeal plates, irregular radiolucent band at meta- epiphyseal junction, physeal “lipping” (cattle with Cu deficiency may have physeal lipping). Need to determine ratio of bone ash:organic matter (bone ash is primarily CaP, normal = 3:2, rickets = 1:2 to 1:3)
• Tx: Supplement with Ca2PO4 (23% Ca, 18.5% P), limestone plus a P source, injectable VitD
• Prevention: balanced diet
• Px: fair to good if ambulatory

• aka ovine hereditary chondrodysplasia
• Etiology: semilethal AR disease in Suffolk, Suffolk crossbred, and Hampshire sheep (lambs must be ss to show CS)
• CS: angular limb deformities (“knock-kneed”, carpus valgus), kyphosis, scoliosis, concavity of sternum, crooked roman nose), failure to thrive
• 2 syndromes: abnormal at birth (stillborn or die within days of birth, or die from scours and pneumonia by 1 month); develop abnormal signs 3-8 weeks (one or more limbs affected, decreased growth rate after 4-8 wks, eventually progresses til lamb can’t walk)
• Dx: rads (widened irregular growth plates w/retained islands of cartilage, esp look at olecranon lateral and flexed); stillborn lambs may not exhibit radiographic changes.
• Prevention: destroy carrier rams (can use carrier ewes to get market lambs or to progeny test rams)
• Breeding stock classification: white - no known spider progeny, gray - sire or dam or sibling has produced a spider lamb but this individual has not, black - individual has produced a spider lamb

• Downer cow with no metabolic or skeletal reasons (i.e., fracture) for being down, and that the cow is alert (i.e., not sick with mastitis, metritis, or other metabolic disease).
• To determine which limbs weight bearing or not (once standing in tank)
• To facilitate faster recovery following development of recumbency (ie, get them up sooner than later!)

• Characteristic knuckling of fetlock; slight dropped hock
• Often secondary to calving paralysis (sciatic paralysis)
• Txt is support wrap...maybe distal limb cast for 2-4 weeks (often more economical than leg wraps)

• BHV1.1
• aka rednose

• IBR (BHV1.1): resp, conjuctiva, ocular
• Repro (BHV1.2): infectious pustulovulvovaginitis/balanposthitis, abortion

BHV2

BHV5

• Caused by: BHV1.1
• Pathogenesis: aerosol, fomites, genital secretions (semen, fetal fluids, tissues)
• CS: abortions (late), conjuctiva, deep corneal vascularization, corneal edema (peripheral along limbus, so not pink eye)
• Dx: paired serology, PCR
• Prevention: vaccination (at 6mo with MLV, annually re-vx)

conjunctival fornix, nasolacrimal duct, under 3rd eyelid

• Photophobia
• Epiphora
• Blepharospasm
• **Limbic corneal ulceration**
• Pinkeye secondarily

• None, but good idea to recheck
• Triple abx eye ointment
• Parenteral antibiotics post removal may help prevent pinkeye but often heal spontaneously
• Inspect under 3rd eyelid

• aka eyeworms
• Caused by: Thelazia gulosa (cattle), T. skrjabini (cattle and horses), T. lacrymalis (horses), T. californiensis (dogs, sheep, and other wild mammals)
• Life cycle: L3 larvae regurgitated from face fly crop during feeding; larvae develop over 3-6 weeks; adult worms can ulcerate eyes
• Dx: direct observation
• Txt: remove worms, levamisole, doramectin (Dectomax)

• Most common eye disease in neonatal lambs
• Congenital (primary): usually lower eyelid and bilateral
• Acquired (secondary): upper or lower eyelid
• CS: rubbing of the eye, ocular and nasal discharge, photophobia, epiphora, blepharospasm, corneal ulceration over lower (or upper if upper lid) half of cornea
• Txt: inject penicillin (1-2 cc) into lower lid, skin staples to evert the lid, place 2-3 vertical mattress sutures

uterus, abomasum, epidural space, right atrium, retrobulbar LNs

• In 10% of Herefords
• Median age: 7.4 yrs
• Cattle with nonpigmented periocular tissues most susceptible (~75% of affected cattle lack pigmentation)
• UV exposure is risk factor

• Plaque: dense white keratinized non malignant tissue located on the corneoscleral limbus or lid margin
• Papilloma: cornified wart-like tissue usually from eyelid
• Acanthoma: keratinized tumor shaped like a horn; the keratin can be removed from the surface of the tumor leaving a small invasive, malignant mass growing off corneal surface

Involves removal of the eye, adnexa, and part of the bony orbit

pseudocowpox, orf, bovine papular stomatitis

• Malignant = smelly
• Metastatic = look for enlargement of submandibular, parotid, prescapular lymph nodes

• Medical: hyperthermia (anesthetize and proptose eye with retrobulbar block, apply electrode probe across tumor, sensor keeps tissue between electrodes at 52°C, then rotate 90° and repeat) or cryotherapy (freeze and thaw x3, for tumors <0.5cm)
• Surgery: 3rd eyelid removal, excise, exenteration (standing or under GA)

• aka pink eye
• Caused by: Moraxella bovis (g- rod) and Moraxella bovoculi (g- cocci), has pili to adhere and cytotoxin
• Peaks: July - Sept
• Transmission: carrier cattle (eyes, vagina, nose), foxtails, flies, concurrent infx, DVMs
• CS: corneal edema that starts centrally; central corneal ulcer
• Dx: corneal swab culture
• Txt: LA-200 and Draxxin are approved, conj inj penicillin, patch eye for comfort
• Prevention: disinfect materials btw cows, fly control, foxtail control, vaccine (must be 4 wks before = June...and Cu/Se supp), ear tags

• Caused by: Mycoplasma (esp M. conjuctivae), Chlamydophila pecorum...M. ovis (g- cocci) is less important and can be found in healthy sheep and goats
• CS: Conjunctival hyperemia, photophobia, blepharospasm, epiphora, becomes mucopurulent
• Dx: corneal ulcer culture (Mycoplasma); conjunctival scrape, cytology or paired serology (Chlamydophila); culture or PCR (M. ovis)
• Txt: self-limiting in a few weeks, tetracycline

• Cattle: in utero BVD infection
• Short horn cattle: large lids/3rd eyelid/entropion
• Jersey calves: autosomal recessive disorder
• Herefords: autosomal recessive encephalopathy, had skull malformation (doming)
• Lambs: from seleniferous pastures
• Piglets: VitA deficiency in sows