BOVINE REVIEW Flashcards by Delaney Garcia

-Actinobacillus, pasteurella, and strep spp.
CS: Tachycardia, anorexia
LESION: Tricuspid and pulmonic valve
GUARDED prognosis

Endocarditis

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Cattle at elevations >2000m
-CS: brisket edema, venous distension, cyanosis, tachycardia
-Can develop Cor pulmonale (R sided heart failure from pulmonary hypertension)
-MURMUR: Pistol shot murmur over jugular furrow
-Get cattle with PAP <41 mmHg (genetic selection

High mountain disease

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-Abomasum is between rumen and abd. wall
-Risk factor: parturition
-CP: metabolic alkalosis with hypochloremia and hypokalemia
-CS: Ping on L side between ribs 9-13, normal TPR
-TX: Roll after casting cow on right side or SURGICAL - R/L omentopexy

Left Displaced Abomasum

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-Abomasum goes from ventral abdominal wall to craniodorsal right abdominal wall
-CP: Mild hypokalemic hypochloremic metabolic alkalosis
-CS: ping on right side between ribs 10-13
TX IS ALWAYS SURGICAL - right paralumbar fossa omentopexy

Right Displaced Abomasum

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-occurs after an RDA where the abomasum rotates CCW and gets stuck in the greater omentum
-Hypochloremic hypokalemic metabolic alkalosis with paradoxic metabolic acidosis with azotemia
-Ping on right side cranial to 10th rib
-Tx is surgical - Right paralumbar omentopexy
-Afib can develop

Abomasal Volvulus

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Type 1: Erosion with no hemorrhage
Type 2: hemorrhagic
Type 3: Perforated with acute localized peritonitis
Type 4: Perforate with diffuse peritonitis
Type 5: perforated with peritonitis in omental bursa
-CS: Bruxism, tachycardia, melena
-common in milk fed calves

Abomasal ulcers

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-Normal gas in a stable foam
-Pasture: Legumes or Feedlot (grains)
-CS: distension affecting the contour of the paralumbar fossa protruding into the vertebral column
-See Bloat line on necropsy - cervical esophagus congested but thoracic portion is blanched
-Dx: No relief by passage of tube, corrected after administering antifoaming agent
-Tx: Poloxalene or rumenotomy if emergent/life threatening

Frothy bloat

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-Caused by esophageal obstruction or pressure from enlargement outside the esophagus
-CS: free gas on top of solid and fluid ruminal contents, gas released and alleviated distension when passing a tube
-tx: trocar and cannula for emergency relief

Gas bloat

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-5 days to 2 week old calves
-Decreased villous height ==> decrease in intestinal SA
-Malabsorptive diarrhea
-Most common cause of viral diarrhea in calves

Rotavirus

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-5 days to 2 week old calves
-Atrophy of colonic ridges (jejunum halfway)
-mucohemorrhagic enteritis, malabsorptive diarrhea, moderate depression

Coronavirus

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->5 day old calves
-F5(K99) or F41
-Pathophys: enterotoxin influences ion and fluid secretion to produce a noninflammatory secretory diarrhea

Enterotoxigenic E. Coli (ETEC)

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-4 days to 2 month old calves
-dissolution of brush border and decrease in enzyme activity
-Mucohemorrhagic diarrhea
-Zoonotic 0157:H7

Attaching and Effacing E. coli (AEEC)

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-2+ week old calves
-CS: fould smelling bloody diarrhea with septicemia

Salmonella diarrhea

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-Few day old calves
-Hemorrhagic enterotoxemia (ABC)
-CS: weakness, bloody diarrhea, abdominal pain
-enterocyte necrosis and submucosal inflammatory infiltrate

Clostridial Diarrhea

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->2 but <1 year old calves
-E. bovis and E. zuernii
-most infected calves show no clinical signs, decreased growth
-can be severe; lethargy, bloody diarrhea, abdominal discomfort, tenesmus
-WINTER COCCIDIA: CNS signs (muscle weakness, clonic-tonic convulsions, nystagmus)
Tx- coccidostats

Coccidiosis

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-5 week old calves
-Self limiting diarrhea
-adheres to apical surface of enterocytes in distal si and results in loss of microvilli

Cryptococcus parvum

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-Failure of reticular groove reflex, results in ruminal acidosis
-Chronic cases can lead to hyperkeratosis of the ruminal mucosa and impairment of ruminal motility with recurrent tympany
-CLAY LIKE FECES

Rumen Drinker Syndrome

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-C. perfringens type A or aspergillus
-Necrotizing hemorrhagic enteritis of SI that leads to intraluminal blood clot
-Occurs 3 months in of lactation
-Risk factor: highly fermentavle feeds
-See dark jelly like feces
-Sx and supportive care
-High fatality, grave prognosis

Hemorrhagic Bowel Disease

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-Fusobacterium necrophorum
-secondary to grain overload
-Seldom see CS, most are occult lesions
-Can rupture into hepatic veins and lead to thrombophlebitis of the cd VC with thromboembolic disease, endocarditis, and pneumonia

Liver abscess

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-CS do not develop until animal is 2 years old
-Can survive on pasture for a long time
-Infects macrophages causing a granulomatous enteritis
-CS: Weight loss, diarrhea, PLE
-Necropsy: thickened and corrugates intestine
-Dx: PCR, acide fast impression smear of ileum
-Cull positives
-Zoonotic -Crohn’s dz

Mycobacterium avium sp. paratuberculosis - MAP - Johne’s disease

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-Oral infection or vertical infections
-Late trimester abortion or PI calves
-CS: Respiratory illness, pneumonia, arthritis, meningoencephalitis
-Dx: necropsy or ELISA
-NECROPSY: pulmonary congestion, suppurative pneumonia, diffuse catarrhal hemorrhagic enteritis, ileitis, hepatomegaly, splenomegaly, gelatinous edema of the gallbladder
-ELISA: detect ab in serum or milk; used for herd monitoring
-Most S. dublin strains are multivalent and antimicrobials that are effective are not allowed in food animals

Salmonella dublin

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-Ingested hardware fall into reticulum and penetrate the wall
-CS: arched bax, groaning and grunting
-as acute inflammation resides, signs of cranial abdominal pain become less apparent and rectal temps become normal
-Dx: Grunt test
Tx: Rumen magnet, PPG, ampi, Ceftiofur
-Prev: rumen magnets

Traumatic reticuloperitonitis

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-Risk factors: cold temps, closed confinement
-CS: fluid diarrhea, nasolacrimal discharge or cough, decreased production
-Dx: PCR and serology
Tx: supportive care

Winter dysentery (bcov)

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Type 1: Failure of eructation
-Hx of pneumonia or inflammatory lesions
Type 2: Failure of omasal transport
-Hardware disease
Type 3: Failure of Pyloric outflow
-DAs or volvulus

Vagal indigestion

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-REPORTABLE DZ -Dermacentor ticks, biting flies -Strong correlation between age of cattle and severity of disease -Carriers for life -CS: EXTRAvascular hemolysis, targets RBC, icterus, anemia, fever, weight loss -Dx: Inclusion bodies on margin of RBC on blood smear -Tx: Tetracycline, imidocarb

Anaplasmosis Marginale

-REPORTABLE DZ -B. bovis and B. bigemina -Boophilus/rhipicephalus tick -CS: INTRAvascular hemoylsis, fever, ataxia, HEMOGLOBINURIA -Tx: Imidocarb

Babesiosis/piroplasmosis

-REPORTABLE DZ -94% of herds contain positives, 46% prevalence in US -Horizontal and vertical transmission -Most animals are PI with no CS -Persistent lympocytosis: (30%); mild reactive changes with normal blood smears; reservoirs for infection -LSA cows: (5%), 4-8 years old, main cause of condemnation in cattle, yellow tan discrete nodules in RA, uterus, spleen, liver, LN, abomasum, and CNS Dx: ELISA on serum or milk -Cull seropositives and retest herd in 30d, no treatment

BLV - Bovine leukemia virus/bovine lymphomas

-REPORTABLE DZ -T. congolense, T. vivax, T. brucei -Tsetse flies PATHO: tsetse flies inoculate trypanosomes into skin of animals -> forms immune complexes CS: fever, anemia, weight loss Dx: Trypanosomes in blood smears, serologic testing for screening Tx: Diminazene, homodium. control of flies

Trypanosomiasis

-Treponema spp -red, ulcerative lesions or grey circular lesions -Prevent with copper sulfate baths -Do not allow infected animals to enter herd -Treat with tetracycline foot wrap

Digital Dermatitis - Hairy heel warts

-Fusobacterium necrophorum, dichelobacter nodosus -Disease of interdigital soft tissue -Fetid discharge -Tx with systemic antimicrobials -Prevent by avoiding contact with rocks, foot baths

Interdigital necrobacillosis - Foot rot

-Dichelobacter nodosus -erosion of the heel bulbs, no lameness -Common finding during hoof trimming -10% Zn sulfate footbaths to prevent -Tx by removing the loose horn

Interdigital dermatits - slurry

-Increased pressure from P3 on the corum leads to changes and weakening of suspending structures due to mechanical and metabolic processes -Lateral hoof in rear legs predisposed -Tx: remove horn around lesion and apply hoof block -Prevent: decrease standing time on hard surfaces

Pododermatitis circumscripta - sole abscess

-Dermatophilus congolensis - GM+, non acid fast -transmitted by contaminated equipment -Paintbrush lesions, crusts or scabs, and wart like lesions Tx: TMS/SMZ, PPG with chlorhexidine -Zoonotic

Dermatophilus congolensis - strawberry heel

-T. verrucosum -Non-pruritic, periocular lesions, scalping and patches with hair loss and grey crust Tx: Remove thick crusts and disinfect with sodium hypochlorite, can use miconazole or clomitrazole

Dermatophytosis - ringworm

-H Bovis: L1 migrate to spinal cord/epidural fat -H. Lineatum: L1 migrate to esophagus -Early summer: attach eggs to legs of lower body -Fall: Migrating around body -Early winter: larvae arrive in subdermal tissues of back of host where they make breathing holes, L3 emerge and form into adults -CS: Gadding, neurologic signs if H. bovis, Esophageal edema if H. lineatum, warbles in tail head or shoulders -Ivermectin in fall to treat

Habronemiasis

-Actinomyces bovis -Penetrating wounds of oral mucosa or from coarse thick stemmed feeds -Granulomatous abscess in mandible or maxilla -See osteomyelitis or pathological fxr on CR -GM+ filamentous bacteria on gm stain -10-20% Sodium iodine IV, antibiotics -Prevent by avoiding stemmy hay

Lumpy Jaw - Actinomyocosis

-dietary deficiency of vit-e or selenium cause acute degeneration of cardiac and skeletal muscle -most seen in rapidly growing calves -seen where soil is deficient in vit-e and selenium -Vit e and selenium have antioxidant function and protect cell membrane from free radical damage -muscle degeneration is the result of oxidant damage to cell membrane -CS: respiratory distress, arrhythmias, muscle weakness, dysphagia, increased CK, AST and LDH -Dx: Low WHOLE BLOOD selenium or liver contents -Necropsy: pale discoloration of muscles, white strands are coagulation necrosis, seen most in LV and septum -Tx: skeletal forms can respond to injectable selenium and oral vit-e, cardiac forms usually cause acute death

White muscle disease

-Listeria monocytogenes -Transmitted by contaminated vegetation and soil -ascends the trigeminal nerve and deposits in the medulla (brainstem) -Can cause placentitis/abortions -CS: circling toward affected side, abortions in last trimester, unilateral signs Facial nerve paralysis: drooping ear, deviated muscle, flaccid lip and lowered lid Trigeminal nerve paralysis -Necropsy: marked autolysis, small necrotic foci in liver, lungs and spleen -dx: INC TP, mononuclear pleocytosis -Tx: PPG and oxytetracycline -ZOONOTIC! can be isolated from milk and can survive certain forms of pasteurization

Listeriosis

-caused by high concentrate diets, bracken fern, amprolium, sulfur toxicity, decreased thiamine intake -CS: ataxia, tonic-clonic seizures, cortical blindness (absent menace with bilateral PLR), dorsomedial strabismus, stargazing -Lesions: cortical necrosis and uv light illumination -Tx: thiamine, dietary modification

polioencephalomalacia

-Lyssavirus, rhabdoviridae -Travels via peripheral nerves to SC and ascends to brain and salivary glands -Skunks, bats, coyotes, foxes, groundhogs -CNS signs 21-80 days post exposure -Introduction by bites of rabid animals -CS: Behavioral changes, paralysis, compulsive tenesmus, bellowing -Dx: Negri bodies in brain -cull animals REPORTABLE

Rabies

-C. tetani - soil found, spore forming -Deep wounds, recent dehorning or castration -Neurotoxin cleaves synaptobrevin - retrograde travel up SC and interferes with inhibitory neurotransmitters from presynaptic nerve endings CS: stiffness, tonic splasms, hyperesthesia, lock jaw, easily excitation, still tail, nares dilate, third eyelid prolapse, sawhorse stance -Dx: clinical evaluation -Tx: tetanus antitoxin, penicillin -Prevention: active immunization

Tetanus

-H. somni -Recently weaned calves -Septicemia needed for brain dz because it causes thrombosis of small arteries and veins in the brainstem and CS -CS: encephalitis, stiffness, ataxia, behavioral changes, exercise intolerance, blindness, dyspnea -Lesions: fibrinous pleuritis, focal myocardial lesions, fibrinous pericarditis, bronchopneumonia, polyarthritis -Dx: Neutrophilic pleocytosis, xanthochromia -tx: oxytetracycline -Prev: monovalent and bivalent bacterins

thromboembolic meningoencephalitis - TEME

-Lush pasture/brassica sp (broccoli) contain high levels of L-tryptophan which is degraded into indoleacetic acid which is then converted to 3-methylindole in the rumen; 3 methyl indole is a pneumotoxin -most seen in adult beef cattle -CS: respiratory distress, loud expiratory grunt, SQ emphysema, frothy nasal dc, no fever -Lesions: pulmonary edema, interstitial pneumonia, large bullae -dx: recent pasture movement, acute resp. distress, necropsy Tx: none -Use monensin - inhibits bacteria that convert tryptophan to 3-methylindole

Bovine interstitial pneumonia - acute bovine pulmonary edema and emphysema - Fog fever

-6-18 mo old calves with recent travel, FPT or stress -Mannheimia hemolytica > Pasteurella > h. somni, trueperella > mycoplasma -acute high fevers, purple mm, herd outbreaks with sudden death, moist coughs, serous to mucopurulent discharge, cranioventral lung sounds -Dx: necropsy -Tx: Tulathromycin, florfenicol, oxytetracyclin, mass administration

Bovine Respiratory disease - Shipping fever

-most frequently isolated in BRD -produces a leukotoxin that results in necrosis, thrombosis and exudation (pneumonia) -Findings: acute, hemorrhagic fibrinonecrotic bronchopneumonia with extensive consolidations cranioventrally

mannheimia hemolytica - Shipping fever pathogen

-MILD fibrinous to fibrinopuruelnt bronchopneumonia and small amounts of necrosis

Pasteurella multocida - Shipping fever pathogen

-myocarditis and pleuritis, encephalitis and arthritis -septicemia

Histophilus somni - shipping fever pathogen

-chronic pneumonia and arthritis -caseonecrotic bronchopneumonia

Mycoplasma bovis - shipping fever pathogen

pulmonary abscesses

trueperella pyogenes - shipping fever pathogen

-Perilla mint (Ketone): affects type 1 pneumocytes causing alveolar and interstitial edema and emphysema -Moldy sweet potato (4-ipomeanol) -CS: sudden death, toxemia -Necropsy: Wet firm dark lungs, sweet potato; enlarged pale lung lobes (perilla mint)

Bovine atypical interstitial pneumonia

-Pasteurella multocida -2-3 month old calves that are stressed -CS: Chronic moist productive cough, mucopurueltn discharge, arthritis, mastitis -Necropsy: chronic abscess formation, firm red cranioventral consolidation -Tx: 3rd generation cephalosporins HIGH Morbidity, LOW mortality

Enzootic calf pneumonia

-BHV-1 -6-18 mo old calves -REPORTABLE -Respiratory, Abortion, Ocular, Infectious pustular vulvovaginitis, neonatal infections, encephalitis -High fever, white plaques in nares, 5-6 month in gestation, red pustules lining vulvas -Dx: PCR or IFA Prev: vaccinate, do not use vaccine in pregnant cows or neonates

Infectious bovine rhinotracheitis

-<6 months old -paramyxovirus -CS: Fever, honking cough, nasal discharge -Lesions: Interstitial pneumonia, syncytial cells -Dx: PCR or IHC

Bovine respiratory syncytial virus

-minor pathogen and associated with mild infection -initiator for other bacterial pneumonia -fatalities rare -CS: pyrexia, serous nasal dc, increased rr/re

Parainfluenza 3 (PI3)

-Actinobacillus lignieresii -pyogranulomatous lesions in the tongue via penetrating wounds -Culture and biopsy -Tx: 10% sodium iodine

Woody tongue - Actinobacillosis

-Otitis media, head tilt, drooped ear, aural dx, facial paralysis, NEURO SIGNS, mastitis, polyarthritis, tenosynovitis, pneumonia, abortion -Dx: Necropsy, PCR/IHC -cull positives

Mycoplasma bovis

-M. mycoides -REPORTABLE and FOREIGN -CS: meningitis, polyarthritis, pneumonia, mastitis, contagious agalactia, watery brown milk, high fever, lowered and extended back, turned out elbows, expiratory grunt -Dx: Fluid clear yellow or turbid fluid with fibrin -Necr: marbled lung cull positives

Contagious bovine pleuropneumonia

-Fusobacterium necrophorum -Closely confined cattle under unsanitary conditions -inflammation of the laryngeal mucosa leading to narrowing of the rima glottidis and inspiratory stridor -results in laryngeal chronditis and pharnygeal invasion leading to painful swallowing -CS: inspiratory dyspnea with stridor, cough, purulent nasal discharge, fetid odor, painful swallowing -Dx: visualization of trachea -Tx: oxytetracyclin, PPG or florfenicol for 2-3 weeks, surgery to remove necrotic granulation tissue and to drain abscess

Necrotic laryngitis - Calf diphtheria

-T. pyogenes, pseudomonas, p. multocida; ascending bacterial infection of the frontal sinus -Immediately after dehorning while wound is open -CS: unilateral; anorexia, fever, nasal discharge, decreased airflow through nasal passages, foul breath -Dx: Skull XR, percussion of head -Tx: Trephination, abx, NSAIDs

Dehorning sinusitis

-M. tuberculosis -CS: weight loss, dysphagia, stridor, most cows asymptomatic -DX: intradermal injection; observe 72 h post; if positive due CCT -No tx, cull positive -zoonotic

Tuberculosis

- Fusobacterium necrophorum >>> -Adult cattle on high carb diets -Thrombus in cd VC, hepatic abscess and suppurative pneumonia -poor prognosis

Vena cava thrombosis -metastatic pneumonia

-Moraxella bovis, UV light, musca domesticalis or autumnalis, stomoxy calcitrans, mechanical irritation, dust or trace mineral deficiency -Summer and fall -Corneal ulceration at center of cornea, blepharospasm, photophobia, and epiphora -Dx: microbial culture -tx: oxytetracycline and tulathromycin

Infectious Bovine Keratoconjunctivitis

-most common neoplasm in cattle -seen most in herefords 8 yo -Cause: heritability, uv light, BHV, papillomaviruses, nutrition -CS: starts at limbal sclera and grows across cornea; starts as smooth plaques and progresses to papillomas -dx: Biopsy -Tx: Surgical excision + cryo or radiation -High rate of recurrence Enucleate for advanced lesions Cull affected animals and offspring to decrease incidence

Ocular Squamous Cell Carcinoma

-bovine papillomavirus -can be pale smooth benign nodules on teat skin or filamentous lesions at the teat orifice -no need to treat -prev with autologous vaccines

Papillomatosis

-cutaneous granulomas -CS: swelling, pitting edema, granulomas, lameness, weight loss -Dx: bacterial culture LESIONS SPONTANEOUSLY RESOLVE IN 2-4 WEEKS

Corynebacterium pseudotuberculosis

-causes metabolic acidosis and renal tubular damage -lethal dose in cattle is 2-10 ml/kg -Impaired alcohol dehydrogenase, causes glycolic acid accumulation and oxalate formation = metabolic acidosis and CaOx crystalluria -CS: depression, paraparesis, recumbency, epistaxis, hemoglobinuria -Tx: emesis, gastric lavage, fluid therapy

Ethylene glycol toxicity

-Ascending infection of the bladder - c. renale colonizes the mucosal lining of the bladder -CS: bloody urine, pyuria, polyuria, fever Dx: Blood, protein and WBC in urine Tx: PPG or TMS for 3-4 weeks, decrease urine pH

Pyelonephritis

-MAP (struvite) - high legume or grass diets, alkaline urine -Ca carbonate - lush, clover pastures, alfalfa -caOx: low calcium diets, white and jagged -Silicate: Western US CS: anorexia, depression, ventral pitting edema Lodges in sigmoid flexure -Tx: Surgical removal or cull -Prevention: increase water intake, ensure Ca:P 2:1 diet

urolithiasis

-Transmission: Culicoides, or attenuated vaccine -Abortion CS: CNS babies, mummified babies -Dx: PCR or pre-colostrum -Control: Reduce midges, vaccination

Bluetongue virus abortion

-D0-40: Embryonic death/abortion -D100-125: PI Calves -D125-150: Cerebellar hypoplasia, hydrancephalo, spinal cord hypoplasia, cataracts, optic neuritis, retinal degeneration -DX: Isolation, PCR -Control: Remove PI Calves

Bovine diarrhea virus abortions

-Abortion at 7 months -Abortion signs: placentitis (necrotic yellow cotyledon, leathery intercotyledon area, normal or autolytic FETUS WITH BRONCHOPNEUMONIA -Dx: Maternal serology and fluorescent ab staining of the placenta; Brucella milk ring test (IF POSITIVE, REPORT AND TEST ALL COWS IN 30D) -PREV: RB51 vaccine

Brucella abortus abortions

C. jejuni or c. fetus -Abortion at 4-8 months -Transmission: ingestion and hematogenous spread -Abortion signs: placentitis (hemorrhagic and edematous), autolyzed or fresh fetus with partially expanded lungs; FIBRINOUS PLEURITIS/PERITONITIS -Dx: Darkfield examination of abomasal contents or culture placenta -Prev: AI and vaccination ZOONOTIC

Campylobacter abortions

-C. Abortus -Abortion during last trimester -Abortion signs: Placentitis (thick and yellow exudate adhered to placenta) -Dx: stained smears of placenta and ELISA ZOONOTIC

Chlamydiosis abortions

-Ornithodoros ticks (pajaroello), California Abortion storms 3-5 mo in -Abortion signs: lymphoid hyperplasia in spleen and LN with granulomatous inflammation, -Cows will not abort in subsequent pregnancies -Prev: expose heifers to endemic areas before breeding

Enzootic Bovine Abortion - foothill abortions

-abortion at 4 months -Abortion signs: unspecific placentitis, autolysis, foci in the liver

IBR/BHV-1 Abortions

-hardjo is probably the culprit -Last trimester abortion; abortion storm -Abortion signs: diffuse placentitis with avascular light tan cotyledons and intercotyledonary areas, autolyzed fetus, dies 2 days before expulsion -Cs: port wine urine, icterus, anemia -Dx: Titers (>1:800 is sus) -cow is a carrier for life and continuously sheds organism -Sourced of infection (lakes, dogs, wildlife) should be eliminated -Vaccinate 2 doses at 4 week intervals followed by annual booster -Tx: oxytetracycline -Zoonotic - urine and milk may be infective for 3 months

Leptospirosis abortions

-L. monocytogenes -Abortions at any stage of gestation -CS: Retained placenta for 2-3d, fibrinous polyserositis with white focu in the liver and cotyledons Dx: Culture from fetus or placenta REPORTABLE, ZOONOTIC

Listeria Abortions

-Abortion at 4 month to term, common in winter -Abortion signs: Severe necrotizing placentitis with enlarge cotyledons that have turned in margins, thick intercotyledon areas, adventitious placentation; NON autolyzed fetus -Dx: fungal hyphae on a necrotizing placentitis

Mycotic abortions - aspergillosis

-Abortion between 4-6 months; abortion storms -Asymtpomatically congenital calves or CNS signs - see inflammation in brain, heart and muscles -Cows are not clinically ill -Dogs are definitive host -No treatment

Neospora caninum abortion

-First trimester abortion; usually only causes infertility -Abortion signs: mild placentitis with hemorrhagic cotyledons and thick intercotyledon areas with flocculent exudate, no lesions on fetus -cows develop secondary pyometra -Bulls are lifelong carriers, cows can clear organism in 20 weeks -No treatment, cull infected bulls

Tritrichomoniasis abortions

Trueperella pyogenes abortion

-Coxiella burnetti; small cell variant -Small cell variant is shed in milk, urine, vaginal secretions, placental tissue and amniotic fluid -gets shed in subsequent parturitions/lactation -Circulated between ixodid ticks and domestic ruminants -Abortions late term -Abortion signs: Placentitis, malaise, anorexia -Dx: PCR/IHC/ELISA -Tx: cull -Prev: abortion management and wind control -ZOONOTIC - highly infectious in humans and can cause hepatitis, pneumonia and endocarditis; transmitted through unpasteurized milk

Q Fever

-Wall is <3 mm diameter and cyst is 25-60 mm wide -Most are 3-8 weeks pp at first attempt of pp ovulation -failure of positive feedback of follicular estrogen on the hypothalamus to release significant gnrh during estrus to trigger lh surge = failure of ovulation at estrus -multiple follicles and cysts form -CS: intermittent estrus, bull like behavior, masculinization, thickened uterine wall with edema/turgid TX: Ovsynch: GNRH -> 7d later: PGF2a --> 48h later gnrh--> AI 24 hours later

Follicular cysts

-PLACENTA is abnormal - RAPID accumulation of fluid into the placenta during late gestation -CS: distended abdomen, uterus above pelcis, round and tense abdomen, CANNOT PALPATE FETUS - DO NOT REBREED

Hydrops allantois

-FETUS is abnormal, SLOW accumulation of amniotic fluid, -CS: piriform abdomen, very little distension, CAN palpate fetus -CAN REBREED

Hydrops amnion

-spread by milking equipment and personnel -best prevention methods are cleaning/hygiene pre and post milking and dry cow IMM management -Pathogens: Step agalactia, S. aureus and Mycoplasma bovis -Can use penicillin for S. agalactiae, but others are hard to tread -Mycoplasma bovis can cause gangrenous mastitis - which can spread from the lungs to the udder and joints -sometimes you may need to cull cattle if too hard to treat

Contagious mastitis

-Sources are water, bedding material, soil and pasture -Can control with hygiene and clean env. -S. uberis, S. dysgalactiae, Lactococcus, Streptococcus faecalis, aerococcus, enterococcus

Environmental mastitis

- Shed in the feces, contact with contaminated environment in milking cows; most common when cows are in dry period or peak lactation due to more pressure on the glands -E. Coli, Klebsiella, Enterbacter, citrobacter or serratia sp. -Causes endotoxin release resulting in increased permeability resulting in edema and swelling

Coliform (endotoxic) mastitis

-Risk factors: abortion, dystocia, twinning, hypocalcemia, stillbirth, heat stroke, aging, premature birth, induction of parturition, increased NEFA - mediated by impaired migration of neutrophils to the placenta interface in the periparturient period, pro-influx macrophages are decreased leading to decreased collagenolysis and fibrinolysis CS: discolored fetid membranes from the vulva >24 hours after birth; foul smelling d/c +/ toxemia Tx: DO NOT REMOVE MANUALLY, DO NOT USE INTRAUTERINE ABx, DO USE oxytocin, estradiol, PGF2a and calcium OR NOT TREAT and let them pass in 2-11 d

Retained placenta

-T. foetus is a protozoan, piriform shape. It invades the vagina and migrates to the cervix and uterus. Induces an inflammatory response that can lead to endometritis, cervicitis, vaginitis and salpingitis - RESULTS IN EARLY FETAL DEATH -Transmitted via live cover or AI infected semen; bulls are clinically normal carriers -CS: irregular calving intervals, post coital pyometra, late gestation abortion -Dx: ID via microscopic evaluation using a bull that has the organism in the epithelial folds or the prepuce and penis -tx: no effective treatment, remove infected bulls

Triochomoniasis

C. venerealis or fetus - GM spiral polar flagellated bacteria -Transmitted by live cover or AI -CS (BULLS < 3 ): transient infection with transmission relying on sexual contact with a noninfected cow due to undeveloped crypts. -CS (BULLS >3): Chronic infections due to deeper crypsts -CS (COWS): mucopuruent endometritis, early embryonic death, prolonged luteal phases, irregular calving interval -Dx: Antibody test, culture and vaginal mucus agglutination test -Tx: vaccinate cows 4 weeks before breeding and revaccinate 1/2 way through breeding season; vaccinate bulls with 2 times the dose 3 weeks apart, can use streptomycin in bulls, cows are not usually treated w abx

Campylobacteriosis

-dairy and beef cattle, tip of the uterus invaginates -Caused by excess traction to relieve dystocia, RFM, hypocalcemia EMERGENCY -Tx: epidural anesthesia, reduce by applying pressure at the cervical portion and and gradually working toward apex; can apply sugar or rinse with hypertonic saline t reduce edema and prolapse

Uterine prolapse

-Risk factors: rumen distension, increased intra-abdominal pressure, fat animals, grazing estrogenic plants (trifolium), brahman cattle -Begins as an intussussception like folding of the vaginal floor CRANIAL to the vestibulovaginal junction -GRADE 1 : intermittent prolapse, only visible when recumbent, normal vaginal tissue -GRADE 2: Continuous acute prolapse of vaginal tissue -GRADE 3: continuous acute prolapse of vagina/bladder/cervix -GRADE 4: chronic prolapse with infection/necrosis -TX: epidural anesthetic, lavage tissues and place buhner suture into the vestibulu

Vaginal Prolapse

occurs during early lactation/1 week pp/fatty liver OR peak lactation/4 weeks pp/NEB -> negative energy balance leads to increased [NEFA] and ketone synthesis in the liver (high serum NEFA/ketones and LOW glucose) -Determination of serum or whole blood [BHB] is the best way to detect and monitor hyperketonemia (1-1.4 mmol/L of blood BHB is diagnostic) -Cows BCS >3.755 at calving are at greatest risk -CS: decreased intake, decreased production, afebrile, CNS signs if nervous ketosis (PICA, bellowing, aggression) -Dx: BHB cowside test -tx: oral propylene glycol drench -Prev: Prevent by maintaining BCS in late lactation, maintaining feed intake, and after calving, promote rapid and sustained increases in feed and energy consumption (ndf 28%)

Ketosis

-NPN undergoes hydrolysis and releases excess ammonia in the GIT which is absorbed leading to hyperammonemia -Sources: Urea, ammonia and monoammonum/diammonium phosphate salts, rice hulls, beet pulp, citrus pulp, cottonseed and straw -0.3-0.5 g/kg urea = adverse effects -1-1.5 g/kg lethal -Formation of 4-methylimidazole = bovine bonkers syndrome -CS: muscle tremors, abdominal pain, frothy salivation, aggression, rumen atony, death -Lesions: bloat, rumen or cecal pH of >7.5 in a recently dead animal -Dx: pH of rumen or cecum, hx and CS -tx: infuse 5% acetic acid and water into rumen to lower pH and prevent absorption of NH3 by converting uncharged NH3 to charged ammonium, and cold water decreaes rumen temp and dilutes rumen media to slow down urease activity -Prev: do not feed >2-3% of grain portion with urea and <1%, NPN should not be more than 1/3 nitrogen

ammonia toxicosis

-B. anthracis = GM+ rod resistant to heat, drying and disinfectants -Causes impaired phagocytosis and vascular integrity leading to sepsis Zoonotic and reportable - causes black eschars, GI dz, flu like symptoms -CS: Bloody discharge from orifices, non-clotting, and acute death without rigor mortis -DO NOT OPEN CARCASS FOR NECx CALL STATE VET -Burn or bury animals, use CIPRO for 60d, prevention via vaccination Show less

Anthrax

-ZOONOTIC - in milk, exposure to aborted fetus or fetal materials -Brucella abortus -Reservoirs: cattle, water buffalo and bison -Transmission: ingestion, large amount of aborted fetuses, fetal membranes and uterine/amniotic fluids via contaminated feed or water or AI -CS: abortion, retained placenta, abscesses in repro of bulls -Dx: culture of stomach contents and lungs, most cows cease shedding organisms from genital tract -BRUCELLA MILK RING TEST: screen cows at 3-6 month intervals to identify infected herds; any positives = test cows individually w blood test within 30 days and cull seropositive cows -Cointrol: RB51 vaccine, vaccinated calves or non pregnant heifer replacement herds

Brucellosis

-Pestivirus - similar to border or classic swine fever -There are cytopathic and noncytopathic types - noncytopathic is the predominant viral biotype -Epitheliotropic: contact with secretions causes invasion of tonsils/GIT - localizes to oral mucosa, intestinal mucos and coronary bands and digits -Most common in young cattle (6-24 months) -PI calves develop when noncytopathic BVDv is transmitted placentally during first 4 months of fetal development -Acute clinical BVD: biphasic fever, decreased production, rapid RR, nasal secretions, diarrhea, leukopenia -Severe clinical BVD: oral ulcerations, lesions of coronary band, diarrhea, leukopenia, fever, petechiation of sclera, thrombocytopenia, ulcerated GIT -Abortion at 4 mo, cerebellar hypoplasia, if INFECTION AT 100-150D -PI Calves INFECTED >125d MUCOSAL DISEASE -fatal form of BVDv occurring in PI cattle occurs when PI calves become infected with cytopathic BVDv -> forms from a mutation of the resident persistent non CP virus -see a profuse enteritis in association with typical mucosal lesions -Dx: Paired Ab serology at 2 time points, ear notch for screening (IHC) -TX: cull positive calves, MLV vaccine at 4-6 mo old and before breeding

Bovine Diarrhea Virus

-C. chauvoei -affects cattle 6mo-2 yo -Transm: endospore ingestion or wound contamination, multiply in an anaerobic env (damaged muscle) -CS: palpable crepitus in muscle, fever, depression, anorexia Nec: Rancid butter muscle with gas bubbles -Tx: PPG -Prev: 7 way bacterin vax

Blackleg

-C. septicum, C. novyi type b, c. perfringens type a -affects any aged cattle -Trans: infected wounds -CS: swelling and edema to dependent portions of the wound, DAF -Necx: Swelling without gas accumulation -Tx: PPG -Prev: 7 way bacterin vax

malignant edema

-C. Haemolyticum; soil organism in alkaline pH -spores embed in the liver; often caused by fasciola hepatica infection -In anaerobic env. spores germinate into vegetative cells and produce PLC and beta toxin that causes intravascular hemolysis, hemolytic anemia and hemogloburia -CS: Death, DAF, port wine colored urine and dark liquid feces -Lesions: anemia, SQ edema, bloody fluid in abdomen, Ischemic infarct in liver -Tx: PPG -control: 7 way bacterin Guarded prog

Bacillary hemoglobinuria

-C. botulinum -Trns: ingestion of contaminated feed like silage -CS: Muscle tremor, ascending paralysis, respiratory paralysis, mydriasis, ptosis, weak tongue -Dx: toxin in serum or feed -NO TREATMENT -PREV: vaccine

Botulism

-occurs when body fat stores are mobilizes and release NEFA into the blood and exceeds the liver's capacity to process NEFAs -NEFAs are re-esterified and deposited inside the liver at TAG -Large amounts of TAG in the liver disturbs function and worsens NEB -Developed before and during parturition; cows that are over conditioned at calving are at highest risk -CS: ketosis, often obese cows, develops with other diseases like DA, metritis, mastiti, no pathog signs dx: liver biopsy is the only direct and reliable method to determine severity -Prev: enter dry period with BCS 3-3.5/5, monensin 4 weeks before calving to modulate rumen fermentation to increase propionate synthesis

Fatty liver disease

-Reportable, ZOONOTIC (vCJD) -Trns: rendered cattle parts in feed, direct contact, through placenta -forms prion -CS: blindness, no menace with normal PLR/palpebral, depression, manic, self mutilation, seizures, star gazing, pruritus, hyperesthesia -Dx: bx third eyelid

Bovine Spongiform Encephalopathy - Mad Cow disease

-eradicated in 2011 -Morbillivirus -similiar to distemper -trans: nasal and ocular secretions -recovered animals have lifelong immunity -CS: fevor, anorexia, depression, oculonasal dc, necrotic lesions on gums, buccal mucosa and tongue, watery/bloody diarrhea (EROSIVE STOMATITIS) -Lesions: erosion of the GIT and URT -zebra striping on rectum -Dx: trPCR allows for analysis to pinpoint re-emerging virus strain -Control: active immunity is lifelong, immunize all cattle with cell culture vaccine (>1 yo)

Rinderpest

-Morbidity 100% - places economic constraints on livestock trade -Picornavirus, Serotype O -Trns: direct/indirect contact with secretions or excretions or by mechanical vectors or by air movement over land and water (can travel 150 mi over water) -infection and replication site is the mucosa of the pharnyx -Ruminants that recover become carriers, but cannot transmit disease to naive cattle -CS: Vesicles in mouth, muzzle, teats and feet, fever -Dx: PCR of vesicular epithelium or fluid -Tx: Cull

Foot and Mouth disease

-Early lactation; lush green pasture -Decreased dietary magnesium = decreased nerve conduction = decreased calcium inhibition -CS: twitching, tetanic spasms, staggering, clonic convulsions, paddling legs,serum -Dx: serum magnesium -tx: oral or iv magnesium

Hypomagnesemia - Grass Tetany

-Used to prevent coccidiosis and improve efficiency by selecting for GM= bacteria that produce propionate -Ld50 = 21-36 mg/kg -MOA: disrupts normal ionic gradients leading to destabilization of the cell membrane and excessive increases in Ca ions -CS: tachycardia, VPC, afib -Necx: pale areas of myocardial fibrosis and pulmonary congestion

Ionophore toxicity

-Cattle gain access to grains (wheat, barley, apples, grapes, bread, potato) Changes in microbial population in the rumen (more GM+ bacteria) - Lactic acid production and decreased rumen pH <5 --> destruction of protozoa/cellulolytic organisms and lactate utilizing organisms leading to impaired rumen motility --> increased lactic acid production leads to increased osmotic pressure in the rumen --> increased fluid quantity in the rumen and acidemia -Consequences include: acidemia (from decreased pH), cv collapse (From increased oncotic pressure in rumen), muscle weakness, shock and death -CS: Acidemia, colic, diarrhea malodorous, sweet feces with undigested kernels of feed, fluid splashing rumen, staggering, decreased PLRs, acute laminitis, anuria -Dx: rumen pH <5.5 -Tx SEVERE cases: rumenotomy, rumen lavage, Sodium bicarb, PPG, thiamine, -tx: MILD cases - mgOH (alkalinizing agent), palatable grassy hay -Do not use milk for 12 hours after last treatment -prev: do not let cattle access to concentrates

Grain overload - lactic acidosis

-occurs when doing harvesting activities when oil and battery disposal from machinery is handled improperly Patho: lead in reticulum dissolves slowly and releases a significant amount in blood -> deposits into bone affecting RBCs antioxidant defenses and tissues rich in mitochondria --> causes cerebral hemorrhage and edema, gametoxicosis/teratogens, nephrotoxins -CS: 24-48 h post exposure ACUTE: ataxia, blindness, salivation, twitching of eyelids SUBACUTE: anorexia, rumen stasis, dull, transient constipation, head pressing, hyperesthesia CHRONIC: dysphagia, aspiration pneumonia, embryotoxicity, poor semen quality -Lesions: oil flakes in git, edema of the cerebral cortex and flattened cortical gyri Dx: whole blood analysis of liver and kidneys - concentrations of lead in blood at 0.35 ppm, liver at 10 ppm and kidney at 10 ppm Blood smear: anisocytosis, anemia, polychromasia ,basophilic stipling, hypochromia, metarubricytosis -tx: not recommended for production animals, cannot treat when animal is neurologic -If caught early can try Ca-EDTA for 3 days, thiamine and mgOH or rumenotomy to remove lead from GIT (rarely successful) -Can excrete into milk, W/d time for milk is greater than 1 year; if lead posioning is confirmed in a cow, all animals should be evaluated

Lead toxicosis

-Host adapted strains: hardjo, guaricura (carried by cattle only, not dependent on env. conditions for transmission) -CS (CHRONIC): mostly hardjo, more frequent cases in cattle, silent infection associated with repro failure and estrus repetition -Dx: Difficult, cannot use MAT because seronegative shedders are common in fected cattle; culture, PCR or immunofluorescence on cervicovaginal fluid is required for individual diagnosis -Incidental strains: pomona, grippotyphosa, icterohaemorrhagiae (carried by other animals, dependent on poor management practices and env.) -CS (ACUTE): incidental strains cause acute cs, seen less frequently as outbreaks, abortions, birth of weak offspring, blood tinged milk -dx: MAT= Ab titers > 800 -Tx -Abx: Streptomycin IM -Management changes: smaller groups of animals, clean env., avoid access to water/puddles or co-grazing with pigs -Vaccine: every 6 months, once before. breeding service season coinciding with BEGINNING OF SPRING when env. is more intense contamination -efficacy to control varies dependent on infecting strain; hardjo and guaricura are impossible to eradicate

Leptospirosis

-Calves need 150g igG and 4L colostrum in 4 hours -Causes of FPT: inadequate colostrum volume, poor quality colostrum, not consumed in a timely manner -FPT leads to septicemia -Agent: E. Coli through umbilicus, GIT or tonsils -Bacteria invades bloodstream and enters WBC - release of cytokines causing sIRS - increased vascular permeability leading to hypotension and poor perfusion and organ failure -CS: lack of suckle, depression, scleral injection, corneal clouding, hypopyon, aqueous flare, hyperemic mm, prolonged CRT, tachycardia -Dx: IgG snap test, TP meter <5.5 g/dL, neutropenia w L shift, toxic change, septic arthritis and meningitis -Tx: plasma transfusion, ceftifur and florfenicol, NSAIDs, IVF and glucose FPT calves are 6x more likely to die

FPT Neonatal septicemia

Onset of lactation = calcium excretion increased from 10g to 30g per day - stresses calcium homeostasis and causes blood calcium concentration to decrease below normal levels (8.5 to 5.5) -Causes hyperexcitability of the nervous system which progresses to decreased strength of muscle contractions and paresis -Most common in cows entering 3rd lactation and jerseys/guernseys -STAGE 1: standing/ambulatory, hypersensitive and excitable, ataxia, tremoring, twitching Tx: Oral Calcium 40-55g -STAGE 2: paretic, cannot stand, obtunded, anorexia, tachycardia, weak pulses, bloat, distended bladder, S shaped curve of neck -Tx: IV calcium, 500 mL 23% Ca gluconate with boric acid to stabilize the ca, put into jugular vein and administer slowly over 20 min; monitor for bradyarrhythmias -STAGE 3: comatose, muscle flaccidity, unresponsive to stimuli, SEVERE bloat, EXTREME tachycardia and no peripheral pulses - All cases will relapse due to transient hypercalcemia - iv calcium shuts down cow efforts to mobilize own calcium by halting PTH and triggering calcitonin - do oral or SQ calcium -prev: feed low calcium diets during dry period by doing an ACIDOGENIC DIET -DCAD= (na+k) - (Cl+S) - acidogenic diets are low in phosphorus and high in chloride -acidogenic diets are associated with decreased DMI - large decreases are at risk for rfm, metritis, fatty liver and ketosis v -Feed diet between -50 to -150 meq/kg of DM to prevent hypocalcemia -acidogenic diets create a compensated metabolic acidosis to increase gi ca absorption

Postparturient paresis - milk fever

-REPORTABLE, FOREIGN, ZOONOTIC -Zoonotic: self limiting influenza virus for 3-5d -Reportable: notify state and federal officials immediately; quarantine premises for 14d -Horses, cattle, swine ,sheeps, goat, llama, alpaca -western states in may to october -trans: black flies, sand flies, biting midges, moving water sources, direct contact -CS: ptyalism, ulcers in mouth and on tongue, on teats, coronitis and secondary lameness, crusting lesions on muzzle and ventral abdomen -Dx: complement fixation test -Tx: resolves in 2 weeks, supportive care -reinfection with second exposure

Vesicular stomatitis

night blindness, decreased growth performance and fertility, abnormal bone development, abortion, still born or blind calves; retained placenta Most common in beef cattle fed primarily harvested feeds Correct through supplementation and nutritional management

Vitamin A Deficiency

‘rickets’ abnormally developed, weak and brittle bones, swollen immobile joints, decreased feed intake, decreased growth performance, stillborn or lethargic calves Allow cattle direct exposure to sunlight Feed suncured forages Supplement with Vit-D

Vitamin D Deficiency

decreased growth rates, impaired immune function, rough or dull colored haircoat, lack of shedding, reproductive failures Feedstuffs are often deficient in copper and require supplementation Overfeeding is easy and toxic

Copper deficiency

decrease in feed intake, decreased feed efficiency and growth, impaired hoof and skin health, decreased fertility and impaired immune function

Zinc deficiency

abortion, stillbirth, skeletal abnormalities, impaired growth and infertility

Manganese deficiency

BOVINE REVIEW Flashcards

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