Cattle

Rotavirus

1-2 wks old possible fiaure of transfer may be end of claving period weak, sternal/alt recumbency, obtunded unresponsive tachycardia increased resp rate(acidotic) sunken eyes, skin tent faiure to suck, cold mm tacky belly bloated and sloshing with watery yellow green diarrhea SNAP test(40% will have it without signs) if outbreak PAGE test or blood gas machine to confirm acidosis virus replicates in SI epithelium causing loss of absorptive cells at tips of villi(crypts ok) loss of K+ Na+ and bicarb and water and sugars not absorbed which ferments to make acids which with loss of bicarb makes acidotic IV fluids with bicarb at signs of acidosis and regular fluid therapy every 4 hours via botle or teat NSAIDs and meloxicam ensure passive transfer, keep enviornement clean and shorten calving period

Cryptosporidiosis

10 days to 3wks or lambs 3-7 days end of calving periodusually, dirty/crowded boxes/pens or change with weather no clear signs or tucked up appearance and reluctant to move, tachycardia if dehydreated, suken eyes and reluctance to suck abomasum tucke dup, profuse yellowgreen diarrhea SNAP test/giemsa stain to confirm oocyte invate brush border of microvilli causing swelling and stunting of villi reducing absorption area causing diarrhea usually self limiting, support dehyardation with oral fluids 4-6 daily halofuginon for outbreaks for 7 days good hygine and not grazing on same pasture every year may occur concurrent to rotavirus

Dairy culling and disease rates

20-24% of herd culled per year(lifespan of 3.04 lactations per cow) Forced cull-must be culled bc death/disese/poor reproduction(>50% of culls) voluntary cull-poor perforamnce/age/temperment Cost for a culled cow is £1328 at end of lactation and 3,307 in early lactation and 3000 for a death(culled cows sell for about £600) Infertility(26.1% of cows in a year), mastitis(37.5%), and lameness(22.3%) are biggest problems also assisted calving, digestive problems, hypomagnesium/calcium, keotosis all issues All referred to as production disease-associated with peripartirition and have many causes and are interrelated all cost money-treatment culling, labor and milk loss

Mastitis basics, costs and prevalence

3.6% of cows are culled each year for it representing 20% of total culls 40 cases per 100 cows per year £100 million costs annually cost can be between £100 and 1700(fatal) multifactoral problem of cow anatomy, mammary defense mechanisms, lactation stage age along with pathgoens, and environemental controls in climate housing milking and feeding along with teat damage

coccidiosis

4-8wks in lambs spring calves in summer or recently weaned dairy calves chronic wasting poor appetite, tucked up with dull coat/fleece, strainiing/groaning normal pulse and resp mucus membranes pale abdomen empty fetid diarrhea and straining in lambs yellow with blood flecks poor grazing due to drought/overgrazing, small dirty paddocks or dirty crowded wet area mcmasters oocyte count, sporulation to find exact feces(may not be shedding) 2-4 days for oocytes to become infective(need humidity and warmth) and may be from ewes or from previous crop move as sporozoites into intestinal epithelium and lyse them invading neighbor cells taking several weeks to cause real signs teat with suphonamides or trimethoprim, and oral fuilds deconquinate or diclazuril in outbreaks good cleaning to prevent

Mastitis control measures

5 point plan Regular mliking machine maintenance post milking teat disinection dry cow therapy prompt treatment/control of clinical cases cull chronic cases Milking machine maintenance- acts as a fomite, may damage teat end, or overmilk thus good liners and routine specialist testing static(no cows being milked testing system pressure regulators ect) and dynamic testing needed Post milk Teat disinefection- removes contageous pathogens and cleans teat sores and improves teat skin, predip disinfects teat reducing bactoscan results can be done via dippping or spraying or with automated teat cleaning systems predip best in high risk periods(housing) for elimination of environmental pathogens

Colisepticiemia and meningitis

<2 wks old possible history of failure of passive transfer, usually dirty calf environment lethargic obtunded recumbent with siezures tachycardia, opisthonus, nystagmus, episcleral congestion and clouding eyes loss of suck reflex, salivation darrhea(agonal, mucoid) hypothermic found PM uuslaly fiaure or partial faiure of passive transfer and exposure to bacteria to oropharynx upper resp or intestines septicemia or bacteremia depending how bad passive transfer was IV antibiotic(marbofloxacin/enrofloxacin) nsaids/steroids and support care generally grave prognosis adequare passive transfer, clean environment and maternal vaccs

Actinobacillosis

A ctinobacillus lignieresii gram- bacterium Wooden tongue salivation, dysphagia, tongue out enlarged submand LN, swellin gunder jaw, painful yellow lesions below mucosa most common form Intestinal affects esophagus/rumen/cardia/reticululum insidious onset chronic runimanl bloat nonpainful but rumination abnormal gurgling and retching rare Cutaneous granulomas of head moutch and chest and lymphadenopathy rare Streptomycin or in NONPREG Sodium Iodide IV

AI in beef herds

AI advantage-best bulls with known ebvs can be used, removes venereal disease risk and can tighten calving periods disadvantage-heat detection can be hard if nto using fixed time AI, labor more intensive/costly ensure cow/heifer good steady nutrition plane and cycling before synch ensure no parasite/element defieicny have good handling to reduce stress and consider double AI to up rates(for single cows 55-65% and heigers 65-75%)

Differences in pharmacology for cattle

Absorptoin-rumen flora catalyse hydrolytic/reductive reactions and will inactivate most oral drugs or flora will be destroyed by oral drugs esp antimicrobials oral modified drug release delivery systems(boluses) can help with this as it can stay in rumen metabolism-major changes in metabalism hepatic metab of anthelminics (benzimidazoles) requires cattle/goats to need more than sheep generally hepatic metab drugs have shorter half lives excretion-urinary ph in herbivores is alkaline compared to carnivore acidic urine thus come drugs through urinary tract like acidic drugs will be ionized and thus eliminate faster than alkaline compared to carnivores pharmacodynamics-receptor level changes dosage in cows is much less for xylazine due to more receptive cell sites

Proteins/peptides/AA related to poisonings

Amanita phalloides-toxic mushroom with aminotoxins causing ab pain, darrhea and eventual coma mistletoe has a similar effect Blue green algae can bloom in water may be hepatotoxic and wont be inactivated by water treatment S-methylcysteine sulfoxide from brassica crops is converted to dimethyl sulfide in rumen and can reduce growthrates and anemia Thiaminase in horsetail and rhizomes of bracket and large ingestion can cause polioencephalomalacia in horses

Types of dry cow therapy for mastitis control

Antibiotic therapy-cloaxcillin for betalactam resit strains cephalonium for both those and gram negs framcetin, penethamate, penicillin for gram negs External teat sealants-give a seal applied twice weekly internal-bismuth subnitrate innto teat cistern/canal so cant help with intramammary infections(low SCC cows only) and must be applied with aspetic technique Culling chronic cases important 3 or more outbreaks or high SCC over 3 months should be culled but also consider age and sources of infection

Mastitis pathogen identification methods

Bacteriology nshould be done prior to antibiotic treatment and taken aseptic clean gloves washed teats dry, predip, dry again, strip foremilk, then disinfect teat, dry and collect sample

Selenium/Vitamin E deficiency and symptoms

Both cell antioxidants preventing lipid peroxidase/free radical damage Muscle is most susceptible as highest oxidative metabolism Selenium/Vitamin E supply along with dietary oxidant levels(Polyunstaturated fatty acids) determine deficiencies Nutritional Muscular dystrophy(white muscle disease)-congenital in stillbirths/weak young or delayed-1-4mo usually bc exercise(turnout at spring) or stress-causing stiffness/discomfort, resp distress/dyspnea, and sudden death from cardiac arrest illthrift-poor fertility, impaired immune system or retained fetal membranes also related

Mastitis-Cogulase negative staphylcocci, strep agalactiae, strep dysgalactiae, mycoplasma

CNS-staph hyicus, simulans, epidermidis, hominis ect colonize teat end and canal often a sample contaminant but may invade during early lactation Strep agalactiae-highly contageous usually enters herd from new animals or relief milkers infects udder and teat canal but easily eliminated with anibiotics strep dysgalactiae-also enivonrmental common to teat sin mycoplasma-rare in UK sudden onset multiple quarters with hardened udder and enlarged lymph nodes with watery to thick colostrum like secretions highly contagious and poor treatement response

Copper deficiency signs and diagnosis

Cattle usually growing post weaning(3-12 mo) depigmentation-greying/borwn coat around ear margin and eyes dry sparse tatty hair coat bone defects-widening of epiphysis poor performance and growth rates anemia/cardiac hypertrophy diarrhea(esp with high molybdenum pastures) and infertility Sheep same but Swayback-enzootic ataxia-pregnant ewes mid to late gestation progressive congenital-stillbirth/weak lambs with neurosigns and ataxia and weakness in hindlimb/staggered gait but otherwise fine delayed-2 to 8 wks of age poor gait discolored fleece and uncrimped stringy wool Signs other than swayback nonspecific dont botherwith checking dietary levels plasma/serum copper good for clinical disease but not body reserves liver levels can find reserves or ceruloplasmin:copper ratio In cattle may just treat and see if works DONT in sheep-copper toxicity

approach to herds with high mastitis

Data collection-examine records for herd recurrence variations ect bulk tank analysis clinical inspection of infected cows(check treatments, bacteriology, teat condition) and farm inspection(biosecruity, milking routine, ben clenliness) Contagious-5 point plan failure most likely evauate milkers, and milking system and culling/treatment method enivonrmental-hygine-dry cool clean areas needed cubibles must be good size and comfortable straw yards changed regularly calving boxes clean/dry everything clean managed, ventilated and not overstocked milking routine and cleaning methods important and minimal teat damage(good milkers) key also low stress/good nutrition and vaccine if needed

approach to high SCC problem

Data collection-strep uberis or contageous pathogens usually inspect farm for 6 point plan(esp milk machine) if strep agalactiae blitz therapy dysgalactie means bad teat managment early dry cow therapy culling-intramammary/parenteral antibiotics culling in lactation treatments milking order discarding milk

Bronchoalveolar lavage technique

Do with a clotted blood analysis 5 animals halter in crush and extend neck tying to fixing in front of iaml lubricate tip of 1m long peice of sterile silone tubing 12mm outside 8mm inside and introduce into nostril advance it through larynx and lubricate 2m long peice 6mm outside 4mm inside and pass through this tube until it lodges in a bronchus flush 60 ml sterile saline in then immediately draw back transfer immediately to sterile sample pot and check for debris ask cleint to take stright to lab and peform PCR or IFAT for iBR RsV and PI3

Parameters of dairy herd management

Dry matter intake-easiest in groups Feed quality-forage/concentrate analysis(good start point) fecal consistency-basic, useful and often overlooked undisturbed cow observation milk production-peak and persistence body condition-esp over stages of lactation(avg of >.75 in early lactation is bad) milk quality-butterfat/protein yeild show roughage and energy status disaese-many nutritionally

Cow selection for sampling of metabolic profiles

Early lactation group-best group, high yeilders will be energy defecient esp 2 weeks post calving. can show if it wil fail to attain peak production or have metabolic diseases/poor late milk quality or repro problems-5-7 cows mid lactation group-over 100 days calved. are at max DM intake and pregnant, good control comparison for early lactation cows and body condidtion and forage contribution to diet monitoring important-5 cows Dry cows-2 weeks prior to calving to check for future problem areas and also about 1-2 months before as well dont take cows over 3 weeks out as early calving group(may have adapted to their diet problems) dont take odd cows, take average ones long standing problem animals will give normal profiles surprisingly get bacground info-cow ID, calving date, BCS, BW, milk stats, diet

Blood sample timing for metabolic profiles

First cows to get new diet/management should be sampled May/june-grass is best quality and availability-shows baseline for rest of year's poorer conditions July/august-summer calving autumn grazing-problems with late stage autumn grasses winter feeding-2-3 weeks into it gives good total diet signs biological variation means that you should do it 2-3 hours after major intake of feed and should be done 2 weeks after any changes made

Practical aspects of pharmacy in farm animals

Food animal rarely treated invidually thus cost/labor effeciency important and minimal carcass damage best choices-bulk feed/water, rumen bolus, multidose injecitors, pour ons, long adcting injections(esp microbials) injection site lesions are bad and will enlarge with age if caused with a calf, so ideally do s/c or IM into neck, and 16gauge

Mastitis detection methods

Foremilking, palpation, behivour, in line mastitis detectors(clot filters) SCC-cells in milk specifically WBC Fossomatic method(automatic) California Mastitis test-crude estimate by gelling reaction good for quick results during milking Bulk or individual cow SCC can be done should be below 200k milk pricing bases on bulk testing with penaltys for above 300k and premiums below 250k mastitis cases, organism base(ecoli give low counts) and age and stage of lactation affect it Bactoscan measures bacteria in milk and also used for pricing with premium for <75k and penalty for over 250k sources include-mastitis pathogens, contamination from environment, poor milk refridgeration/milking equpiment

Calf Diphtheria(Oral/Laryngeal Necrobacillosis

Fusobacterium necrophorum calves 1-3 mo Oral-swelling of cheeks necrotic halitosis, anorexica, pyrexia,salivation, lesions and cheeks/tongue treat with systemic antibiotics(oxytetracycline, penicillin) laryngeal-anorexia pyrexia cough, stridor, dyspnea long term high dose antibiotics(lincomycin) and corticosteroids to drop edema and possible tracheostomy

Mastitis Cause and epidemiology

Herd problem, some pathogens contagious and some environmental Contagious live in cow transmit during milking bacteria have adhesive properties High SCC low bactoscan staph A, strep a/dysgalactia, mycosplasma environmental trasmit between milking(usually just after via passive movement up canal, or from teat canula ect) Milking routine, and post milk teat dip are main control for contagious and environmental hygine and premilk teat dip for environemental

Beef heifer replacement breeding management

Homebred replacements are best-least biosecurity risk Have calving down at 2-21/2 years old to good EASY calving bull just ahead of rest of herd ensure adequate nutrition during mating(esp trace elements) ad check for freemartins/nonbreeders ect aim for weight at mating of 65% expected mature weight PD and remove all nonpregnant heifers after 6-7 weeks try to manage in separate group through first year If from oustide source isolate from main herd and screen for bvd, vacc for lepto/bvd/ibr if not from known disease status herd(TRY to get them from a neg herd)

Bovine respiratory disease pathogens

Infectious Bovine Rhinotracheitis-bovine herpes virus 1-purulent trachitis lots of noise in trachea at exam, hypersalivation/serous oculonasal discharge may also have conjunctivitis or corneal edema bovine respiratory syncytial virus-paramyxovirus necrotising bronchiolitis and interstital pneumonia with lesin s on caudodorsal lung lobes, severe dyspnea possible may need corticosteroids parainfluenza type 3-paramyxovirus mild bronciolitis impairing immune system and secondary bacterial infection bovine coronavirus-16% of cases positive uknown otherwise bovine viral diarrhea-pestivirus that while primarily GI in persistent infections will cause predisposition mannheimia hemolytica-gram neg rod faculattive anerobe-necoritizing fibrinous pleuropneumoni-12 serotypes usually A1 is cause also a commensal common in NA in 7-14 day cattle after shipping pastuerella multocida-gram neg rod/coccoid necoritizing fibrnous pleuropneumonia potential zoonotic commensal too histophilus somni-gram neg rod fuclative anerobe-high range of pathogenicity some comensals may cause myocarditis polyarthritic meningitis too mycoplasma bovis-no cell wall(thus betalactams useless)pleomorphic cells-exudative bronchopneumonia may be intracellular, mild on infection but syntergistic with others(IBR, H somni) and variable signs, may be transmitted via milk

Dairy disease costs

Infertility-one of the largest sources of loss, failure for cow to get back into calf soon enough(not following the 365day calving interval) each extra day is about £3 cost Mastitis 40 cases per 100 per year treatment cost-minor,discarded milk cost,lower milk yeilds, culling costs average cost of £201.20 per case and between 168(mild) and 1709(fatal) Lameness-£80 million poor fertility, high culling, low milk yeild and welfare issue actual cost likely higher given indirect loss £178 avg cost, 80-324 between Milk fever-treatment costs fairly low £40 but can go up to 209 per case

Dairy calf preventative medicine

Keep records of treatments(volume given, doses, animal ID) check calves twice daily and consider calf scoring congenital problems not uncommmon, check heart when can and look for other deformities digestive problems(milk overflow, esophageal groove closure ect) common esp with poor feeding husbandry post weaning scour common as are trace element deficiency

Other environmental mastitis pathogens

Klebsiella pneumonia-from damp sawdust psuedomonas-contaminated water used to wash cows ect can be chronic or peracute with gren/blue udder secretions, poor response to treatment step uberis-common to straw yards and skin of cow common infection in dry period and may become systemic and often bcomes recurrent Bacillus, yeats(candidia/aspregillis)

Actinomycosis

Lumpy jaw, actinomyces bovis gram+ Firm bony swelling on jaw at central cheek teeth region around painful soft tissue, dysphagia and emaciation and discharge from sinus common and may cause tooth displacement or fractures treat with streptomycin or sodium iodide iv poor response aim for remission then slaughter

MRL/ADI

Max residue limit based on an acceptable daily intake withdrawals are established to ensure that it will be below that residue limit very large safety factor for an ADI-assumes 500g meat, 1.5L milk, 2 eggs 20g honey per day

Photosensitizing agent poisoning

Metabolites build up under the skin and react to sunlight causing necrosis, edema and serous oozing and sloughing of skin of nonpigmented skin in cow/horse in sheep only wool free areas of face/ears/limbs usually Primary is from movement of poor pasture to lush green that increases cholorphyll uptake st johns wort/buckwheat may too usually 2-3 days exposure Hepatogenous-biliary phylloerythrin excreition(from the chlorophyll) is obstructed from liver disease and goes into circulation bog asphodel/ragwort also related esp scottish lambs in early summer

Milking routine

Milker hygine-gloves/disinfectants foremilking-detect mastitis teat prep-clean and dried predip dont overmilk post milk teat disinfection good milking order(high yeilders fresh calvers first) mastitic cows last

Building symptoms and solutions for calves

Moisture-dirty water lying dirty catttle damp floors and poor helath Draiginge 1in 60 or 1 in 20 below straw, drainage in pen and good manure/straw management Fresh air too little-ammonia smell dark damp corners high temperatures air inlets and outlets Too much air speed-animals huddling or avoiding areas, having hairy coat and low production air inlets and outlets above animal height, perforated wall cladding

Bovine respiratory disease treatment

NSAIDs-reduce pyrexia inflammation and improve analgesia usually melociam also flunixin and carprofen bromhexine as a mucolytic injectable or oral powder IV or oral fluids for dehydrated animals vaccs only good for prevention really but intranasal IBR vaccs can help wiht outbreak antibiotics for primpary/secondary should be done empirically after culture/sensitivity Betalactams(penicllin, amoxycillin), macrolides(tylosin, tulathromycin), tetracycline(oxytetracycline-usualy first line), fluoroquinolones(enrofloxacin also last resort), trimethoprim, florofenicol-also first line oxytetracycline and florofenicol preferred as act for 4 days tilmicosin(vet inject only), tulathromycin, gamithoromycin, tildipirosin good ong lungs and long acting consider scoring systems but rectal temp is best choice anything over 39.5c retreat often required few days later

copper deficiency treatment and prevention

Oral compound-copper sulphate 8-4 weeks before lambing, copper oxide needles in capsul allowing slow absorption of 2-3 mo ruminal bolus for slow release up to 6 mo injectable-high variability in absorption and activity-Methionate Glycinate slow, EDTA heptonate inclusion in compound feeds(banned in UK) free access minerals mineral fertilizer or reduced molybdenum/iron swayback is progressive and irreversble but mild lambs can be treated and on detection all ewes should be given coper prevent in future using supplement feeding

Record keeping

Owner musthave proof of purchase and supplier info and batch number of drug and purchase date and quantitity and withdrawal and must note name/amount/date of administration and withdrawal and ID of animals and vet should note down involvement disposal must also be noted Vet for POM-V/VPSmust note date and transaction, product ID quanitity, address of recipient, and any perscriptions and batch number Cascade Date of animal exam, owner info, ID of animals, diagnosis, trade name of product, batch number, name/quantity of active ingredient, dose, duration and withdrawal

Clinical mastitis signs

Peracute is only a small percentage In milk it often be lumpier and clotted with watery or yellow color mastitis reduces butterfat, caesin and lactose and total protein calcium and phsophrous also reduced keeping and milk yeild higher RBC/WBC and NaCl and pH up from 6.7 t about 7 SCC/bacteria count will show increase in sublinical cases and milk changes are detected before signs show hot painful swollen udder Set into grades from noninfected to sublinical(high SCC/bacteria detected) to clinical grades 1-3 (milk shows clumping grade 1-udder damage grade 2 and systemic problems grade 3)

General principles of trace element deficiencies

Phases: Depletion-loss from storage sites but blood levels normal deficiency-blood levels drop dysfunction-decline in enzymes of metabolism causing impaired body function but no clinical signs disease-clinical problems apparent Can be primary lack in diet or secondary due to other factors clinical exam(looking for characteristic signs), pasture/soil content, and animal sampling for analysis key to diagnosis

breeding soundness evaluation

Physical exam Repro exam-scrotal shape scrotal CIRCUMFERENCE OVER 15MO=>31CM OVER 2YO >34CM(SOME BREEDS HAVE OTHER STANDARDS) palpate testicles and epididymides carefully for infection/degeneration palpate accessory sex glands and sheif and inspect tip of penis(trauma, phymosis, papilloma SEMEN EVALUATION COLLECT SEMEN VIA ELECTO EJACUATION OR ARTIFICIAL VAGINA/RECTAL MASSAGE GROSS AND PROGRESSIVE MOTILITY >60% PROGRESSIVE AND MORPHOLOGY >70% NORMAL HANDLE SEMEN WEL service capacity-observe bul mating females to ensure good libido and normal intromission

Esophageal Obstruction

Potatoes, chopped swede/turnip common causes salivation and repeated swallowing and progressive bloating assess rumenal typany may need to trocharize relax esophagus then gag animal and try to massage it up to pharynx and remove if in thoracic inlet consider using gastric tube to push into rumen

Preventative Medicine aims and objectives

Prevention of disease and minimal loss from subclinical disease, increased productivity, longevity, good welfare and husbandry and maximize production and profitability Objectives Specific-clear aims to all individuals involved Measurable-objective results should be recorded to find progress is made Achievable-dont set unrealistic goals Relevant-should be related to overall production aims of a farm Time-based

Iodine deficiency

Primary-low in many soils in west UK Secondary-goitrogens-thiocyanate-impairs iodine uptake to thyroid by competitive inhib(brassicas/legumes) thiouracil-distrupts iodination of thyroid hormone keeping it inactive(oil seed rape) Selenium is part of process so it too may affect it Goiter-thyroid enlargement via compensation may only be histopathologically obvious not physically still birth/weak young-often born iodine deficient and will have goiter and alopecia/subcut edema poor production/fertility common Diagnose on Soil/pasture iodine, goiter,thyroid iodine levels and iodine levels of blood/urine/milk will show short term intake levels and thyroid hormone or controlled supplementation trials Thyroid histopath is best diagnosis tool Direct treatment-oral iodine salts, or intrarumenal bolus(6 mo) painting of iodine into skinfold of cattle injectable long term iodized poppyseed soil(2 yrs unavailable in UK) inclusion in feeds or free access salt blocks indirect via fertilizers(ineffecient) and reduced goitrogens(NO RAPESEED)

Selenium/Vit E deficiency diagnosis and treatment

Selenium status and creatine kinase(realted to muscle damage) and AST(may elevate with liver problems too) to diagnose, also PM necrotic heart and skeletal muscles Soil/pasture levels(very well correlated, and blood/liver selenium(short term only) Glutathione peroxidase in blood-standard test as contains selenium in enzymes and shows long term status Plasma a-tocopherol levels show WMD risk Direct-treat with oral sodium slenate or intraruminal bolus(lasts 6-12 mo) injections of sodium slenate(3 mo) or barium selenate(long term 9-12 mo) add to ration indirect-apply fertilizer to pasture can last up to 3 years Vit E should be supplemented with selenium by same methods or tablets, and may need weekly intervals both can cross placenta and enter via colstrum so good for dam and offspring in late pregnancy

Esophageal stenosis upper alimentary squamous neoplasia

Stenosis congenital or from neoplaia/lymph node enlargement regurg and ruminal tympany Neoplasia bracken toxin causing pailloams wasting coughing salivation bloat cull

Stomatitis, papular stomatitis

Stomatitis/Pharyngitis physical injury from dosing gun stomach tube ect salivation, halitosis, quidding, swellling treat with antiinflams/antibiotics Papular stomatitis Parapoxvirus(ZOONOTIC) calves 1-12 mo, papular rings on muzzel nostrils and buccal mucosa anorxia and mild pyrexia Self limiting heals within 4-7 days

Copper defieicny factors and copper metabolism

Sulfur-converted to sulfides that react to form insoluble CuS molybdenum-form thiomolybdate with sulfur to bind irreversibly to copper-affected by soil content and pasture improvement like liming or late maturity grasses Iron-inibits copper uptake by binding or in combination with sulfides-common with soil contamination Zinc/cadmium sometimes Brassicas/cereals good sources but root cops/poor grazing related GI parasites Genetics-Texels have high absorption, blackface sheep poor Liver main storage(70%) caeruloplasmin main transport protein(80% copper bound to it) clinical signs only show after liver stores depleated and copper drop at tissue sites may take 3-6 months to appear

mastitis targets

Targets BMSCC-below 150k proprtion scc above 200k <10% bactoscan below 20k <20 per 100 per year infected less than 15% infected overal per year recurrence bleow 10% culling below 2%

Defense mechanisms against mastitis

Teat skin-uncut unchapped no warts teat canal barrier-forms keratin seal after milking genetic factors-conshaped pendulous udders bad udder defenses-lactoferrin-binds iron to reduce bacterial growth when dry lactoperoxidase-bacteriostatic to gram+ and cidal to gram- iducible defenses-wbc migration ect

Mastitis control dry cow therapy

Treat existing infections and prevent new ones(summer mastitis) and ecoli duration of action and activity during dry period-esp done during last 2 weeks residues-antibiotics that last longer do have more residue type of bacteria-staph aureus and strep uberis main ones to be treated and ecoli complete cure of sublinical infections(parenteral antibiotics if needed) dry cow tube hsould be put in aseptically

Ecoli mastitis

Usually due to poor housing/hygiene peracute mastitis-usually early lactation and life threatening intially anorexia, pyrexia, diarrhea, with generally normal udder and milk develops to hard hot udder with yellow watery secretions and low temp and deyhdration that may become fatal subclinical common with just increased SCC chronic recurrent masttis-poor immune response leads to second run about 10% of time may infect in dry period laying dormant in udder then starting up in early lactation(likely cause of 50% of total subclinical cases)

Housing ventilation for calves

Ventilation biggest priority as fresh air keeps dampness down and minimizes cold(keeping above lower critical temp) Steep roof with an open ridge at the top is best stack effect and on still days it will warm the air and there should be an open ridge at the top to allow this to leave and pull fresh cool air in On the sides its should be at least 10 m cube per calf up to 90kg 13 m cube up to 150 and 15 cube for anything above that Oulet ridge should be minimum .04 sq m per calf and .1 sq m outlet per cow test with smoke tests inllet should be 4x area of outlet

animal pharmacy legislation and drug cascade

Veterinary Medicines Regulations 2005 main document cascade if there is a product is liscensed for codition and species it must be used Cascade options-if it liscensed for another condition in same species or another species in same condition or a UK liscensed product or in accordance with import certificate or produced by a vet/pharmascist or other authoraised individual or a vet product outside the EU

Enterotoxigenic ecoli - k99 antigen positive

Young calf <1wk old, history of passive transfer failure or precalving vacc failure usually housed rarish but can become an outbreak dehydration to rapid decline to recumbancy and rapid heart rate suken eyes and skin tenting with tacky mm bloated looking and sloshing from gut stasis, profuse yellow/white diarrhea without mucus or blood pyrexia and evenutal hypothermia snap test, culure, serum tp to diagnose ecoli adhere to gut mucosa and release toxin causing hypersecretion of water into lumen causing osmotic diarrhea without much villi damage treat with IV/oral bolus fluid and support care and cover antibiotics if septicemia prevent with clean pens, yards and feeders/bottles/teats ensure good colstrum intake and consider precalf vacc

identification and treatment of clinical mastitis cases

accurate record keeping important and may be investigaed must have cow ID, date, quarters infected and bacteriology results and treatments for htem Antibiotics-amoxycillin clauvanate cefquinome framyeticin(wont work against betalactamase) pirlimycin(wont work on gram neg also 5 day withdrawl) 48-84 hr milk withdrawal in all cases all treated MUST be IDed and withdrawn from milking Grade I-usually farmer treated with intramammary tubes Grade II-vet often contacted-parenteral therapy and nsaids needed penicillin(no gram neg b-lactam resistant), amoxycillin, cefquinome, trimethoprim, framyectin, tylosin)gram+ only) nsaids-flunixin, ketoprofen, meloxicam grade III-coliform or staph aureus-vet needed aggressive treatment

Food animal extra drug reqs

additional food animal reqs must be used for only animals on one holding it must be licensed for food animal if from another state ensure it is listed on the EU table of permitted substances(ex metronidazole/chloramphenicol arent listed) Withdrawal periodmust be specified (min 7days milk/eggs, 28 for meat and 500 degree days fish) Records should be kept 5 years w name of owner, animal IDs, dates, diagnosis, drug and dose and duration and withdrawal

In feed medication

all are pomv/vps and must have a medicated feed stuffs perscription and standard perscription with following info of perscriber and qualifications owner info species/id/number of animals to be treated premesis of animals date of perscription, signature of prescriber, name and amount and dosage/administration instructions warnings/withdrawal, manufactuerer of feedstuffs and amount/type of feedstuffs being used and inclusion rate of vet product and any instructions

Best antimicrobial,nsaid for cost

amoxicillin then trimethoprim then ceftiofur(really expensive in pigs), then ceporex finadyne then metacam then ketofen

Oxalates

beet rhubarb sorrel free oxalate absorbed into rumen and calcium oxalate forms in arteries damaging lung capillaries and cause pulmonary edema and continued will cause nephrosis from crystals ni renal tubules and plasma Ca may drop causing hypocalcemia sheep more than cows/horses but can adapt to high oxlate diets via rumen flora usually diagnose on history and signs as well as PM oxalate cyrstals in kidney borogluconate therapy may help but most die of acute renal failure

Tannin poisoning

bind to protein and cause asringent reaction in mouth oak leaves and acorns which become toxic in cattle adn sheep digestive tract some animals crave them signs show up days later, dullness anorexia constipatoin and anuria and dystentery/diarrhea urine dark and serous oculonasal discharge acorns in rumen and abomastitis and uremic smelling carcass and edema found PM treat with liquid parafiin and milk and appetite stimulants avoid saline/IVs

goitrogenic glycoside poisoning

brasica and white clover goiter reduced growth rate and diarrhea depending on composition sudden blindness in cattle and sheep and digestive disturbance in growing cattle grazing on rape especially in seeds brassica has variable amounts of that in glucosinolates interfere in thyroid synth and thyiocyanates impair iodine uptake(can be treated with extra iodine)

Targets for heifer rearing

calve at 22-26 mo conception at 15 mo 60% adult weight at service 85% adult weight at calving 40kg calf to 700kg means .8 kg/day to service

Beef suckler aims and must haves

calve herd over short season of 9-12 wks at the same time each year and wean one calf per cow compact caving pattern ensures easier management and efficient feeding of animals ensuring better calvings milk and healthier calves Requires fertile cows cycling at breeding period good replacement heifer breeding fertile bulls during breeding period no infectious infertility diseases introduced

Acute lead poisoning

calves death w/in 12-48 hours blindness, muscle tremors, colic, frothing of mouth, staggered gait become recumbant and convulsive and hyperreactive to touch/sound adult cattle can become aggresive frenzied and pyrexic

Welfare of farmed animals regulations 2000

calves <6 mo colustrum within 6 hr of birth iron to keep hemoglobin above 4.5 mmol/L >2 wks 100g/day fiberous food up to over 250 g/day 20 wks feed twice daily and have sufficient rining water every day and unlimited access in summer or druing illness

Coliform mastitis case treatment

clinical exam-severe depression, recumbency, low rectal temp, diarrhea, hard quarter common fluid therapy-endotoxemia causes hypovolemia so up blood vol- up to 50L fluids needed oral, IV(saline usually only do 10-15L nonsterile) IV hypertonic fluids to induce drinking Nsaids antibiotics-high dose broad spectrum(sulphonamides, cefquinome, amoxycillin, oxytetracycline) calcium borogluconate(hypocalcemia common) quarter stripping and oxytocin to help letdown

approach to high bactoscan problem

combo of mastitis pathogens, environmental contampination, dirty milk parlor and poor refridgeration look for patterns in data and bulk tank analysis to find source must be below 4C to prevent bact growth Bactoscan for bacteria, Total bacterial count for viable bacteria, theroduric count-for pasteurisation resistant bacteria(washing up problems), coliform count(environ mental problem), psychotroph indicator value-poor premilking teat infection or direct bacterial counts Udder pathogens=reduce mastitis and id animals and separate their milk environmental-high coliform/pyschotroph=keep cows clean, clean teats/predip, dry them too dirty milk plant-high bactoscan/tbc and theroduric count-rarer now but cleaning process may be at fault, high water volume, cleaning solution high temp, good detergens used poor refrdigeration-bactoscan/phsycotrophs high-cool milk beter

Bovine respiratory disease aetiology

compromise of the mucociliary escaltor, leukocytes, and antimicrobials allows colonization of resp and commensals to extend with large number of organisms as possible secondary source of infection primary usually virus and may do so without seconadry infection but secondary infectors may occur without primary if defends reduced for other reason

Components of preventative medicine plan

details of farm, current production data, production targets, repro performance, nutritional management, replacement policy, disease control, infectious disease control(status of various diseases and vaccines), parasite control, neonate care, biosecurity, medicine records, stockmanship, and calendar of health plan(routine procedures)

Metabolic profile use

dont replace technique but provide extra info on nutritional balance of groups of cow in a herd as far as energy protein and minerals go most successful when integrated with larger planned preventative medicine program and find problem areas before they show up in production loss or health problems

Estrus synch in beef herds

double prostaglandin injection-cows/heifers injected twice with PG 11 days apart and fixed time AI 72 and then 96 hours folowing injection best for maiden heifers as results can be poor in cows progesterone releasing device CIDR-device inserted 8-10 days with prostaglandin injection given 1-2 days before device removed AI at 48 and 72 hours after removed or once at 56 hrs progesterone based synchrony is better in beef herds as can help in anestrus and degree of synch is better than double programs esp if GnRH used

Nitrates/nitrites

droughts can cause it to build up in soil and if there is a heavy rain in no sun after it will retain in plants or overuse of nitrate fertilizer especially clover/brassicas in root/stem usually in cattle or sometimes store lambs that re poorly fed combines with hemoglobin to make methemoglobin causing dyspnea, tachycardia tremors weakness and in severe cases mucosa will brown then become cyanotic then anoxic death few hours to few days blood Pm is chocolate colored and tissue is brown and pulmonary congestion/petechia in heart treat with methylene blue every 6-8 hours 4.4 mg/kg in 2% solution and remove animal from nitrate source and feed high carbs

Best start for dairy calf

dry cow nutrition importnat, consider precalving vacc good clean dry well lit calving pens navels dipped after birth and good colosturm(10% bw by 6hrs and 3.5% more by 12hrs) test colostrumf or quality and monitor passive transfer using serum total protein should be at least >5.2g/dL, ideally 5.5g/dL after feed twice dayfrom buckets/bottles or teat feeder/robotic feeders milk replacer should be made to right temp and centration and creep feed by 2 weeks of age 24hr acess to water drining 4-6L water per 1kg concentrate eaten dont feed waste milk or from dirty basins

Summer mastitis

dry cows and heifer disease varies in incidence by region arcanobacterium pyogenes, peptostreptococcus, and strep dysgalactiae and others transmited via head flies swollen hard painful hot udder with enlarged teat secretions thick and clotted yellow green pyrexic lame stiff edema on leg/udder and may abort parenteral antibitocis(penicilin, sulphonamide or tylosin) intramammray antibiotics(pencillin/erythromycin) and nsaids and udder stripping to treat Fly treatment and sealing teat canal key control

Cardiac Glycoside poisoning

foxglove, lily of the valley, oleander Act on myocardium increasing contractility and slowing heart rate. Moderate intoxication results in bradycardia, depression regurg and diarrhea higher causes cardio irregularities brady/tachycardia, dysrythmia within 4-12 hours of ingestion and 2-3 days toxicity will retain even if dried/boiled fluid support+atropine and propranolol and charcoal/rumenotomy can help

alkaloid poisoning

generally bitter tasting and thus rarely eaten but can become addictive poisoning is usually fatal and if not recovery is often incomplete mimic and block ACh dopamine and serotonin excess salivation vomiting, ab pain diarrhoea convulsions coma yew, hemlock ragwort, lupin

Beef herd fertility analysis/benchmarks

good records important for iding for culling and analyzing fertility, in theory 60% will calve in 21 day period, 25% in 43 days 10% at 63 and 5% in the rest construct histogram using dates bulls run with cows to find theoretic start of calving and use that as day 0 then wok out cows that calve in each 3 week period, from that you should expect barren cows to be <5% cows in first 3 weeks to be >65% and calf crop to be >94%

Ideal calf rearing environement

healthy environment open sunny location with not too many calves in one airspace with adequate ventilation and protection fro draughts and dust and no vermin newly arrived calves should be kept apart from others and if individually penned must be able to see others and must be group penned by 8 weeks small groups of equally sized animals good dry bedding with pens that drain directly out the building not into other pens must be large enough for calf to lay at least 1m wide and 1.8m long individual pens ready access for feed prep and cleaning with nearby storage areas is best. allow time between crops to rest facility and clean out best to have an original facility and not have to modify it

Beef bull selection

ideal should produce easily born calves with rapid growth and good conformation EBVs(estimaed breeding values) for common breeds to aid in bull selection and BLUP(best linear unbiased prediction) to use performance of animal istles and relatives and progeny to maximize data new puchased bulls should be screened for BVD and if >2yrs Johnes and try to source from disease free herds Hire bulls and nonvirgin bulls are major disease risk

Feeds with high copper content

pasture/silage/roots grown on pig/poultry manure distillery byproduct feeds w/ copper stills concentrate feeds w palm oil or mollassed sugarbeet milk-high copper availability cattle minerals, copper sulphate foot baths low copper antagonist(molybdenum, sulfur, iron) feeds

Bovine respiratory disease significance

£80 million per year as of 1997 £43 per dairy calf, £82 suckler weight loss biggest cost 40% of cost in suckler 25% in dairy avg mortality/morbidity both higher in suckler than dairy £300 if calf is lost also costs of long term damage growth rates vaccine cost and reduced lactation ect

Bovine respiratory disease outbreak approach

if not a dyspnic calf brought up go for thorough history and exam of buildings for risk factors and state of animals random sample of 10-20 animals pyrexia esp important 39.5 or even over 41), tachycardia, tachpnea/hypernea/shallow breaths, dry cough(interstitial pneumonai) or prdocutive(bronchopneumonia) ocular/nasal discharge and type(serous/hemorrhagic/purulent) auscult trachea and lug fields(lack=considlation/pleurisy) reluctance to move/grunting/pain concurrent disease(gi pathogens like scours) H somni linked with depressed animals IBR with high temps dead animals should be PMd(may not find clear agent look for cranioventral lung and get samples) and conjuntival swabs for IFAT/PCR IBR diagnosis Pyrxic without purulent discharge and were normal yesterday are ideal animals to sample bronchoalveolar lavage(better than nasal swab if done well) clotted blood sample and serology<-use for older calves return in 2 weeks for second serology if BAL fails always check BVD status and consider lungworm or poor passive transfer

Carbohydrate overload(lactic acidosis)

imbalanced concentrate roughage ratio or carb gorging after accessing feed store or feed change cho ferments and gas up and ph drops killing cellulolytic bacteria acid tolerant bacteria survive that produce more acid and cause acidosis and water is absorbed into rumen from system dehydrating animal then gut stasis and bloat followws mild discomfort anorexia, reduced ruminal activity ruminal distension maybe diarrhea severe-anorexia, dpression, dehydration, tachycardia, rumen stasis, pain lamintitis may see toxemia with pyrexia or acidisosi-tachpnea, weak, ataxic coma death pull over 100bpm and rumen pH below 4.5=slaughter or rumenotomy if gorging mointor over 48 hours IV fluids, antacids, Ca/glucose, penicillin/oxytetracycline and vit B1 all help clin cases prevent with min 10% roughage in diet, dont over grind grain and keep bins locked

Trace element deficiency prevention/correction methods

indirect application of mineral fertilizer to pastures(only works really for primary deficiency) minimizing factors interfering with uptake(for secondary problems like soil contamination reducing copper) genetic selection-some breeds better than others Direct inclusion in compound feed(best choice) free access mineral block/licks medicated water oral drench/bolus injectable compounds

Cyanogenic glycoside poisoning

linseed and cherry laurel convert glycosides to hydrocyanic acid and has glycosides in the plant thus during decomposition or ruminal digestion makes production of it drying material doesnt reduce toxicity but can cut down on cyanide content it inactivates cytochrome oxidase system starving cells of oxygen thus brain and mycoardium having highest oxygen use are first to die blood becomes bright red and dyspnea convulsions and death soon follow feed hisotry bright red mucosa and smell of bitter almonds in rumen to diagnose treatment must be rapid and requires IV sodium thiosulphate and sodium nitrite repeatedly

subacute lead poisoning

more common to sheep than cows dullness, inappetence, incoordination, blindness, gait problems(circling and immobility) hyperaesthia, salivation, teeth grinding, muscle tremors ruminal atony/ab pain and constimpation and later fetid diarrhea palbepral eye reflex absent or reduced(differentiation from polioecephalomalacia) abortion or paralytic lambs common clinical signs and detection in blood/feces/urine/milk using lithium heparin tubes fecal levels show unabsorbed/excreted from bone lead and are of little vlaue without blood levels kidney lead concentrations gold standard but liver biopsy possible

Lead poisoning treatment

must be done early but usually disease progressed too far by time of diagnosis calcium versenate at 12.5% driop 110-220 mg/kg over 12 hours blindness may persist wont reduce tissues levels thus food safety wise will still require natural eliminiation

maximizing beef cow fertility

nutritional management most important as ovary recycling is related to body condition and energy of the cow winter rations should accomodate pregnancy/lactation and allow cows and good condition to use body fat to reduce feed costs BCS<2=less likely to concieve during mating period separate thin cows to feed extra and feed less to fat cows(periparturient problems) ensure trace elements supplemented(esp copper/selenium) avoid sudden diet changes have control measures for fertility diseases(lepto, bvd, ect) Spring calves 3.5 bcs at weaning in winter, 2.5 6 weeks precalving in early spring autumn calves-3 at servicing, 2.5 at spring turnout

Lead poisoning

once common rarer now, cattle esp young lead paint, soil contamination, inudstrial lead, petrol lead, metallic lead or sprays/building materials all sources Most is GI or resp absorbed but only 2% ingested lead is absorbed some excreted in bile/milk/urine initial deposit to kidney/liver and then also bone(esp growth plates) causing osteoporosis and may be a reservoir for lead that can be released into circulation at times like preg/poor nutirtion/illness lead binds to RBC causing fragility and mild anemia with immature RBC binds to endothelial cells of brain capillaries causing edema via high permeability v bad for young animals can readily cross into placenta-tertogenesis/abortion

Plant poisoning associations

poor pasture-drought or snow forcing animals to eat weeds/hedges overgrazing allowing weeds to establish forage conservation-toxic plants may if conserved with other forage become palatable accessibility to poison-isolated cases are usually from duping hedge cuttings or waste or from storms grazing experience-young animals or new animals are more likely transportation-tired and hungry animals are more likely environmental factors-drought/shade or overuse of herbicide animal species

Staph aureus mastitis

primary reservoir in udder may be on teat skin can transmit to next 6-8 cows that use same milker most produce B-lactamase peracute gangerenous mastitus-pyrexia, pain, redness, swelling of udder systemic illness recumbent severe systemic illness and depression udder will be black blue clammy with reddish brown secretions must cull acute mastitis-clotted milk chronic-hard to treat fibrose indurate udder 25-40% success rates antibiotics dont penetrate the fibrosis well and most are resistant to betalactam antibiotics

Chronic Copper poisoning

sheep mostly sometimes cattle Suffolk sheep and Angus cows predisposed occurs after lysosomal copper storage capacity in liver has been exceeded causing intravascular hemolysis+jaundice Subclinical from 8000 umol/kg to 15000(lysosomal capacity) stress like sales ormetabolic problems may lower capacity Blood copper levels may reach 38-200umol/L during hemolytic crisis and debris may block renal tubules causing renal failure and brain damage progressive ataxia, jaundice and hemoglobinuria and anemia followed by death Rare in adults usually young calves anorexic enophthalmos and dehydration with rapid breathing/HR subcut ammonium tetrathiomolybdate can be used but no longer allowed antiinflam support and IV fluids+antibiotic and molybdenum or sulphur added to diet efficiency of copper uptake compared to iron sulphur ect are more related to poisoning than just high copper feeds

Bovine respiratory disease risk factors

sourcing calves from mutiple farms-more pathogens with group mixing, establish good relationship with sources and avoid markets/collection centers transport-stressful esp with group/diet changes illegal if navel hasn't healed or under 7 days old and cant go to market more than once in 28 days large group sizes-more mixing and more nimals establishing heirarchy and therefore more stressed. less than 40 weaned per pen mixed age groups-increases bullying and even if separate in same airspace may passively pass on disease to younger cows group changes-stess and spread poor colostrum management-good protein status of dam and ensure suckling 3L at birth and 3L at 6 hrs. monitor quality if possible changes/extreme temperature-changes in weather esp outside 10C and 29C require energy change damp/draught-increase lower critical temp making cows cold at higher temp insufficient airflow-relative humidity <75% nutrition-malnutrition=immunosupression esp common with milk replacer water-dehydration=immune drodrying of mucociliary escalator dust stockmanship-gentle handling=less stress others-housing weaning castration disbudding all stressful and all reduce immune, good analgesia important dont do all at once

Acute copper poisoning

sporadic in both sheep/cows gross overdose via IV/oral copper to prevent deficiency symptoms overwealms hepatic removal/storage capacity signs w/in 24 hrs of admin stress or other treatments may influence ability to remove generalized edema, GI inflam, petechia sudden depression anorexia, rapid HR/resp and low temp blue green mucoid diarrhea collapse/death w/in 24 hrs dysentery/juandice appearant erosion/ulceration of abomasal/intestinal muscoa and edema found PM and high liver/kidney copper concen found

Indigestion

sudden diet change upsets rumen microflora or excess carbs or antibiotics rumenal atony, inappetance, milk drop, colic, diarrhea no pyrexia clinical exam and history to diagnose rumen stimulants and better forage, and probiotics to help

Basic biosecurity

to prevent introduction of disease to farm and minimize spread in herd 1. Maintain closed herd 2.Operate isolation for pruchased stock 3. provide cleen feed/water 4. control visitors/vehicles 5. control wildlife 6. monitor health status and operate disease control program

saponin poisoning

very slow absorption thus large amounts needed may cause gastroenteritis found in ivy

Bull cow ratios and general management

young bull 20-30 cows max mature 40-50 cows max nutrition-young bulls <2 1/2 yo rewquire fed for normal maintence(fit not fat) housing in wellfenced outdoor paddock or pen with exercise area lameness common good foot trimming needed dont forget to include in vacc/worming