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261 Cards in this Set
- Front
- Back
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qualities of colostrum |
high solids content
high fat content Ig cells fat sol vitamins laxative |
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milk composition
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lactose- glucose and galactose
proteins (3.1-3.5%) - casein - whey fat droplets (3-10) cells |
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physiology of lactogenesis
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hormonal control with neuronal imputs
prolactin promotes milk production oxytocin facilitates milk ejection- contraction of myoepitherlial cells stressful stimuli interfere with oxytocin binding |
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lactation curve/ schedule
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peak lactation 4-8 weeks post calving
typical lactation 305 days 60 day dry period- rest/ recovery of mammary tissue production manipulated by photoperiod and BGH |
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what influeces milk composition
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genetics, stage of lactation, breed, diet, environment, season
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wht effect does SARA have on milk fat
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depresses milk fat
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Milk gland defences
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1. teak canal- primary physical barrier- firmly keratinized, no glands
2. regular milking- keratinized cells in teak canal trap bacteria and sheared off by force of milk coming through canal 3. teat sphincter- contracts from teat base after miking- wringing out milk so onky thin film left- dries and closes teat 4. phagocytes- 50,000-200,000/ml in normal udder 5. humoral response 6. cell mediated response 7. lactoferrin- limits iron availability- antibacterial |
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av milk prod of cows
av calving length 1L increase at peak= |
7000l
13m 200L extra in lactation |
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clinical manifestations of mastitis
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enlarged supramammary lnn
abnormal secrtions- colour, consistency, smell abnormal size palpable abnormalities agalactiva- suually secondary to systemic dz blind/ non functional glands- severe mastitis hungry neonate pain/altered gait teat and skin lesions |
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palpable abnormalities of the mammary gland
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temperature- increased or decreased
crepitus- anaerobic infections nodules- chronic inflamm- fibrosis, abscessation |
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how to examine mammary gland
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1. restraint- xylazine, footrope
2. visual- teat end, skin 3. palpate- udder 4. palpate- supramamm lnn 5. milk secretions- clots, watery milk, colour, odour +/- sterile milk collection rapid mastitis test- mix with equal detergent.. viscosity correlates with SCC 6. adjacent skin- udder sores 7. mamm vein- phlebitis, rupture |
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Disorders of the mammary gland
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udder oedema- usually physiologic- first calf heifers, late pregnancy. if severe- breakdown of median suspensory lig, difficulty walking
high sodium or potassium in diet, high grain blood in milk- usually rupture of vessel by direct trauma galactorrhea- udder developmet and lactation in absence of preg- usually goats gynecomastia- boys get boobies- adrenal dz/ hormonal imbal |
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conditions affecting teat
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1. milking equipment- over miking, excessive teat end vacuum, pulsator malfunction, poor fitting liners. Oedema, hyperkeratosis, scaly, irritated skin
2. teat dips- too conectrated- drying and cracking 3. teat cracks- poor envieonmental conditions, poor emollient in dip 4. pseudocowpox- heal in 2-3 weeks. xzoonotic 5. herpes mammilitis- BH2,4- usually first calf heifers. raised oedematous plaques, calves may get oral lesions 6.photosensitisation- generalized 7. warts- common- papilloma 8. teat peas- amyloid 9. teat spiders- tissue membrane 10. frostbite 11. exotic dz- FMD, vesicular stomatitis |
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importance of let down
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depends on cistern capacity vs alveolar capacity
only 30% in dairy cattle compared to 80% in dairy goats first calf cows even more important because cistern capacity less- reason for them responding well to more regular milking and requiring better milk letdown |
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components of milking machine
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teat cup- rubber or silicon liner enclosed in shell
milk line to remove milk pulsator supplies alternating vacuum and atmospheric pressure at 60 times a minute |
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phases of milking
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massage phase- inside liner at milk vacuum at all times- atmospheric air enters between shell and liner, collapsing liner- massages teat and prevents oedema in teat
milking phase- pulasotir creates vacuum between shel and liner- same vacuum on both sides of liner so it opens- milk drawn out through teat opening. ideal end vacuum is 37-42 kpa |
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milking procedue
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1. cows move in themselves
2. ensure teats are clean and dry 3. apply cups to plump teats- routine= optimal oxytocin release/timing 4. remove cups by cutting vacuum when milk ptod is at a dribble 5. post teat dip |
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losses incurred due to mastitis
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discarded milk
mik quality penalties based on scc early culling treatment cost vet cost increased labout risk of vat AB contamination deaths |
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major contagious pathogens
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str. agalactiae
s aureus mycoplasma increasing prevalence |
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mastitis- environmental pathogens
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st. uberis
str. dysgalactiae e.coli klebsiella enterobacter citrobacter strep bovis arcanobacter pyogenes yeast corynebacterium bovis prototheca still important to examine teat- damage during milking process with predispose |
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what athogens are most commonly associated with subclinical mastitis and how is it monitored
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s.aureus, s.agalactiae, st. uberus, coag neg staphs
SCC /ml milk a bulk tank SCC of 200,000 indicates that 15% of cows are infected in 1 or more quarters 400,000 35% |
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definition of clinical mastitis
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grossly abnormal milk beyond first 3 swuirts+/- evidence of varying degrees of mammary gland inflamm
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signs of actue mastitis
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hot swollen gland
flakes or clots in milk- can be watery, serous, purulent anorexia, depression, fever in severe cases- tachypnea, hypoCa, recumbency |
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pathogens causing acute gangrenous mastitis
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clostridium spp
staph aurus occasionally coliforms |
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signs of acute gangrenous mastitis
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initially hot, hyperaemic and swollen, within hours becomes cold, secretions watery and sanguinous, blue discolouration from teat to various areas of the gland, slouding of skin within 10-14 days
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signs of chronic mastitsi
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chronically elevated SCC
periodically flakey, clotty, fibrin scarring- palpable changes decreased milk yiels |
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properties of s aurues mastitis
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s. aureus- not obligate- poor milking, colonises unhealthy teat skin, unhealthy quarters, farmers hands, fly bite. facultatively intracellular so chronic, unresolving infections are a problem. most comm cause of acute gangrenous mastitis- vasocontrictive alphatoxin. major reservoir is subclinical infections
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st agalactiae mastitis
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st. agalactiae- obligte parasite of mamm glands- few clinical signs, chronic destruction of ductal system. can be eradicted
sensutuve to treatment large numbers of bacteria may be shed in milk |
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mycoplasma mastitis
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highly contagious
facultative intracellular fibrosis of glandular tissue large numbers shed in milk spread by improper intrammamm tx fresh cows at risk |
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coliform mastitis
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faecal contamination
LPS incites rapid inflamm response mild to severe signs most spontaneously clear 10% remain chronically infected endotox in severe cases- induces hypoCa- mortality common |
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pathogenesis of dry cow mstitis
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occur during dry period- increased incidence in muddy, wet, filthy environment- putulent infection and abscessation of the gland
can be spread by flies caused by truperella pyogenes |
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principles of mastitis control
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ensure healthy teats
reduce numbers of mastitis pathogens in contact with the teat |
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strategies to reduce transmission of contagious mastitis
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1. adequately sized, properly functioningmilking equipment abd appropriate milking technique
2. ensure hygienic milking practices- gloves 3. disinfect teats post milking 4, milk clinical cases last, use separate cluster for them 5. use dry cow therapy- treat each quarter at drying off 6. cull chronically infected cows (s aureus, mucoplasma- poor AB response, reservoir) 7. maintain closed herd. PCR or milk culture of new animals before introducing to herd 8. backflush the cluster after a chronically infected cow is milked 9. avoid feeding heifer herd replacements with mastitic milk- transmit mycoplasma, s. aureus, coag neg streps, str agalactiae |
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controlling environmental mastitis
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1. milking equipment, teat spray
2. herd environment clean and dry 3. sheltered calving paddocks 4. avoid muddy tracks 5. diets adequate in vit A and E, beta carotene, Se, Cu, Zn |
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Herd mastitis surveillance
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1. herd recording- yield, milk fat, protein, individual SCC
2. BMCC- high- lots of subclinical cows, clinical cows put into milk vat some pathogens raise BMCC more than others- staphs may take a while to elevate alarmingly whereas a few heavily shedding agalactiae cows will significantly elevate BMCC 3. Bactoscan- number of bacteria present in each ml milk after incubation. results in 5 mins 4. coliform count 5. thermoduric count- elevated= poor cleaning |
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treating staph aureus mastitis
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lactational therapy produces cure rate of less than 40% but will decrase shedding and SCC. Betalactams most commonly
dry cow treatment more successful- reduce exiting inection and decrase incidence of new infection cull persistently infected cows consider c&s intramammary and possibly macrolide |
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treating agalactiae, dysgalactiae, uberus
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respond well to ABs (40-80%). lactating cow therapy should be based on individual quarter or composite samples. Penethamate also good option. SCC not good measure of active infection- may have overcome infection (falsely high) or be low in chronic infection. reinection common if teat lesion unresolved. High rate of spontaneous clinical cure, only 20% bacteriological cure
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tx coliform mastitis
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not responsive to lactational, dry cow therapy. Self resolving usually, systemic ABs to prevent endotoxaemia. Supportive therapy. Frequent milking (1-2hrsin acute) to flush out inflamm mediators, bacteria (4-6 hours in chronic). NSAIDS with intravenous or oral fluids to prevent dehydration. May need to addresss hypoCa or hypoK
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benefits of dry cow therapy over lactational therapy
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1. higher cure rate
2. higher dose can be used 3. retention time of ab is longer 4. incidence of new infections during dry period Is reduced 5. tissue damage by mastitis regenerated 6. clinical mastitis at freshening may be reduced 7. reduced risk of contaminiating milk with drug residue |
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mastitis is goats
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1. caprine arthritis encephalomyelitis- hard udder cuased by intersitisal mastitis. no tx. DFK
2. mycoplasma-, no tx, don't feed to kids 3. arcanobacterium pyogenes- following wound, causes abscess 4. c. pseudotuberculosis- mastitis rarely 5. s.aureus- similar to cattle 6. C- strps- cmmon 7. str. agalactiae- uncommon 8. coliforms |
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sheep mastitis pathogens
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s aureus
p haemolytica |
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zoonoses shed in milk
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listeria monocytogenes
nocardia mycobacterium salmonella brucella |
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management of severe acute mastitis
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1- euth
2. tx - fluids- hypertonic saline - ca (caution) - antiinflamms- NSAIDs - antimicronials- broad acting - freq milking 1-2 hrs |
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antimicrobials reported to be beneficial for acute coliform mastiss
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oxytetracycline
TMS ceftiofur |
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ideal AB
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low MIC doe bacterial pathogens
bacteriocidal activity not reduced by presence of milk ph of milk 6.9- weak bases accumulate in milk lipid solubility extent of binding to udder proteins ionization |
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disadvantage of intramamm tx
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uneven distribution
risk of contqamination irritation to tissues ab might disturb phagocytosis |
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macrolides
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narrow spec- gram pos only
weak base, lipid sol -static milk interferes with activity |
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Penicillin G (penethamate)
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MIC low
weak acid lipophilic no interference from milk |
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choosing ab for mastitis
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know pathogen profile of the farm
BMCC pathogens likely to be assoc with late lactation consider cost, WHP, amount of milk discarded, likelihood of contam, likelihood of cure |
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when would you use both intramammary and parenteral tx of mastitis
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valuable cow
known s.aureus cows younger cow- want to mazimise chance of cure vs chronic infection |
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mastitis in sheep
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staph aureus- blue bag
p. haemolytica- blue bag less important Coag neg staph c. pyogenes streptococcus coliforms p. mltocida bacillus |
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milk cultures
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s,. agalactiae- prolific shedder- CAMP test
staph aureus- improved detection from frozen sample mycoplasma- special media, frozen sample coliforms- often culture neg |
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musculoskeletal physical exam
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Note size, shape, and symmetry
• Stance • Look for muscle fasiculations • Observe the animals gait looking for evidence of lameness, weakness, stiffness, pain, and ataxia. • Palpation (tone, consistency, sensitivity) • Temperature (warm / cold). • Percussion |
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altered muscle tone ddx
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Increased muscle tone
– Neural (tetanus, strychnine poisoning, seizures) – Periodic spasticity and spastic paresis in cattle. – Myopathy • Decreased muscle tone – Reduced neural inputs associated. – Severe electrolyte imbalances. |
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muscle atrophy ddx
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• Denervation
– Complete denervation of a muscle results in more than a 50% loss of muscle mass within a 2 to 3 week period. • Disuse • Injury. |
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forelimb injury epidemiology
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distal fractures more comm
muscular injury less comm than in hind limb |
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common hind limb injuries
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• Ruptured gastrocnemius
• Avulsion of the adductor muscles • Coxofemoral luxation • Ruptured peroneous tertius • Femorotibial instability • Sacroiliac luxation/instability |
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principles of gastrocnemius rupture
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- Common in post partum cows.
– Metabolic muscle weakness (hypocalcemia) increases the risk. – Slippery surfaces increase risk – Occasionally observed in goats – Can be a complication of lumbosacral epidural |
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ddx gastrocnemius rupture
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• Partial Ishiatic nerve paralysis
• Tibial Nerve Paralysis |
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principles of avulsion of the adductors
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• Obturator, gracilis,
pectineus, and adductor muscles. • Parturition • Contributing factors – Metabolic disease – Poor footing – Nerve damage (Calving paralysis) • Prognosis guarded • Rx: flotation or deep bedding with good footing. |
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coxofemoral luxation- epi, risk factors, tx, px |
• Common in dairy cows. |
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ddx coxofemoral luxation
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• DDx: pelvic fractures, femoral fractures, separation of the femoral epiphysis, and sacroiliac luxation.
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signs, dx peroneus tertius
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Originates between the femoral condyles and inserts on
the metatarsus. • Part of the reciprocal apparatus. • No abnormalities apparent at rest. • During ambulation the limb may be dragged with the claws scrapping the ground. • Dx: Extension of the hock with concurrent flexion of the stifle. |
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causes of femorotibial instability, dx, rx
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Cruciate injuries
– Bulls most common – The menisci are usually damaged – Anterior draw with acute injuries – Effusion of the stifle. • Collateral Ligament Injuries – Damage to the medial collateral ligament more common – Lateral to medial instability of the stifle. – The medial meniscus is usually torn. • Dx: Physical findings Rx slaughter |
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ddx femorotibial instability
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septic gonitis, distal femoral or proximal tibial fracture
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sacroiliac luxation and subluxation- causes, signs, mx
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• Generally associated with parturition
• Physiological relaxation of pelvic ligaments • Clinical Signs – Mild ataxia – Weakness in the hindquarters (subluxation) – Severe posterior paresis and recumbency (luxation) – The lumbar spine and sacrum appear dropped relative to the sacral tuberosities of the ileum. – Reduced dorsoventral diameter of the pelvic inlet • Management: Rest, good footing. |
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ilium fracture signs, cause, px
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most common site wing of the ilium- knocked on gateway or post
- degree of lameness varies- usually minor - asymmetry of the pelvis- 'dropped' hip - dx rectal palp- swelling, haemmorhage or fracture site simple uncomplicatd f#- no tx and good px confinement- callus formation might cause calving issues in future- should examine per rectum at a later date to check for callus |
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what is compartment syndrome
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The weight of a recumbent animal on dependent
muscle groups creates significant increases in intra‐ muscular pressure and subsequently decreased perfusion and ischemia of muscles and nerves. If sedating or lying down an animal- make sure there is a soft surface or thick bedding, not just concrete |
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treatment of compartment syndrome
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• Correction of the underlying cause of
recumbency • Fluid therapy to maintain renal perfusion • Nonsteroidal anti‐inflammatories • Nursing care • Provision of adequate footing and bedding • Flotation |
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prevention of compartment syndrome
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Careful positioning and judicious use of padding.
• Front leg forward to relieve pressure off the triceps. • Support the upper limb to reduce pressure on the lower limb. • Minimize down time. • Maintenance a light plane of anesthesia • Administer IV fluids during longer procedures. • Monitor blood pressure during anesthesia. |
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fracture first aid
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analgesia- caution ataxia
prevent further damage distal- splint proximal- protected by muscle mass confine animal apply pressure bandages to reduce swelling |
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what is the px of SDF rupture
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recover by fibrosis- will have to wait a couple of month to assess- cost/guarded px
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what do you need to consider when giving px of fracture
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structure involved- damage to nerves, vessels, tendons, joints
open v closed (poor px) prox vs distal (prox harder to immobilise) size of patient (ability to cast/splint) patient temperament |
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principle/ options for immobilisation
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• Immobilise
– Joint above and below fracture – Avoid constriction with foot protruding from the end of the cast – Judicious use of padding • Options – Splint – Cast – Thomas splint – External fixation |
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approach to a distal # in a calf
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1. may need splint until swelling subsides
2. sedate with diazepam/xylazine 3. apply cast to immobilise- dont overextend, plenty of padding oin pressure areas 4. cast needs to be changed in 2-3 weeks for rapidly growing calves. 5. any regression- remove cast |
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Myopathies (8)
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1. Se/Vit E deficiency- asociated with volcanic soil types, higher winter rainfall
Toxic 2. Ionophores- Monensin (bloat prevention, anticoccidial, increase feed efficiency by inc propionate, dec butyrate) 3. Gossypol- cotton seed (natural insecticide) 4. Toxic plants 5. Muscle necrosis- clostridial dz Metabolic 6. HypoCa 7. HypoK 8. Botulism |
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types of copper deficiency
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primary- <5ppm in diet
secondary- high level of Mo, S, Ca, Zn, Fe in diet Ca:Mo hould be 6-10:1 |
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clinical signs Ca def
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1. Young animals are more susceptible- calves with brottle bones running through yard and breaking bone
2. Achomotrichia (loss of coat color) 3. Enzootic ataxia / swayback 4. spontaneous fractures 5. Physeal enlargements / Physitis 6. Diarrhea 7 Illthrift (failure to thrive) 8. Decreased immunity 9. Anemia, falling disease 10. Reproductive inefficiency |
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pathophys of cu deficiency
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•Neonates born to copper deficient dams have reduced copper stores.
• Colostrum is rich in copper • Milk is low in copper • Osteoporosis secondary to depressed osteoblastic activity. • Copper is a component of many enzymes – Lysyl oxidase, (Connective tissue) – Tyrosine kinase (Coat color) • Diarrhea is secondary to villous atrophy |
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dx of cu deficiency
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evaluate at least 5 animals
clinical signs fdont always correlate with cu levels hx, demographic clinical signs erum copper (drops after liver depleted) liver cu hair |
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cu deficiency tx and cx
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Oral supplementation
– Intra‐ ruminal boluses (depress wt gain in feeder cattle) – Top dressing of pastures – Addition of copper to salt mixes, 0.25 – 0.5% copper sulfate for sheep and 2% for cattle. – Addition of copper to the total ration - Copper requirements dependant dietary Mo, S, Zn, Ca, and Fe • Copper injections (Copper glycinate) – Toxicosis has been reported in selenium deficient cattle |
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what are the ways in which Ca: P ratio can be disturbed
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Ca:P should be 2:1
Absolute calcium deficiency- les common • Relative phosphorous excess- more common • Phosphorous deficiency • Vitamin D deficiency or Carotene excess |
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signs of Ca deficiency
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Decreased growth rate and dental
maldevelopment. • Lameness / stiffness, rickets • Soft bones, tendency to fracture • Reduced fertility |
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dx absolute,/ relative Ca deficiency
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– Dietary history (high concentrates / low forage)
– Clinical signs – Response to supplementation – Pathology • Osteoporosis • Parathyroid hyperplasia |
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signs of a P deficiency
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• Primary deficiency
• Geographical distribution • Clinical signs – Pica (May result in high incidence of botulism) – Poor growth – Rough coat – Infertility – Osteodystrophy / stiffness / fractures, rickets • Under range conditions lactating cows most commonly affected. • Young animals grow slowly and develop rickets |
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dx abd cx of phosphorus deficiency
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• Diagnosis
– Location – Clinical signs – Response to supplementation • Control – Supplemental phosphorous • Bone meal • Dicalcium phosphate • Disodium phosphate •Superphosphate (fertilizer, may contain excess fluorine) |
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common neuro diseases in cattle
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Listeria |
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common neuro disease in sheep
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• Listeria
• Botulism • Plant staggers • (Lead toxicity) • Cerebral corticonecrosis/Polioencephalomalacia • Hepatic encephalopathy • Neurogenetics: inherited disease more likely to show in adults FSE |
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Exotic neuro disease in cattle and sheep
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cattle- BSE, rabies
sheep, Scrapie, raies, Visna |
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cause of lead poisoning
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innate curiosity, indiscriminate feeding, relative susceptibility
- calves licking foreign objects most effected- more readily absord lead if on a milk diet - adult calves- intake of contaminated pasturem, indiscriminate feeding (silage with lead shot, pain, old battery) |
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signs of lead poisoning
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depression
blind, head pressing aimless, staggering gait muscle tremor seizures hyperirritability salivation, frothing, rumenal atony sudden death- esp calves |
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treatment of lead poisoning
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Calcium Sodium Versenate (Ca‐EDTA)
• Symptomatic – anticonvulsants, fluids |
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signs and pathogenesis of botulism, dcx, pxx,
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Highly fatal |
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signs of polioencephalomalacia
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sudden onset blindness, aimless wandering |
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causes of thiamine deficiency
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thiaminases in the rumen- thiaminase producing acteria
ingetion of thiaminases- bracken fern, Nardoo ferm |
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symptoms of hepatic enceph
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dullness, increased vocalisation, |
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what most commonly cuases suppurative leptomeningitis in calves
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e.coli
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causes of non-suppurative leptomeningitis/ encephalitis
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- IBR- calves <6mo
- sporadic bovine encephalomyelitis- chlamydophila pecorum |
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pathogen, signs, tx of SBE
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Disseminated vasculitis and serositis |
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what causes thromboembolic meningoencephalitis, what is the typical dz progression
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Haemophilus somni- acute onset, rapid course and high fatality.
Peractue cases- sudden death more commonly show marked pyrxia early in dz, a range of neuro signs (depresed weak, droopy eyelids 'sleepy sydrome', tremors, nystagmus, recumbent, may progress to opisthotonos), may be preceded by resp disease (7 days) but not always |
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what is cause, manifestation of hypoVitA in young cattle?
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insufficient supply of Vit A in diet, usually feedlot calves
in young animals- manifestations are those of compression of the brain and spinal cord. Vit A also play a role in enhancing the immune system- higher susceptibility to infectious d anorexia, ill thrift, diarrhoea, blindness, dialted pupils, tapetal bleeding (papillary oedema and CSF pressure), slight exophthalmos, absebces of menace |
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Manifestation of hypoVitA in adult cattle |
night blindness, weight loss, infertility |
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causes of bilateral visual defects |
hypoVitA
neurovisceral ceroid- lipofuscinosis lipofucinosis- plant alkaloid poisoning |
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signs and ddx cerebellar dysfxn
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hypermetria, head tremor, wide stance
pestivirus storage disorder - a-mannosidosis (angus, murray grey) - toxic- darling pea abiotrophy- rapid degeneration (angus) |
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ddx vestibular dz
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peripheral- metastatic SCC
central- listeriosis |
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pathogenesis of listeria monocytogenes infection
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Listeria moncytogenes –
intracellular; in macrophages, secretes haemolysin, resists intracellular killing mechanisms ubiquitous, multiply in soils, rotting vegetation; silage pH > 5.5 association with silage feeding Encephalitis: medulla microabscesses Abortions |
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CS, necropsy findings, Tx, Cx of listeriosis
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Clinical signs: vestibular
– dullness, head tilt, circling, unilateral facial paralysis – recumbency, death in 3 - 8 days Necropsy: medulla oblongata – haemorrhagic meningoencephalitis with microabscessation Treatment: early, penicillins +/- aminoglycoside high dose, prolonged treatment Control: avoid poor quality silage (pH> 5.5) & rotting vegetation |
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epidemiology of phalaris toxicity
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only affects ruminants, mainly P aquatica
• signs may develop days to months after grazing • Phalaris aquatica is a valuable introduced winter-growing temperate perennial pasture plant • Several harmful alkaloids, esp. fresh shooting pastures |
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sydromes of phalaris tox
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1. Staggers: most common
indole alkaloid storage Cobalt preventative: autumn-winter Risk areas: limestone soils Co deficient 2. sudden death Cardiac: <1% PE-like sudden death: 5-15% |
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stagger/ tremorgenic syndromes
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1. Phalaris toxicity- neuro or sudden death |
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NMJ disorders
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presynaptic- botulism, ixodes
synaptic- competitive release of Sux post synaptic- Op poisoning |
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signs of tetanus
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stiffness |
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bacteria associated with clostridial myonecrosis
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c.chauvoei (blackleg)
C. septicum (malignant oedema) c. sordelli novyi and perfringens A may be involved in mixed infection |
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causes of peripartum neonatal loss
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foetal infection/abortion
dystocia starvation hypothermia poor colostral transfer sepsis D+ (e.coli) |
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foetal infection/abortion aetiologies
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Neosporosis
• Toxoplasmosis • Trichomoniasis • Leptospirosis • Vibriosis • Listeriosis • Chlamydophilosis • BVDV • Border disease • IBR • Akabane • Plant toxins (eg. nitrite) • Genetic |
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maternal and foetal factors leading to dystocia
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Parity (heifers vs cows)
• Conformation • Metabolic – Obesity, HypoCa, negative energy balance • Sex ‐ 2 / 3 dystocia with male calves • Birth weight • Number – twins • Presentation & position – eg. breech • Deformity – eg. arthrogryposis |
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vitals adult vs calf
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Adult
T 37.8-39.2 HR 40-80 RR 12-36 Calf T 37.8-39.4 HR 100-140 RR 30-60 |
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Assessment of the neonate
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1. PE
2. BCS 3. CV under 90 is bradycardia 4. respiratory rate/effort 5. maloderous breath 6. GIT- cleft palate, brachygnathism, atresia coli/recti/ ani, melena, scours BLOAT? succuss- delineate boundaries, stomach tube- ruminal vs abomasal bloat 7. Urogenital- patent urachus, urine at umbilicus, omphalitis, 8. MS- septic arthritis 9. neuro- hydrancephaly (BVDV, akabane), cerebellar dysplasia(BVDV), PEM, FSE (kid, lambs), depressed mentation (sepsis, D+, bacterial meningitis 10. assess transfer of maternal antibodies |
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ddx bradycardia/ tachycardia in neonate
|
brady- stress, hypothermia, hypoglycaemia, hyperkalaemia (more common)
tachy- cardiomyopathy, hypoMg, iomophore tox |
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main ddx maloderous breath in the neonate
|
necrotic pharyngeal injury, necrotic laryngitis, calf diptheria, apiration pneumonia- common in calves less than 1 week.. may be iatrogenic
enzootic pneumonia 4w-6m. mycoplama outbreaks maydecelop in calves <4w |
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CS neonatal sepsis
|
Lethargy
• Depressed mentation • Poor suck reflex • Weakness • Dehydration • Diarrhoea • Recumbency • Tachycardia & Tachypnoea • (Rectal temp, HR & RR are not reliable predictors of sepsis |
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Host factors in the neonatal sepsis
|
HOST
• Perinatal stress (in utero hypoxia, dystocia, prematurity, birth asphyxia) • Inadequate transfer of MATERNAL ANTIBODY |
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Pathogen factors in neonatal sepsis
|
HOST
• Perinatal stress (in utero hypoxia, dystocia, prematurity, birth asphyxia) • Inadequate transfer of MATERNAL ANTIBODY PATHOGEN • Opportunistic bacteria that normally live in the genital tract, on skin or in the environment. • 80% of sepsis is caused by GRAM NEGATIVE bacteria (eg. E.coli) • Entry is via the GIT, Respiratory tract, placenta or umbilicus |
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Environmental factors in neonatal sepsis
|
ENVIRONMENT
• Unsanitary conditions • Overcrowding • Poor ventilation • Contamination of the environment with pathogens (eg. sepsis secondary to neonatal calf scours). |
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neonatal sepsis may be associated with:
|
Septic arthritis
• Osteomyelitis • Omphalophlebitis • Bacterial meningitis • Diarrhoea • Uveitis |
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treatment of septicaemic calf
|
Treatment:
• 80% of sepsis is GRAM NEGATIVE, so a broad‐spectrum antibiotic (including gram negative coverage) should be used: • Trimethoprim‐sulfonamides • Oxytetracycline • Ceftiofur • Neomycin (But beware meat residues! and remember that all streps are intrinsically resistant) • ENDOTOXAEMIA is also an important part of pathogenesis. • FLUID THERAPY • ANTI‐INFLAMMATORIES (eg. Flunixin meglumine, Meloxicam) • Prognosis for septicaemic neonates is poor |
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main causes of neonatal calf scours
|
Enterotoxigenic E coli (<4d)
Rotavirus (4 -14 days) but can occur in older and younger calves Coronavirus (4 -30 days) Cryptosoridium parvum (5 -30d) Salmonella (any age but typically 7-28 days) |
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preventing neonatal scours
|
1Ensure adequate colostral intake (Time, Volume & Quality)
2.Provide adequate nutrition 3. Provide a clean and comfortable environment 4.Boost specific immunity 5.Minimise pathogen exposure |
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preventing disease in calves
|
regular rotation of calving paddocks- free from effluent withgood drainage
isolation of animals with diarrhoea remove from adult cattel as soon as possible avoid overcrowding maternal vaccinations- E. coli K99, salmonella- increase Ab in colostrum calf hutches removal and disposal of faeces nutrition colostrum |
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5 mechanisms for D+
|
1. omotic- overfeeding of indigetivle feeds- eg milk replacers containing less digestible plant proteins
2. exudative diarrhoea- increase in fluid production secondary to inflammation of the intestinal mucosa eg salmonella 3. secretory D+ eg ETECs 4. reduced surface area for absorption- malabsorption eg rotavirus, coronavirus, crypto 5. abnormal intestinal motility- increased peristalsis |
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pathophys of ETECs
|
mainly calves under 4days
attach with fimbrial antigens, secrete enterotoxins that stimulate secretion of water, sodium and chloride ions into the intestinal lumen. No mechanical pathology- villi are not damaged Diarrhoea, dehydration, weakness. rapid course- progress from recumbency to death in 6-12 hours Dx- culture, demonstrate K99 antigen by ELISA or agglutination |
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Salmonella pathophys + common strains
|
Dublin, Typhimurium
- any age but typically 7-30 days can cause diarrhoea, septicaemia (.Dublin can produce pneumonia 3-8w) transmission- orofaecal, vertical, aerosol, saliva, milk, nasal secretions, saliva invade lamina propria- inflammation, haemorrhage, fibrinous sloughing of mucosa. Can migrate to lnn, intermittent shedding, can have lifelong carriers shedding in milk and faeces |
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Salmonella lesions and dx
|
Catarrhal or haemorrhagic enteritis
• Fibronecrotic ileotyphlocolitis • Inflammation of messenteric lymph nodes • Fibrinous cholecystitis • Splenomegaly • Pulmonary congestion & bronchopneumonia with chronic cases of S. Dublin. • Necrosis of extremities (eg. necrotic ear tips) can also be observed with S. Dublin. Diagnosis by culture of faeces, intestinal contents or viscera |
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other main E coli causing calf scours
|
Attaching and effacing e coli (EHECs)
Distort and destroy the microvilli brush border. • Enterohaemorrhagic shiga‐like toxin cause a mucohaemorrhagic colitis • EHECs are K99 negative! |
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Clostridial neonatal scour
|
Usually C. perfringens type C in calves under 10d
Haemorrhagic enteritis, colic, weakness, prostration and death. Cl. perfringens type A may also cause diarrhoea in calves, Cl. perfringens type B in lambs. |
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bacterial scour in neonates
|
ETECs
Salmonella c. perfringens EHECs |
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Rotavirus a cause of neonatal scours
|
• The most common causes of neonatal calf scours.
• Typically causes diarrhoea in calves 4 – 14 days old (but may be younger or older). Transmission by the faeco‐oral route. • Invade the small intestinal epithelial cells leading to villus atrophy. • Infection is short‐lived, but it takes time for the villi to repair. • Replacement enterocytes have reduced lactase activity, further contributing to maldigestion and malabsorption. • Diagnosis by antigen ELISA, fluorescent antibody testing, histopathology, electron micro |
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Coronavirus as a ause of neonatal scours
|
typically 4-30d
inade the absorptive epithelium of both the small intestine and large intestine, causing villous atrophy (SI) and destruction of the colonic ridges (LI) - may also be clinical signs associated with large intestinal disease (haematochezia and straining) - can cause a mild interstitial pneumonia - excreted by asymptomatic adults, increasing around partutrion DIAGNOSIS - ELISA, FAT, histopath |
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VIral diarrhoea in neonates
|
rota
corona BVDV- transient |
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protozoal calf scours
|
crypto- PPP2-7d
sporozoites infect brush border of vili in ileum, caecum and colon- villous atrophy, fusion and crypt hyperplasia= malabsorption coccidiosis- not common, typically 1-2m Giardia- mild, pasty scours ddx float, ELISA for crypto |
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when can milk cause a nutritional scour
|
1. mldigetion, absorption due to enteric pathogens
2. milk replacers- cheap plant proteins (less digestible), plant carbohydrates (even though calves can only digeset lactose). Large amounts replacer or off milk replacer can cause osmotic D+ Give sick calves whole cow milk |
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Assessing dehydration in the calf
|
•
MILD (5 – 6%): Dry MM, No visible sinking of eyes, Skin tent < 5s • MODERATE (7 – 8%): Slight sinking of the eye, Skin tent > 5 sec • SEVERE (> 8%): Space between the globe and orbit Severe cases are estimated to have lost 8 – 10% of body weight |
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required immunoglobulin intake in neonates
|
120-150g IgG within first 3-6 hours of life and ideally the same amount 12hr later. Amount of colostrum will depend on quality.
Often natural intake is insufficinet- best to take calf from dam and feed 4L of high quality (>50g IgG/L) colostrum in first few hours via nipple feeder (encourages oesophageal groove closure) or oesophageal feeder (rumenal pooling) |
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main causes of peripartum death and what can high peri[artum mortality reflect
|
dystocia, starvation, hypotehermia (60%)
mismanagement of maternal nutrition or the maternal environment during the last trimester and or the pre and peripartum period |
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Assessing neonate
|
1. dehydration
2. Macidosis- based on clinical signs rather than BGA- CNS depression, decreased sucking reflex, ataxia, recumbency 3. lyte imbalance- total body deficit Na, Cl and K, hypoNa, normoCl 4. hyperK- 2` to acidosis. exchange of IC K for EC H 5. Bradycardia. arrythmia and clinical Macidosis suggests hyperK. Total K deficit, but secondary hyperK- just treat the Macidosis 6. Hypoglycaemia- weakness, lethargy, convulsion, opisthotonos, coma 7. sepsis- all calves with D+ will have E coli overgrowth |
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Treatment of systemically ill, scouring calf
|
1. FLUID AND ELECTROLYTES. IV bicarb if macidosi, hyperK suspected
2. Energy- milk or IV glucose 3. warmth 4. ABs 5. NSAIDs |
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|
Determining fluid/electrolyte therapy in scouring calf+ determining administration of fluids
|
1. calculate fluid deficit
+ 4-6ml/kg/hr maintenance + ongoing losses 2. calculate bicarb deficit - give bicarb if bae deficit over 10mEq/L - 1L isotonic = 156mmol should get half of calculated deficit over first 6 hours, rest over following 12-24 hours faster if in hypovolaemic shock or septic If IV difficult- use interosseus admin (head of femur/ humerus) L required= deficit/156 3. potassium deficit- avoid isotonic NaCl 0.4xBWxKdeficit 4. hypoglycaemic- CRI 5-10% dextrose or hypertonic bolus |
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|
calculating bicarb deficit
|
base deficit = [30- serum bicarb (mmol/L)] or [30-TCO2]
bicarb deficit 0.6 x BW x [30-serum bicarb] if base deficit <10mEq/L dont need to administer bicarb, just fluids |
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Fluids that can be used for critical neonate
|
sodium bicarbonate
hartmanns hypertonic saline for resusc isotonic saline- beware in hypoK patients CRI dextrose 5-!0% |
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when to use oral fluids, how much?
|
- able to nurse or drink
-in mildy affected calves - if suck reflex is weak, stomach tube can be used - scouring calf needs twice daily intake- i.e scouring holstein that usually has 4L of milk will require another 4L of electrolyte solution |
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Composition of electrolyte solution
|
sodium
Potassium chloride alkalinising agent- acetate, propionate (A+P preferred), bicarconate, citrate glucose or glycine (helps na absorption) SID= 60-80 (Na+K-Cl) |
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|
nutritional requirements scouring calf
|
ideally switch from replacer to whole milk
50kg calf needs 2000kCal/day (3.3L) for maintenance and 3500 (5.7L) for 0.5kg daily weight gain if moribund/ unable to drink- 5-10% dex infusion |
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Antibiotics and NSAIDs for scouring neonate
|
80% sepsis G neg
- ceftiofur - trimethoprim ulfonamides aminoglycosides need to be bacteriocidal- rules out oxytetracycline Flunixin meglumine meloxicam |
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|
antiprotozoal treatment for crypto
|
Halofuginone- registered in calves
reduce oocyt shedding and shortens course of dz- only if tx early LOW SAFETY MARGIN- oeophageal ulcers if dose exceeds 1mg/10kg |
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Why is colostrum intake so important?
|
ruminants have a epitheliochoral placenta- 6 layers between maternal and foetal blood. Means neonates rely entirely on colostral Ig transfer for immunity
Absorbed via pinocytosis- very efficient first 6 hours, drops dramatically after 12, stops at 36 |
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Ensuring clostrum quality
|
cows on 3rd+ lactation have the highest quality of clostrum. IgG density less in heifers and less in induced cows.
FREEZE EXCESS GOOD COLOSTRUM use first milk colostrum measure using colotrometer (want reading over 22%) |
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|
how to measure calf PT effectiveness
|
refractometer- total serum protein >5.2g/dL (52g/L)
want less than 1 in 6 calves to drop below 5.5 |
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neonate nutrition
|
16% of body weight as milk needed to
achieve 0.5% body weight per day. • Milk replacers often contain less ME per DM than whole milk – may need to increase the amount of milk replacer fed to compensate. • Avoid mastitis milk – may increase disease risk / transmit Mycoplasma • Avoid pooling milk – Salmonella, Johnes, EBL, Mycoplasma • Provide creep feed from 3 days – grain important for rumen development |
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environmental prevention of neonatal disease
|
•Provide fresh, clean water.
•Hygienic use of feeders and feeding utensils •Shelter / protection from the elements •Clean, dry bedding material |
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prevention of neonatal disease: boosting specific imunity
|
vaccinations:
E.coli K99 Salmonella Rotavirus and coronavirus colostogenesis begins 5 weeks before calving- booster at least 5 week before calving to boost supply of igG against specific antigens. 2 doses 4-6 weeks apart then annual booster |
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|
how does the E.coli maternal vacc work?
|
Anti K99 antibodies- not only aborbed passivlet into circulation- IgG and IgA also present in the gut at the same time that calves are susceptible to K99
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how effective is the salmonella maternal vacc
|
partial protection- maternal antibodies wane at 6w and older cattle can be affected
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How to minimise neonatal pathogen exposure
|
1. remove calves at birth and feed only clean, un pooled colostrum
2. maintain clean calving environment 3. house calves away from effluent and adult cattle 4. staff- clean clothes in calf shed 5. calving hutches 6. All in/all out- dont mix age groups 7. isolate sick calves 8. clean and disinfect feeding utensils 9. control rodents, protect feed 10. chill or freeze colostrum if not being used immediately 11. avoid pooling of whole milk or pastuerise 12. mix fresh feed daily |
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|
preventing contact with adult faeces and controlling supply of colostrum helps control:
|
1. calf scours- salmonella, crypto, corona
2., Johnes 3. Enzootic bovine leukosis 4. mycoplasma 5. Joint ill, pneumonia and sepsis (due to inadequate maternal transfer) |
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pathogen minimisation focus points
|
1. avoid adult faeces
2. other calves 3. biosecurity 4. pests 5. feed |
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|
what is weaner throughput?
|
rate with which weaners ae produced by an enterprise
depends on number of weaners and kg of product produced |
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factors contributing to weaner throughput
|
1. stocking rate
2. fecundity (number of live offspring per breeding female) a. pregnancy rate b. lambing/ calving rate c. marking rate d. weaning rate 3. minimised calving/ lambing spread 4. early weaning- without compromising growth rate 5. cull and replace policy- maximise pasture use 6. minimising weaner loss (<10% is goal) |
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challenges faced by weaner animals
|
1. separated from dam
2 need to fend from themselves nutritionally 3. immune systems not fully developed- susceptible to dz |
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|
weaning sheep
|
- between 60& 150 days
- can wean as early as 2w - by 3 weeks- rumen has developed so feed conversion can be maximised by direct feeding as alternative to feeding from ewe- common practice in drought years - WEIGHT IS CRUCIAL- small increases in growth rate dramatically decreases mortality rate- accumulate more body reserves increase in 0.25-5kg/m can decrease mortality by 74% weaner at 20kg liveweight has approx 1kg of fat stores- increases with increasing liveweight. Any energy deficit in lamb under 20kg will be met by mobilising body protein stores and will have deleterious effects on strength and resilience of the animal |
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benefits of early weaning
|
- take stress off ewe
- greater feed conversion- better utilisation of supplements. Dam produces disproportionate milk to an increase in DMI - stimulates oestrus in cow - gives cow a break- better production - safe pastures |
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susceptibility of weaners
|
- low fat stores to meet deficits- energy and protein deficits lead to weakness, death and disease
- high requirement for minerals and trace elements due to growth- first on the farm to show deficiencies - at time of weaning- young, recently muelesed, separation distrwes, learning to graze efficiently, and in late winter, often wet and cold. - high risk helminthosis, fleece rot, dermatophilosis, fly strike, pustular dermatitis, pneumonia and arthritis |
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common llamb weaner diseases
|
yersiniosis
coccidiosis eperythrozoonosis campylobacterosis enteritis red gut grain poisoning helminthosis fasciolosis blacks dz enterotoxaemia dermatophilus fly strike fleet rot contagfious pustular dermatitis malnutrition se/vitE, Cu deficiency rickets |
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minimising weaning stress
|
move lambs and ewes so they cant hear each other
dont drastically change ration for 2 weeks keep weaning groups together and monitor for disease |
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weaning strategies
|
1. early weaning
lambs about 13w, 20kg beef 6m, 100kg 2. vaccinate- clostridial +/- cheesy gland 3. parasite control worm, hold in yards 24 hours 4. attend to tail end of mob 5. wean onto clean, high quality paddock 6. introduce grain before weaning 7. weigh- keep lambs with highest adjusted weaning weights for breeding |
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WEaner vaccination programs
|
2 injections 4-6 weeks apart. If dam vacc'd do from 10w. Earlier if surgical castration or dehorning
sheep 3 in 1- pulpy kidney, tetanus, cheesy gland 5 in 1- pulpy, tet, black dz, black leg, MO 6 in 1- pulpy, tet, black dz, black leg, MO, CG Cattle 5 in 1: pulpy, tet, black dz, black leg, MO 7 in 1: pulpy tet black dz black leg MO, L. pomona, L. hardjo |
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benefit of late weaning
|
lambs, ewes less stressed
lower risk mastitis less pens and pasture fields pasture gains more economical than feedlot gains |
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|
effect of length of joining period
|
may need separate weaning for tail of the mob- twins and late born
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|
how to select weaning time for calves
|
age of calves
weight of calves condition score of cow availability of pasture- wean earlier in drought and supplement weaners when cows are due to calve again |
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|
benefits of yard weaning
|
socialisation
adapt to confinement adapt to concentrate feed and water dams can remain nearby until they disperse |
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|
what else is done at weaning
|
parasite control
boosters cu, Se need to consider amount of stress placed on animals at this time |
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|
aim of weaner and dairy replacement management
|
produce a heifer that
mates at 55% adult live weight calves at 24mo calves at 85% of mature herd body weight (416 jersey, 552 holstein) calves at BCS5-5.5 adjusts to lactating cow ration short calving interval for second mating period achieves the above at minimal input costs |
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|
efficient dairy replacement with minimum input costs, need to aim for:
|
good performance with minimal disease and mortality
optimum growth rates minimum feed costs minimum labour req |
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|
what is measured to track heifer growth . when doe a group of heifers enter breeding group?
|
weight at mating, calvings
wither height- indication of stature growth rates heifers enter breeding group based on minimum age of 13m and weight of 375kg |
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|
heifer nutritional requirements
|
1. protein
bypass proteins for lean body growth- even top qual pasture may not be sufficient 2. supplementation to meet energy requirements for growth |
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|
when is it vitcal to get liveweights right
|
mating and transition period
|
|
|
strategies to meet heifer target growth rates
|
leader- follower grazing system
graze on irrigation supplementary rain feed restriction/ compensatory growth agist heifers off farm |
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|
calving target weights
|
mate 14-15m at 360(Fr)/270(J)
1st calving 550 (f) 415 (J) |
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|
properties of a well reared heifer
|
less chance of calving problems
will produce more milk in her lifetime (.5-.7L perkg above 400kg over first 3 lactations back into calf quicker less likely to be culled if heifers calve at 24 months you need less replacements |
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|
families of dz causing ill thrift
|
1. mineral deficiency/imbalance
2. parasitism 3. nutrition related 4. infectious 5. toxins |
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|
parasites causing ill thrift in weaners
|
GIT nematodes
lungworm fasciolosis paramphistomes (rumen fluke) coccidiosis external parasites |
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|
nutrition related causes of ill thrift
|
poor feed requirement estimation
poor quality feed inputs subclinical acidosis skewed growth rates due to competition poor transition phase management PEM- thiamine deficiency laminitis |
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|
infectious causes ill thrift
|
yersinia
salmonella BVD Dictyocaulus pneumonia necrotic pododermatitis pink eye IBR Lepto |
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|
toxin as cause of ill thrift
|
- fodder with high N
- fodders with cyanogenic glycosides - mycotoxins/ endophyte - contaminated water- cyanophycae - incorrect dosage of ionophores - ingested hepatotoxins, bracken fern |
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|
when do you see yersiniosis
|
weaners- failure to thrive, associated with intercurrent dz
late winter, stress, oral exposure- attach to gut via surface proteins. resist phago and form microcolonies- produce enterotoxin- secretory D+ |
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|
Hx tht suggests coccidiosis
|
synchronous onset of D+ within a few weeks of confinement. Poor nutrition and nematodes
|
|
|
tx od coccidiosis
|
sodium sulfadiminidine
|
|
|
pathogenesis salmonella
|
adherence with fimbrae
enteric colonisation invasion of m cells- internalised necoris of epithelium- infiltrates lamina propria, intracellular survival and dissemination- overwhelm defences and enter systemic dissemination- septicaemic shock |
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|
weaner diseases of cattle
|
Yersiniosis
Coccidiosis BVD Grain poisoning Ostertagiasis Fascioliasis Paramphistomiasis Pneumonia Malnutrition Trace element deficiency: Se/Vit E, Cu |
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|
ddx ill thrift in weaner cattle
|
trace mineral deficiency- Se/vit E, Cu
parasites- ostertagia, fasciola, paramphistomiasis infection- yersiniosis, coccidiosis liver injury grain poisoning BVD malnutrition pneumonia |
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|
how is eimeria alabamensis an emerging problem
|
oocysts overwinter on pasture- found in hay
tunour onto pasture leads to outbreak detec oocysts a few days later reinfection not clinical- clean paddocks with older stock |
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|
pathophys ostertagiosis
|
Larval damage to abomasal mucosa
inflammation, hyperplasia of glandular epithelium with mucous metaplasia loss of parietal cells decreased hydrochloric acid release increased abomasal pH reduced conversion of pepsinogen to pepsin poor protein digestion Type I Calves during first grazing season Ingestion of a large number of infective larvae Steady trickle of emerging larvae with mild disease Type II Yearlings Post-hypobiotic emergence of many organisms in spring More pronounced disease |
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|
mot common mineral deficiencies leading to ill thrif
|
•
Copper • Cobalt • Selenium • and less commonly with –Calcium, phosphorus and vitamin D imbalance –Zinc –Potassium predisposing factors- high rainfall, lush pasture |
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|
means of cu supp
|
SC: copper glycinate,
Cu salts (sulphate or lysinate) in licks blocks or water Rumen boluses |
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|
soil type assoc with Co deficiency
|
• Granite, calcareous, sandy and high Mn soils likely Co deficient.
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|
|
selenium supplementation
|
Oral selenite or selenate(less toxic),
– Rumen bolus. • Oral or injectable should be @ 0.1mg Se/kg LW. – Paddock dressing • 10g/ha Se as superphosphate or prills. |
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|
effects of Zn deficiency
|
Reduced intake and growth
– poor reproduction • degeneration of seminiferous tubules • abnormal leydig cells, abortion • mummification, teratogenic • reduced myometrium contractility – weak hoof horn – Perakeratosis – immunosuppression |
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|
main effect of Mg def
|
poor conception rates
|
|
|
effect of Mo toxicity
|
Cu deficiency
|
|
|
when is iodine deficiency most seen
|
last 3 month of gestation- weak hairless dead calves,
due to thiocyanates |
|
|
approaching a potential mineral deficiency
|
good hx
nutrition analysis what supplementation- precisely fertilisatin practices for last 5 years known deficiencies on or around farm length of time on current paddock/ farm sample affected and unaffecte |
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|
acute infections causing sudden death (10)
|
Enterotoxaemia
Black Disease, Blackleg Anthrax Babesia Septicaemic salmonellosis Haemorrhagic Septicaemia Leptospirosis Shipping fever Endocarditis Metritis/Mastitis |
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|
toxic causes sudden death (10)
|
Snake bite
Monensin, OP’s, Lead Aflatoxins, Plants… Nitrate/nitrite (e.g. sorghum) Oxalates (e.g. oxalis) Cyanogenic glycosides (e.g. sorghum) Phalaris, Cardiac glycosides PA alkaloids Green Cestrum Blue-green algae |
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|
nutritional/ metabolic sudden death
|
Polioencephalomalacia
Hypomagnesaemia Ruminal acidosis Bloat Milk Fever Ketosis |
|
|
'other' causes of sudden death
|
Electrocutions, lightning strikes
Internal haemorrhage, Trauma Cardiac, Hardware (TRP) Anaphylaxis (e.g. after vaccination) Heatstroke / exposure Endoparasitism |
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|
what to sample if toxin suspected
|
Formalin-fixed samples of all major tissues
Brain – half formalin-fixed, half fresh Urine – if present Stomach/rumen content Liver Kidney Body fat food |
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|
pathogenesis of MCF
|
most important in deer
gamma herpesvirus acute, fatal, usually sporadic dz necrotising vasculitis, lymphadenopathy peracute, alimentary- fever, D+ tropism for lymphoid tissue- lymphoid hyperplasia, vasulitis with terminalDIC and consumptive coagulopathy. erosive, ulcerative lesions of the mucosa and cutaneous structures usually 12-24 months- can be older head and eye form most common- profuse oculonasal discharge, corneal opacity, ulcerations and erosions of the mouth dx Hx (sheep), CS, PCR - EDTA blood |
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|
ddx MCF
|
rinderpest
BVD IBR sporadic bovine encephalomyelitis jembrana (indonesia) |
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|
when to suspect anthrax
|
anthrax belt
no rigor mortis rapid gaseous decomposition/bloat tarry, unclotted blood discharges |
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|
Anthrax toxins and dx
|
lethal toxin, protective antigen, oedema factor
LT causes macrophage death Gram pos, endospore forming rods polychrome methylene blue stain |
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|
pathophys enterotoaemia
|
c perfringens D proliferates in response to high starch diet, releases epsilon toxin- sudden , severe toxaemia, endothelial damage, extravasation, endocardial haemorrhage
rapid renal autolysis, FSE, mayonaise intestinal contents |
|
|
immunisation for clostridial disease
|
ewes 2w before lambing, at maeking, 6 weeks later (weaning)
annial booster |
|
|
bacteria causing malignant oedema, pathophys
|
Clostridium septicum, novyi type A (Swelled head), chauvoei (also causes Blackleg), perfringens type A, sordellii
- provides focus in subcut tissues for anaerobic necrosis- severe systemic intoxication |
|
|
clinical/ necropsy signs of MO
|
Clin. signs - soft doughy swelling, local heat, pain, high fever, emphysema, death 24 to 48 hours
Necropsy - rapid post-mortem changes, oedema fluid; bubbles of gas except Cl novyi, putrid odour, especially Cl perfringens & Cl sodellii Wounds are typically, gassy = crepitus, Cl novyi - oedema |
|
|
necropsy dx of black disease
|
At necropsy: extravasation, subcutaneous venous congestion, straw coloured fluid in body cavities
liver engorged with area(s) of necrosis Lab diagnosis - presence of Cl novyi in liver lesions presence of toxin in peritoneal fluid fluorescent antibody detects organism falso positive in animals dead over 12hr |
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|
vaccinate for FULL protection
|
maternal booster -2w
1. marking 2. weaning 3. [booster 7m] to prevent enterotox 4. booster 12m 5. annual booster- close to shearing |
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|
pathophys red gut
|
intestinal torsion- lucerne or clover pastures
|
|
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diagnosis of nitrate poisoning |
history- sudden death, resp distress, ataxia, D+ blood changes (must be collected within 1-2hrs) aqueous humour levels (lasts 24 hrs) plant nitrate levels tissues and urine brown
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differentials nitrate poisoning 6 |
sudden death- blue green algae, urea tox, acute brassica poioning, hydrocyanic poisoning
brown blood- nitrates, acute copper poisoning bright red cherry blood- hydrocyanic poisoning
Dyspnoea- Acute bovine pulm oedema, nitrate, cyanogenic |
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therapy for nitrate poisoning |
remove from paddock feed high quality CHO IV methylene blue (q6-8hr)- 6m WHP fluids, supportive therapy
+-/ vasocontrictor (Ad) |
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Preventing nitrate poisoning |
- dont put young hungry stock on high nitrate pastures - test pastures first - feed extra CHO to reduce rumen pH and slow -ate to -ite conversion - lknow plants that accumulate- supply alternate feed |
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plant commonly associaed with nitrate poisoning |
ryegrass cereal grasses (oats, barley, maize, wheat) sorghum, millet, kikuyu, brassica |
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plant factors leading to hydrocyanotic acid poisoning |
young, rapidly growing stressed (herbicide, frost) plants. sorghum can remain toxic |
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Clinical signs of cyanide poisoning |
SUDDEN DEATH animals become affected within 10mins of eating toxic material and die within 2-3 mins of first showing signs
other signs- bright reb blood and mm, respiratory distress, fasciculations, recumbency, terminal convulsions
chronic tox- posterior ataxia, U incontinence syndrome, arthrogryposis, poor production
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diagnosis cyanogenic glycoside poisoning |
- history bright red blood, doesnt clot analyse suspect plant PM- mm membranes pink, cyanide analysis (<1hr) of rumen content, muscle (20h), liver (4hr) |
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treatment of cyanogenic poisoning |
IV sodium nitrite followed by sodium thiosulphate- repeat latter as required
also give orally to detoxify rumen (q1hr) give to in contacts |
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prevention cyanide poisoning |
sorghum needs to be over 75cm sialge has decreased HCN but not hay salt/ mineral with added sulfur reduces tox |
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pathogenesis of cardiac glycoside poisoning |
: Compounds, including digoxin, inhibit cardiac Na/K
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clinical signs, diagnosis of cardiac glycosides |
sudden death, salivation, arrythmia, muscle tremors, sweating, struggling, convulsions, D+ (SLUD)
History, arrythmia, focal myocardial necrosis |
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therapy for cardiac glycosides |
activated charcol +/- atropine +/- propanolol prevent access |
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Plants causing sudden death |
nitrate pisoning cyanogenic glycoides cardiac glycosides green cestrum fluoracetates (1080)
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plants causing hepatic disorders |
green cestrum pyrrolizidine alkaloids lupinosis sporodesmin
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plants causing dermatological disorders |
st johns wart sporodesmin ergot alkaloids
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plants causing CNS disorders |
paspalum staggers perenial rye staggers annual rye staggers phalaris staggers oxalates
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signs of green cestrum poisoning |
Sudden death/die within hours or over several days Dx history and PM changes to the liver. Survivors have liver damage |
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signs of Fluoracetate poisoning, tx |
plants found in northern australia, qld and western australia
– Inhibits citric acid cycle. Sudden death, convulsions, cardiac
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diagnosis of pyrrolizidine alkaloid toxicity |
History |
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presentations of phimopsin tox |
Fungi on stubble of lupin crops- produced after plant dies AUTUMN- ftty liver syndrome due to inappetance cattle- sudden death, abortion, icterus, photo, ill trhift sheep- actue
WINTER- cirrhotic liver syndrome inappetance, cachekia, lethargy, severe photosensitisation, Cu tox, PM smal fibrotic liver |
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pathogenesis of sporodesmin |
facial eczema - perennial ryegrass dead leaf litter warm, humid weather, comonly after spring rain. Cattle more susceptible fungal spores damage to bile caniculi causing cholangitis and fibrosis phtosensitisation around muzzle, white areas, teats, vulva, swollen legs, kicking belly |
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diagnosis sporodesmin and prevention |
elevated GGT, hepatic lesionss pasture spore counts
prevention- fungicides, Zn supplementation |
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pathogen, CS and prevention of st johns wort dermatitis |
Pathogenesis: Hypericin, photosynthetising pigment, not detoxified
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Patho, CS, Dx, Tx ergot alkaloids |
• Ergot alkaloids (fescue foot; summer slump) |
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signs of acutemucosal disease |
depression anorexia pyrexia tachypnea tachycardia profuse watery D+- mucus, blood, fibrin straining, perineal staining oral lesions- mucosal necrosis and sloughing erosive lesions- vulva, interdigital cleft affected animals usually die 3-7days |
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signs of chronic mucosal disease |
erosions of oral cavity, on muzzles, nares mucopurulent nasal and ocular discharge inappetance emaciation coarse hair erosive lesions at mucocutaneous junction intermittent diarrhoea +/- bloat may surviv up to 18m
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BVDV/MD ddx |
MCF oral acrinobacillosis bovine papular stomatitis |
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BVDV dx |
Antigen- ear notch- IHC Antigen- whole blood- ACE (antigen capture ELISA)- commercially availble, might not pick up acute transient infections
Antibody- AGID (agar-gel immunodiffusion) quantified on a scale of 1 to 3 depending on when the animal was exposed >3+ exposed in last 3-9m
to dx acute infectio need paired sample or virus isolation
PCR- bull screening of milk to detect persistent infection 1-2+ unlikely last 12 m |
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BUlk milk PCR for BDVD |
Used to ID PI’s |
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control of pestivirus |
Exposure of heifers to a PI before mating |
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when should cows feet be trimmed? why? |
ideally twice a year- at dry off and 3-4 months in milk
reduces incidence of lameness, restores normal shape and weightbearing |
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aims of foot trimming |
restore balance between the claws restore correct dorsal wall length (toe length) restore correct sole depth and thickness- weight bearing surface
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where does claw overgrowth occur most? |
abaxial wall, toe, sole
weightbearing claw grows the fastest- lateral on hind, medial on front
leads to backward rotation of P3 and increased pressure on the heel
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Basic order of foot trimming- Karl Burgi style |
Wash the foot first often more needed on the back feet start with medial claw- serves as template for the opposite claw 1. remove buckle if present 2. measure + cut dorsal wall length (6-8cm) 3. trim sole flat, perpendicular to shinbone 4. leave 6mm sole at toe 5. spare heel to achieve 52 degrees (measure angle)
Step 2 Move to lateral claw- remove bucke 2. trim lateral claw and sole to match medial 3. balance heel- look down from hock
Step 3 save and respect toe triangle model sole - medial claw 1/3 or less lateral sole- 2.3 or more equalise flat distance between claws
ALWAYS LEAVE TOE TRIANGLE
front foot- start with lateral claw
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