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320 Cards in this Set
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what is watery mouth caused by?
what are the clinical signs? |
reduced or delayed colostrm intake = generalised endotoxaemia
lethargy, profuse salivation abdominal distension hypothermia collapse dehydration extremities cold mm congested, scleral blood vessels dilated abdominal palpation resented |
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what age of lambs does watery mouth affect?
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1-3 days old
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how do you treat watery mouth?
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not economical
IV flunixin oral dextrose/electrolytes enema or 1mg/kg metoclopramide broad spectrum antibiotics |
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how do you prevent watery mouth?
|
correct nutrition of ewe
managing abortion and dystocia 50ml/kg colostrum in firsdt hour maintain clean lambing environment AMINOGLYCOSIDE PO WITHIN 15 MINS OF BIRTH |
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list 5 causes of neonatal enteritis
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viral diarrhoea
crypto lamb dystentery salmonella typhimurium/dublin enterotoxigenic E. coli k99 |
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what age do lambs get crypto? what are teh clinical signs and how do you treat and prevent it?
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2-20 days old
acute onset, pale green coloured watery diarrhoea (sometimes blood stained) if oocyst contamination high oral fluids and improve hygiene / move susceptible lambs to clean environment |
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what are outbreaks of almonellosis in lambs usually associated with
|
purchase of infected carrier sheep or calves
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what are teh clinical signs of salmonellosis
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depression
profuse green/brown diarrhoea variable pyrexia dehydration dyspnoea recumbency death |
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how do you diagnose salmonella?
how do you treat it? |
faecal culture from liver, gall bladder, SI, mesenteric LN
fluids, BS Abs, flunixin - RECOVERERS ILL THRIVEN AND MAY BE CARRIERS |
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what age of lambs get enterotoxigenic E. Coli? is this disease common? how is it controlled?
|
2 days old - watery brown diarrhoea and most die without prompt fluids
hygiene, adequate colostrum VACCINE - give with clostridial |
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which bacteria tend to be involved in non specific bacteraemias in neonates?
|
E. coli
p. haemolytica p. multocida arcanobcaterium poyogenes staph strep |
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what age do you tend to see meningitis
|
2-4 weeks
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what are teh clinical signs of meningitis
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isolate from dam and don't suckle
episcleral congestion lack of suck reflex weak chagned gait depression and stupor hyperaesthesia to auditory and tactilestimuli opisthotonus |
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what age do you see joint ill
|
5 days
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which bacterium associated with polyarthritis particularly in lowland flocks
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strep dysgalactiae - from dams tests or milk: high morbidity despite good hygiene and colostrum management
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what are the clinical signs of navel ill
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hunched back
poor body condition - poor suckling moist navel that is painful may be purulent swelling continues around round lig of bladder or falciform ligament to liver - pain on palpation |
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how do older lambs become infected with erysipelothrix rhusiopathiae
|
docking
castration wound abrasions from dipping |
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what happens in neonates infected with E. rhysiopathiae?
|
bacteraemia --> settle in joints causing fibrinopurulent polyarthritis ina ddition to osteomyelitis and sometimes endocarditis: mortality low but morbidity high: stiff and pyrexic.if chronic joitns can get ankylosed
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how do you treat E. rhysiopathiae?
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parenteral penicillin high dose
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if E. rhysiopathiae flock problem how can you prevent it?
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vaccinate dam 2 doses 4-6 weeks apart in first year
booster 3-4 weeks before lambing |
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where does f. necrophorum spread to from liver_
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joints and lungs
poor hygiene and passive immunity |
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when are you more likely to see a production response to ioding supplementation?
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when thyroid:body weight of newborn lambs > 0.4g/kg
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what are the clinical signs of iodine deficiency in newborn lambs?
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pot belly
scant wool without crimp goitre |
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what crops is iodine deficiency associated with, part in merinos (AUS!!!), when fed to ewes in late pregnancy?
|
brassica
contain thiocyanate goitrogen precursors |
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when and to who can you administer iodine supplementation?
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pre tupping
mid pregnancy 4 weeks before lambing ewes |
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what are the other options aside from oral supplementation of iodine?
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cutaneous
injection: q 2 years in ewes sustained release ruminal bolus |
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what is the cause of congenital swayback? what are the clinical signs?
|
severe copper deficiency of mid to late pregnant ewes
stillbirth small and weak lambs with fine head tremours incoordinated, fine boned and dull coated lambs with HL weakness clinical signs induced when handling susceptible to neonatal ifnections |
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what are the clinical signs of copper deficiency in grown sheep?
|
swayback
osteoporosis and bone fractures steely wool wool discolouration increased disease susceptibility ill thrift |
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what are the clinical signs of white muscle disease
|
stillbrith
weak lambs that fail to feed difficulty sucking sudden onset semiparalysis death from resp failure or startvation ill thrifty survivors can be delayed - gathering, dockking, transport can induce |
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how do you prevent congenital white muscle disease?
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supplement selenium to dam before lambing
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what are the differentials for white muscle disease?
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joint ill
pneumonia spinal abscessation |
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what are teh PM findings of White muscle disease
|
necrotic lesions on myocardium
symmetrical myonecrosis of HL |
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how can you diagnose WMD?
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histop
CK over 500iu/l |
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what are some of the non specific PM findings that support diagnosis of watery mouth?
|
abomasal distension with clear and mucoid fluid contents
gas filled SI congestion of viscera multifocal fibrinous hepatitis and focal supprative pneumonia and diffuse meningoencephalitis in some cases |
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what are the 2 main infectious causes of mastitis in ewes?
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staph a - from skin
P. haemolytica - from lambs mouth |
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what are the underlying causes of mastitis in ewes?
how can you prevent it? |
ewes milk supply insufficient: excess suckling by lambs
orf lesions cold winds ADDRESS protein nutrition of ewes and BC during last trimester of pregnancy to enhance milk prod vaccine for orf tilmicosin injection or dry ewe mastitis tubes |
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which 2 organisms cause coccidiosis in 4-8 week old lambs?
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e. crandallis
E. ovinoidalis |
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what are the clinical signs of coccidiosis? who contributes to environmental contamination?
|
acute diarrhoea
dullness anorexia dehydration w weight loss healthy ewes early born lambs: not ingest sufficient amount to get sick, so develop imunity but contribute significantly to contamination --> dz in later born lambs |
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what is the main important ddx of coccidiosis
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GI parasitism: nematodirosis in particular
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how long after infected are oocysts shed in faeces?
how do you treat coccidiosis/prevent it? |
2-3 weeks til shed in faeces
treat whole flock with sulphonamides and avoid intensive grazing. keep later born lambs on different areas to early born decoquinate in lamb creep feed or to ewes to reduce contam: but dont develop immunity = danger when stopped diclazuril to lambs as single preventative treatment in anticipation of problem (once PO) |
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2 sites of urethral obstruction
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vermiform appendage
sigmoid flexure |
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what 2 types of calculi mainly seen
|
calcium magnesium phosphate
magnesium ammonium phosphate |
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which diets are likely to increase problem of uroliths
|
cereal diets and beep pulp: low in calcium and high in phosphorous --> increased urinary output of phosphorous
compounded by magnesium added to diet> DO NOT FEED EWE RATIONS TO HOUSED WHETHER LAMBS |
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what are the clinical signs of severe urolithiasis
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ventral abdomen and prepuce swollen due to leakage of urine into subcut tissues: slough
abdomen distended following leakage of bladder |
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how do you treat urolithiasis?
why is prognosis poor? what should you check for in ration? |
amputate urethral process
pelvic urethrotomy acidify urine: withdraw feed for 24 hours and dose with 10g ammonium chloride to reduce likelihood of calculus formation. unrestricted access to fresh water poor prognosis due to hydronephrosis check ration for phosphate and magnesium levels and alter accordingly |
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which species of tick is most important vector of disease
|
ixodes ricinus
- virus - rickettsia - bac - preotozoa |
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where are dermacentor reticulatus and haemaphysalis punctata found in UK (ticks)?
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S England and Wales
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at what temperature and humidity is tick feeding activity optimal?
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at 7 degrees (quest for meal when over 7 degrees) and over 85% humidity
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what is life cycle of ixodes?
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tick mate on host and femal feeds then drops to ground. eggs laid in vegetation. larvae then feed for 5-7 days and then drop to gruond and moult to nymphs. nymphs feed for 5-7 days then drop to ground and moult to adults and cycle restarts
= 3 host life cycle! enables transmission of disease non feeding tages need high humidity: dense mat of vegetation with mod to high rainfall |
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what are predilection sites for ticks
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head, neck, groin, axilla
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how can you control ticks
1) dip: protection how long? 2) pour on: protection how long? |
1) diazinon: 3-8 weeks cover - not advised
2) deltamethrin or high cis cypermethrin pour on:6/8 week protection |
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what is the causative agent of tick borne fever?
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E. phagocytophila
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what is the pathogenesis of TBF? what are the clinical signs?
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intracellular infection of WBC: get neutropaenia and trhombocytopaenia
sudden fever of 4-22 day duration pregnant abort potentiation to other infections: louping ill and tick pyaemia, resp disease, haemorrhagic enteritis |
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which groups of sheep ar ate greatest risk of TBF?
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newborn lambs and bought in pregnant ewes> most young lambs infected first 2 weeks of life
MOST INFECTED BECOME CARRIERS / can get periodic spontaneous recrudescence |
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how do you diagnose TBF?
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knowledge of tick activity
giemsa stained blood smear see rickettsia positive serology IFAT or ELISA: exposure splenomegaly PM and tick bite sites |
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how do you prevent TBF?
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pour on flumethrin or high cis cypermethren when new borns introduced to hill
can combine with single prophylactic injection of LA oxytet |
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what is WD time for high cis cypermethrin?
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3 days
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what is louping ill caused by? what does it result in?
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flavivirus
non suppurative meningoencephalomyelitis: transient ataxia or sudden death --> recumbency, convulsion within 24-48 hours NON FATAL CASE: RESIDUAL TORTICOLLIS OR POST PARALYSIS FOR MONTHS |
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which sheep are immune to louping ill? which are susceptible?
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older sheep immune
lambs not protected by colostral antibody = die in first spring if protected by antibody will be susceptible in second spring: endemic farm losses therefore seen in ewe lambs retained for breeding |
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when is mortality much higher in louping ill and what may you see in these cases?
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if co infected with E. phagocytophila - in addition to nervous signs may see dysentery due to superinfection with fungi
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what is the pathogenesis of louping ill? how long is animal viraemic and why is this important?
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viral replication in lymph node draining tick bite site - animal viraemic for 3 days (time period when larval and nymph stage ticks can get ifnected and transmit next year when they feed as nymphs and adults respectively).
virus then enters purkinje cells of CNS and get clinical signs |
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how is louping ill diagnosed?
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clinical signs and hx of tick activity
histo of brain virus isolation from brain ELISA serology: positive = exposure |
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how do you control louping ill?
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control ticks
remove susceptible sheep at timse of tick activity vaccination |
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what is the vaccination protocol for louping ill?
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any animals retained for breeding get single SC injection in autumn or following spring before tick active
all purchased sheep vaccinated once, at least 28 days before exposure to tick infested pasture blanket vaccination over 2 years |
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how can humans get infected with louping ill?
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skin cuts and blood from viraemic animals - vets PMing!
via uncooked meat or infected sheep milk |
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which other animal aside from sheep develop level of viraemia of louping ill that allows transmission of infection to ticks?
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red grouse
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what does control of louping ill in red grouse depend on?
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controling infection in sheep
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what is the causative agent of tick pyaemia? what are the clinical signs?
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S. aureus - potentiated by E. phagocytophila
bacteraemia and joint ill posterior paralysis: spianl abscesses abscesses in internal organs |
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what are the clinical signs of babesiosis? how is it diagnosed and treated?
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seldom clinically significant
pyrexia tachypnoea tachycardia, pale and jaundiced mucus membranes diagnose by detecting babesia in giemsa stained blood smear treat with IMIDOCARB DIPROPRIONATE OR DIMINAZENE ACETURATE |
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how is Q fever (C. burnetti) diagnosed? what maintaines infection in sheep?
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ticks maintain infection in sheep (sheep can spread to humans via foetal fluids frmo aborting or ignestion of milk/faeces or via aerosol --> flu, pneumonia, hepatitis or endocarditis)
diagnosed Ziehl Neelsen stain of foetal stomach or placenta serology for exposure SMALL RED INTRA AND EXTRACELLULAR COCCOID BODIES |
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what is the ifnectiuos dose of B. burgdorferi related to?
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time which infected tick feeds: remove asap!
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when does Cl. perfringens multiply rapidly in the abomasum and SI?
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when anaerobic conditiosn combine with presence of large quantities of fermentable CHO> suddenc change in diet overflowing undigested feed to SI
conditions resulting in gut stasis and low fibre or severe PGE may also contribute to toxin build up in SI |
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how are clostridial protoxin converted to toxins
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by enteric digestive enzymes
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which clostridial species causes
1) black led 2) malignant oedema 3) black disease 4) braxy 5) abomasitis 6) botulism |
1) C chaeuvoei
2) C. septicum or novyi type A 3) C. novyi type B 4) C. septicum 5) C. sordellii 6) C. botulinum C and D (cf horses B and C) |
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lamb dysentery
- age seen in - clinical signs - % loss if extreme |
under 2 weeks
sudden death of stronger singletons acute abdominal pain, die in 4 hours faeces can be semifluid and blood stained, often normal 20-30% loss in extreme non vaccinated |
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what are PM findings of C. perfringens type B
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dark red distended intestines
intestinal mucosa ulcerated serosanguineous peritoneal fluid pale and friable liver kidneys enlarged |
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how C. perfringens type B diagnosed
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gram stain from int scraping
culture for int content ELISA (toxins from int or peritoneal fluid) - specificity not good |
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what age do you see pulpy kidney in? what age is it most common in?
what is it associated with? |
assc with change in diet
fatal in sheep of all ages commonest in 4-10 weeks old or fattening lambs 6mo to 1 year old |
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cs of pulpy kidney
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hypereastesia
ataxia recumbency opisthotonus convulsion death diarrhoea if live longer focal symmetrical encephalomalacia |
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what is seen on PM in pulpy kidney?
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excess pericardial fluid
endocardial haemorrhage swollen viscera congested and friable liver pale and swollen to autolysed kidneys |
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what are the clinical signs of struck?
what do you see pm |
enteritis
peritonitis sudden death pale pink pericardial, throacic and abdo cavity fluid haemorrhagic enteritis proximal intestinal tract |
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how do you manage an enterotoxaemia outbreak?
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instigate vaccination programme
restrict feeding inject C. perfringens beta and epsilon toxins in valuable animals |
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what is abomasitis caused by? what age do you see it in?
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caused by clostridium sordelli resulting in bloated and depressed lambs
see in 3-10 week olds that are creep fed looks like lamb dysentery on PM just seen in older! |
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what are PM changes seen in abomasitis? how else can you diagnose it?
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abdominal distension
pale or congested mm enlarged lymph nodes subcut oedema abomasum distended and displaced and wall thickened and emphysematous gram stain necrotic lesions in abomasal folds culture from necrotic lesion IFAT on air dried smear |
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what is the agent involved in braxy and how does infection come about?
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clostridium septicum
via ingestion of frosted food in late autumn: affected seldom seen alive |
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what organism causes black leg? when do outbreaks tend to occur?
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clostridium chauvoei
outbreaks follow: docking catration shearing under unhygienic conditions use of dirty needles wintering on root crops poor lambing hygiene and dystocia |
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what may be seen if blackleg associated with parturition injury? what may you see in fighting males?
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malignant oedema in fighting males: whole face swells and epistaxis
parturition injury may see erosion of vulval mucosa, vulval and perineal oedema with dark red gassy necrosis extending to adjacent muscle, blackquarter metritis before lambing> entire uterus oedematus and foetus dead and anasarcous |
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what organs does visceral blackleg affect?
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myocardium
pericarditis pleurisy meninges |
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how can you diagnose blackleg?
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PM changes fresh carcass
histopath from formalin fixed section from edge of lesion FAT from unfixed tissue from periphery of lesions smears of BM from rib gram positive rods in smears of oedema fluid or of the margins of muscle lesions |
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what are the clinical signs of blackleg in cattle if still alive?
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pyrexic, depressed, tachypnoeic and anorexic at first
stiff and lame *upper limbs and spinal muscles) vulva and perineum can be affected as in sheep wounds discharge rancid smelling serosanguinous fluid over 12-24 hours get tremors, ataxia, recumbency, coma and death. |
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what is infectious agent of black disease
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clostridium novyi type B
= normal flora in int contents> lodge as spores in lvier of healthy - liver fluke --> necrotic debris and exudate that is suitable for multiplcation and toxin prod by C. novyi |
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what do you see PM in black disease?
|
engorged subcut blood vessels if fresh carcase: black carcase
dark liver with distinct paler necrotic areas evidence of recent fluke migration blood tinged fluid in pericardium and peritoneum myocardial petechial haemorrhages ecchymotic haemorrhages on omentuma nd serosa necrotic foci in mesenteric lymph nodes |
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how may you diagnose black disease
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gram stain of cut liver
FAT on fresh air dried smears of liver tissue |
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what PM agent may confuse diagnosis of black disease?
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invasion of C. septicum
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what is the causative agent of bacilliary haemoglobinuria (red water)?
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clostridium novyi type D
- also invovles migrating lvier fluke |
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what are the clinical signs of bacilliary haemoglobinuria
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mainly in cattle
fever ruminal stasis abd pain anaemia jaundice dark red urine death after 2-3 days |
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when is tetanus commonly seen in sheep?
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following rubber ring use - docking wounds
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what is the incubation period of tetanus
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1-3 weeks
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what are the clinical signs of tetanus
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cant swallow or eructate
saw horse appearance tailedhead out in cattle |
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which botulism species associated with poultry litter contamination? what are the clinical signs in cattle?
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C and D
flaccid paralysis and incoordination starting with pelvic limbs: recumbency and death in 24 hours |
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list 10 causes of ill thrift in weaned lambs
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poor nutrition
PGE cobalt deficiency selenium deficiiency liver fluke respiratory disease lameness sheep scab coccidiosis border disease |
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if investigating ill thrift on a farm what should you include in your history
|
farming system and feed management throughout year
times of lambing and weaning lambing percentage worming regime and anthelmintics used trave element problems and supplements used scouring, coughing, lameness or skin disease weather conditions |
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what is a practical diagnostic tool when investigating ill thrifty lambs?
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human destruction and PM of one or two of the worst affected as will be of low financial value
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what diagnostic tests should you do when investigating ill thrift
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faecal sample for wec, fluke eggs, coccidia oocysts
serum blood samples for vit B12 and glutathione peroxidase |
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what has cobalt deficiency been associated with in pregnant ewes?
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poor reproductive performance
poor milk prod high perinatal lamb mortality rates |
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what are the clinical signs of cobalt deficiency in lambs
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empty and pot bellied
watery ocular discharge: low grade conjunctivitis pale and anaemic: check haemonchosis poor wool quality - "open fleece" |
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what is cobalt required for and why is this essential?
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production of vitamin B12
vit B12 needed to utilise rumen derived propionic acid in energy production and to metabolise amino acids necessary for optimum growth and wool production. poor utilisation of propionic acid results in reduced dry matter intakes --> ill thrift |
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when is pasture cobalt high and low
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low in spring and high in winter
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when are clinical signs of cobalt deficiency most common
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weaned lambs in summer
newborn lams of deficient dams in spring |
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which soils are low in cobalt?
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those derived from granite
those containing manganese, iron and nickel (interfere with cobalt uptake by plants soil with pH over 6.3 |
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which pasture species contains higher levels of cobalt than others
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clover
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what can rseult in elevated serum vit B12 concentrations skewing blood vit B12 analysis?
|
yarding for more than 6 hours before sampling
liver damage poor handling |
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how many blood samples for vitB12 should you take and why? how many liver samples should you take?
|
10 blood samples due to individual variation. less variation with liver vit B12so 3 samples adequate
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what accumulates in plasma cobalt deficient sheep
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methylmalonic acid> use as support of cobalt deficiency
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which animals should you try to get liver biopsies off to get an indication of vit B12 reserves
|
lambs at weaning
ewes pre lambing |
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what is a good method to diagnose cobalt deficiency
|
dose response trial
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how can you provide short term cobalt supplementation?
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1) drench wean lambs - 7 days
2) foliar liquid application spraying - 6 weeks silage paddocks can also be sprayed at early growth stage vit B12 injections: last 1-4 weeks |
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how can you provide long term cobalt supplementation?
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intraruminal cobalt bullets or pasture top dressing
overseas long acting injection available |
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what can ovine white liver disease be caused by?
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cobalt deficiency: fatty infilatration associated with low vit B12 status of lambs
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what are the clinical signs of ovine white liver disease?
|
HE
lack of menace sudden depression stupor fine muscle fasciculations ataxia haed pressing death |
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which breed of sheep can lamb all year
|
dorset horn
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what are the advantages of synchronising sheep (4)
|
compact lambing
more accurate feeding and ration control even batches of lambs AI |
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how long do you keep progestagen sponges in sheep
|
12-14 days --> in season in 36 to 48 hours so get rams in 40-48 hours (remove in 2 ays and return 2 weeks later to catch those that failed to conceive and raddle them this time to know which are early and late lambers)
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what is your target for abortion
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should be under 2%
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what are the differentials for CCN (4)?
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focal symmetrical encephalomalacia (weaned)
adult coenurosis lsiteriosis pregnancy toxaemia |
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what are the clinical signs of CCN
|
cerebral in origin so
first blind and wander aimlessly dorsiflexion of neck: star gaze hypereasthetic to auditory and tactile stimuli can --> seizure dorsomedial strabismus and spontaneous horizontal nystagmus trauma to facial nerve can result in ptosis and drooped ear lat recumbency and opisthotonus followed by death in 3-5 days if untreated |
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how do you treat CCN
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high dose thiamine for 3 days - stand and eat in 24 hours and normal vision in 5-7 days
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what is CCN assc with?
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2 weeks after movemnt on pasture or dietary change
routine anthelmintic treatment |
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what are the clinical signs of sulphur toxicity (3)
|
lack of menace bilaterally
depression head pressing |
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what is the main differential for brain abscess. what age you see it in
|
see in 3-6 month old lambs and calves. main differential is coenurosis but this is uncommon in sheep under 6months of age
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what are the clinical signs of brain abscess?
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head turned towards chest
contralat blindness proprioceptive deficit depression compulsive circling but often stand motionless or trapped in corner of pen |
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how long after eating bad silage can animals develop listeriosis
|
10 days post eating. sometimes present 2 weeks after removal of bad silage
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what age do you tend to see listeriosis in sheep?
|
21-24 months as premolars erupting
4-8week old lambs with acces to bad silage |
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what are the clinical signs of listeriosis?
|
depression and anorexia
propulsive movement circling facial paralysis lack of blink (unilateral usually can be bilat in growing lambs if infection in brain spreads) profuse salivation and food impaction: loss of sensation of trigeminal ipsilateral hemiparesis lat recumbency with involuntary running movements terminally unable to rise DEATH 24-48 hours after onset of CS |
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how do clinical signs differ in cattle with regards to listeriosis?
|
may msis cranial nerve signs> 50% recover cf 30% of sheep
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how do you diagnose listeriosis?
|
virus isolation from brain or placanta or foetus
on PM may see congested meninges |
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what are the differentials for listeriosis in cattle (if no facial nerve signs)
|
peripheral vestibular lesion
basillar empyema BSE thromboembolic encephalitis CCN lead poisoning fracture of horizontal ramus rabies ketosis |
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what are the differentials of listeriosis in sheep
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ketosis
brain abscess nephrosis |
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how do you treat listeriosis
|
penicillin G 300000iu?kg IV BID for 3 days
can give IV dex at first presentation but controversial. supportive treatment with feeding via orogastric tube if having difficulty eating |
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how do you treat vestibular disease (middle ear infection)
|
procaine pen 44000 iu/kg sid for 5 days
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if you see a sheep that is healthy with an ear droop and ptosis on same side what may come to mind?
|
that it may have had otitis media in the past causing damage to the VII
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what age do you see sarcocystis? what are the clinical signs?
|
6-12 month old lambs
get HL ataxia and paresis: dog sit |
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what are the differentials for sarcocystis
|
compressive SC lesion
delayed swayback |
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which breed of sheep and cow do you see cerebellar abiotrphy? what age?
|
charollais lambs
holstein calves 3-4 month old |
|
|
what are the clinical signs of cerebellar abiotrphy?
|
lowered head carriage
intention tremors wide based stance atazia preservation of strength dysmetria progressive deterioration in neurological function (cf BVD and borders) |
|
|
how do you diagnose cerebelar abiotrophy?
|
histo of brain: purkinje cell degen - inherited
|
|
|
what age do you typically see scrapie? any breeds overrepresetned?
|
4yo
cheviots and suffolks |
|
|
what are the clinical signs of scrapie?
|
fleece poor condition: loss on flanks and tail head due to rubbing, if regrow will be black
nibble response and lip smack and sway hindlimbs if stimulate skin over dorsal sacral area depression with hyperaesthesia collapse when stressed for 5 to 10 minutes HL ataxia, dysmetria, hypdermetria, wide based stance: trot down or turn hopw with hindlimb bruxism due to decreased rumination and impaction |
|
|
what are the clinical signs of the brain form of visna?
|
head tilt
circling ataxia hypermeetria lesion is in lateral ventricle |
|
|
what are the signs of the spinal form of visna?
|
unilateral HL proprioceptive deficit to paralysis
decreased flexion of distal joints dorsal hoof contacts ground: knuckles of fet lock |
|
|
how do you position sheep for CSF collection. where do you collect and what are landmarks?
|
sternal recumbency with hips flexed and Hl extended along abdomen
lumbosacral> landmarks midway between last lumbar spinous process and first sacral dorsal spine go 2 to 3 cm caudal to the line that joins the wings of ilium |
|
|
how much LA should you put subcut for CSF colelction and how should you hold needle?
|
1-2 mls of LA subcut and keep hub 5 degrees caudal: pop when penetrates ligament and get CSF in hub
|
|
|
what gauges and size needle do you use for CSF colelction in
1) lambs 2) ewes/calves 40-80kg 3) rams?calves over 80 kg 4) cattle |
1) 21g, 2.5 cm
2) 19g, 4cm 3) 19g, 5cm 4) 18g, 10cm |
|
|
which ovine neurological conditions (3) are associated with diffuse cerebral signs?
|
polioencephalomalacia
bacterial meningitis pregnancy toxaemia |
|
|
what clinical signs may you see with pregnancy toxaemia?
|
depression
bilateral loss of menace frequent bleating (communication?) |
|
|
what is required to mitigate risk of scab introduction from stray sheep?
|
a minimum of one autumn acaricide treatment, ideally before tupping.
|
|
|
how long are handling pens considered a source of re/infection of sheep scab?
|
at least 17 days after removal of untreated sheep: if return sheep to these fields a residual acaricide treatment must be used
|
|
|
how can you treat sheep scab?
|
plunge dip for one minute in diazinon> head dipped twice
- care regarding faecal and soil contamination: will bind the chemical - don't dip in hot weather - rain will dilute it will kill mites in 24 hours flumethrin dip has residual protection for weeks. high cis cypermethrin does not but calso controls headfly, blowfly and lice (still licensed?!?) 2 subcut injections of IVM 7 days apart at 200ug/kg - no residual protection single IM doramectin at 300ug/kg - less than 17 days residual protection single subcut moxidectin 1% 200ug/kg protects for 28 days - but 2 injections 10 days apart recommended for scab outbreaks single s/c moxidectin 2% LA - gives 60 days residual protection with all injectable types takes 7 days until mites killed |
|
|
what should be done following dipping (for scab)?
|
stand in drainage pen for 5 to ten minutes and then turn out to shaded pasture - never pen in closed building after dipping
|
|
|
what weight must sheep be in order to use systemic endectosides
|
over 15kg
|
|
|
how much fleece growth should sheep have for optimum control of flystrike with regards to plunge dipping?
|
at least 3 weeks fleece growth
|
|
|
how do you achieve best results with plunge dipping?
|
remove dags
sheep yarded overnight feet cleaned by running over slats |
|
|
what dips do you use for flystrike prevention?
|
high cis cypermethron: protection for 3 to 8 weeks , usually around 6
organophosphate cyromazine and dicyclanil pour on provides 10 to 16 weeks protection respectively |
|
|
how long do pyrethroid pour ons take to disperse around body and kill lice
|
about 6 weeks - if treat within 6 weeks of lambing will fail to prevent infection of newborn lambs
|
|
|
how do you prevent louse infestation
|
single off shears application of pyrethroid pour on in summer provides all year round protection - louse numbers increase slowly
|
|
|
what is moxidectin 1% incompatable with?
|
footrot vaccine
|
|
|
what are the 2 most common causes of lameness in sheep?
|
interdigital dermatitis
foot rot |
|
|
what are the agents involved in footrot and how is infection brought about?
|
F. necrophorum penetrates stratum corneum and dichelobacter nodosus proteases cause hoof separation and allows depper penetration of fusobacterium. wet conditions and trauma of interdigital skin allow this penetration to occur.
|
|
|
what are the clinical signs of footrot
|
mixture of interdigital dermatitis, under run heels and severe under run hooves
under running spreads from axial heel, laterally and anteriorly under sole to abaxial wall and toe characteristic smell |
|
|
what is footrot impossible to differentiate from early on?
|
interdigital dermatitis
|
|
|
what do you see in mild strains of footrot
|
separation at heels and back of sole - if virulent get complete separation of horn and hoof wall
|
|
|
what do you seen in chronic cases of footrot?
|
extremely lame, recumbent, flystrike on foot and flanks
|
|
|
how many in flock should you examine if investigating foot rot
|
10 to 40
|
|
|
how do you topically treat footrot?
|
gentle paring and application of oxytet
clean feet then foot bath 3% formalin - hardens foot 10% zinc sulphate will cure 80% of feet (doesnt work for severe) if very severe may need parenteral antibiotics e.g. oxytet or high dose pen and strep |
|
|
how else can you treat footrot
|
with vaccination - some respond to first injection, 50 to 100% respond to second vaccine. cross protection limited *multiple group infection common*
parenteral antibiotics if severe and dry conditions for 24 hours post treatment |
|
|
how do you control and prevent footrot?
|
vaccine and footbaths
|
|
|
how much protection does footrot vaccine give and what is protocol
|
give 2 doses. 2-6 months protection : for high risk groups mainly e.g. rams before mating as reactions and reduced LW gain can occur which is not ideal for fat lambs
|
|
|
when is footbathing essential to prevent footort
|
from May if not too dry weekly or fortnightly
|
|
|
what is scald?
|
interdigital dermatitis
|
|
|
what is the aetiology of interdigital dermatitis
|
F. necrophorum alone / indistinguishable from benign footroot> long wet grass predisposing factor and straw bedding may play role in housed ewes
|
|
|
what proportion of flock can be affected by ID dermatitis in extreme cases?
|
up to 90%!
|
|
|
what are the clinical signs of interdigital dermatitis?
|
interdigital skin inflamed and swollen
layer of white necrotic material may get erosions of skin no under running of horn, no smell lameness can persist for several months if untreated |
|
|
how do you treat and control interdigital dermatitis?
|
oxytet spray
move to dry pasture ideal manage areas around troughs and gates 10% zinc sulphate or 3% formalin bath and dry for 1 hour repeat 5-14 day intervals throughout risk period |
|
|
what is the aetiology of ovine digital dermatitis?
|
think spirochaete - not sure. may be orf, but not consistently identifed in scab material from lesions
F necrophorum and D. nodosus often present and may increase severity as do FORMALIN FOOTBATHS |
|
|
what are the clinical signs of ovine digital dermatitis?
|
severe lameness
initially full thickness skin ulceration at CORONY BAND hoof wall under run from coronary band and shed to expose laminae that may bleed profusely 1cm diameter circular areas of hair loss and ulceration sometimes seen on skin below fetlocks |
|
|
how is ovine digital dermatitis treated?
|
oxytet spray> lesions heal quickly
footbathing for 20 minutes in tylosin or lincomycin antibiotic solutions followed by dry standing. individual cases may benefit from systemic antibiotic treatment |
|
|
where does distal interphalangeal joint capsule lie and how is this important with regard to septic arthritis of P2 and P3 joint (pedal arthritis)?
|
close to interdigital skin: septic arthritis with footrot!
|
|
|
what are some of the clinical signs of footrot?
|
aside from obvious foot swelling and discharges at coronary band, weight loss, etc
can get pregnancy toxaemia, and poor reproductive performance in rams |
|
|
how do you remove an ovine digit? what gauge needle and length? how much local?
|
tournique above hock or below carpus
clip and scrub over superficial vein - recurrent tarsal on hindlimb laterally, or cephalic on forelimb found medially 5ml LA into superficial vein with 9g 1 inch needle anaesthetised in 5 minutes - prick heel to test clean foot and interdigital skin - make interdigital cut and insert embryotomy wire - remove digit 15 degrees above horizontal to cut through middle of P2 debride any rinfected tissue apply oxytet spray, non adherent dressing and well padded pressure bandage long acting oxytet Im if needed change dressing after 2 days change again after 4 to 5 days and leave on for 5 days |
|
|
what predisposes to tow abscess (aka white line abscess)
|
F necrophorum
shelly toe foot rot |
|
|
how do you treat a toe abscess?
|
careful paring to release trapped pus
remove under run horn |
|
|
what is shelly toe?
when is it seen and when does lameness occur? |
separation of superficial hoof wall close to white lone at toe
commonly seen in sheep grazing on lush pasture lameness when impacted with soil and faecal material |
|
|
when is laminitis seen in sheep?
|
in concentrate fed
following metritis/mastitis systemic viral disease e.g. FMD and bluetongue stand hunched with all feet placed under body. may resolve in a few days on own can result in pregnancy toxaemia |
|
|
what are the clinical signs of a toe granuloma?
|
proliferation of granulation tissue!
extremely lame lesions bleed when handled smooth or strawberry like growths upt o 3cm across associated with sole or axial hoof wall close to toe often covered with overgrown horn |
|
|
what is toe granulome often diagnosed as by clients?
|
foot rot
|
|
|
how do you treat toe granuloma?
|
pare overgrown horn with help of local
apply tissue bandage |
|
|
when do you get toe granuloma?
|
after foot paring
sequel to footrot or toe abscess |
|
|
what are interdigital fibromas
|
fibrous overgrowths of one or more foot usually in terminal sire breeds - prone to interdigital ifnections! many regrow if removed
treat secondary infections with oxytet spray |
|
|
what are 3 problems over fat ewes may be faced with
|
pregnancy toxaemia
vaginal prolapse copper poisoning |
|
|
how much liveweight does 0.5 unit of BCS =?
how much energy is required to gain 0.5 units of CS in a month? |
5-6%20MJ of maintenance energy
|
|
|
what should the BCS be of lowland ewes
1) at tupping 2) mid preganncy 3) lambing |
1) 3 to 3.5
2 and 3) 2.5-3 |
|
|
what should BCS be of hill ewes at
1) tupping 2) mid pregnancy 3) lambing |
1) 2.5 to 3
2) and 3) 2 to 2.5 |
|
|
what should be brought to mind when faced with thin ewe(s)?
|
whole flock nutrition and management problems (lameness, scab)
johne's fluke PGE tooth problems parasites and management of gimmers triplet ewes chronic pneumonia> MVV, SPA< pasteurella chronic lamenes> DJD, septic arthritis chronic abscess endocarditis scrapie want to know number of animals affected, stage of production, management and nutrition, previous diseases |
|
|
what samples may you take from a thin ewe?
|
faeces: fluke, worms, johnes
blood: BOH butyrate, urea, albumin, globulin (total protein), GLDH, GGT, possibly serology for maedi and Johnes scin scrap or bacteriology fo footrot if needed can do PM - liver, int, lungs interesting |
|
|
what age is johnes usually seen in? what may trigger clinical disease?
|
stress triggers disease, e.g. lambing: 3-4 yo
|
|
|
what does multibacillary johnes indicate
|
numerous Map in macrophages: weak cell mediated immunity but strong antibody
|
|
|
what does paucibacillary johnes indicate?
|
Map sparse or absent, within lymjphocytes, granulomata and giant cells> strong CMI but weak antibody
|
|
|
what % of cases of Johnes does a faecal smear pick up
|
50%
|
|
|
does johnes spread from cattle to sheep?
|
appears to be little cattle to sheep spread
|
|
|
what are the costs of johnes disease?
|
loss of ewe
cost of replacement death/poor growth of lambs estimated to be 50 pounds if ill and 80 pounds if upland per clinical case. |
|
|
how can you control johnes on a farm
|
remove clinical cases from flock
don't keep lambs from affected ewes for breeding good farm hygiene treat PGE good nutrition have compact lambing period and remove replacement lambs from high risk pastures early and avoid high risk stocking rates as lambing is high risk period purchase sheep from free herds can use vaccine> 90% reduction of shedding in australia: 2 to 3 pounds per dose so makes sense if over 5% prevalence |
|
|
how is johnes eradicated in aus?
|
cull susceptible animals
pasture left free for over 15 months including 2 summers - but still have problems with wildlife reservoirs, water course contamination and re introduction via infected stock purchase |
|
|
how do you manage broken mouth
|
draft to lowground pastures with good sward height of pasture, supplementary concentrates
|
|
|
what can cause incisor tooth wear?
|
soil ingestion
calcium and copper deficiencies --> enamel defects parasites trauma soil acids and pasture juices |
|
|
what are differentials for food impaction in cheeks?
|
cheek teeth disease
actinobacillosis diphtheresis |
|
|
how can you alleviate weight loss caused by cheek teeth disease to allow sale
|
2-3 months of appropriate concentrate feeding may restore some body condition
|
|
|
name 2 worms found in abomasum
|
teladorsagia circumcinta
haemonchus contortus |
|
|
name 4 worms found in small intestine
|
trichostrnogylus vitrnius
nematodirus battus cooperia strongyloides paipillosis |
|
|
name 3 worms found in large intestine
|
oesophagostomum venulosum
trichuris ovis chabertia ovina |
|
|
how many T. circumcincta worms cause clinical dz?
|
5000
|
|
|
when do you see nematodirus battus?
|
may through june
|
|
|
when do you see haemonchus contortus
|
june through september
|
|
|
when do you see T cricumcincta
|
juen through november
|
|
|
when do you see T. vitrinus
|
september through to december
|
|
|
when do you see acute fluke
|
september through december
|
|
|
when do you see chronic fluke
|
january through march
|
|
|
how much weight should lambs gain a day?
|
240g/day
|
|
|
what are 3 main categories involved in poor anthelmintic efficacy?
|
underdosing
(underestimate weights, inaccurate dosing guns, mathematical error, poor technique) poor anthelmintic efficacy (out of date product, poor product storage, poor quality product) anthelmintic resistance |
|
|
what does FECRT involve?
|
performing faecal egg count before and 7 and 12 days after treatment with anthelmintic
used to detect resistance |
|
|
what is a target selective treatment?
|
partial flock treatment aimed at maintaining a population in refugia
|
|
|
what is metaphylactic treatments?
|
whole flock treatments administered following appearance of clinical signs e.g. scouring
|
|
|
what is strategic prophylactiv treatment?
|
giving whole flock treatment at appropriate times
|
|
|
what is neosuppressive treatment?
|
whole flock treatments given at regular intervals close to prepatent period of parasite> does little to maintain a susceptible population in refugia
|
|
|
when is type i ostertagia disease seen
|
in young cattle late summer and autumn in first grazing season
|
|
|
when is type Ii ostertagiasis seen
|
yearling cattle in late winter or spring following their first grazing season
|
|
|
what is the period between PGE egg shedding and max number of infective larvae on pasture
|
3-6 weeks
|
|
|
how long can L3 survive for on pasture
|
10-12 weeks, some can survive for a year
|
|
|
what does quarantine treatment of new sheep for PGE involve
|
dose all animals an dyard for 48 hours, then put on contaminated pasture
prevent entry of strays and have general good biosecurity |
|
|
what is a drench check
|
fresh faecal sample from 10 lambs 10 to 14 days after treatment to heck if worked
|
|
|
what is the life cycle of dendrocoelium dendriticum
|
adult flukes in bile ducts shed eggs that are voided in faeces. miracidium already present in egg!!!
egg eaten by land snail where asexual multiplication occurs to form cercaria cercaria extruded in slime balls that are eaten by ants. metacercariae develop in ant body and brain and sheep eat the ants --> infection in sheep. migrate along main bile duct to liver: NO PARENCHYMAL MIGRATION |
|
|
what is the life cycle of paramphistomum cervi?
|
fluke eggs shed in faeces. miracidia develop in egg and then hatch and swim until find snail host. multiply asexually and hundreds of cercaria released (looks like a cross between mushroom and sperm). cercaria swim and encyst as metacercaria on vegetation that are ingested by final host
|
|
|
what happens to paramphistomum cervi metacercaria when in host?
|
excyst in duodenum - immature flukes attach and plug feed for 6 week - migrate to forestomach where they mature
adult flukes attach to forestomach wall using sucker and feed on blood may see haemorrhagic enteritis involving duodenum and upper ilium. paramphistomum seen attached to reticulum and rumenal/omasal mucosa |
|
|
what is the infective stage of tapeworm called?
|
oncospheres: from canid faeces penetrate gut wall and travel to organs via circulation
|
|
|
which species of tapeworm causes coenurosis (gid, aka coenurus cerebralis)
where in brain do most cysts form? hwo long until clinical signs after infection? what age of sheep? |
taenia multiceps
90% in cerebral hemisphere, 10% cerebellum clinical signs in 2-6 months post infection mainly 6 to 234 month old sheep affected |
|
|
list 7 differentials for coenurosis
|
brain abscess
listeriosis louping ill sarcocystosis polioencphalomalacia hypomagnesaemia pregnancy toxaemia |
|
|
which tapeworm causes cysts in the abdomen - particularly omentum, mesentery or visceral peritoneum?
what is the cyst stage called |
taenia hydatigena
cysticercu tenuicolis |
|
|
what is the cyst form of taenia ovis called? what does it infect and how is it spread?
|
cysticercus ovis: muscle and diaphragm (heart)
further spread by flies |
|
|
how long may hydatid oncospheres survive in environment?
|
up to 2 years
|
|
|
what causes hydatid cysts and where are they found?
|
echinococcus granulosos: liver and lungs or peritoneum massive cysts = life threatening zoonosis
|
|
|
how often should you treat farm dogs with praziquantel
|
every 6 to 8 weeks
|
|
|
which tapeworm has man as final host?
|
taenia saginata
|
|
|
how are dairy cows infected with ostertagiasis
|
L3 ingested by adults in late summer (eggs deposited in april develop to L3 by late summer) which results in type I disease in 18 days
low temperature in autumn inhibit L3 at L4 stage in abomasal glands. in late winter or spring these emerge and result in type II ostertagiasis |
|
|
what increases the risk of type II ostertagiasis?
|
dry summer with autumn rain
anything that delays exposure of susceptible calves to high levels of L3 |
|
|
what rae the clinical signs of ostertagiasis
|
scour and ill thrift with sub optimal weight gains and drop in milk yield
|
|
|
what is the pathogenesis of ostertagiasis in beef spring calves? how does this differ to autumn born?
|
overwintered L3 killed by immune cows. those on pasture die before calves eat them. L3 in late summer and autumn when graze the following season is when they are susceptible.
autumn born calves will be out without dams so will be susceptible in first grazing season like dairy calves |
|
|
when and how often do you treat cows for ostertagiasis if
1)dairy/autumn born beef calves 2)spring born beef calves |
1) treat during 1st grazing season with benzimidazoles every 3 weeks or IVM/DOM/mox every , 6, 7 and 7 weeks respectively starting 3 weeks after turn out
2) treat at housing after 2nd grazing season to prevent type II ostertagiasis developing |
|
|
how long may an anthelmintic bolus last? what is meat withdrawal period?
|
may last 90 to 147 days, withdrawal up to 8months!!!
|
|
|
which drugs treat type I ostertagiasis?
|
all anthelmintics
|
|
|
which drugs treat type II ostertagiasis?
|
albendazole, fenbendazole, oxfendazole and macrocyclic lactones - work against early
also treat with fluids |
|
|
what has been seen to a problem with IVM treatment of ostertagiasis?
|
ostertagie die and cooperia survive - have some resistance. thankfully only cause clinical problems with massive infection which mainly include inappetance and poor weight gain
|
|
|
what time of year to you see D. viviparous outbreaks?
|
july through to september/October
|
|
|
what is the lifecycle of D. viviparoues?
|
infectious dose very small!
adults in bronchi lay eggs that are coughed up: Li hatch and swallowed and passed in feaces--> L3 in 5 days (increase rapidly if in warm conditions e.g. faeces in warm weather: L3 ingested with grass and penetrate intestinal mucosa. moult to L4 in mesenteric LN and then travel to ventral parts of caudal lung lobes via lymph and blood. enter alveoli where moult to L5 and cycle starts again may be spread via fungi some L3 overwitner on pasture and some inhibited L5 survive in carrier |
|
|
what is prepatent period of D viviparous
|
28 days
|
|
|
how do you treat D viviparous?
|
with Levamisole and broad spectrum antibiotics> levamisole better as paralyse bug - BZM and ML kill and thought to result in massive inflammatory response
px: can vaccinate calves over 2 months 92 doses 4 weeks apart, 2nd before turnout) - still contribute to contamination so need to vaccinate all |
|
|
which cattle cannot receive D. viviparous vaccine?
|
those that have had pneumonia in the past
|
|
|
what is the cycle of fasciola?
|
mature fluke in bile lay eggs> miracidia develop in egg and then leave in 6 weeks when 15 degrees. they swim and find snail host where they multiply asexually and form cercaria> leave snal and encyst on vegetatino as metacarcaria. metacarcaria ingested by final host.
|
|
|
what temperature is required for miracidia tod evelop ine gg
|
over 10 degrees: april through november
|
|
|
when is
1) acute 2) subacute 3) chronic fascioliasis seen |
1) september through december
2) december through march 3) february and march ` |
|
|
when do you want to control fascioliasis?
|
late spring: remove adults
jaunary: remove immature and adults october: remove immature high risk extra dose given 4-6 weeks after standard treatment |
|
|
which drug works against all stages of fluke?
|
triclabendazole: if resistant focus only on treating in late spring as opposed to every 3 weeks during risk period (autumn and early winter)
|
|
|
which drugs work against larvae over 6 weeks and adults?
|
closantel
nitroxynil |
|
|
which drugs only removes adult fluke?
|
clorsulon
albendazole |
|
|
list 7 differentials for respiratory disease in neonate sheep?
|
septicaemic pasteurellosis
dystocia: fractured ribs and upper airway oedema congenital heart defect neonatal respiratory distress syndrome: immature lungs inhalation pneumonia anaemia: haemolytic with cow colostrum feeding nutritional myopathy: misdiagnosed because weak |
|
|
list 4 differentials for acute respiratory disease in growing lambs
|
acute pasteurellosis/viral inf
inhalation pneumonia from drenching nutritional myopathy phenolic dip aspiration |
|
|
list 4 differentials for chronic respiratory disease in growing lambs
|
chronic pasteurellosis/pleurisy
atypical pneumonia parasitic bronchitis oestrus ovis:nasal bot fly (south UK) |
|
|
what are the 3 main differentials for acute respiratory disease in adult sheep?
|
acute pasteurellosis/viral infection
phenolic dip aspiration laryngeal chondritis: texels and suffolks |
|
|
what are the 4 main differentials for chronic respiratory disease in adult sheep?
|
maedi visna
sheep pulmonary adenomatosis chronic pasteurellosis/pleurisy (chronic suppurative pneumonia) chronic nasal obstruction |
|
|
what are significant clinical findings of respiratory disease in sheep
|
coughing
nasal discharge of mucopus, blood or copious serous discharge dyspnoea adventitious crackles and wheezes (c.f. abd breathing as is normal!) dx often PM |
|
|
list 3 viruses that affect the respiratory tract
|
Pi3
adenovirus RSV, reovirus |
|
|
at what point have most hseep been infected with PI3
|
at 12 onths of age
|
|
|
what does Pi3 predispose lambs to
|
infection of mannheimia haemolytica
Pi3 vacine trials demonstrate a reduction in prevalence of pneumonia> give half cattle dose to ewes before tuping and lambs at 6 weeks of age |
|
|
which sheep do you see adenovirus?
|
primarily young lambs
|
|
|
what does M. haemolytics cause in
1) young lambs 2) growing lambs 3) adult ewes |
1) septicaemia
2) pneumonia 3) mastitis |
|
|
what does pasteurella trehalosi cause?
|
septicaemia in 6 to 10 month old lambs
|
|
|
what rae the clinical signs of M. haemolytica?
|
sudden death: CONSOLIDATED LUNGS
|
|
|
what are the 3 main differentials for acute respiratory disease in adult sheep?
|
acute pasteurellosis/viral infection
phenolic dip aspiration laryngeal chondritis: texels and suffolks |
|
|
what are the 4 main differentials for chronic respiratory disease in adult sheep?
|
maedi visna
sheep pulmonary adenomatosis chronic pasteurellosis/pleurisy (chronic suppurative pneumonia) chronic nasal obstruction |
|
|
what are significant clinical findings of respiratory disease in sheep
|
coughing
nasal discharge of mucopus, blood or copious serous discharge dyspnoea adventitious crackles and wheezes (c.f. abd breathing as is normal!) dx often PM |
|
|
list 3 viruses that affect the respiratory tract
|
Pi3
adenovirus RSV, reovirus |
|
|
at what point have most hseep been infected with PI3
|
at 12 onths of age
|
|
|
what does Pi3 predispose lambs to
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infection of mannheimia haemolytica
Pi3 vacine trials demonstrate a reduction in prevalence of pneumonia> give half cattle dose to ewes before tuping and lambs at 6 weeks of age |
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which sheep do you see adenovirus?
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primarily young lambs
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what does M. haemolytics cause in
1) young lambs 2) growing lambs 3) adult ewes |
1) septicaemia
2) pneumonia 3) mastitis |
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what does pasteurella trehalosi cause?
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septicaemia in 6 to 10 month old lambs
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what rae the clinical signs of M. haemolytica?
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sudden death: CONSOLIDATED LUNGS.
sudden onset anorexia, dullness, pyrexia with hypernoea/dyspnoea, serous ocular and nasal discharge or frothy fluid at month if terminal may lead to ill thrift |
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what age do you get sudden death in lambs with septicaemic pasteurellosis?
what do you see PM? |
up to 12 week s of age
pleurisy and pericarditis petechia in myocardium, spleen, liver, kidney, big LNs and hepatic fatty change |
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what is differential for M haemolytica
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clostridial disease
autolysis hypostatic congestion |
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what are predisposing factors for triggering clinical disease of M. haemolytica (as natural inhabitant)?
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temperature extremes
handling stress PI3 SPA mycoplasma or bordetella |
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when do mortality of M. haemolytica tend to occur
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first few days of disease
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when can you vaccinate lambs against pasteurellosis?
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2 doses of vaccine from 3 weeks of age - time vaccines with expected otubreak
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when do you see P. trehalosi infection (sudden death)?
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July through to December
usually following movement onto rape, turnips or improved pastures - GI ulcers port of entry |
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how does P trehalosi infection differ from M. haemolytica?
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no consolidation
also have necrotic erosions in pharynx around tonsils, nasal mucosae and upper alimnetar tract and infarcts in liver, kidney and spleen |
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what are the differentials for systemic pasteurellosis (P trehalosi and the septicaemic form of M. haemolytica)
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clostridial disease
ruminal acidosis redgut acute fluke brassica poisoning nitrite poisoning dog worry phenolic dip aspiration rhododenron poisoning |
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what is the caustive agent of atypical pneumonia?
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Mycoplasma ovipneumoniae, poss C. psittaci
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what are teh clinical signs of atypical pneumonia
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under 1 year old, chronic soft cough with mucopus and nasal discharge, dull tachypnoeic, and growth rates affected
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which bacteria may be i9nvolved in chronic suppurative pneumonia?
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M haemolytica
A pyogenes P multocida E coli corynebacterium other causes of lung abscesses psuedotuberculosis tuberculosis |
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what do you hear on auscultation with chronic suppurative pneumonia?
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muffling on thoracic auscultation
may have dyspnoea and purulent nasal discharge or no resp signs!!! |
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what is seen on US in SPA?
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severe ventral consolidation
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how do you control SPA?
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prompt culing of lean or dyspnoeic sheap
offspring also develop so do not retain as replacements maintain sheep of different age groups separately reduce clinical disease |
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what age do you see maedi?
what are the clinical signs? |
over 3
exercise intolerance during gathering stand with neck extended, increased respiratory rate, flared nostrils and abrominal component to breathing wasting and dyspnoea obvious at rest severely stressed can get cyanosis auscultation unrewarding - continue to eat despite dyspnoea and weight loss |
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what are the clinical signs of visna?
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nervous: drag HL, knuckle, ataxia, incoordination collapse, death
indurativ e mastitis: flabby udder with diffuse hardening, milk prod decreased but milk looks normal, ln big |
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maedi/visna arthritis?
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in US, not identified in UK
stiff striagh legged gait, swelling of carpals, lymphocytic proliferation over synovial membranes |
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how does maedi differ from SPA on PM?
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entire lung is affected and firm, rubbery and heavy. some cases only gross chagne is increase in weight
have smooth muscle hyperplasia (see with lungworm), diffuse interstitial pneumonia and lymjphoid infiltration and (see with atypical pneumonia) prolif of alveolar septae CAN BE MASKED BY PASTEURELLA OR SPA ON PM! |
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how do you diagnose maedi?
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agar gel diffusion test antibody detection> but some never develop antibodies!
ELISA higher sensitivity |
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how is maedi transmitted?
why is vaccination not an option? |
colostrum and milk
vx not an option as mutates around immune response> biosecurity best way to control - keep closed flock, test serologically and cull or remove lambs from dams immediately after birth strict culling policy and increased replacement rate can aid control (get from MV free stock) |
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which breeds do you see laryngeal chondritis in? what age and when?
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texels and suffolks - usually 2 yo
late summer or autumn during breeding season and related to concentrate feeding |
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what is cause of laryngeal chondritis?
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conformation, trauma, dust and infection
get oedema and respiratory distress with mucosal ulceration resulting in arytenoid abscessation |
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what are the clinical signs of laryngeal chondritis?
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head lowered
neck extended tachypnoea and tachycardia inspiratory stridor salivation cyanosis |
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how do you treat laryngeal chondritis?
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dex
7-10 days synulox, micotil or lincomycin tracheostomy BUT RECUR WITHIN MONTH GUARDED PX! |
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what is oestrus ovis?
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nasal bot fly --> sneezing, head shaking, pneumonia death possible
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