Cattle past questions

a) Describe the pathophysiology of ketosis (5 marks) b) LIST the clinical signs of ketosis. (4 marks) c) Explain the difference between primary, secondary and tertiary ketosis. (3 marks) d) Write short notes on the treatment and management of an individual cow that you have diagnosed with primary ketosis.

*Draw diagram* Essentially what is happening is that the level of lactation we require from our cows costs them a massive amount of glucose. - Much is used in the mammary gland because the udder of high-yielding dairy cows has an enormous demand for glucose for lactose synthesis. Additionally due to the high energy demands in lactation, the cow is in negative energy balance. -Mobilisation of lipid from adipose tissue is the main mechanism by which cows that are in negative energy balance attempt to meet their total metabolic needs. However maintenance of adequate supplies of glucose at this time is essential since, in addition to the demands for lactation, glucose is required for the proper metabolism of fatty acids. (A glucose derived precursor is also needed in the Krebs cycle) Sources of glucose: Ruminants dietary carbohydrates are converted by the rumen microflora to the volatile fatty acids (VFA), acetic acid (acetate), propionic acid (propionate) and butyric acid (butyrate). Butyrate and acetate go into the krebs cycle to form energy. Propionate can be converted to glucose. However during lactation, there may be inadequate proprionate due to inadequate feed intake etc. Where the supply of VFA or NEFA exceeds the ability of the animal to oxidise them, they are converted into ketone bodies or reesterified into TG in the liver and kidney. (Since the acetyl coa produced from free fatty acids cant go into the krebs cycle, it turns into ketones.) = ketosis

You screen a mob of calves to remove any BVD PIs using the ear notch test. The ear notch test has a sensitivity of 99% and a specificity of 99.9%. The prevalence of BVD PIs in herds is about 1% so you use this as your pre-test probability of disease. a) Using the nomogram provided on the next page, calculate your post-test probability of BVD PI if the ear notch test is positive? Likelihood ratio = sensitivity / 1 - specificity (3 marks) b) Given your updated post-test probability of BVD PI, what action would you take now? (1 mark) c) The calf you have identified as a PI is potentially very valuable so you want to be absolutely certain that it is not a false positive. What additional testing could you do? (2 marks) d) Define Sensitivity as applied to a diagnostic test. (3 marks) e) Define Positive Predictive Value (PPV). f) Explain how a test's sensitivity, specificity and the disease prevalence affects the PPV.

.99/.01= 99 Likelihood ratio= post test probailitya a)90 c) Test in series. • Sample blood for the presence of virus 1. BVD ag ELISA 2. BVD ab elisa 3*. BVD PCR* A positive result confirms an animal is PI in most cases. However, some transient infections can also be detected by these technologies, so any positive animal should be re-sampled three or four weeks later. Two positive results confirm a PI. A positive followed by a negative result is consistent with a TI animal. d)Sensitivity: proportion of true positives that test positive e) Proportion of animals that test positive, that actually have teh disease f)Positive and negative predictive values are influenced by the prevalence of disease in the population that is being tested. If we test in a high prevalence setting, it is more likely that persons who test positive truly have disease than if the test is performed in a population with low prevalence. Using the same test in a population with higher prevalence increases positive predictive value. Conversely, increased prevalence results in decreased negative predictive value. need to add to this about sensitivity and specifiity. If we have high sensitivity, we have few false negatives. We also have more false positives. Therefore positive predictive value will be lower. If we have high specificity, we have few false positives Therefore positive predictive value will be higher. Test with high sensitivity= allows you to rule out whatever you are testing for snout Test with High Specificity = A positive result allows you to rule-in whatever you are testing for spin Using more than one diagnostic test Series / Confirmatory -Run two or more tests sequentially -Used to confirm a positive test with a low positive predictive value (low specificity or low prevalence) -A negative result in either results in a negative conclusion Parallel Run two or more tests concurrently Used to find positive cases when the test has a low negative predictive value (low sensitivity or high prevalence) -A positive result in either results in a positive conclusion

Using bullet points: a) List the FIVE (5) principles of paring a lame claw. (3 marks) b) List traits of cow behaviour that need to be considered when investigating a lame herd problem. (6 marks) c) List features of human behaviour and the physical environment that may contribute to a lame herd problem.

1. Cut off all under-run hoof 2. Feather thehoof edges. 3. Shift weight bearing. 4. Always dig a hole with an exit route. 5. avoid unnecessary disruption of underlying soft tissue. b) list traits of cow behaviour. 1. Cows are heirachial. dominant vs submissive. need to take this into consideration when thinking about putting cows in close confines- submissive getting pushed around etc. (yard too small?). dominant like to go into shed first. -young cows will get more injuries front feet, older back feet. 2. Avoidance of areas 3. Cows dont show there lame until it really hurts- why its a seriousu welfare issue. so if you can see its lame something is really wrong. 4. If heads are up when going into milk shed- means there being pushed c) Humans 1. Impatience -Pressuring cows to go faster, makign them turn sharpy, shoving them together, race design, on concrete long period of time 2. Humans using dogs. muddy wet environment, gravel, upslopes- topography Physical environment

You have undertaken a fetotomy of a calve with a head back which required just one cut. there is some vaginal damage. list the drugs you would use (from teh start of fetotomyto what you prescribe for the farmer to continue treatments with) and for each explain what you are trying to achieve with treatment

1. Epidural 2. Tocolytic 3. NSAIDs After 3. Oxytocin 4. Antibiotics 5. vitamin b12/drench Pad out more with cattle book Monitor her

You are called to a dairy farm late on a sunny afternoon in March to examine a 6 year old Friesian cow that is kicking at her abdomen. Her temperature is 39oC, she has had a dramatic decline in milk production, her (unpigmented) teats are reddened and there is no evidence of mastitis. You note that recent rain after a prolonged dry spell has resulted in a flush of fresh grass on the farm. a) What are the THREE (3) most likely differential diagnoses you might consider? (3 marks) b) Write short notes on the pathogenesis of one of your differential diagnoses. (6 marks) c) What further testing might you carry out to refine your diagnosis? (3 marks) d) How would you treat this case while waiting for your test results? (3 marks)

1. Facial eczema - Mainly in NI between Jan and April. Facial eczema needs to be differentiated from other causes of secondary photosensitisation, from primary causes such as St. John's Wort (usually found in wastelands), buckwheat (not common in Australasia), ngaio, panicum and lupinosis, and from congenital porphyria. or does he want other ddx for colic such as intussusception. Diagnostic aids Serum concentrations of the enzyme GGT give the best indication of the severity of bile duct damage.

a) What are the predisposing factors for white line disease in NZ dairy cows? Outline the pathogenesis of this condition. (6 marks) b) Briefly describe how you would investigate a herd problem 5 predisposing factors

1. Herding pressure on cows close to the shed or in the yard, or @ damaged sections of the track- impatient handling 2. Increased twisting pressure (slippery concrete, being tightly packed etc) 3. Standing on concrete/hard surfaces for excessive amounts of time 4. Wet and dirty underfoot conditions that soften the horn 5. Overgrowth of the toe and laminitis Investigation of a herd problem 1. Determine prevalence 2. Clinical examination 3. Environmental examinaton -size of yards for number of cows (too small collecting yard a common problem) -stocking rate - shiny back gate? - pasture conditions- wet, soggy land? -track condition (tight narrow bends often a problem) -housing? 4. Stockmanship and management- watch it happen -impatient/abusive? -use of barking dogs -standing on concrete for excessive amounts of time? -cow flow into milking shed?

A farmer presents you with a down cow that has had two bags of calcium IV and one bag of mix SC. The cow is bright and alert. a) Describe using bullet points the process of clinical examination of the cow (5 marks) b) You identify no significant issues. What treatment would you give the cow? Justify your treatment choices.

1. History- has she calved recently? feed? other cows affected? . 2. What the problem is (what farmer thinks it is) 3. environmental exam. 4. Clinical examination- take from jennys notes. mentation etc. b) If she can swallow it may be beneficial to give an oral drench- zoe thinks starter drench (glucose, calcium, mag, b12 to get her eating). Contact the farmer again tomorrow to check on progress. Also discuss nursing care- hip lifters. • Vicious circle of pressure damage • Location, location, location • Shelter • Lift her and move her • Food and water • Assessment. Nursing of the Down Cow 1 Needs to be comfortable - on a soft surface, straw/sawdust > paddock > dirt > concrete. Shelter to protect against the wind and the rain. In a barn if possible, sheltered by a hedge or haybales, protect with a cover but may eat better outside on grass. Keep her propped in sternal recumbency. Access to water and an energy dense feedstuff such as silage or meal. The digestion of hay provides heat for warmth. Supplement with ketol or molasses and other tonics. Treat the initiating cause Roll the cow from side to side to minimise pressure necrosis. Alternate which side she spends the night on. Consider rubbing and manipulating the limbs to restore circulation. Assist her to stand for periods of the day. Other options include: The use of acupuncture to stimulate nerve function and aid in recovery.

2013 2. a) In October a dairy farmer has found 2 adult milking cows (out of a group of 50) dead in the paddock one morning. They were last seen 12 hours ago, at which time none seemed obviously abnormal. List TEN (10) reasonable differential diagnoses for this case and for each possible diagnosis describe a key feature in the history or post mortem findings which would increase the likelihood of it being the correct diagnosis.

1. Ketosis -ketones in urine 2. Hypomag -aqueous humour- check mag levels 3. Same for hypoca -likely older, high producing cows 4. Rumen acidosis 5. Bloat -what crops are -check rumen 6. Toxicity - can look at gut contents and aroundpaddock. - can test liver. -copper toxicity? 7. Type 2ostertagiosis 8.Lightning -storm last night 9. Cast -paddock topography, ditches? etc 10. Organophosphate poisoning

What do you consider to be the most common causes of a low 3-week submission rate in a seasonal, spring-calving, pastoral dairy herd? (6 marks) b) Explain in detail the steps that you would take to help the manager of such a herd improve its 3-week submission rate. *** still need to do this one.

1. Low bodycondition score. 2. Post partum anoestrus (late calvers). 3. anouestrus cows. - cyst, persistent follicle, persistent corpus luteum 4. poor heat detection. 5. metritis/endometritis. 6. Plane of nutrition. - dont want to be losing weight. 7. Genetics- poor fertility. selecting for higher milk yield details- look at body condition, watch farmers doing heat detection, look @ records, use seeders. vet check etc etc

QUESTION 7 Oral electrolytes are crucial for treating diarrhoea in calves. Farmers will often make their own glucose and salt solutions for treating calf diarrhoea; however these are less effective than properly researched commercial electrolytes a) List FIVE (5) ingredients you could find in a commercial electrolyte in addition to NaCl and glucose; and for each ingredient list one reason why it should be there. (10 marks) b) List the advantages of continuing to feed milk to calves with neonatal diarrhoea alongside oral electrolytes.

1. Sodium (chloride) - to correct losses (cause there losing alot of this) Low blood pH is very common in calves with diarrhoea and is due mainly to a combination of intestinal loss of sodium (hyponatraemia), loss of bicarbonate into the gut lumen, lactic acid production in shocked tissues and volatile fatty acid production in the colon from fermentation of partially digested foodstuffs. It has recently been suggested that D-lactic acid is the major product of colonic fermentation, which is important since calves are unable to efficiently metabolise and clear D-lactate. The metabolic acidosis results in progressive CNS depression, decreased suckle reflex, ataxia, recumbency, coma and, finally, death The combination of intestinal loss of electrolytes and reduced milk intake results in a total body deficit of Na+, Ct and K+. Untreated scouring calves usually have hyponatraemia and normochloraemia. However, there may be hyperkalaemia secondary to metabolic acidosis, due to the exchange of intracellular potassium for extracellular hydrogen ions in an attempt to buffer the extracellular fluid. Bradycardia (less than 70 beats/min), cardiac arrhythmias and the clinical prediction of acidaemia (low blood pH) are suggestive of hyperkalaemia Sodium Both to replace losses and to restore tissue fluid osmolarity, and to assist with the uptake of water, through coabsorption with glucose/amino acids. 2. Glucose - to correct hypoglycaemia -rather than the total energy needs of the calf -also important for the uptake of sodium Glucose To correct hypoglycaemia, provide a source of energy and assist with the uptake of water. Adding enough glucose to a solution to provide some nutritional support usually requires that the fluid is hypertonic, rather than isotonic. Hence, compromises between the amount of glucose and the osmolarity of the fluid are usually required. 3. Potassium - to correct net loss -despite paradoxical hyperkalaemia Potassium Although diarrhoeic calves are hyperkalaemic, potassium is needed l:o restore the net loss that occurs during diarrhoea 4. Alkalinising agents -Direct - NaHCO3 (sodium bicarbonate) 5. -Indirect - lactate, citrate, acetate -calves that are significantly acidotic wont recover without an alkanalising agent 5. Amino acids (glycine, alanine) -Assist with uptake of sodium and water Alot of the fluids that are sold are only ok for mildly affected calves WE WANT THESE 5 KEY THINGS IN OUR TREATMNET 6. Dextrose - - to correct hypoglycaemia b) Neonatal calves have very limited energy stores. Anorexia and maldigestion/malabsorption of nutrients rapidly results in an energy deficit. There is continued debate as to whether milk should be fed in addition to oral electrolyte solutions. Many authors recommend that milk feeding should be completely discontinued for 24 hours in diarrhoeic calves while commercial oral electrolyte treatment is instigated. If milk is to be withheld and replaced by oral electrolyte solutions, it should not be withheld for more than 24 to 48 hours, because many of the available electrolyte solutions do not contain sufficient energy to meet the calf's needs. A number of authors recommend the continued feeding of milk to diarrhoeic calves and, in several studies, this has been associated with uninterrupted weight gain and superior mucosal regeneration as compared to calves from which milk was being withheld. However, milk should not be.mixed with oral electrolytes, nor should it be given within. 2 to 3 hours of electrolyte administration. One recommendation is to alternate!.' electrolyte and milk feeds; this is particularly applicable when 3 or 4 feeds per day are required to meet the calf's total fluid requirement. Bicarbonate-containing fluids should not be fed with milk and preferably not within 1 hour of milk feeding.

d) Write short notes on the treatment and management of an individual cow that you have diagnosed with primary ketosis.

1.Dextrose i/v. -500 mL of 40% solution -Only effective for ~2h Rememebr they will be hyper responsive to IV. he lost 3 teeth giving to one nervous case. so sedate her first** put local over the vein before you put local in. *DO NOT EVEN PUT ANYTHING THAT has 40% GLUCOSE SUBQ. will cause rotten cow disease (anything glucose subq= bad)* 2.Propylene glycol, oral -200 mL b.i.d on Day 1 -100 mL b.i.d for 2-3 more days 3.Corticosteroids -E.g. 40 mg dexamethasone, i/m, once Corticosteroid injections (e.g. 40 mg dexamethasone) have been widely shown to be effective in the treatment of ketosis. Glucocorticoids do not appear to induce gluconeogenesis in ruminants, but rather their use is associated with a repartitioning of glucose in the body. Corticosteroids are also known to decrease blood ketone body concentration and milk production in ketotic cows. -Work from Israel, as well as local experience, suggests that combined intravenous glucose and intramuscular corticosteroids is the treatment of choice, with the lowest relapse rate. Anything that makes the cow feel like eating could be good e.g. vitamin b12- appetite stimulant Lastly address the primary issue: lack of feed/energy. Need to ensure cows are getting enough feed (buy in concentrates etc?)

a) What synchronisation programme would you recommend for dairy heifers? Include details on timing. (3 marks) b) Compare and contrast, using a table format, the advantages and disadvantages of synchronisation of dairy heifers so that 60% get pregnant on one day (one week before planned start of mating for the main herd) with natural mating starting at the same time.

Advantages and disadvantages Advantages: 1. Short calving period- amount of stressful time reduced 2. Early calvers will also be earlier next season 3. Heifers mated to AI- good genetic merit. Lots of good replacements. 4. With synchonrisation= get more pregnant early (put as first point) 5. Makes it easier to detect Disadvantages: 1. Huge feed demand at the same time + since its early wont match up to feed supply/demand 2. Huge labour demand all at once (especially if dystocia etc) 3. No cows will be going into milking shed- heifers may panic.

DairyNZ have defined FIVE (5) different farm production systems which are used on New Zealand dairy farms. Describe the THREE (3) main components used to define those farm systems. (5 marks) b) Using several examples, show how interactions between these components influence decision making, animal productivity and farm profitability

As New Zealand pastoral farming is about profitably balancing feed supply and demand, five production systems have been described by DairyNZ primarily on the basis of when imported feed is fed to dry or lactating cows during the season and secondly by the amount of imported feed and/or off farm grazing. The definitions do not include grazing or feed for young stock. System 1 - All grass self contained, all stock on the dairy platform No feed is imported. No supplement fed to the herd except supplement harvested off the effective milking area and dry cows are not grazed off the effective milking area. System 2 - Feed imported, either supplement or grazing off, fed to dry cows Approx 4 - 14% of total feed is imported. Large variation in % as in high rainfall areas and cold climates such as Southland, most of the cows are wintered off. System 3 - Feed imported to extend lactation (typically autumn feed) and for dry cows Approx 10-20% of total feed is imported. Westland - feed to extend lactation may be imported in spring rather than autumn. System 4 - Feed imported and used at both ends of lactation and for dry cows Approx 20 - 30% of total feed is imported onto the farm. System 5 - Imported feed used all year, throughout lactation & for dry cows Approx 25 - 40% (but can be up to 55%) of total feed is imported. *Note: Farms feeding 1-2kg of meal or grain per cow per day for most of the season will best fit in System 3.

What criteria would you use to determine whether a farm had a high risk of environmental or contagious mastitis?

Best practice for teat scoring • Within 60 sec of cluster removal. • Observed and recorded in regular pattern. • Use head torch. • Score all teats of 80 cows or 20% of herd. • Representative sample (parity, stage of lactation) Look at environment- muddy paddocks etc- think strep Strep uberis tends to be acute in spring. Look at milking hygeine etc- then think staph. Things were different in my lecture, go on this Low con, low en , low cow risk= ITS Low con, low en, high cow risk=DCT Low environmental, high con, low or high cow risk= DCT High con, high enviro= use both no matter cow risk.

Compare and contrast the presentation, clinical signs, prognosis and methods of treatment for: • Left abomasal displacement and • Right abomasal displacement and torsion. Answer this question using annotated diagrams wherever possible.

Clinical signs LDA: 1. Sudden onset drop milk yield and anorexia 2. Cow bright(ish) mild constipation, shiny surface to faeces 3. No temperature 4. Ketones possibly in urine (he always gets urine from sick cows****) 5. Hypochloraemia, hypokalaemia, hypocalcaemia 6. Concomitant illness (metritis, mastitis) 7. Slab sided left para-lumbar fossa (instead of rumen coming out- will be more flat looking) -the paralumbar fossa is sunken, because the rumen is smaller than normal and displaced medially. • High pitched ping over left ribs 10-13 (almost pathogonomic) on a line from elbow to tuber coxae -flick hard Left displaced abomasum -Methods of fixation •Non surgical rolling or bumpy ride in float 20% success rate •Standing right flank omentopexy (gold standard) 90% success rate •Cast percutaneous toggling (most kiwi friendly- cheap) 80 to 90% success rate Follow up treatment options • Procaine penicillin 20,000 iu/kg for 3 to 5 days • Dextrose IV • Propylene glycol (ketol) drench for 5 days • Get the cow onto good quality forage to fill rumen • 20 litres of oral fluids by tube Prognosis: pretty good with surgery/toggling Clinical signs of RDA and torsion: *RDA is much less common than LDA. Probably has a common aetiology to LDA Signs 1. Cow may have diarrhoea, but signs can be vague with anorexia and weight loss -The onset is insidious, with inappetence, reduction of milk yield and varying degrees of ketosis. 2. Often more fluid sounds than LDA 3. If torsion develops cow rapidly becomes desperately ill RDA occurs primarily in adult dairy cows, mostly within 3 to 6 weeks after calving, although right-sided displacement can occur at any time. Rumination ceases and rumen contractions are weak and irregular. There is a gradual distension of the right side of the abdomen. Percussion and simultaneous auscultation over the right middle to upper third of the abdomen commonly elicits a characteristic high-pitched ping Abomasa/ volvulus (AV) -This is a much more acute condition - Once AV occurs, there is a sudden onset of abdominal pain -The heart rate rapidly increases, -Due to the onset of peripheral circulatory failure, the animal feels cold, has a subnormal temperature and pale mucous membranes Auscultation/percussion and auscultation/ballottement reveal the presence of a large gasfilled viscus high in the right abdomen The grossly distended abomasum can usually be palpated per rectum in the upper-right quadrant of the abdomen. Diagnosis is by demonstrating the presence of high-pitched pings on percussion, and fluid splashes on ballottement of the right abdomen. In cases of volvulus pings extend over a large area of the right flank and the abomasum can often be palpated per rectum. • Treatment for uncomplicated displacement can be surgical or medical. Treatment of volvulus must be surgical, in combination with appropriate fluid/supportive therapy. Treatment • If long standing, pulse >120 or cow down consider euthanasia •Standing right sided omentopexy, good(ish) success rate if early -• Decompress, may need to remove fluid too, stomach tube purse-string suture • Check viability of abomasum • Correct displacement by pushing greater curvature cranially and ventrally • Anchor with omentopexy • Vagal indigestion is a potential complication of the more severe RDAs •Medical use of metoclopropamide (care) and buscopan and baytril (see Stefan Smith) Prognosis: Untreated animals usually die within 48 to 72 hours from dehydration, shock and toxaemia. Up to one third of animals survlVlng AV develop a vagus indigestion syndrome due to pressure and tension damage to the ventral vagus nerve near the site of the volvulus. In our experience, the prognosis for animals with an AV is reasonably good if the animals are diagnosed at an early stage. However, it becomes progressively worse as the animal becomes more dehydrated, as the heart rate increases, and if there is a large build-up of fluid in the abomasum, which necessitates drainage before correction. Guarded prognosis overall

Cryptosporidia is a common cause of diarrhoea in calves and also a common zoonosis seen in veterinary students. Massey is currently revamping its calf treatment facilities. a) List the measures that you think we could take to limit spread of cryptosporidia from calves to students.

Cryptosporidia Infective oocysts, containing four sporozoites, are excreted in the faeces of infected animals. Because they are already sporulated, the sporozoites of cryptosporidia can be released in simple aqueous solutions, rather than requiring the presence of reducing conditions, pancreatic enzymes or bile salts (as do most other protozoan parasites). Hence, following ingestion (or possibly inhalation) by a suitable host, The life cycle of the parasite means that persistent infections can be established in a host animal and that infection spreads rapidly between anim~ls and persists within the environment. 1. Provide masks that veterinary students can wear while they are cleaning/ doing things in infected environemnt Provide gloves- make it part of protocol 2. Make the pens easily cleanable (e..g concrete floors- cleaning supplies outside, good drainage as crytpo can be in water) 3. ensure hand cleaning facilities are nearby. 4. posters on walls reminding risk- how to wash hands etc. 5. clean boots with disinfectant between sheds- facilities for this. 6. clearly label issolation wards and what the animal is suspected of having. have ifnormation for protocol e.g. do not touch 7. Good ventilation 8. Foot baths 9. separate cleaning supplies for healthy and sick animals 10. Wash your hands 11. Education/induction foreveryone in the area

a) Describe a vaccination protocol to protect dairy cattle and the people in contact with them from developing disease due to leptospirosis. Justify your recommendations. (5 marks) b) Would your recommendations from part a) above differ if your target population was beef cattle? Explain why there are or aren't any differences. (2 marks) c) List the risk management factors, other than the vaccination of cattle that should be implemented on dairy farms to protect people who may come onto the farm and write BRIEF bullet point notes about what you would recommend. (8 marks)

Dairy First course of vaccination (2 injections within 4 weeks) - 1st vaccination (sensitizer): at disbudding (10-14 weeks after start of calving, Sep-Oct); - 2nd vaccination: before transfer to runoff or replacement rearing farm (14-18 weeks after start of calving, Oct-Nov). st annual booster: 5-7 months after 2nd vaccination when 10 months old (May), or as soon as convenient thereafter, to align with adult stock. Annual whole herd vaccination in May - Lactating herd at dry-off - Replacement heifers In new-born ruminant animals, the primary mechanism for protection against leptospiral infection is effected by the passive transfer of maternal antibodies against Leptospira in the colostrum: the level of antibody protection, as measured by MAT, is dependent on the antibody level in the dam. The optimal timing of dam vaccination for calf protection was assessed in a report by Virbac New Zealand Ltd. (Pulford, 2006), using results from an in-house study that showed lower levels of MAT Hardjo titres in new-born calves of dams vaccinated less than 50 days compared to more than 50 days before calving. Combining these results with additional serological data from new-born calves of dams vaccinated between 54 and 90 days pre-calving led to the conclusion that, for optimal calf immunity, dam vaccination should be carried out at least 70 days before calving. (if we do it in may- 70 days before calving that starts in july) The annual herd booster strategy is to vaccinate prior to autumn rainfall, as a high water table is believed to be the most important risk factor for L. Hardjobovis/ L. Pomona infection, at the time of highest challenge. This timing is not ideal in maximising L. Copenhageni maternal antibodies to be passed on to the calf, assuming that maternal antibodies are protective. Combine with above lepto Q Beef First course of vaccination (2 injections within 4 weeks; 1 and 2 in Figure 3) - 1 st vaccination: at ear-marking (4-6 weeks old, Oct-Nov); - 2 nd vaccination: 4-6 weeks after 1st vaccination (10-12 weeks old, Nov-Jan). Annual whole herd vaccination in July-August pre-calving (4 in Figure 3) Biosecurity measures Assume that all bought in stock are unvaccinated. Vaccinate all young replacement stock before they leave the property for rearing. Vaccinate all purchased stock (cows, breeding bulls) at least 6 weeks before entering the property. Where this is not possible or was not done, keep new stock on a separate run-off that will not be grazed by the resident stock for at least 12 weeks (quarantine). 1. Avoid areas with effluent 2. dont let kids go in ponds 3. induction plan 4. good hygeine 5. milking equipment (gown, gloves, sometimes even googles) 6. Wash equipment as you come thorugh 7. Vaccinate dogs 8. No pigs in area 9. Control rodents.

Write a brief disease illness script for "blackleg" - a rapidly fatal clostridial infection using the following headings: • Epidemiology • Time Course • Pathophysiology • Key clinical signs or features

Epidemiology: Epidemiology: Well conditioned and fast growing animals are most susceptible, history of recent yarding (bruising occurs). unvaccinated herd. usually 1 animal at a time but over a week or two you might get severeal Time course: Acute Pathopphysiology • Clostridium chauvoei spores eaten and remain dormant in oxygenated muscle • Traumatic muscle injury results in muscle hypoxia • Spores germinate and bacteria proliferate • Toxins cause vasoconstriction resulting in more muscle hypoxia and inhibiting inflammation • Animals die rapidly due to toxemia Clinical signs Dark muscle containing numerous gas bubbles (emphysematous necrosis). A rancid butter smell would have been present. Swollen Lame Dead cows

2014 S1- Penny question It is March and your client is worried that pasture quantity and quality is not sufficient to maintain the level of milk production and body condition score of their herd. a) Describe the process you would use to ascertain if the current level of feeding is sufficient to meet the goals of your client. (5 marks) b) You decide the cows are being underfed. List options available to the farmer to rectify the problem. (5 marks) c) Using your knowledge of the 'whole farm model', discuss what you think would be the THREE (3) main factors to take into account when making a recommendation on the options available. (5 marks) d) Describe the implications for farm productivity and profitability if no changes are made to the current feeding levels.

Feed required = 16 kgDM/cow daily. Need to use a plate meter or some other method to decide what the average pasture cover is. Then must calculate. Rule number 1: feed demand vs supply 2: quality vs quantitiy 3. Margins. Feed demand -e.g. cows pg 9 facts and figures food feed supply: pre-post. palt emeter, sward stick, visual b) fertiliser, supplements, sell off stock, dry off stock . d) if you milk off your cows back, then dry them off when super skinny. Long term effects: 1. reduced fertility 2. reduced production next season, 3. Higher empty rate = more cull cows 4. ^ risk of disease e.g. retained fetal membranes and lameness = more money spent on animal health 5. they are anoestrus for longer- so get a larger calving spread = less days in milk and therefore less money. example exam q discussing the 3 main compoonents of a farm system model. tell me what do you think are the most important factors that are going to impact a persons decision to buy supplementary feed in or not. 1. production system 2. people 3. farm business she thinks knowledge and skill are she thinks knowledge and skill are going to be really important if your thinking about price of milk solids. need to realise if you dont get supplementary feed you lose production but if price of milk solid is low you migh tnot be making money anyway\ goals are also important. how stringently do you want to stick to your goal? some people dont want to deter at all even though it could be more profitable to dry off cows. Values is important. -some people will panic and they dont buy in supplements cause dont think they can afford but they still want profit -they milk off their cows ba All covered Values Skill Knowledge- Vets are a very trusted source of information. For skills and knowledge: a farmer is more likely to do something hes confident in communication --quite a lot of farmers are quite independent- work on there own. -very wide range of communicaton skills - some close to zero. have to be really clear on expectations- especially when your a farmer employing someone. Relationships - e.g. many farmers want to keep the farm in the family- pass the business on to there kids to run when they cant anymore. can be more difficult to assess these aims as there more personal. Harder to articulate relationships. Attitudes: some farmers can have incredible skill and knowledge but be very risk adverse and therefore its difficult to implem;ent change. Goals - goals are generally less personal and therefore easier to assess. However its not just a business, its a way of life. Maximising profit is not always the number one important thing to the farmer. therefore must always discuss goals - dont assume.

a) List the criteria you would use to determine that a lame cow needed a claw amputation. (5 marks) b) Describe, with illustrations, how you would amputate a claw of a cow. Include details on preparation, anaesthesia and post-operative care

How to do the amputation 1. Sedate the animal (xylazine) and ensure animal is restrained (cast etc) 2. Put a touniquet on half way up the cannon bone 3. Inject local into one of the vessels for regional analgesia. (regional intravenous analgesia) -It does not matter which vein is chosen for the injection. However, the veins most commonly used (Figure 18.3.20) are the medial branch of the cephalic vein on the metacarpus (forelimb) and the lateral branch of the saphenous vein on the metatarsus (hindlimb). 4.Examine digits to check that infection has not reached the level of the fetlock joint and that sepsis is confined to the distal part of the proximal phalanx and more distal structures 5. Clip from the coronary band to above the fetlock 6. Perform a surgical scrub 7. Put a clean glove over the toe that is going to be amputated (as difficult to remove all dirt etc from hoof and this way it can be handled by the surgeon) 8. A circumferential skin incision is made at an oblique angle over P1 9. Using fetotomy wire, cut at an oblique angle through p1. care needs to be taken not to enter the fetlock joint. 10. perform haemostasis by clamping and twisting major vessels. 11. the wound is not closed to allow drainage 12. bandage tightly in a figure 8 to prevent haemorrhage but not too tight so the remaining claw is still perfused. *remove tourniquet Post-operative care A long acting AB is given (oxytetracycline) and the dressing changed after 2 or 3 days. At that time a lighter and less tight bandage should be applied, which is left in position for 2 to 3 weeks. The stump surface may then safely be left exposed for further granulation to occur. Complete healing is usually achieved in 5 to 6 weeks. Animals should be kept in reasonably dry surroundings, either housed or outdoors on dry ground, during the 3-week recovery period.

QUESTION 3 You are working in rural mixed practice in New Zealand and your boss has asked you to write a short article for the practice newsletter about leptospirosis risk management. You have a lot of spring-calving dairy clients but also some sheep and beef clients, deer farmers and lifestyle blocks. Your article should introduce the topic, recommend a vaccination programme and outline other risk management strategies. Your answer to this question will be your first draft of the article (up to 10 marks will be given for content and up to 5 marks will be given for appropriate language and writing style).

How to protect YOU and your herd from lepto Introduce topic: Leptospirosis is a bacterial disease that affects a wide range of animals ( including deer, sheep, cattle) and can be transmitted to humans. Infection can result in production losses (e.g. milk drop, decreased growth), decreased reproductive performance and further animal health costs (mastitis, inappetence, fatalities). Additionally many animals infected with leptospirosis may not exhibit clinical signs and will these animals will remain invisisble in the herd- shedding the bacteria acting as a source of infection for other animals or humans. Leptospira organisms are shed in the urine of infected animals. Human infection usually occurs by contact with urine (e.g. urine splashing into eye or mouth, contact with abrasions). Initial signs of leptospirosis in humans are fever, chills, muscle aches. If untreated fever will occur and organ damage may occur (liver failure, kidney damage). Therefore due to the serious animal and human impacts leptospirosis poses, it is vital to minimise the risk of infection. Incorporating a vaccination programme is a key factor in minimising risk. All classes of stock need to be vaccinated. Calves require two shots 4-6 weeks apart and this should happen before maternal antibodies wane. Additionally previously unvaccinated cattle should recieve 2 vaccinations, 4 weeks apart. The annual herd booster should be given before autumn, as the high rainfall then increases the risk for infection. Other risk management strategies Vaccinating your herd is a positive step in reducing the risk of leptospirosis, but it will not give you full protection. Further methods that should be incorporated into your farm management practices are: Hygeine Leptospira organisms are passed in the urine of an infected host. Humans can become in Human infection is most likely to occur by contact with infected urine (such as urine splashes into the eye, nose and mouth) or kidneys. Routes of infection are usually considered to be skin abrasions, lacerations and the conjunctiva -Splashes at milking (eyes, mouth) Avoid rubbing eyes, nose, mouth Wash hands wiitth diisiinffecttantt Avoid harsh scrubbing off hands Use disposable towels Use plasters over cuts >>practice good personal hygeine Appropriate clothing -apron, keep mouth closed, gloves. -one farm uses visors. If your picking up an aborted foetus- wear gloves. -carry a towel in your ute. Include education: farm stuff must be aware of these risks and prevention measures Staff Visitors • Hazards awareness Family members More copies of the book available Ensure all staff are aware, every year Prevent spread of lepto onto the farm 1. Only buy bulls that were vaccinated as calves 2. control rodent population Farm dairy Silos Feed pads Calf milk powder and meal >> Rodent bait, tidy feed management is important Pigs Unvaccinated pigs - Often infected -Ideally should not be kept Vaccination 6 monthly Buy from Lepto free piggery Unknown status - Antibiotic treatment Effluent management -Bug can live in wet conditions for up to 6 months -Spray effluent during dry conditions, graze sprayed pasture when dried -Reduce stagnant water buildup -Fence ponds and sumps >>Manage effluent with care

a) What is the standard operating procedure for inserting an intramammary product? (3 marks) b) What is the difference between clinical cure and bacteriological cure? (1 mark) c) Why is it important to treat a case of clinical mastitis for long enough, especially if staphylococci are involved? (3 marks) d) What are the usual reasons for apparent treatment failure? (4 marks) e) What are the options for managing a cow where achieving a clinical cure proves impossible? * go over this question again.

Hygiene is critical when using intramammary products 1. NEVER put tubes directly into water 2. Have a clean working area and everything you need before you start -use one side of the shed to bring the cows in, the other to keep your gear to stop it being contamianted 3. Wear gloves- wash and dry between each cow 4. Clean, disinfect and treat one teat at a time. -vigorously rub the tend end several times. If the wipe still appears dirty, repeat with a new teat wipe until it is clean 5. Carefully inject treatment into teat 6. Lactating antibiotics can be massaged into the udder - DO NOT massage dry cow antibiotics or internal teat sealants.- 7. Spray the cows teats with teat spray -high concentration 8. Clearly mark her so you know she has been treated b) A clinical cure occurs when the appearance of the milk returns to normal. Bacteriological cures occur when the bacteria causing the mastitis are eliminated from the quarter c) staph very contagious- will spread from cup to cup. Can also spread from one udder to the others. Therefore do not want to infect the rest of the herd. - can spread even when subclinical d) Product was not adminsitered in a hygeinic manner Insufficient contact of antimicrobials with bacteria Incorrect dose Incorrect duration of treatment Incorrect storage of product Re-infection e) Dry off Cull. Sell her Could use her as a nurse cow

Draw the table below into your answer book. Complete the table by comparing and contrasting the conditions hypocalcaemia and hypomagnesaemia using the following headings: • Predisposing factors • Clinical signs • Treatment • Prevention

Hypocalcaemia: Predisposing factors: Farm level risk factors 1. Inadequate feed on farm e.g. Low Ca in diet - eg Maize silage 2. Reduced intake due to Poor weather, bulling cows, transport etc 4. Poor transition managemnet (feeding high calcium precalving, inadequate mg, high DCAD) 5. Feeding diets with nutritional interactions e.g. -If cows have been getting lots of zinc for a long time over summer you will occasionally see a cow go down with milk fever -Fathen b) Cow level risk factors 1. High producing cows (have higher calcium req's) 2. Older cows (will generally be high producers + calcium homeostasis not as effective) 3.Concurrent disease (will decrease feed intake) 4. Breed: Within dairy breeds the Jersey is the most susceptible; Clinical signs Clinical signs First stage: HypoCa - Clinical signs First stage • First stage of clinical signs: • Restlessness • Excitability • Anorexia • Tongue protruding *This stage is hardly ever seen by vets and is often missed by farmers as it progresses rapidly to......* Second stage: • All muscle tone diminished • Skeletal muscles - weak, ataxia, sternal recumbency, sigmoid curve of neck • Cardiac muscle - faint heart beat (reduced cardiac output) so increased heart rate. • Smooth muscle (gut) - decreased gut sounds, bloat, constipation, lose swallow reflex. • Smooth muscle (uterine) - uterine contractions do not occur if the cow is in the process of parturition, can lead to dystocia and/or retained foetal membranes. • Pupils will dilate (loss of smooth muscle function). • Lose ability to regulate body temperature, usually become hypothermic.** Stage 3 • Lateral recumbency • Bloat, may aspirate rumen contents. • Comatose • Death Other 2 are talked about elsewhere. Hypomagnesaemia: Predisposing factors: -high producing cows especially older cows -Generally worse with age but can affect first-calvers (very rarely) Reduced intake - inappetance due to other disease conditions or Eating less due to -calving -heavily pregnant -drying off (should supplement then) -transport -bad weather 2. Reduced absorption - high potash, high nitrogen levels, high CP(crude protein) in spring grass -Nutritional interactions (lots of Cu2+ ingestion) -K+ ingestion/effluent. -The disorder occurs in animals grazed primarily on fresh, lush, rapidly growing pastures, which have often been heavily fertilised with nitrogen and/or K, and have a low DM and Mg content. -poor transition management (not enough mg etc) Clinical signs: • Hyperaesthesia, irritability in the shed (kicking cups off, urination / defaecation), aggression, charging • Muscle tremor, twitching, general uncoordination • Increased jaw tone, eye movement • Increased heart rate and strength (may be complicated by hypoCa) • Sternal then lateral recumbency with limbs extended, hard to sit up into sternal • Convulsions (involuntary neural discharge) likely to be hyperthermic • Death - may be sudden with signs of a struggle IF THEY HAVE hypophos they crawl. she showed a video legs are at weird angles when crawling. Other covered elsewhere.

QUESTION 2 In mid August you are called to a case of clinical grass staggers in a 5-year-old dairy cow that has been calved 3 weeks. When you arrive she is laterally recumbent and convulsing. a) Outline how you would treat this cow. (7 marks) b) The herd is being supplemented with magnesium chloride at the rate of 30g per cow per day via the water supply. What options would you consider recommending to prevent further cases in the rest of the cows?

Hypomag= = Grass Staggers = Grass Tetany a) Treatment: • Magnesium +/- energy source -generally just need mg. if close to calving give some ca aswell. • Anaesthesia? - in severe cases • Intravenous Mg - extreme care required! -cant give high conc mg into the vein • Subcutaneous -usually give a mix of IV and subQ • Oral and enema - attack both ends • Is this a herd problem? • Mag sulphate 20% - should not be given I/V, good for S/Q or as an enema so probably 2 bags under the skin mg sulfate as an enema also good also give oral (MgO drench) Afleet enema from pharmacy works (give IV) relatively short. Treatment consists of slow (over ~ 10 min) intravenous administration of Ca and Mg solutions. It requires berween 1.5 and 2.25 g of elemental Mg to return serum Mg concentrations of a cow with clinical hypomagnesaemia to normal (Goff, 2004). Most of the commercially available intravenous Mg preparations are combined with Ca, because hypomagnesaemia is often accompanied by hypocalcaemia. Commercially available 4-in-l 'solutions in Australia typically contain 4.7 g Mg/L. Insertion of a needle (or catheter) into the vein of a convulsing cow can present a challenge. The heart should be closely monitored during infusion because these solutions can cause severe cardiac arrhythmias. In addition, subcutaneous Mg sulphate can be used (500 mL of a 20% solution for an adult cow) to reduce the risk of relapses. In severe cases, 50 to 100 mL 20% Mg sulphate may be given by slow intravenous injection. Alternatively, the more bioavailable compound of Mg pyrrolidone carboxylate acid (Energomag®) can be used (80 mL intravenously and 80 mL subcutaneously). In some cases, tranquillisation might be necessary to prevent selfmutilation; 3 to 5 mL of 325 mg/mL pentobarbitone solution (euthanasia solution) works well; the use of acepromazine or xylazine is not recommended. Parenteral Mg treatment should be followed by oral therapy using 100 g MgO daily for 1 to 2 days, followed by 50 g for at least another 5 days. An enema of a 30% MgCl2 solution (60 g of MgC12 in 200 mL of water) can also be used as a treatment. b) Most cases of clinical hypomagnesaemia occur in the early postpartum period. The disease continues to be a common problem in dairy and beef cattle in Australasia, causing significant morbidity and mortality. Generally, relatively few cows in a herd will show clinical signs of grass tetany, even though a large percentage may have decreased serum Mg and Ca concentrations. Subdinical hypomagnesaemia is associated with an increased incidence of milk fever (hypocalcaemia) and lowered milk production. Clinical signs are not usually apparent until the acute disease is precipitated by adverse factors such as inclement weather. I would recommend taking blood samples to check if the supplementation is adequate MUST BLOOD SAMPLE TO CHECK THAT IT IS WORKING. CAUSE THER EIS SO MUCH INDIVIDUAL VARiation • Subclinical hypoMg has significant effects on production and health If inadequate consider 1. dusting • Mag oxide is used • Can only really spread one day in advance • Assume 50% losses (not eaten by cows - falls onto soil) • Easy to apply • Often spread 60 - 100 g/c/d 2. Drenching -• Drenching with mag oxide. It is important that supplementation is started at least 2 to 3 weeks prior to calving to allow the digestive system time to adjust to the supplement and to ensure that the supplement is effective when lactation begins. This will also reduce the incidence of other metabolic disorders over calving (i.e. hypocalcaemia). Options for Mg supplementation include the following. Individual drenching. This requires suitable handling facilities. In some situations treatment may be included with bloat therapies. Suitable sources of Mg include MgS04 or MgC12 (both at 100 g/cow/day), and micronised (300 mesh) MgO (at 20 to 30 g/cow/day, used as a suspension). In situations where cattle are receiving concentrates (either grain or pellets) on a daily basis, the required amount of Mg can be readily incorporated into the concentrate mix. This provides a very easy and cost-effective method of Mg supplementation. Hay feeding. The feeding of hay, especially legume hays, will help avoid hypomagnesaemia. Hay treated with MgO (50 g/ cow/day) is an effective means of supplying extra Mg. Pasture dusting. A dusting grade (i.e. 60 mesh) of MgO should be used at a rate of 75 to 100 g/cow/day. For better adherence it is best to dust early in the morning when the grass is still damp. Paddocks can be dusted several days ahead, but should be redusted after heavy (>25 mm) rain. Mixing into maize silage or other supplementary feed. Usually MgO is used for this at a rate of 30 to 40 g/ cowl day. Water trough treatment. MgC12 and MgS04 can be added to the sole source of the drinking water supply with a measured, maximum amount of 60 g/cow/day being recommended. Higher rates will make the water unpalatable. Cows need to be trained to accept the treated water. Summary: prevention is by incorporating mgO into feed (dusted on to pasture, given with feed or as blocks) giving it as a drench, or as intraruminal bullets. mgcl and mgso4 can be given through the drinking water but are relatively unpalatable and intakes are relaible. also Avoiding excess applications ofK fertiliser and any application of K from June to October. Testing for mag: • Don't test single unwell animals to get idea of herd status - Mg declines quickly with anorexia. - Test a group (10) of animals, 3 weeks b4 calving for Mg, 7 days after calving for Ca.

a) Write short notes on the aetiology of white line disease in dairy cattle in New Zealand. (5 marks) b) Briefly describe the pathogenesis of the disease along with possible sequelae. (5 marks) c) How would you treat a case that has resulted in rupture of the junction between the caudal heel bulb and the skin?

In general, the term 'white line disease' refers to the conditions of haemorrhage (Disc Figure 18.5-2.10), fissure and abscess formation that most commonly occurs in the abaxial white line. Separation, followed by impaction penetration of the corium, infection and abscessation of the white line are the commonly recognised clinical lesions. Abscess formation occurs once penetration and infection of the white line has taken plac Aetiology of whtie line disease: This condition is common in herds where there is either herding pressure on the cows close to the shed, in the yard, or at damaged sections of the track. Twisting pressure is likely to cause white line disease. Mostly seen in the back foot outer claw in adult cows and the front foot inner claw in heifers (these claws take the most weight). Predisposing factors -excessive walking on hard surfaces -wet and dirty underfoot conditions that soften the horn -overgrowth of the toe -laminitis Pathogenesis of the disease with possible sequelae: Damage to the soft junction (white line) between the wall and the sole, causing a split that works its way up under the side wall of the hoof. • Even before lifting the foot there is often a "break out" visible at the coronet. • Under the foot there is a splitting away of the wall from the sole, filled with sand and gravel if it is severe. From book The white line forms the junction between teh wall and the sole and as such , is a point of weakness. Sequelae If untreated, infection can track up in the soft tissues of the foot, commonly resulting in discharging sinuses at the coronary band, retro-bulbar abscesses or septic arthritis. Tenosynovitis is a less common sequel. Can lead to septic laminitis if the infection tracks proximally along the direction of the dermal lamellae of the wall 2.12). Likewise, heel abscesses may occur as a consequence of white line disease If the infection tracks inward, may get deep digital sepsis. (e.g. retro-bulbar abscess and septic arthritis of the distal interphalangeal joint) White line abscesses occurring towards the toe are more likely to under-run the entire sole rather than track proximally up the lamellae to discharge at the coronary band. How would you treat a case that has resulted in rupture of the junction between teh caudal heel bulb and the skin? no idea. are we gonna amputate or treat like normal..?

Construct a decision tree to show how you would distinguish, in a 3-year-old lactating Friesian cow, between: a) Right abomasal torsion b) Intussusception c) Systemic salmonellosis d) Caecal torsion Text only should be used to annotate the diagram. Do not write an essay.

Intussusception - Initial classic colic signs may disappear after 12 hours Cow can adopt rocking-horse stance Heart rate initially high may drop Cow may groan and/or collapse On rectal distended bowel and if lucky feel fistshaped mobile mass to right Shock, dehydration, metabolic acidosis May get ping over right PLF -If within reach, an intussusception can be felt rectally as a rather firm, slightly coiled mass. History and presenting signs The cow goes completely off her milk and becomes anorexic. Rumination stops and, in most cases, the rumen is atonic. The right side of the abdomen enlarges as a result of stasis and distension of the small intestine. Clinical findings and diagnosis The symptoms of intussusception are sudden in onset. Initially colic may be the most prominent feature, although this is not always noticed by the owner. This is due mainly to acute congestion and oedema of the intussusception. This early pain is intense (Figure 3.4.1) and manifests by paddling of the hind legs, kicking at the belly, the frequent passage of small amounts of faeces and occasionally, recumbency. After the initial colic, respiration and heart rate fall to normal, but as the condition progresses the heart rate becomes increasingly fast and weak and it may reach 140 beats/min at the terminal stage. The rectal temperature soon becomes subnormal. Splashing sounds in the fluid-filled portion of the intestine may be heard on simultaneous auscultation/ballottement of the lower right flank. In most cases the animal starts to pass blood and mucus with the faeces, and soon passes only small quantities of tenacious blood-stained mucus or dark clotted blood (Figure 3.4.2). On rectal examination multiple loops of tightly distended small intestine may be felt in the right abdomen Systemic salmonellosis •peracute:- septicaemia and death •acute enteritis/dysentry, bacteraemia, pyrexia Caecal torsion -Similar signs to RDA May get fluid sounds more caudal and dorsal to RDA On rectal will feel French loaf projecting into pelvis -In case of caecal volvulus or torsion, the clinical onset is relatively acute, with the animal showing anorexia, typical signs of abdominal pain and a sharp decline in milk production. Heart and respiratory rates are increased and usually there is a complete absence of rumen contractions. The right abdomen becomes markedly distended and varying degrees of dehydration develop depending on the severity of the volvulus. Very scant faeces are passed, followed by a complete absence of defecation in the later stages. On auscultation/percussion, a high-pitched resonant ping can be heard in the right paralumbar fossa - the ping extending over a greater area than in the case of simple caecal dilatation. On rectal examination the distended body of the caecum is usually palpable at the entrance to the pelvic cavity, whereas the apex is displaced cranially and laterally or medially, out of reach. In cases involving the colon and caecum, distended loops of colon can also be detected per rectum. Right abomasal torsion -This is when the abomasum floats up on the right side and then flips backward Inflow and outflow obstruction -If torsion develops cow rapidly becomes desperately ill Abomasa/ volvulus (AV) RDA is probably a common, although not essential, precursor of abomasal volvulus. This is a much more acute condition than simple right-sided dilatation and displacement. Once AV occurs, there is a sudden onset of abdominal pain, which may only last a few hours (Disc Figure 3.3.18). The heart rate rapidly increases, usually to 100 to 120 beats/ min, but sometimes as high as 140 beats/ min. Due to the onset of peripheral circulatory failure, the animal feels cold, has a subnormal temperature and pale mucous membranes (Figure 3.3.19). The abdomen is distended on the right side. Auscultation/percussion and auscultation/ballottement reveal the presence of a large gasfilled viscus high in the right abdomen (Figure 3.3.20). The grossly distended abomasum can usually be palpated per rectum in the upper-right quadrant of the abdomen

Write short notes on how you would investigate an outbreak of mastitis on an organic dairy farm at calving time. What measures might you put in place to limit new cases and keep the bulk somatic cell count under control?

Mastitis - staph aurerus and step uberis are still the problems Investigation - what stage of lactation are they in, how old are the cows affected, strip/test/culture History Environmental exam Look at hygeine Clinical exam Treatment/management/separation/prevention strategies Manuka honey can be used as an intramammary treatment -should be medical grade (not suprmarket) Dose- 5 to 10 ml. warm it up first. -If nothing works, dry off quarter Limit new cases 1. Dont keep cows in overcrowded, muddy paddocks (more environmental contamination of streps) -have good drainage 2. Manage stand off areas/races- keep hygenic 3. Reduce stress- have shelter, feed adequately. 2. Hygeine while milking- wear gloves, clean if get dirty, clean cups if get soiled etc 3. iodine teat after milking (allowed) Breed for disease resistance select to keep calves from animals that have mastitis resistance -Although heritability for resistance is low, can make rapid progress if selection pressure high enough. -cull animals with consistently high SCC and MRST - separate so they dsont infect more! Lastly, vigilance in monitoring! striping etc

For the condition that you placed at top of your list of causes of haemoglobinuria: (i) Briefly describe the pathogenesis of the presence of haemoglobin in the urine. (ii) How would you treat an animal affected by this condition, whose PCV was 14%? (iii) How would you manage this condition at the herd level? Justify your answer.

Nutritional haemoglobinuria This condition is also known as Brassica redwater, kale anaemia, rape and kale poisoning, or SMCO toxicity The toxic factor is SMCO, which is converted by rumen bacteria into dimethyl disulphide, a haemolytic agent So intravascular haemolysis From path Cattle, sheep and goats grazing Brassica crops such as kale or rape sometimes develop intravascular haemolytic Heinz body anaemia. S-methylcysteine sulphoxide (SMCO) in the crop is converted to dimethyl disulphide by rumen microorganisms. After absorption this compound interacts with reduced glutathione in erythrocytes to induce Heinz body formation. In severe cases there is haemoglobinuria, icterus and even death. ii)Blood transfusion if PCV is <15% https://www.youtube.com/watch?v=cml7tyQdqJU&feature =youtu.be iii) Management Affected animals should be removed from the crop and given alternative feed such as pasture, hay, baleage or silage. Brassica feeding should always be introduced gradually. An adjustment period of 7 to 10 days is recommended with grazing initially limited to 1 hour and later to only a few hours each day. The total amount of Brassica crop fed should not exceed 20 kg wet weight (or 'as fed') per cow per day; 25 kg is considered toxic. Restricting access by strip grazing, as well as the simultaneous feeding of hay or straw, reduces the likelihood of problems occurring.

You have just finished a simle fetotomy on a schistosome What post op care would you give the cow? took 40 minutes

Oxytocin nsaid's antibiotics starter drench b12 injection to get her eating. monitor for illness *check this. put her on the list to monitor for anoestrus.

c) Explain the difference between primary, secondary and tertiary ketosis.

Primary: Not enough energy and/or gluconeonegic precursors in the diet. Primary under-feeding ketosis: Where cows are not being offered sufficient feed of acceptable quality, i.e. insufficient propionate precursors are available. Secondary under-feeding ketosis Where the cow's voluntary feed intake is inhibited by another disease, leading to insufficient intake of propionate precursors. Secondary: Another condition is reducing feed intake e.g. lameness, LDA, post partum infections Tertiary: Alimentary or ketogenic ketosis : Where animals are fed excessive amounts of highly ketogenic feeds, e.g. silages high in butyric acid

Pic for step 5

Remember the 5 principles of trimming -Remove all under-run horn -Don't create holes without an exit route -Smooth out the edges of all holes -Minimise disruption to underlying soft tissue -Shift weight bearing away from any lesions or areas of instability. -Consider when to use a block. As a guide a block should always be used when soft tissue is exposed.

(a) List the FIVE (5) key changes which occur in the rumen during the development of rumen acidosis. (5 marks) (b) List the clinical signs you would commonly see in cows with rumen acidosis. (4 marks) (c) What tests can be performed to confirm a diagnosis of rumen acidosis? (2 marks) (d) List FOUR (4) strategies that would assist in preventing rumen acidosis.

Rumen acidosis is a common disorder that occurs as a result of the fermentation of excessive amounts of carbohydrate (such as grain, fruit, root crops or maize silage) in the rumen. In acute rumen acidosis, the carbohydrate is fermented into lactic acid. This causes a decrease in rumen pH and increase in the osmolarity of rumen contents, resulting in chemical rumenitis, metabolic acidosis and dehydration from loss of tissue fluid into the rumen, to an extent that depends upon the severity of the rumen acidosis. b) Clinical signs hours. Cows are completely ~anorexic, very dull, weak and ataxic, show signs of colic and often grind their teeth -Later in the disease process, body temperature and resplfatory rate may be below normal, but heart rate is usually elevated (> 120 beats/min) . Rumen motility may be decreased or absent, causing marked rumen distensi -Eyes become sunken and sclera injected as dehydration and toxaemia develo c) Rumen pH, appearance and other characteristics _of the rumen Buid may provide additional diagnostic information. In severe cases, the pH of rumen Buid decreases to 4.5 or less -rumen fluid is coloured milky-green to brown, with the pH usually being <5 d) Acute rumen acidosis can be prevented by denying cattle access to feed storage areas and maintaining adequate control of feeding ~~- . The condition of SARA often goes undetected and emphasis should be placed on prevention rather than treatment. Most importantly, cows should be adapted gradually to carbohydraterich feeds. The adaptation of rumen microflora and rumen papillae from forage-predominant rations to . high-ene:gy lactation rations requires time, and the change m the ration should be carried out gradually over a period of more than 3 weeks. Also, it is recommended that a good-quality fibre source, such as pasture, cereal or legume hay, is offered as part of the animals' diet. Additonal dietary controls for SARA used frequently in lactating dairy cow rations include buffers (e.g. NaHC03), neutralising agents (e.g. MgO)

You are called to a farm 4 weeks after the start of calving to treat several lame cows. On examination you find that some have laminitis. Close by is the feed pad where there are two groups of cows. One group is the "springer" mob being fed 2 kg of grass silage and 2 kg of maize silage per cow (average condition score 5.5) and the other group is the milkers being fed 6 kg of maize silage per cow (average condition score 4.2). All the maize has 'Triple Mix' (lime flour, 'Causmag' and salt) added. Each mob spends 2 hours on the pad and is then given access to paddocks which had di-ammonium phosphate (DAP) and chipped potash applied in late April. On questioning, the farmer is concerned his production levels are below average, the milkers are not eating to capacity and that there has been a high incidence of clinical milk fever this year. a) What problems may be occurring in this management system? (4 marks) b) What further investigations might you carry out? (4 marks) c) What recommendations would you make? (7 marks)

Subclinical hypomag Signs include restlessness and irritability. • Reduced appetite. • Reduced milk production. • Higher incidence of hypocalcaemia. Hypoca causes similar symtoms... a) Problems 1. Maize silage is low in calcium. - inadequate calcium supplementation? 2. Only maize going to the milkers shoudl be supplemented with lime flour. -if give too much ca before calving, down regulates mechanism, more likely to get milk fever. so you want to feed a low calcium diet before calving. will turn on the homeostatic mechanism, and will be able to cope 3. High potash reduces absorption of magnesium. - seasonal pasture Mg levels (normal range 0.16 to 0.22%) are lowest in the late winter/ early spring period. -Potassium ions may inhibit Mg transport across the rumen wall and therefore increase Mg loss in the faeces. Dietary K concentrations >4% DM, which may occur as a result of the use of K fertilisers to increase spring pasture growth and yield, can completely inhibit Mg absorption from the rumen -It has been demonstrated that small reductions in blood Mg concentrations may result in a greatly impaired capacity to mobilise Ca in response to hypocalcaemia. Hypomagnesaemia affects Ca metabolism by reducing PTH secretion in response to hypocalcaemia and by reducing tissue sensitivity to PTH. b) -Take blood samples and test for mag and calcium levels. - c) Increase calcium supplementation? Look at DCAD- Options for Mg supplementation include the following. 1. Individual drenching. This requires suitable handling facilities. 2. Hay feeding. The feeding of hay, especially legume hays, will help avoid hypomagnesaemia. Hay treated with MgO (50 g/ cow/day) is an effective means of supplying extra Mg. 3. Pasture dusting. 4. Mixing into maize silage or other supplementary feed. Usually MgO is used for this at a rate of 30 to 40 g/ cowl day. 5. Water trough treatment. MgC12 and MgS04 can be added to the sole source of the drinking water supply with a measured, maximum amount of 60 g/cow/day being recommended. Higher rates will make the water unpalatable. -this will also lower dcad. Intra-ruminal Mg bullets. Whats causing the laminitis?? found an article saying acidosis not an issue in nz... The role of nutrition and feeding management in the development of lameness has received much attention, particularly in the Northern Hemisphere. Despite the possible over-emphasis on nutrition, it has become clear that in the Northern Hemisphere feed inputs may be a factor in herd lameness. This is probably also the case in Australasia, particularly where there are feeding regimens that result in a significant and prolonged drop in rumen pH. These may result in a dramatic increase in lameness, associated with an acidosis-induced laminitis??? feeding finely chopped silage (in particular maize silage) are common factors in the development of laminitis because of their propensity £or inciting SARA. Adding buffers to rations containing finely chopped silage may help if saliva production is low. The addition of buffers at 0.75% of total ration dry matter is common with maize (corn) silage-based rations. Sodium bicarbonate should not be fed at levels greater than 1 % of the ration because palatability will be affected. maybe ask someone about this. - email lecturer?

a) List the FIVE (5) principles of paring a lame claw.

The 5-step foot trimming Method The five steps are: 1. Length 2. Levels 3. Model 4. Height difference 5. Remove under run horn. These steps are explained below. The majority of foot lameness in cattle occurs in the back outer claw. Front foot lameness is more common in the inner claw. These lame claws will often require much more horn to be removed than would be the case for routine trimming. So, in the hind feet the inner claw should always be trimmed first to act as a template for the outer claw, and in the front foot the outer claw should be trimmed first. 1. Length -Lift the foot and clean Cut the first claw to 7.5cm long. Cut the second claw to equal length, take account of any buckling of the toe. Levels -Trim the first claw flat, leaving 5-7mm thickness at the tip. Spare the heel. Trim the bearing surface of the second claw to the same level (if possible). Model Trim out the horn from around the interdigital space on both claws. This reduces the trapping of debris between the claws, and allows the entry of light and air. 4. Height Difference If a hind outer or front inner claw is damaged, make this claw lower towards the heel. These are the common sites for white line disease in New Zealand. This partly transfers the weight to the healthy claw. 5. Remove under run horn -Loose and under run horn is removed from the heel of the first claw and the heel and bearing surface of the second claw. In lame cows all black marks will have to be followed until they end. All loose and under run horn at white line lesions and around ulcers must be entirely removed. Need a hoof trimmer and a sharp knife

While you are at a beef farm pregnancy testing the cows, the farmer expresses concern about the poor reproductive performance of her herd. This has been a problem for a number of years and she has spent a lot of money on lab tests trying to get to the bottom of the problem but with no success and asks for your help when you are scanning the cows. The farm has a herd of 400 Hereford x Friesian cows (300 mixed age (MA) and 100 heifers). The in-calf rate of the MA cows is 80%, in contrast, the rate for the heifers (which calve as 2-year olds is 90%. However the heifers appear small for their age and amongst the MA cows a high percentage of second and third calvers are not pregnant. Cow body condition is generally poor. Reproductive system Bull out with cattle (heifers and cows) for 14 weeks. Calving date 1 August - cows and heifers are break grazed on pasture during calving. Bull to cow ratio 1 to 30. Multiple sire mated. Describe your approach to improving the management on this farm to improve reproductive performance.

The problem: Although mating 2 year olds can be economically profitable, it requires good management so that the rebreeding problems at 27 months and future matings do not occur -a heifer that calves needs 40% more feed then an empty heifer until next mating. ** -extra feed over winter required to grow heifers -huge amount of growth needs to occur between the first mating and 2nd winter. Conception rates • Cow condition at calving is most important Feeding • End winter to mating - High LWG (0.7-1.0 kg/day) feed 10-12 cm pasture or 2000-2500kg DM/ha • Keep LWG high over the joining period and into the summer and autumn So in this case we need to focus on pasture management • at high stocking rates animal intake declines because pasture intake depends on herbage allowance -so we need to decrease stocking rate so animal intake can increase. • We need to focus on pre and post grazing residuals to maintain pasture quality and ensure high animal intakes • Better farmers will increase post grazing residuals and decrease pre grazing levels • Pre grazing controls pasture quality • Post grazing controls animal intake When to Condition Score • There are five times where it may be beneficial • weaning time - watch young cows • 30 -45 days after weaning - see how feeding is going • 60-90 days prior to calving - last opportunity to get things correct prior to calving • Calving - separate cows on condition? • Mating - planning next years production Could use crops to increase feed energy/herb pasture Lower % of heifers pregnant as 3 year olds -often one of the costs is a lower pregnancy rate (5-10%) as three year olds -this lower rate is more than compensated for if lifetime production is considered Calving date? is this a good time Bull cow ratio is good 14 weeks is way too long •All heifers that enter the herd should calve over no more that 42 days •this ensures the main herd will have a calving duration of 52-63 days •Use restricted heifer joining periods as method of tightening the calving duration in main herd •join for 42 days at the same time as cows -(negates long post-partum oestrus of early calving heifers and cows) Delayed PPOI if calf early and poorly feed cows counter intutitive.. i think that means post partum anouestrus interval So we want to calve in LATE september- shes calving too early! Why strive for a compact season? • Fewer anoestrus cows at start of breeding • More uniform sized calves at weaning (more saleable) • More uniform replacement heifers at 15 mo • More efficient feed budgeting • Easier supervision of calving • A compact spring calving period is the key to maximising reproductive performance • With compact calving it is essential to match calving dates with spring grass growth • Mid to late September some in October****

b) LIST the clinical signs of ketosis.

The signs we see either relate to hypoglycaemia or hyperketonaemia Hyperketonaemia 1. Diuresis (inc urine) 2. Dry, mucus covered faeces ** shiny poo- characteristic 3. Dull, glazed sunken eyes 4. Harsh coat (dry and sticking up) 5. Paradoxical decreased appetite 6. Preference for fibrous feeds 7. Smell of ketones on breath/milk Hypoglycaemia (wasting form- most common) 1. Loss of BCS, ↓ milk yield - Can be rapid- loss of condition can be quite rapid 2. Can be "subclinical" with mild, chronic loss 3. Cardinal signs ~normal •May self-limit as milk production drops -so they dry themselves of you may see them after this has happened so wont be ketotic anymore. •ALWAYS check for other diseases (LDA especially) Signs resulting from hypoglycaemia: (Nervous form of ketosis) •Occurs in ~10% of cases •Presents as a NEUROLOGICAL case, rather than metabolic •Licking/chewing bars •Depraved appetite •Salivation •Wandering •Hyperaesthesia, staggery gait, mm tremors •Aggression - can look similar to lead poison cow •Appears blind, may head press •Or may be depressed and dull

Write short notes on: a) Programmes for the management of bovine leptospirosis (e.g. Leptosure™).

Together, using the Leptosure® programme, the farmer and veterinarian will: Vaccinate livestock Identify the hazards that may lead to contracting leptospirosis Assess the significance of each hazard Enact a risk management programme that eliminates, isolates or minimises significant hazards Monitor and assess risk on an ongoing basis. So just write same shit as above

Clinical Examination of the cow. (i) Having established that a cow has recently calved, what further follow-up questions should you ask when taking a history for a "sick cow"? (3 marks) (ii) With the help of a diagram describe how to perform the Williams' test for traumatic reticulo-peritonitis (TRP) in a cow. (3 marks) (iii) What additional tests could be used to assist in the diagnosis of TRP?

Traumatic reticulo-peritonitis. Rarely, a soft grunt may be heard by auscultation over the trachea during reticular contractions (if there are any) . This sign, also known as the Williams' test, is diagnostic ofTRP, if it is present (Figure 3.2.31). iii) Diagnostic aids In the case of TRP, the associated peritonitis is localised and the pain response to deep firm palpation may be detectable over only a very small area. Several methods can be used to elicit a grunt in cattle with pain due to TRP. 1. The standard technique for small cows is a controlled upward push, with a knee or closed fist, of the ventral abdominal wall caudal and slightly left to the xiphoid of the sternum while listening over the trachea with a stethoscope. • In large cows and bulls, particularly if the peritonitis is abating, it may be difficult to produce a grunt, using the method described above. The best method is to use a heavy pole held horizontally under the area immediately caudal to the xiphoid to provide a sudden lift (upward pressure). carried out by people holding the pole on either side. 3. Strongly pinching the withers at the level of the 8th thoracic vertebra (which causes lowering of the back, thereby exacerbating any pain from the anterior region of the abdomen), while auscultating over the trachea is also a reliable technique, especially for people with considerable clinical experience. Rarely, a soft grunt may be heard by auscultation over the trachea during reticular contractions (if there are any) . This sign, also known as the Williams' test, is diagnostic ofTRP, if it is present (Figure 3.2.31).

d) Treatment of hypocalcaemia. (4 marks) e) Prevention of hypocalcaemia. (4 marks)

Treatment: Animals found in lateral recumbency should immediately be moved into sternal recumbency to minimise the risk of regurgitation and subsequent aspiration pneumonia. 1. Give one bag of calcium IV into the jugular vein. -give relatively slowly (never squeeze bag). Monitor heart rate at the same time for arrythmias. -Accordingly, when given by the intravenous route, Ca solutions should be infused slowly and the heart monitored throughout the duration of the infusion (Figure 12.3.14). Some degree of cardiac arrhythmia is not uncommon during Ca administration, but infusion should cease if it becomes more severe. In severe cases of cardiac arrhythmia induced by infusion of Ca solutions, 10% Mg sulphate (100 to 400 mL) can be given intravenously to antagonise the cardio-excitability effect of the Ca. This treatment can at times be life-saving -Give a second bag of ca/mg IV. (will maintain ca levels for around 6 hours) -Calcium borogluconate is the most commonly used treatment for hypocalcaemia in cattle. The most rapid response is obtained by giving this treatment intravenously. During cold weather Ca solutions ideally should be warmed to bqdy temperature 2. Give a ca/mg bag subq (will slow release over ~12 hrs) 3. Give an oral calcium treatment (ensure she has a swallow reflex) 4. Need to get the cow eating. -Try vitamin B12 and/or Mederantil. 5. • Maybe leave more for 8-12 hours time (subq im guessing) Prevention: refer to above The cattle are supplemented with Mg over this period. The most important mineral for dry cows is Mg. It is essential in the prevention of milk fever and should be added to the diet for at least 2 weeks precalving. In many cases, Causmag (magnesium oxide) at a rate of 50 g/cow/day is mixed with a small amount of water, which is then sprinkled over the supplementary feed that is being offered. • Once cows have calved, the concentrate fraction of the diet should contain 1 to 2% limestone to provide an adequate source of dietary Ca. So talk about dcad, mg levels, adequate ca in diet, not too much ca before calving. From lecture- 3 key things 1. Ensure adequate blood magnesium levels (transport of Ca into extracellular fluid is achieved by a Ca-Mg-ATPase pump). 2. Do not feed diets that are high in Ca precalving. 3. Reduce the DCAD over the last few weeks of the dry period if possible.

question 1 2013

What are the important criteria to be used when buying bulls for use in this herd? 1. Tested and vaccinated for BVD 2. Are they clean? 3. BV- calving ease, growth to weaning Direct vs indirect calving ease cause theyll be keepign the daughters also. 4. breeding soundness- libido, lameness. b)Main criteria the farmer should consider if he chooses to finish teh cattle on some flat alnd on the farm? 1. Castrate vs bull beef. 2. Stock management: Dont mix groups, rotational grazing/break feeding? 3. Supply vs demand - pasture species, KgDm pre and post. crop? 4. Parasites 5. Vaccinations c) Management keys to successfully change to calve -look @ lecture 1. Bull selection

A farmer has presented you with a cow with an eye problem pictured below. a) What is the most likely cause? (2 marks) b) What FOUR (4) clinical checks should you perform before presenting the farmer with a treatment plan? (4 marks) c) What is your restraint and anaesthetic plan if you decide to perform a third eyelid removal? (2 marks) d) Describe, using bullet points your approach if you decide the animal needs an enucleation?

What is the msot likely cause? Cancer eye- squamous cell carcinoma. 4 clinical checks? Check the other eye can still see Feel the mandibular and parotid lymph nodes are not enlarged (as cancer travels in lymph). Also feel the bony orbit for any abnormalities (cancer can invade bone) Do a general thorough clinical examination of the cow- want to make sure its otherwise healthy is she pregnant? restraint and anaesthetic plan for eyelid removal? Restrain with a head bale and a head rope. If the animal is fractious, use a nose twitch. Dont always need to sedate but if you do, use xylazine. Which 5%? Xylazine comes in 3 percentages- 2%, 5% and 10%. Remember ruminants are very sensitive to xylazine, so only use the 2%. Anaesthetic plan Inject local into the affected nictitating membrane and then surgically remove the tumour along with a liberal area of surrounding, normal tissue enucleation? Restraint plan as above. How do we prep for surgery? clear around the eye with just water shave the hair around the eye clean again with water inject local in the skin 1cm above and below the eye and one cm away from the medial canthus. Inject local as your drawing out.. use Clamps to shut the eyelids together use a spinal needle to do a four point block- north, east, south, west. Remember it is hard to puncture the globe but still feel you are running along the bony orbit use iodine to properly scrub make an incision 1cm above and below the eyelid (no wider otherwise you will not beable to close the gap start blunt dissecting around the casing of the eyeball (shouldn't enter through the white material) dissect around the tear duct so that will be removed also cut the optic nerve/blood cells with it. d) Finally, the optic nerve is severed and the entire contents of the orbit are removed, thereby avoiding spillage of potentially cancerous cells pack the eye with gauze. Closure of the defect by suturing together the remains of the eyelids give nsaids+ antbiotics.

Write short notes on Dry Cow Therapy, including management of cows from late lactation to the early dry period.

Whats it for? 1. Eliminating infection (mostly cow associated) 2. Preventing new infection (there is a big risk of infection at dry off) Dry cow therapy is much much much more effective than when in milk Which antibitoic? Cloxacillin is the best against staph aurues - massey uses this. cloxacillin is a b lactamase resistant penicillin. their antimicrobial efficacy is aimed at b lactamase producing strains of gram positive cocci, particulary staph aurues. cephlaonur commonly used but no better Cephlaonur -most popular dry cow treatment, lasts 70 days -will be in udder at calving, rise in antibitoics in milk but cow is sealants stop bacteria from getting in. (environmental) If teat sealant, do you need antibiotics? Does a 40 day ab teat seal work as well as 70 day Do you still need long acting dry cow therapy if you teat seal? -if a high level of infection then yes its likely you do 70 day is better. has a higher conc of drug initially. teat seal is 12$ per cow. pays for itself. very useful. Antibiotic is 7 dollar saving if using short vs long acting farmers like long acting dry cow + teat seal but standard protocol is short acting cloxacillin + teat seal. this way you save 7 dollars per cow 100 days or up to 33 days after calving cows treated with teat seal had less clinical masitis. (even though teat seal is lost in 1-2 day of lactation) Managing drying off 1. Stop at 5L a day: -Cows producing less than 5 L/day (or less than 0.4 kg MS/day) may significantly increase bulk milk SCC even when they do not have mastitis. - This practice may also reduce the likelihood of mastitis infections at the following calving 2. Dont starve -Feed 'maintenance' diet for the first 7-14 days after dry off. Restricting feeding after dry off helps accelerate the udder involution process. 3. Dont prevent from having water -To comply with animal welfare codes, water must not be restricted. 4. Dont milk once a day. -It is advisable to maintain the same milking frequency up until dry off. Reducing the frequency of milking will increase the bulk milk SCC, particularly for cows with a higher SCC (Holmes et al 1996). Milking 'once-a-day' has not shown significant impacts, or benefits, on the risk of mastitis after drying off. Intermittent milking (i.e. milking every other day) should be avoided as this can significantly increase the risk of mastitis 5. Put cows in clean areas after giving DCT or ITS. -Cows should be put in dry, clean paddocks (not heavily soiled with manure, little bare ground, no exposure to dairy effluent) for 7-14 days after dry off. This is because the numbers of coliform and streptococci bacteria in the environment are important predictors of new infection rates 6. dont want very high stocking density -dont want cows on mud (inc strep uberis risk)

Discuss the advantages and disadvantages of the following three bedding materials for use in a calf rearing facility: • Straw • Sawdust/Shavings • Stones

Wood shavings (not tanalised), sawdust (Figure 17.1.8), or shredded paper works well in warm/mild conditions. A deep litter of rice hulls or wood chips, 40 to 50 cm thick on a concrete floor, provides excellent bedding. Such materials generally have good moisture removal properties allow the calf to create a microenvironment

Q5 a)Describe the process you would use to establish teh feed requirements of herd during spring If this feeding level is implemented, how would you see if your recommendation is sufficient ? c) The farm has a Spring pasture surplus. Discuss the different ways you can manage this surplus.

a) 1. Calculate the energy requirement (maint, milk, walking) 2. Discuss how much energy is in the feed per kg DM. how much dm is in the feed. how much pasture is there. 3. could maybe mention minerals b) What are pre and post grazing residuals? magic number 1600? * check this. How much condition are they losing- before and after. One condition score over the entire spring is ok- check this. no lower then 4- 4.5. we want them 4.5 at mating. 5.5 at calving. c) e.g. if its spring. what are you going to do. she wont be impressed if we say to bring on new stock. ** 1. Turn into hay, baleage 2. Turn into silage 3. Rotational grazing- high stocking rate, short rotations. 4. Take out poor performing paddock and get re-seeding of ryegrass 5. wilt it and feed it- so better utilised. We want to do this because if we have too much will lose quality and slower growth? We dont want to buy in new stock in spring because wont have enough feed in summer and winter etc. Long term: can manage calving dates so peak lactation is when the most grass is on the ground. d) 3 things 1. knowledge- do they know how to make 2. profit? 3. Grass... look at 1st slide.

You are presented with SIX (6) collapsed 10-day-old calves that are unable to stand and have no suckle reflex. a) List the differential diagnoses for this presentation. (2 marks) b) Describe how you would distinguish between these differential diagnoses. Include clinical examination and diagnostic findings. (6 marks) c) You have decided that rotavirus is the cause of the problem. Outline, in bullet points, a preventative regime for next year to reduce the likelihood of this occurring again. (7 marks)

a) 1. Cryptosporidium (4 days to 4 weeks) 2. Salmonella (7+ days) 3. Rotavirus = up to 10 days 4. Corona virus (1-3 weeks) Clinical examination: Affected calves exhibit diarrhoea with various degrees of dehydration. There are differences in the characteristics of the faeces and of secondary clinical signs that are present in 'typical' cases of each pathogen yet, on the whole, attempts to diagnose the cause of diarrhoea by simple clinical examination are generally unrewarding Points that mayhelp: Salmonella: Acute cases are typically initially pyrexic (with temperatures reaching 41°C), anorexic and are depressed, recumbent or prostrated. Temperatures often return to normal at the onset of diarrhoea but are often subnormal at the time of clinical examination. Evidence of septicaemic spread includes central nervous system (CNS) signs, ocular lesions (hypopyon) and polyarthritis. The faeces range from a profuse to a moderate diarrhoea (Figure 17.4.9). Dysentery is often present and faeces are mucoid, may smell obviously necrotic and may contain fresh blood and shreds of mucosa (Disc Figure 17.4.1 Rotavirus: Morbidity is high, but mortality is generally low in uncomplicated cases. There is an incubation period of 1 to 3 days, after which diarrhoea typically lasts for 1 to 3 days (longer if concurrent infections are present). Faeces are yellowish and watery (Figure 17.4.11). Sometimes they are frothy, although this is not a definitive diagnostic criterion. Other clinical signs include depression, reduced sucking response and dehydration Crypto: deaths are uncommon Corona: mortality low Affected calves ate initially only mildly depressed and continue to drink. They subsequently become weak and lethargic as they become dehydrated and hypoglycaemic. Because the enteritis results in maldigestion and malabsorption, calves can appear grossly emaciated and, consequently, misdiagnoses of underfeeding/ starvation have been made Diagnostic findings For salmonella you need to culture a faecal sample ELISA on a faecal sample for rotaviarus (want at least 3-4 affected calves) ELISA on a faecal sample for coronavirus Cryptosporidium: floatation of oocysts. Preventative regime: developing high standards of management and husbandry systems, which take cognisance of the major predisposing factors and implement strategies to prevent them from occurring/ mitigating their effects. Probably the most important aspect of control is a management attitude that believes that 'calves are important'. Where calves are regarded as of secondary importance, a nuisance or are relatively expendable, disease is hard to control. Conversely, management that attaches a high value to the individual animal usually results in a low incidence of disease. 1. Bedding 2. Hygeine - changing bedding, disinfecting pens between calves, having solid fences between pens, feeding healthy first, sick last 3. Colostrum management 4. Environment- cold? draughts? 5. Dont mix ages. 6. Measures to minimise the exposure of young calves to potential enteric pathogens • Good batch management of calves; i.e. an all-in/all-out policy and avoiding the mixing of calves of different ages. • Meticulous attention to detail during the period of milk feeding. Hygiene, handling of CMR and storage of colostrum are amongst the most important areas to consider during this period. Careful observation of the calves' behaviour during this period will help to identify sick animals before they become debilitated. • All utensils used for feeding calves and storing milk should be thoroughly cleaned on a regular basis. Utensils used to feed sick calves should not be used for healthy calves. • Provision of high-quality hard feeds (compound feed and roughage). Avoiding faecal contamination of feeders. Careful monitoring to ensure that intakes are appropriate. Maintaining good growth rates. • Provision of clean, fresh water in drinkers that cannot become contaminated with faeces. • Personnel hygiene. Particular care should be taken to avoid the risk of carrying contaminated material from sick calves into the pens of healthy calves. • Pen hygiene, including cleaning, spelling and/or disinfection between batches of calves. • Provision of isolated 'hospital' pens to minimise the spread of disease from infected animals. • Prompt, effective, vigorous treatment of sick animals. Calves with diarrhoea should be promptly removed from the remainder of the healthy calves. Two approaches have been taken with vaccination against rotavirus and coronavirus infection in calves. The first approach involves oral vaccination of neonatal calves with a modified live vaccine. The vaccine must be administered immediately after birth and before the calf has suckled, because the colostrum of most cows contains virus-neutralising antibodies that interfere with the vaccine. The second approach involves intramuscular vaccination of pregnant cows with either a modified live or an inactivated vaccine in order to stimulate the production of high concentrations of specific virus-neutralising antibodies in colostrum and milk during the first few days of the cow's lactation. Although, there are reports of successful field trials of cows that have been vaccinated against bovine rotavirus alone, or against both rotavirus and coronavirus, negative results have also been reported. There is a lack of vaccinespecific data supporting the efficacy claims for these vaccines. Rotavirus + coronavirus vaccines are not available in Australia. A combined bovine rotavirus + E. coli K99 bacterin (Rotavec K99®) has been registered for use in cattle in New Zealand for several years.

Diarrhoea in neonatal calves is a multi-factorial condition. a) LIST the factors that contribute to this being a problem on a farm. (3 marks) b) How would you carry out an epidemiological investigation of a calf diarrhoea problem on a farm? (7 marks) c) Describe your approach to the treatment of a calf with diarrhoea, which is depressed, dehydrated and no longer has a suckle reflex.

a) 1. Failure of passive transfer (inadequate colostrum storage or management practices) 2. Cold environments (draughts, inadequate bedding) 3. Heavily contaminated environment ( 4. Mixing of ages of calves (increased challenge) -when born are naieve/sterile cant take threats from older ones. c) Firstly I would give IV fluids over 4-6 hours. I would give NaHCO3 (1.3%) to correct the metabolic acidosis followed by Ringer's or Hartman's I would then give a broad spectrum antibiotic (e.g. amoxycillin) as there will always be bacterial (i.e. E. coli) overgrowth even if this wasnt the primary pathogen. I would give NSAIDs for pain relief. I would then ask the owner to rotate giving milk and oral electrolytes 4 hours apart. •Oesophageal tubing for calves that won't/can't suck *Ensure isolation protocol is good.

You are called to a farm in mid-spring at afternoon milking for a down cow. When you get there you find a 3-year-old cow that has been calved for 2 weeks, in lateral recumbency in the yard showing the classical signs of an epileptiform seizure. (a) List the differential diagnoses for this cow and indicate which is the most likely. (2 marks) (b) How would you treat her for the most likely diagnosis? (4 marks) (c) In order to prevent more cases in the herd, what questions would you ask the farmer, what diagnostic testing might you carry out and what options might you put forward?

a) 1. Hypomag 2. early stages hypoca( jennys never seen) 2. Lead poisoning -The disease is characterised by an acute encephalopathy. 3. Tetanus 4. Listeriosis -"Other potential effects of listeriosis include proprioceptive deficits (brainstem damage), tremor and collapse (cerebellum)" 5. polioencephalomacalacia (PEM) Lead and urea poisoning, PEM and infectious neurological diseases are also differentials for hypomagnesaemia. With lead poisoning animals may demonstrate maniacal excitement and continuous convulsions that lead to paralysis. Abdominal pain, blindness, diarrhoea and constipation are sometimes observed. b) Most likely hypomag c) 1. Transition management? diet etc 2. Stressors? 3. Fertiliser? K+? 4. Mg supplementation? Diagnostic testing: mag and calcium.

You suspect a problem with excess negative energy balance (NEB) in a group of 250 Holstein-Friesians being fed a diet of 4kg DM grass silage, 2kg DM palm kernel and 15kg DM grass. Outline your investigation and approach for this herd focussing on: a) The signs that you would see in herd with excess NEB b) How you would confirm the problem c) The likely underlying causes of the problem d) Identifying some potential solutions for the problem

a) 1. Loss of condition/ weight loss 2. Increased disease due to increased stress 3. Metabolic disease (e.g. ketosis) 4. Poor production (decreased milk yield) 5. Poor fertility- high level anoestrous 6. Poor calf growth b)Calculate requirement vs what is offered Calculate demand of cows (milk + maintainence+ walking + preggerz?) Test silage and grass for energy -Pre and post grazing levels (plate) -Are they ruminanting? or are they hungry- bellowing, standing at gate. c) Poor quality (low ME) in feed on offer Not able to eat the feed on offer -Inadequate management (not rotationally grazing fast enough etc) -feeding the concentrates (already filled up on grass). -think about palm kernel problems cause penny doesnt like palm kernel d) fertilier Buy in better quality feed Educate farmer on grazing praactices- how to keep pasture quality high -did they make the silage themselves? education on producing it Herb crops/replant grass Decrease requirements -once a day milking -decrease stocking rate (culling)

You are called to a 300 cow dairy farm that you have not previously visited to treat some lame cows. While waiting for the farmer to bring the cows in to the yard you note that, although the race seems in good condition, the yard seems rather small for the size of the herd and that the hock rail on the backing gate is very shiny. (a) What do these observations suggest about the type of lameness you are about to see? (3 marks) (b) Outline the pathogenesis of this condition. (6 marks) (c) What recommendations might you make to reduce the number of further cases?

a) A predisposing factor for white line disease is pressure being put on cows whiel going into the shed (shiny backing gate implies its being used inappropriately- shouldnt be used to physically push, its just to stop them from going back). b) white line disease!

a) Which key pathogens cause enzootic pneumonia in calves in New Zealand? (3 marks) b) Which key factors reduce the risk of disease in dairy calves in New Zealand? (2 marks) c) You are called to see an outbreak of coughing in a mob of 60 calves, 5 have died and 15 are clinically ill. i) Outline your approach to this clinical problem using bullet points (5 marks) ii) What treatment would you give the calves? Justify this treatment. (5 marks)

a) Enzootic pneumonia is usually associated with a combination of one or more respiratory virus infections, commonly complicated by secondary bacterial invasion with Mannheimia haemolytica, Pasteurella multocida, Arcanobacterium pyogenes, Fusobacterium necrophorum or Histophilus somni. The viral agents commonly incriminated include parainfluenza Type 3 virus (PI3), bovine respiratory syncytial virus (BRSV) and bovine herpesvirus 1 (BoHV-1). bovine herpes virus 1 causes IBR b) • Predisposed by bad housing: - Correct housing faults - especially ventilation/condensation -Adequate fresh air flow into the calves' environment is important for limiting humidity and reducing the concentration of noxious gases and pathogens. -Barns or sheds for rearing calves should be airy bur draught-free and be twice as deep as they are wide or high. -The narrow opening should be the front entrance ifthe barn faces the prevailing wind. -so no draughts but still ventilated. -NO WET BEDDING. • Correct bad management: - Batch management, pen management -are they bringing them in 1 at a time to pens. this is bad. all in, all out policy -An 'all-in all-out' policy should be practised -Don't overcrowd pens -Should be similar ages in pens -remove/isolate sick animals -Multiple stressors should be avoided or reduced as far as possible, e.g. combinations of weaning, drenching, vaccination, dehorning and castration etc. Although there are vaccines available • COLOSTRUM i) Outline your approach to this clinical problem using bullet points 1. History -Age of the calves -Previous history on farm -Colostrum management -Management of calves (e.g. all in all out) -Vaccination protocol -Isolation protocol 2. Environmental exam -Is the bedding wet? -Are there draughts in the shed? -Condensation? -Overcrowded? -Stale air? poor ventilation? -Smell of ammonia in air? 3. Clinical examination -Distance first- any other obvious problems? diarrhoea? navel ill? Clinical examination of sick animals Respiratory signs include coughing, dyspnoea and tachypnoea. Pyrexia is usually evident. Later on, there is inappetence, dehydration and recumbency. Mucoid/mucopurulent oculo-nasal discharge is usually present. Consolidation of the cranio-ventral region of the lungs is usually present and may be evident on auscultation/percussion of the chest. The area of affected lung tissue is often much enlarged and the loud harsh respiratory sounds (due to congestion and oedema) are followed by crackles and a pleuritic friction rub, indicating chronic suppurative pneumonia. When there is marked lung consolidation, few sounds are present. Samples: Nasopharyngeal swabs to detect pathogens + get AB sensitivity PM: If it is necessary to confirm the diagnosis, this can be done by observing characteristic lung lesions at necropsy of a moribund calf iii) Treatment • Sick animals need prompt, vigorous and prolonged treatment -isolate the ones coughing etc into a different airspace. • Antibiotics - Amoxicillin, ceftiofur, florfenicol, marbofloxacin, tilmicosin, trimethoprim/sulphadiazine. - Are not the answer...just a stop gap • Corticosteroids or (better) NSAIDs e..g flunixin Therapy should be continued for 3 to 5 days depending on the drug used and the response to treatment, but a longer period of treatment will often be necessary. If a large percentage of the calves in a group is affected at one time, it is probable that many other 'healthy' animals are incubating the disease and it may be a good policy to treat all the cattle in the group. Affected animals should be removed from the in-contact group, and provided with adequate nursing Treatment is with antibiotics and NSAIDs. A successful prognosis is more likely to occur when aggressive treatment is instigated early in the course of the disease. -justification- can be fatal without.

Hypocalcaemia is a common metabolic disturbance of dairy cows. Write short notes on: a) Farm level risk factors for hypocalcaemia. (1½ marks) b) Cow level risk factors for hypocalcaemia . (1½ marks) c) Clinical signs of hypocalcaemia. (4 marks)

a) Farm level risk factors 1. Inadequate feed on farm e.g. Low Ca in diet - eg Maize silage 2. Reduced intake due to Poor weather, bulling cows, transport etc 4. Poor transition managemnet (feeding high calcium precalving, inadequate mg, high DCAD) 5. Feeding diets with nutritional interactions e.g. -If cows have been getting lots of zinc for a long time over summer you will occasionally see a cow go down with milk fever -Fathen b) Cow level risk factors 1. High producing cows (have higher calcium req's) 2. Older cows (will generally be high producers + calcium homeostasis not as effective) 3.Concurrent disease (will decrease feed intake) 4. Breed: Within dairy breeds the Jersey is the most susceptible; c) Clinical signs First stage: HypoCa - Clinical signs First stage • First stage of clinical signs: • Restlessness • Excitability • Anorexia • Tongue protruding *This stage is hardly ever seen by vets and is often missed by farmers as it progresses rapidly to......* Second stage: • All muscle tone diminished • Skeletal muscles - weak, ataxia, sternal recumbency, sigmoid curve of neck • Cardiac muscle - faint heart beat (reduced cardiac output) so increased heart rate. • Smooth muscle (gut) - decreased gut sounds, bloat, constipation, lose swallow reflex. • Smooth muscle (uterine) - uterine contractions do not occur if the cow is in the process of parturition, can lead to dystocia and/or retained foetal membranes. • Pupils will dilate (loss of smooth muscle function). • Lose ability to regulate body temperature, usually become hypothermic.** Stage 3 • Lateral recumbency • Bloat, may aspirate rumen contents. • Comatose • Death

a) List the possible causes of bovine abortion that you would be likely to encounter in New Zealand. (5 marks) 10 in total b) From your list choose ONE (1) infectious cause and ONE (1) non-infectious cause and write brief notes covering: i) Presentation / likely clinical findings / possible sequelae ii) Diagnosis iii) Treatment / Prevention / Control (if applicable)

a) Infectious causes 1.Neospora caninum -most common cause 2. Salmonella Brandenberg 3. Leptospirosis 4. BVD 5. Listeria 6. Oppurtunistic bacteraemia Non infectious 1. Macrocarpa 2. Nitrate toxicity 3. Abnormal uterine environment (e.g. twins in one horn) 4. Iatrogenic Corticosteroids -how we induce parturition orXylazine in later pregnancy b) Infectious: Neospora caninum Presentation/likely clinical findings/possible sequelae: -Likely several cows aborting- causes 'abortion storms' -Abortion mainly in 5th - 7th months gestation -Abortion is the only clinical sign observed in adult cows.(so systemically fine) - Within herds abortions may be sporadic, clustered or epidemic. -Cows of any age may abort (immunity is not lifelong- ab's wax and wane) Sequelae: Abortions in future due to vertical transmission -which may result in abortion or the birth of a congenitally infected calf which will maintain the infection within the herd. =poor herd reproductive performance Diagnosis: 1. Histopathology of fetal: brain, heart, skeletal muscle, liver, showing scattered foci of non -suppurative cellular infiltrates with occasional foci of necrosis 2. Maternal serology: just cause positive doesnt mean it was the cause. Provides evidence for infection but Infection ≠ cause of abortion, Compare aborting vs. non-aborting cows, Titre may not go very high and may drop rapidly (within a couple of months) Not all infected cows will abort - depends on the stage of gestation at which parasitaemia occurs (tachyzoites) Treatment/prevention/control 1. General hygiene and biosecurity (minimise contact between cattle and dogs) 2. Test and cull seropositive animals (if you can afford to do it..cant cull 80% of cows) -put big red ear tags on them and dont breed them with the good AI so you don end up keeping them cause the baby will likely be neospora positive Instead breed with a hereford so they are born with big white faces and you sell/bobby them -Reduces herd seoprevalence -Costs associated with whole herd testing -Issues with test sensitivity (do it at a time they have most likely see neospora recently) -May not be feasible to cull them all -At least identify infected cows and don't keep replacement heifers from them -Often find familial lines of infection 3. Minimise other stressors (e.g. BVD, mouldy feed) 4. Reproductive management (embryo transfer will prevent vertical transmision) Vaccination and chemotherapy had crosses through them. Macrocarpa Presentation / likely clinical findings / possible sequelae -Abortions occur in the last trimester of pregnancy. -The incidence of abortions depends on the number of cows that have access to the trees, the quantity of material ingested and the overall plane of nutrition of the animals. -Abortion normally occurs 2 to 3 days after ingestion of toxic plant -Weak uterine contractions and incomplete dilation of the cervix are typical signs of exposure to pine needles. -Fetal membranes are retained in the majority of cases Sequaela: -metritis is a common sequel. Diagnosis: -There is no diagnostic laboratory test to confirm abortion due to macrocarpa/pine needle ingestion. Therefore, diagnosis should be based on clinical signs and a relevant history. However, it is widely held that there is a characteristic smell to cows that have aborted due to macrocarpa/pine needles ingestion which is a helpful aid to diagnosis. Management Prevention consists of avoiding access of pregnant cattle to macrocarpa and pine needles. Losses can· continue for up to 2 weeks after preventing access to this toxic material.

QUESTION 2 a) Define the term "compact calving season" for a hill-country beef cow herd. Explain why it is an important production target. (5 marks) b) Explain how you would condense a prolonged calving period for a hill country beef farmer. (5 marks) think of bull and cow factors for this (5 for each) c) Describe how breeding beef heifers for the first time at 15 months of age can contribute to a compact calving pattern.

a) What defines a compact calving season? 1. Breeding season 42-63 days (2 or 3 cycles) 2. Calving - add 7 days for prolonged gestation cows and heifers Why strive for a compact season? • Fewer anoestrus cows at start of breeding • More uniform sized calves at weaning (more saleable) + heavier!* • More uniform replacement heifers at 15 mo • More efficient feed budgeting • Easier supervision of calving *• A compact spring calving period is the key to maximising reproductive performance* b) 1. • With compact calving it is essential to match calving dates with spring grass growth • Mid to late September some in October Compact Beef Calving Season Management of cows 1. Breed to suit the farming system 2. Adequate nutrition (energy, magnesium, Cu and Se) 3. BCS (at calving) 5 (2.5) or greater 4. Calving date to coincide with feed supply (Oct may be better than Sept) Bull Management 1. Ensure bulls are sound 2. Observe mating groups regularly (at least once a week) 3. Rotate bulls during mating 4. Consider topography of mating paddocks 5. Adequate bull:cow ratio (1:30 - 1:50 usual range) Gradually change 1. Restrict mating to 63 days and cull empty cows (especially if decreasing cow numbers) 2. Gradually restrict the mating period by 2 weeks each year for 3 years and cull empty cows 3. Delay start of mating such that calving coincides with spring flush of grass 4. Calving period is often determined by the first two calving seasons of replacements heifers c) Describe how breeding beef heifers for the first time at 15 months of age can contribute to a compact calving pattern **Calving period is often determined by the first two calving seasons of replacements heifers** So have the same strategy for your 15 months. only keep bulls in for 42 days. cull empties as there going to have lower reproductive perforamcne in the future ensure your feed management is good

QUESTION 4 a) Briefly outline the timeframe over which you will detect BVD antigen and antibodies to BVD in a newly infected animal. (2 marks) b) Use bullet points to discuss the different laboratory tests that are used to detect BVD antigen and antibody in individual animals. (6 marks) c) A dairy farm in your area has had poor reproductive performance for the past few years. Briefly discuss how you could assess whether BVD infection is part of the problem.

a) • An animal will be viral antigen positive from about days 3 to 10 post-infection • 2 - 3 weeks after initial infection should become antibody positive • No guarantee that natural immunity will be lifelong but continued exposure to field virus will boost immunity see low levels of antibodies at 14 days. So at 9 days to 14 days, its antibody negative and antigen negative. b) Virus/antigen tests 1. PCR (detects DNA) - sensitive 2. Ag ELISA -can be done as an ear notch test or test serum. • For PCR can pool samples and test 10-15 at once • PCR is incredibly sensitive and more likely to detect a TI • ELISA is less likely to detect a TI For ELISA you get maternal AB interference until older then 35 days. 3. Bulk milk testing - Ag (PCR) • Now for any size herd, may detect a TI • Your PI must be milking - and into the vat, PIs more likely to be sick and in the penicillin mob Antibody tests 1. AbELISA - serum • Only means animal has been infected (may have been in utero) • Main use is to test 15 rising 1 y.o. animals as if more than a couple are positive then probably been in contact with a PI (may have been in utero) 2. Bulk Milk Testing - AbELISA • Provides an average figure for the herd antibody levels and therefore an indication of how widespread infection is. High levels of antibody would be suspicious of exposure to a PI http://www.controlbvd.org.nz/sites/default/files/domain-23/Testing%20for%20BVDv%20Unravelling%20the%20options.pdf c) hx- weak calves, congenital abnormalities? abortions? Has it been this way awhile? have new stock come in? Testing- antigen and antibody testing on milk. Could test calves once >35 days old.

a) List SIX (6) advantages to having a mixed species beef-and-sheep system rather than a solely sheep farm. (3 marks) b) How are efficiency and productivity defined in a beef cow herd? (2 marks) c) Outline the key criteria limiting efficiency and productivity.

a) 1. Maximising profit per hectre so for money. 2. Not labour intensive 3. Pasture control 4. Welfare friendly 5. Animal health benefits because the internal parasite that infect cattle do not infect sheep 6. Diversify income 7. They are hardy b) Productivity= Number weaned x weight of CALVES / number cows mated Efficiency= productivity /cow liveweight at weaning Efficient conversion of pasture to calf? how do we measure this? • Ratio of calf weaning weight/cow live weight at weaning - Cow live weight a proxy for feed eaten

On a 650-cow spring calving farm you are talking to the farm manager and he is saying how he has fewer milk fever cases this year than last year. He says the only change he has made is to add a special springer mineral to the diet. He shows you the packet (see left column in the table below). The cows are being fed a diet of 2kg DM maize silage and 8 kg DM grass. a) What is DCAD, and why is knowing DCAD a useful aid in designing diets to prevent milk fever. (3 marks) b) Outline whether you think this mineral could be useful in preventing milk fever. Explain your reasoning. (1 mark) c) Is a marked difference in milk fever incidence in this year compared to last, when the only reported change is the use of this product, good evidence that this product is responsible for the difference? Explain your reasoning. The second column in the table provides the recommended intakes for the active ingredients in the product. Comment on whether this product is a useful additional supplement for: i. Chromium ii. Copper iii. Cobalt iv. Vitamin D (6 marks) e) What alternative supplement could you add to the diet of these cows to replace this supplement? (1 mark) f) Assuming the impact on milk fever of your alternative is equivalent which product will, have the best cost-benefit

a) DCAD is the Dieterary cation anion difference. Importance of PTH: Parathyroid hormone is a key hormone in the homeostasis of calcium levels. When blood calcium levels are low, PTH is released. It functions in multiple ways to increase blood calcium levels (increased bone resorption, increased renal resorption, activation of vitamin D) In mild metabolic acidosis PTH activity is increased. Manipulation of the diet to lower DCAD causes a mild metabolic acidosis. Therefore lower DCAD= increased PTH activity = hopefully less incidence of milk fever b) Yes because it had a negative DCAD value therefore will lower the DCAD therefore increase PTH activity. Additonally the supplement has magnesium in it. -Transport of Ca into extracellular fluid is achieved by a Ca-Mg-ATPase pump (but could hav emore mg in it) c) No. The incidence of milk fever is going to vary year by year. The nutrient value of grass and maize silage will vary each year. Additionally the number of 'at risk' cows is likely to vary each year (older, high producing cows, concurrent disease etc) However the ancedotal evidence is a good starting point for further research but correlation is not causation. Comment on whether this product is a useful additional supplement for: i. Chromium: No proven response to supplementation- so therefore from a scientific view, we have no justification to include it in the diet. ii. Copper: Has 50 mg more than recommended daily intake. Toxicity risk. iii. Cobalt: 10mg in it. .6 recommended. wasteful? iv. Vitamin D: low but cow can produce itself? so maybe not an issue? (6 marks) e) Add MgCl2 to water • MgCl2 and MgSO4 are acidotic and may be useful for lowering DCAD pre-calving f). Not given the cost of supplement. Assume mgcl2 would be more efficient as your not buying extra minerals that are not needed to lower dcad.

For a heifer that is expected to be 500 kg as a mature cow, what are the recommended liveweights at: a) 6 months. (1 mark) b) 15 months. (1 mark) c) 22 months. d) List the likely outcomes in the medium term (1 - 3 months) if your heifers are on average 80% of target bodyweight at 15 months e) List the likely outcomes until the end of the first lactation if your heifers are still, on averagec 80% of target bodyweight at 22 months. f) What body condition score should heifers be at calving (1 - 10 scale)?

a) 30% b) 60% (mating) c) 90% Target weights for your young stock should be relative to the weight that they will grow to as mature cows: 30% of mature liveweight at six months of age, and 40% at nine months; 60% of mature liveweight at 15 months (mating); 90% of mature liveweight at 22 months. -from dairy nz At 6 want them to be At 15 months they should be 300kg 22 months 450 d) Because there in good body weight hter emre likely to have early puberty and therefore more likely to get in calf. higher pregnancy rate and higher conception rate. eproduction Achieving the 15 month liveweight target will help minimise the incidence of non-cycling heifers at mating. e) They are 50kg underweight So they will be less bodyweight at calving Less likely to get in calf Will need to dry off earlier Heifer f) Calving= 5.5 Mating= 4.5 Mature cow Calving=5 Mating= 4 Average loss of BCS in early lactation should not be more than 1.0 BCS unit, because greater average losses indicate that too many cows have lost 1.5 or more BCS units. If calving BCS is right, not more than 15% of cows should be below BCS 4.0 at planned start of mating *checked from dairy nz

One of your dairy farm clients has signed up this season for bulk milk BVD testing (no herd level testing had previously been carried out). The results from the first sample show high levels of antibody and virus present in the milk sample. a) What do these results indicate about the BVD status of the farm? (1 mark) b) List the animal welfare and economic costs that might be occurring on the farm? (3 marks) c) If the farmer decides to control BVD on her farm outline the course of action you would pursue. (8 marks) d) List the recommendations you would make about on-farm biosecurity in the future to prevent reintroduction of BVD virus.

a) Antibodies in herd indicate the herd has been infected with BVD and the virus present indicates there are currently cow/s shedding bvd (infecting more cows) within the milking herd. Bulk milk antibody indicates level of past exposure in the herd, PCR tells you if there is a PI (or TI) currently milking into the vat. There is an active infection in the herd (PI or TI) and some cows are mounting an immune response (could have already had it). b) Young bunnies 1.Diarrhoea therefore weight loss in young stock - could die if left untreated, Growth check for about 4 weeks • Also immunosuppressed for several weeks around the time of infection • So more likely to get other disease and the disease is likely to be more severe than usual • In young stock will commonly see pneumonia and other gastrointestinal infections such as coccidiosis and yersiniosis Older animals -Reduced milk yield (economic loss) • Abortion, high MT rate (EED) -poor herd reproductive performance • Weak, dummy or stillborn calves -Congenital defects- cerebellar hypoplasia- ataxia, unable to rise Increased susceptibility to other disease --Pneumonia, mastitis Bulls • Infertility in bulls for weeks-months c) jenny If there are very high levels of antibody then it is quite likely that there has been a PI in contact with the herd quite recently. That PI might now be dead or gone. Do the bulk milk PCR to determine if there is a PI in the milking herd. The PI might be a bull! If the bulk milk PCR is positive then need to assess the lowest producing cows with individual blood tests to try and identify the PI. IF they have been testing for a few years and it has only just gone PCR positive then the PI would have to be a cow that is new to the milking herd - most likely a first calved 2 y.o. 1. Define 2. Assess 3. Action 4. monitor Action: -vaccinate -screen and remove PI's -monitor 1. Identify the PI's • If positive then you have to find the culprit - test the lowest producers first (bottom 10%) -If the bulk milk PCR is positive then need to assess the lowest producing cows with individual blood tests to try and identify the PI. -Request pooled serum BVD PCR tests on these animals. -If the BVD virus is detected in one or more animals, remove these PI cows from the milk supply. If no cows are identified as PI in the first screen, select the next 10% of low producers and repeat the process until a PI cow is found. 2. Arrange another BTM PCR test once the PI cows have been removed. Record all cows not contributing milk to the vat at the time the BTM sample was collected. (you need to have sampled these cows not contributing also as bvd cows are likely to be in the sick herd) - If the BVD virus is not detected in the BTM sample and in the individual samples from the cows not contributing milk to the vat, all the PIs have been identified. *Make sure you test cows not contributing to milk pen also- e.g. masitits separated cows as cows with bvd can be immunosuppressed and therefore are more likely to get masitis etc. • Then re-test the vat again by bulk milk antigen testing (PCR) (PCR test on BTM) 2. Test all bulls for BVD viral antigen, also keep them vaccinated Cull positives Do I need to test the calves? Calves In this method, either blood (serum) or an ear notch sample is taken and examined for the presence of the BVD virus. PCR and/or ELISA technologies are used for this purpose. The decision on which sample to take and which test to request will depend on the relative importance of convenience and cost. However, as colostral antibody can interfere with the ELISA test on blood and ear notches it is important to wait until calves are older than 35 days of age before sampling. Cull positives Annually monitor the farm (bulk milk tank antigen test- pcr) d) For this question think about the 5 ways BVD can get on to the farm and think which of our 3 controls are suitable 1. detect and cull 2. vaccinate 3. stop them coming in..? 3. Insist that all animals coming in for grazing are vaccinated Biosecurity 1. Should test bought in animals to make sure they are not PI + vaccinate them. 2. If practical, prevent contact between your cows and the neighbours. (avoid adjacent grazing etc) -Double-fencing, temporary hotwires and hedges are all likely to prevent direct contact with neighbours' stock. 3. All bulls should be tested + vaccinated -All bulls should be tested for the BVD virus before contact with the herd and ideally before arriving on the farm. It is recommended that the farmer request a veterinary certificate for each bull to show that it has been tested virus-free and is not persistently infected. 4. Minimise bringing in stock or if you do you must test before mixing with other stock -All calves to be kept from bought-in cows should be tested for the virus as soon as possible after birth, and definitely before leaving the calf sheds. (could be a trojan) Control by management If you do not buy cows, you will not be at risk from bought-in cows. One option to avoid having to test all their calves if cows are bought-in is to cull or euthanise the calves as quickly as possible after birth, and take care to not carry infection from any PI calves to other classes of stock before they depart. To minimise the risk of keeping a calf by mistake due to mis-mothering, bought-in cows should be calved as a separate mob. Vets/fomites/people coming onto farm BVD virus can survive for up to a week in the environment. As there is a risk of the BVD virus being transmitted via fluids and/or faeces, by use of shared equipment, shared yards/raceways and common grazing paddocks, management events should be separated by at least a week to ensure the virus is not spread via fomites. Anyone coming on to a farm could be a risk for introducing BVD if they are in contact with animals on other farms as well. Embryo transfer has additional risks that must be managed. Any equipment used with other animals should be considered a risk for at least a week unless it is well cleaned and disinfected. Vaccinating cows grazing off the farm in the first four months of pregnancy will protect foetuses so they don't become PI and threaten the herd after birth. Grazing weaner calves in isolation from the milking herd will minimise the risk they pose to the herd. Calves, heifers and cows that are going to graze away from the home farm can be protected with vaccinations before they leave. When developing a BVD-control programme on a farm, there may be a group of cattle whose risk of exposure cannot be minimised. If this is the case, it may be a good idea to vaccinate the group. This will often be the case when: heifers and/or carry-over cows go off farm to graze. These animals may co-mingle or be next to cattle with an unknown BVD status. Vaccinating this group before it leaves the farm and again 12 months later will protect it from any health effects from transient BVD infection. Vaccination before mating will also protect the group from impaired reproductive effects during mating and pregnancy and, most importantly from a disease-control perspective, minimise the chance of a PI calf being born on the milking platform cattle go to shows or are leased out for a period while pregnant introduced cattle that are naïve or of unknown BVD status go on to a known infected farm. This most commonly occurs with rising twoyear- old cattle returning home from grazing where the dairy farm is known to be infected. It also applies to bulls coming on to an infected property. Essentially, any cattle that go off the farm and become pregnant should be fully vaccinated while off farm if there is any chance they could become exposed to BVD during pregnancy. Screen all keeper calves for PI- annually screen dont let kids play in farm pond water

Jersey question 2014

a) Calculate the amount needed using the dairy nz book for walking, milk production, maintainence, pregnancy b) 11-12 mj/kg c) Unlikely- find more info. how much space is in one tummy? e) 1. Supplement with high energy food e.g grain 2. Have food with a higher % of DM- wilted grass, silage, PKE 3. herb crops f) farm tools (ability to feed out) -labour avaliable -cost of feed -milk price (if shit wwont buy in feed)

For each of the following scenarios list FIVE (5) possible (and relatively likely under New Zealand farming conditions) causes for "sudden" death. For each, list risk factors and post-mortem findings which may make you suspect a certain diagnosis. a) One dairy calf in its first week of life (being reared indoors) found dead, was apparently normal 16 hours ago. b) Three out of a group of 50 beef calves die over a period of two weeks following weaning, they are only checked every 3-4 days. c) Eight adult dairy cows suddenly dead out of a group of 350, all appeared normal 12 hours ago. d) One adult dairy cow, apparently normal 48 hours ago, was noticed to be recumbent 4 hours ago and now dead.

a) Calf and sudden 1. Atresia ani -dilated abdomen -wont have a hole for anus 2. Twisted gut 3. Hypothermia 4. Salmonella -Can be any age, more common in younger calves in teh first week or 2 of life. Can be peracute, acute Clinical presentation: enteritis, severe diarrhoea , fever then hypothermic. PM: inflamed abomasum, diarrhoea staining around perineum. 5. Clostridial disease- tetanus 6. PDA 7. navel ill Say i had had multiple calves 1. salmonella 2. E.coli: occurs in calves around 1-4 days old. 3. Coronavirus - calves aged 1-3 weeks*** 4. Rotavirus = calves less then 10 days old 5. Cryptosporidium: occurs from 4 days to 4 weeks b) 1. Black leg- clostridial disease -activation of latent cl chavoei spores in response to low oxygen conditions (muscle damage- then they begin multiplication and produce a toxin, leading to expansion of the lesion. -should have swollen limbs on PM and gangrenous myositis -will become rapidly bloated and autolytic -areas of dark red to black swollen muscle which contains foam and gas 2. Sudden death syndrome (clostridium sordellii) -sudden death of rapidly growing cattle (usually beef) -activation fo bacteria may be associated with a relatively acidic rumen pH: animals typically on good quality, highly digestible feed -toxinproduced causes intravascular haemolysis and a fatal septicaemia PM: anaemia signs, must culture for definitive diagnosis. 3. Bloat Primary(frothy) - extremely important -Grazing pastures with high legume content. Proteins stabilise gas bubbles produced by rumen fermentation producing a foam. Difficult to eructate. -Rumen pressure increases and pressure on thoracic organs impairs cardiopulmonary function. PM diagnosis is difficult. Rumen is clearly distended and there will be foamy rumen contents. Look for a bloat line. Congested cervical versus blached thoracic mucosa. Secondary (free gas) bloat- less common. -Due to physical or functional defects in the eructation of gas e.g. -foreign body (turnip stuck in oesophagus) 4. Parasites- ostertagia, haemonchus 5. Salmonella? 6. Copper toxicity? c) Lightning strike Copper toxicity -likely a group if its an overdose. have they been supplemented or fed palm kernel? Intravascular haemolysis- hypoxia etc. Bloat Choke (seoncdary bloat i thin..) Rumen acidosis d) 1. Metritis 2. Hypoca 3. Hypomag Ketosis 4. Fracture 5. Cast cow Epi: older cow, pregnant , overweight, rough ground. likely an individual acute tiem course presentation: down cow, bloated, frothy mouth Mechanism: cant eructate, results in bloat. rumen compresses diaphragm, cant breath, respiratory arrest Milk vein rupture

penny 2012 Productivity on a dairy farm is determined by stocking rate, calving and drying off dates, feeding levels and use of supplements. Your client's herd has an average BCS 3 (1-10 scale) and are producing 1 kg MS post-calving. Considering the factors above (using bullet points), a) Discuss what may have occurred in terms of feed demand and supply. (4 marks) b) Describe what are the implications of this in terms of animal and farm productivity. (4 marks) c) What steps would you take to: i) Estimate the current level of feeding. ii) Check it is sufficient. iii) Modify feed demand and/or supply if necessary

a) Demand was higher then supply. Negative energybalance. b) implcaitons on productivity: milking off there backs, will ger really skinny, low fertility etc etc. c) send samples to lab- ag research. calculate etc etc. plate meters. iii) dry some off. supplements. nitrogen fertiliser. sell/cull. either increase the amount of feed or decrease the amoutn of mouths. could do once a day milking - would decrease feed demand.

Your client has a 350-cow dairy farm with a planned start of calving of the 24th July and a planned start of mating (PSM) of 10th October and a mating period of 16 weeks. As a result of this, 20% of the herd will calve within 4 weeks of PSM. a) What implications does this have for future mating management? (5 marks) b) What management practices can be implemented to have a more compact calving spread? (5 marks) c) What is the financial impact of a long vs. compact calving spread?

a) Implications 1. Long calving spread 2. Lots of late calvers. late come into heat again >> cycle for next year. remember 6 week anoestrus period, will also likely be in poorer body condition score for next PSM. 3. Less calf selection for replacement calves 4. Fewer going to concieve or AI or have to do AI longer (this is expensive to do AI- typically only do it for 4 weeks) - therefore getting less genetic gain 5. Long tiem for farmer to check for heat. - gonna end up paying attention less cause frustrated. 6. Feed difficulty- we want our cows hitting peak lactation when pasture growth is starting to peak. Effects of a high proportion of late calving cows •High proportion of anoestrus cows at the start of mating -Few, if any, observations of oestrus activity -Low SR at 3 and 4 weeks -Low CR at 4 weeks -Low in-calf rate at 6 weeks •Calving pattern is not concentrated -late calving dates the following season -short lactation lengths b) 1. • observed for oestrus for 3‐4 weeks before the start of mating - if anoestrus, then get a vet check. (also if RFM, or aassisted calving etc) 2. CIDR/synchronisation programs 2. Metricheck. treat if they have endometritis and its 4+ weeks post calving 3. Cull late calvers (also use PD for culling) 4. Have good nutrition and BCS for cows - want a body condition score of 5 at calving! -might need to bring in supplements/use fertiliser etc. 5. Train in heat detection 6. Bull management and bull effect 7. Want calves and heifers meeting target weights. c) Compact calving= can feed budget more effectively, labour intensive period is for less time, genetic value of the newborns would be decreased.= long term effect on milk production. also have more empties for next tiem since 6 week rule = less milk and more cull cows. + more vet costs for anoestrus cow visits To maintain a tight calving spread, conception must occur within 12 weeks of calving •Time for uterus involution and at least one cycle before mating

QUESTION 10 a) What are the aims of good transition management of dairy cows in the pericalving period? (4 marks) b) What farm management practices need to be implemented as part of good transition management?

a) To decrease the incidence of calving- related diseases that commonly occur (, RFM, hypocalcaemia, displaced abomasum) Relatively recent developments in animal breeding have produced dairy cows that experience enormous losses of body nutrients in order to support their milk production. Production diseases of the modern dairy cow are associated with a level of production inconsistent with nutrient intake, provision of an unsuitable diet or an unsuitable environment. These diseases constitute a major proportion of the common health problems in cattle occurring on many dairy farms. While traditionally regarded as encompassing the significant metabolic disorders of dairy cows (hypocalcaemia, hypomagnesaemia and ketosis), the term production disease has been broadened to include conditions such as retained fetal membranes, displacement of the abomasum and laminitis. There are three major areas of metabolic disorders that are experienced by dairy cows: disorders of energy and protein nutrition; disorders of calcium, magnesium and phosphorous nutrition; trace element/micronutrient disorders. The first two are primarily diseases of late pregnancy and early lactation, although disorders of energy metabolism can occur at any stage of lactation as secondary complications of alimentary disease. Likewise, disorders of calcium (Ca), magnesium (Mg) and phosphorus (P) can occur at any time that dietary intakes are inadequate or intake is compromised by confounding dietary factors. Nonetheless, these situations are of relatively limited importance in comparison to the occurrence of such disorders during the peri-calving period. Consequently, before considering the specific nutritional disorders in detail, an overview of the management of the transition period will be given. The transition period extends from 3 weeks before calving to 3 to 5 weeks after calving; representing the period of time during which the cow completes her transition from being a dry, pregnant animal to a lactating cow. Most metabolic disorders (e.g. milk fever, ketosis, displaced abomasum) primarily impact on cows during the periparturient period, as do disorders of reproduction (retained fetal membranes [RFM], metritis) , lameness and many other infectious diseases. The transmon period represents a period of massive change for the dairy cow. During it, she must alter her nutrient partitioning from tissue deposition (body condition score [BCS] gain) to tissue mobilisation (BCS loss). Nutrient demand increases hugely in response to the requirements for the final stages of fetal growth and the onset oflactation, yet cows undergo a significant decline in dry matter intake (DMI) at the same time as this increased demand is occurring. Moreover, although cows increase their DMI in response to the demands of lactation, the response is delayed so they spend a significant period of time in a negative energy- balance. The depth and duration of negative energy balance are generally (although not universally, see Grummer et al, 2004) considered to be important determinants of many aspects of production, reproduction and disease during early lactation. Thus, where negative energy balance is excessive, conditions such as fat cow syndrome or ketosis can result; other direct complications of negative energy balance at this time can include RFM and displaced abomasum, whilst subfertility and increased predisposition to infectious disease are also sequelae of unresolved negative energy balance. Summary: the transition from late pregnancy to aerly lactation is a critical period because it is when cahnges in the metabolic status have long term effects upon the health fertility and productivity of dairy cows. these include changes in glucose metabolism, mobilisation of lipid stores and uptake and reabsorption of calcium The ultimate goals of management udring the transition period can be summed up as -minimise the extent of body fat mobilisation around calving -maximise the appetite of the cow jus tbefore and at calving -promote high feed intake after calving -maintain serum ca at and after calving -maintain immune function b) 1. Ensure adequate blood magnesium levels (transport of Ca into extracellular fluid is achieved by a Ca-Mg-ATPase pump). 2. Do not feed diets that are high in Ca precalving. 3. Reduce the DCAD over the last few weeks of the dry period if possible. -Lots of people put MgCl2 in the water. 4. Feeding a diet containing adequate amounts of fibre of adequate length is one of the most important ways recommended to decrease the incidence of displaced abomasum. "Correct transition cow management, including introduction of post-calving feeds, achieving adequate precalving intakes, paying attention to the dietary cation-anion difference (DCAD) and magnesium status and stimulating the return of appetite after the day of calving." In late pregnancy the cow has to meet both her own requirement/ for maintenance and the nutrient costs of her rapidly growing fetus and udder. It is commonly recommended in Australian systems that the transition cow diet should contain some concentratesV (commonly around 3 kg/cow/day) to increase the metabolisable energy content in the ration. This will help meet the increasing requirements of the cow and her developing fetus. It also provides the rumen with an opportunity to adapt to the type of feed that the animal is likely to receive after calving, since inclusion of a higher proportion of non-fibre carbohydrates (NFC) should promote rumen microbial adaptation to NFC levels typical of diets fed during lactation. It should also provide increased amounts of propionate to support hepatic gluconeogenesis. Since post caling diets are likely to contain higher quanatities of nfc, nfc should be introduced in teh dry period to allow the rumen microflora to adapt to the diet bfore calving. benefits include higher post scalving dmi and reduced risk of rumen acidosis. The management of the transition diet to reduce the incidence of milk fever is discussed in detail under Hypocalcaemia, p. 520. Because high-quality pasture is commonly relatively high in potassium (K) and sodium (Na), it is usually recommended that the intake of such pasture should be limited and cereal hay (preferably obtained from paddocks where no K fertiliser or effiuent has been used) be available to transition cows at all times. Maize silage can also be used in this situation Cows should be provided with at least 8 to 10 kg DM feed providing 10 mj/kg dm during the last month of gestation to allow growth of the fetus without depletion of body stores. However should not overfeed (want them at condition score 5 when tehy calve) Hypomagnesaemia also affects Ca metabolism by reducing PTH secretion in response to hypocalcaemia and by reducing tissue sensitivity to PTH. The Mg content of the close-up, dry cow ration and early lactation ration should be between 0.35 and 0.4% OM. Likewise, P content of the prepartum diet is a significant predictor of milk fever, as increasing P cdncentration increases the risk of hypocalcaemia. Ideally, the ration should supply between 35 and 50 g P daily, so' the diet must contain about 0.4% dietary P. Cows are relatively immunosupressed immediately before and during and after calving therefore more susceptible to dz. There is also evidence to suggest that this periparturient relaxation of resistance to disease might be accentuated by inadequate trace element nutrition. It is therefore important to aim for optimum levels of the minerals that are involved in modulating immune function, especially selenium (Se), copper (Cu) and zinc (Zn). From dairy nz - Feed springing cows 80-90% of their requirements for metabolisable energy if BCS 5 or greater (Table 1) - If less than BCS 5, feed springing cows 100% of their metabolisable energy requirements (Table 1) - Do not over-feed springing cows! • Supplement springing cows with 20 g magnesium/cow/day Mature cows that are thinner than BCS 4.5 or fatter than BCS 5 at calving are at an increased risk of metabolic and infectious diseases after calving, like mastitis and metritis. Therefore, not only is the average BCS of the herd important, the range is equally important. The herd must be managed from March onwards to identify thinner and fatter cows for preferential treatment. Restricting food intake: Restricting a cow's metabolisable energy intake to 80-90% of their requirements in the weeks before calving increases blood calcium on the day of calving and the day after calving, reducing the risk of milk fever. The mechanism by which this works is, as yet, unknown, but the effect is consistent across pasture-based and TMR-based diets. Calcium supplementation: Supplementing cows with calcium (e.g., ground limestone) during the colostrum period increases blood calcium and reduces the risk of milk fever6 . The majority of milk fever occurs in the 24-48 hours after calving. If cows can be supplemented with calcium during this period, the risk of classical milk fever decreases.

A hill country sheep and beef cattle farmer with a 400 cow Angus herd, that have first calves at 3 years of age, seeks advice on the following: a) What are the management keys to a successful outcome of calving heifers for the first time at 2 years of age? (5 marks) b) What are the important characteristics in the angus bull chosen to mate heifers to calve for the first time at 2 years of age? (5 marks) c) How can calving heifers for the first time at 2 years of age be used as a means of achieving a compact calving in the adult (mixed age cows) herd? (5 marks)

a) fill in as revision from above b) focus on calving ease c)

a) Using bullet points compare and contrast the TWO (2) milk production curves shown in the graph above. Assume there has been no change in herd size. (5 marks) b) List the factors that may have contributed to the shape of the production curve from mid-October to late December 2011. (3 marks) c) List the additional information you would require (both available data and on farm observations) to confirm which of the factors in part b) were most important. (3 marks) d) For ONE (1) of the factors you have identified in part b), briefly describe what advice you would give to prevent this happening in the future. (4 marks)

a) red= earlier peak lactation. higher peak lactation. blue= peaklactation occurs later and the peak is less high Peak production is later in the year. Could have been a drought - not enough food Could have been later calving (later peak lactation) Different weather conditions Could have increased supplemetnation for the herd. MOre older cows= therefore higher producers Could have changed AI bulls to select for sooner calving Could have used CIDRs -done good anoestrus checks Better BCS c) Fertility records Supplementation/feeding . post/pre grazing levels AI dates/start of mating BCS at mating - were they milking of there back? d) Body condition score goals for calving and for mating Using in calf to increase herd fertility Feed- demand vs supply Use CIDRs, identify anoestrus cows

A somewhat agitated farmer phones you at 4pm one afternoon in March, after a few days of unusually warm wet weather, to say his cows are kicking cups off and some are passing blood-stained urine. His farm is at relatively high altitude and he has taken no precautions against facial eczema. a) Explain to the farmer what you think his cows have got and why you think his cows are showing the clinical signs that they are. (4 marks) b) How would you treat the affected cows? (3 marks) c) How would you monitor the situation and what preventative measures would you put in place for the rest of the herd? (4 marks) d) What are the likely sequelae for the worst affected cows and how could you monitor their recovery?

a)•Caused by sporidesmin, a fungal mycotoxin • The fungus is Pithoymyces chartarum • The fungus is a saprophyte (grows in dead litter at the base of the grass) • The fungus requires warm, moist, humid conditions to grow • Animals ingest spores when grazing • Sporidesmin causes liver and bile duct damage •The damaged bile ducts prevent the excretion of waste products from chlorophyll metabolism - phylloerythrin •These build up in the blood stream and react with sunlight in non-pigmented skin and muco-cutaneous junctions causing the signs of photosensitisation • Marked inflammation of white areas (distinctly thickened, may be exuding serum) and exposed un-pigmented skin (teats) -LOOK AT THE EYES ALSO. WILL BE SWOLLEN Will be kicking off cups as teats will have photosensitization- will be irriated and sore and the cups will be further irritating them. Photosensitisation tends to occur about 2 weeks after exposure to spores or sporidesmin. Facial eczema is characterised by irritation, reddening (Disc Figure 7.3.4) and oedema (Disc Figure 7.3.5) of exposed hairless or non-pigmented skin. The animals are restless, will seek shade and may lick or rub affected areas as photosensitisation develops Blood stained urine: •The toxin concentrates in the bile ducts and urine •Causes the release of free radicals • These damage the lining of the bile ducts and bladder lining (causing cystitis) Haemoglobinuria (Disc Figure 7.3.9) and jaundice (Figure 7.3.10), associated with an acute haemolytic crisis, may also be observed in cattle during the facial eczema season in New Zealand and Australia. There seems to be little doubt that such cases are related to sporidesmin toxicity, but the mechanism is unknow b) Treatment 1. Pain relief -NSAIDS + Antimine 2. Remove from affected pasture -Although insult may have been 2 weeks ago 3. Shade- dry her off and keep her in shade. (paddocks with trees) -Use cow coats if no shade (dont worry about cow getting too hot- she needs shade!!) 4. Antibacterial sunscreens -Systemic antibiotics may be required as well 5. Manderson's mix (drench animal with it) -Mix of olive, castor, cod-liver and linseed oils -he doesnt know how it works, has something to do with free radicals. buy from RD1. does seem to help 6. Euthanasia -they cant go to the wroks with open wounds. so will be months and months before they can go...never cruel to shoot a cow 7. Dry off severely affected cattle c) •We over-rely on zinc products •Often ignore pasture based treatments •Often ignore alternative strategies 1. Can use spore counting to assess risk at farm level •Choose same 4 paddocks and sample repeatedly through season to give average farm score Risk assessed as: < 30,000 slight, 30 - 60,000 moderate, > 60,000 high 2. Use alternative grass species, chicory, tall fescue 3. There are FE tolerant breeds of sheep, nothing similar tried in cattle as far as I know 4. Grazing strategies to reduce grazing too low (keep residuals higher) 5. Zinc has two effects •It prevents the production of free radicals •It blocks the uptake of copper, the enzyme catalyst Available zinc products •Zn oxide (drenching) - reliable - every animal gets its dose. May also be fed on supplement or pasture dusted (less reliable) •Zn sulphate (water supplies) - less reliable (self help) - greater risk of toxicity. Need an exclusive water supply! In-line or in-trough dispensers •Zn oxide in feed can also lead to toxicity issues but when done well could be the best method •Slow release intra-ruminal bolus eg 'Time Capsule' - reliable but expensive. Lasts 4 weeks. Popular for dry stock *care with toxicity for zinc 6. Pasture treatments •Thiabendazole 150g/Ha d) Many animals affected by facial eczema do not show outward signs. However, there will be some degree ofliver damage in these subclinical cases and overall well-being and milk production will be affected. It has been estimated that for every clinically affected cow in a given herd there will be 4 or 5 animals that are affected subclinically (i.e. only about 20% of affected animals show clinical signs of the disease). These animals may survive multiple episodes of subclinical facial eczema before eventually succumbing to the stress of calving and early lactation. If they survive long enough their productive life is likely to be cut short as farmers usually cull on individual production figures. Other animals are culled as a result of the neoplastic cutaneous 'horns' that develop in white skin that has been damaged by photosensitisation There appears to be a significant negative association between GGT concentrations after a facial eczema challenge and cow survival. It has been found that survival of animals to the end of the second lactation in exposed herds is about 10% lower in heifers with serum GGT >200 IU/L than in those with lower GGT values. In general, young stock tend to recover better than older animals. b)

Bovine Viral Diarrhoea (BVD) is a commonly encountered disease in New Zealand cattle. Write short notes on: a) Methods for BVD antigen testing of individual cattle and what a positive result means. (4 marks) b) Methods for BVD antibody testing of individual cattle and what a positive result means. (4 marks) c) Methods for assessing level of BVD infection in a herd of dairy cattle. (4 marks) d) Methods for assessing level of BVD infection in a herd of beef cattle.

d) Beef cattle: The purpose of this step is to determine if the herd is currently infected with BVD. This information has a bearing on the type of control plan that is devised for your farm. To define the BVD status of a beef herd: 1. Get your vet to collect 15 random blood samples from each category of breeding stock run separately on the farm. Just sample the cows, not their calves. 2. Your vet will request that a pooled BVD antibody test is performed on each group of 15 samples. 3. Groups of calves less than 10 months of age that have been reared separately need to be sampled for the virus. Your vet will advise you on this. The level of antibody in the blood sample is proportional to the level of BVD exposure in the herd. the more antibodies present in the pooled sample, indicating a higher prevalence of infected or previously infected cows in the herd. This test can only be applied to cattle older than 10 months of age once maternal immunity has waned.

Currently halofuginone is the only licensed treatment for Cryptosporidia in cattle, but it is not very effective and its safety margin is low. One of your clients, Bilbo Baggins, comes to you with a magic new treatment, hobbit oil, for Cryptosporidia; he wants some advice on how to show the world how good his product is. b) Summarise, using bullet points, how you would test how effective hobbit oil is as a treatment for Cryptosporidia in calves. Ensure you cover all the key areas of trial design.

1. Confirm its a case (take a faecal sample- test) 2. Randomise groups 3. Treat (ideally double blind study) - one group new treatment. one old treatment. 4. Define teh standard of improvement - monitor think of 7 steps of epi

As part of a full clinical examination there are often one or two essential history questions that are highly correlated with a diagnosis. For the following conditions please give the one or two questions that are essential for supporting your diagnosis: f) Coccidiosis in calves.

1. How old are the calves? coccidiosis usually occurs in calves older then 3 weeks. 2.

2013 Sem 1 1. a) Draw a simple diagram representing the component factors of a dairy farm which have to function well for a farm to be profitable. (4 marks) b) On your diagram annotate those areas where a veterinarian can exert significant influence on the health and productivity of the animals on that farm. (4 marks) c) Identify which single area of veterinary involvement is likely to have the most significant impact on the dairy farm. Use bullet points explain why this is the case. (4 marks) d) List the important points of the farms history and the clinical examination of the herd you would require to identify the main factors limiting performance in the area you have chosen.

a) b)the farm -knowledge- , profit, skill, values (if educate about welfare), cows, environment c) I think knowledge. then explain that you can increase the amount of good decisions etc etc. zoe thought health d) History -any diseases. prevention measures put in place? -any outbreaks -scanning %'s -Submission rate Clinical -bcs of animal

A standing right-sided flank laparotomy is a generic approach for a large number of bovine abdominal surgeries a) Describe in detail, including drawings, how you would perform a standing right sided laparotomy in a cow. Include in your answer an assessment of the handling facilities required, your approach to analgesia and minimum standards of patient aftercare. (10 marks) b) Describe, using bullet points, one surgery of your choice that could be carried out as an extension to this generic right sided approach. Be careful to highlight any necessary alterations in incision site or technique where applicable.

a) For handing, a crush is required. Use a head halter and tie the head toward the right side (so if it collapses it will fall on the other side) Most commonly local anaesthetic is used and it is a standing procedure. Perform a Perineural technique: paravertebral block- count forward from back. Paravertebral block: In cattle, T13, L1 and L2and L3 supply sensory and motor innervation to the skin, fascia, muscles and peritoneum of the flank. Regional analgesia of thesse nerves= paravertebral block. Dont block L3. Walk the needle off the caudal edge of the transverse process. By doing this you can deposit local close to the intervertebral foramen where the nerve is most localized. When the transverse process has been located, a line is drawn from its cranial edge to the dorsal midline. The site for injection is 3cm from the midline. A vertical incision is made 1/2way between last rib and tuber coxae in cattle. Modified cut external abdominal oblique. Grid cut the internal abdominal oblique and transverse abdominal muscle. Grid cuts get better healing and bleed less. To "grid" means to split the muscle layers manually along their fibres. When suturing the muscle : Take wide bites and should be full thickeness. b) An nsaid (e.g. flunixin) is administered preoperative. a right lap is performed in teh standing cow under paravertebral analgesia without sedation. The surgeons left arm is directed toward the cows tail head over the dorsal sac of the rumen, then around behind the omentum into the left sublumbar fossa. the abomasum is football sized and lies high up on the left side under the costal arch, buoyed by its gas content. the abomasum is punctured and delfated using a 14 gauage needle connected to a suction pump. release of gas causes the abomasum to sink toward the ventral midline. Near the midline teh greater omentum is grasped with the left hand and pulled up the ventral margin of the incision. an omentopexy is performed. A continous suture taking bites of omentum is used to close the peritoneum and transversus msucle layer, picking up a deep bite of omentum with each needle pass. https://books.google.co.nz/books?id=0r4r5qR0NVAC&pg=PA78&lpg=PA78&dq=right-sided+flank+laparotomy+cattle&source=bl&ots=XhQouuYp8U&sig=CyTo5bg6p9qwDkwvOv9qIOL7NQw&hl=en&sa=X&ved=0CE0Q6AEwCWoVChMIoZiKzMiCyAIVAaqUCh11DQcR#v=onepage&q=right-sided%20flank%20laparotomy%20cattle&f=false

A farmer with a 400 cow Angus self-replacing herd that calves heifers first at three years of age and sells all male calves at weaning seeks advice on the following: a) What are the important criteria to be used when buying bulls for use this herd? (5 marks) b) What would be the main criteria the farmer should consider if he chooses to finish the male cattle on some flat land on the farm? - didnt know how to answer this, would it be growth performance, FCE? (5 marks) c) What are managements keys to successfully change to calve heifer first at 2 years of age in this herd?

a) Important criteria to be used when buying bulls for use this herd We want to select bulls on EBV. If you just look at the cow, you don't know what proportion is environment or genetics. -EBV's are used to separate genetics from environment - we want to know the genetic potential of a bull 1. Calving Ease Traits • Gestation length EBV days - a prediction of days from conception to birth • Calving Ease (DIR) EBV % DIR= direct. - a prediction of calving ease from 2 year heifers • Calving Ease (DTRS) EBV % - a prediction of ease of calving of 2 year daughters -maternal contribution to calving ease . so this the BULLS daughters • Birth Weight EBV Kg - a prediction of birth weight of a bulls calves 2. Growth Traits • 200 -Day Growth EBV (kg) - a prediction of calves to growth to weaning • 400 - Day weight EBV (kg) - a prediction of growth from weaning to yearling weight -if you want early slaughter you want 400 day weight. • 600 - Day weight EBV (kg) - a prediction of growth from yearling to mature weight All fairly highly correlated anyway** Remember we want short gestations, low dystocia, high growth 3. Maternal Traits • 200- Day milk EBV kg - prediction of a bull's daughters milking and mothering ability Extra weight at 200 days due to this effect -dont actually milk them to find this out • Mature Cow Weight EBV kg - a prediction of cow weight at 5 years of age (roughly when a cow reaches mature size- generally the emphasis is to reduce mature cow weight so there more efficiecnt) 4. • Scrotal circumference EBV (cm) - an estimate of age at puberty in daughters - larger scrotal size bulls more semen production • Days to calving EBV (days) - a estimate of the time taken to conceive after joining - measured in number of days from start of joining to subsequent calving 5. Carcass Traits • Carcass weight EBV kg - a prediction of carcass weight (untrimmed hot carcass) • Ultrasound eye muscle area (cm2) - a prediction eye muscle area at 12/13 rib site • Intra-muscular Fat (Marbling) % - a prediction of intra-muscular fat % at 12/13 rib 6. Cost of the bull -need to get an economic return from its superior genetics. 7. Also should have a reproductive exam done on it, ensure not lame etc. 8. Does he need to stick with angus for selling to a certain market? otherwise could take advantage of hybrid vigour.. + combining best traits of breeds c) How to calve heifers first at 2 years of age Firstly need really good management of heifers from weaning to get them to adequate liveweights -need to get them to puberty. it happens at about 50-60% of mature weight. -so if we have a 500kg mature lw cow. we need her to reach 300kg for mating. • Post weaning to the end of winter - moderate LWG (0.2 kg/day) feed 6-7 cm pasture around 1500-1800 kg DM/ha • End winter to mating - High LWG (0.7-1.0 kg/day) feed 10-12 cm pasture or 2000-2500kg DM/ha • Keep LWG high over the joining period and into the summer and autumn To successfully mate heifers at 15 months 1. Set a growth pathway from weaning to a minimum joining liveweight at 14 month -300 kg for Angus, Hereford etc., 320 kg for later maturing breed types (or 60-70% of mature liveweight) •Use a small breed type (eg ----) and select a bull with an EBV for birthweight below the breed average -hereford would be alright, angus also alright. MUST look at EBV •join for 42 days at the same time as cows -(negates long post-partum oestrus of early calving heifers and cows) •overmate (join more heifers than needed as replacements) then cull after pregnancy testing •cull late 2nd cycle heifers and ensure 75% calve in first 21 days of calving •Appropriate nutrition levels from 6 -30 months of age •Having realistic expectations Heifer breeding and shortening the calving period •All heifers that enter the herd should calve over no more that 42 days •this ensures the main herd will have a calving duration of 52-63 days •Use restricted heifer joining periods as method of tightening the calving duration in main herd •Calving pattern (number in first 21 days is crucial to this) Aim for: •85% pregnant after 42 day joining period •60-75% calve in first 21 days •90% calf survival •90% pregnant as rising 3 year olds *also make sure your mating date is good cause you want babies to be born so you can have lots of feed*??

a) What are the likely reasons for treatment failure in cases of clinical mastitis? (5 marks) b) What are your options for hopeless mastitis cases? (2 marks) c) A client contacts you in late September wishing to treat 30 high cell count cows out of his spring-calving herd of 300. Due to contractual obligations, culling is not an option at least until December. His bulk milk cell count (including those cows) is hovering around 280,000. What would you advise?

c) MRS T. 1. Mark the infected 30 cows. (spray paint etc). 2. Record the affected cows. 3. Separate the affected cows into there own paddock/group. 4. Treat with antibiotics- e.g. amoxicillin. -Could do culture and sensitivity but usually a waste of money . Milk them after the rest of the herd has gone through- then clean everything thoroughly.

Clinical Examination of the cow. (i) Having established that a cow has recently calved, what further follow-up questions should you ask when taking a history for a "sick cow"? (3 marks) (ii) With the help of a diagram describe how to perform the Williams' test for traumatic reticulo-peritonitis (TRP) in a cow. (3 marks) (iii) What additional tests could be used to assist in the diagnosis of TRP?

i) Supplementation levels? Feeding levels? Other cows affected? How old is the cow? What breed is it? Difficult calving? - did anyone pull etc

a) List, in descending order of importance, the main differentials that you could consider in an ADULT dairy cow for: (i) haematuria (ii) haemoglobinuria. (6 marks) b) How would you differentiate between haemoglobinuria and haematuria in the field.

i) Haematuria 1. Pyelonephritis 2. Cystitis 3. Enzootic haematuria (Bracken-fern poisoning) 4. Urolithiasis 5. Malignant Catarrhal Fever 6. Severe/acute septicaemia 7. Sporidesmin toxicity (but Hb-uria is more common) 8. Renal infarction Haemoglobinuria 1. Acute leptospirosis(only calves apparently) "Conditions resulting in haemoglobinuria Leptospirosis (due to Leptospira interrogans serovar Pomona; only in calves)."- from cattle book 2. Postparturient haemoglobinuria -will be within a very short period of calving 3. Nutritional haemoglobinuria - SMCO/brassica toxicity *revise path of this - Allium spp (onion) toxicity 4. Copper toxicity (rare in cattle, more common in sheep) 5. Bacillary haemoglobinuria (Cl. haemolyticum) 6. Blood parasites (anaplasmosis, babesiosis) Haemoglobinuria signs • Pyrexia, if infectious • Pale mucous membranes, low (very!) PCV • Exercise intolerant... may collapse • "Anaemic murmur" b) Haematuria= right. blood cells settled out Haemoglobinuria= left. colour of red wine. never clears Haemoglobinuria • Deep red to brown colour of the urine. • No erythrocytes in urine sediment. • Usually associated with visible discoloration of plasma. Haematuria • Clots may or may not be present in the urine. • Erythrocytes in the sediment. From cattle book

Owing to a slight mix up with times, when you arrive at the knacker's yard to post mortem a cow with a wasting condition only the abdominal viscera remain for you to examine. Using bullet points list the conditions you could rule in/out and the signs/tests you would look for/apply.

knacker=slaughter house. yohnes= thickened intestines + enlarged lymph nodes. TB= enlarged lymph nodes and liver lesions. parasites= morrocan leather appearance. facial eczema= look for liver lesions. lymphoma= lumps and enlarged lymph nodes. hardware disease- could check reticulum for a hole. rumen acidosis. test liver for deficiencies?

List the criteria you would use to determine that a lame cow needed a claw amputation.

werent savable by antibiotics or by trimming Claw amputation. When is this indicated? 1. septic arthritis of the distal interphalangeal joint 2. severe trauma to the claw 3. septic tenosynovitis of the deep digital flexor 4. Osteomyelitis of the distal sesamoid 5. osteomyelitis of the pedal bone 6. sepsis of the coronary band Claw amputation should not be performed in herds where the cows have to walk over a slatted or grated area to be milked. Careful consideration regarding this procedure is also required in the following siruations: • large-framed, heavy animals; • hind claws in breeding bulls (because of problems with mounting); • medial claws in both hind- and forelimbs (often there is difficulty in adjusting the proper placement of the remaining digit). Amputation provides immediate relief and a good prognosis for performing for quite a few years in a commercial herd. (1 -2 years) im from cattle book

another diagram

• prior to calving on rising plane of feeding (6kg/day) (need to check ME content these are Average ie. 10.5 MJME)) • large increase at calving (up to 8-9 kg/day) • increase 30 days after calving up to 12kg/day (can eat up to 16-18 kg/day) • fall after weaning to maintenance level • can keep at maintenance until 6-8 weeks before calving