PVMPH

how bad is lamb mortality?

Apparently 10-25% by day 3. dystocia, stillbirth, hypothermia/starvation, infection, and non-infectious disease are almost evenly split (except hypothermia is 25%). However these figures are from 1982. There is an acceptable level of preventable losses that is too high.

In January you visit a farm with 150 Red deer hinds used to breed young deer for venison production. The owner is concerned because a few of the hinds have lost a considerable amount of weight over the past month. The hinds are outdoors grazing on average quality pasture plus silage. They have not received any animal remedies recently and are 2-3 months pregnant. On distance examination they are all bright and alert but you note that 5 hinds are in considerably poorer body condition than the others. Which hinds would you select for full physical examination?

As this problem appears to be restricted to a sub-group of hinds you should direct your efforts at examining them. However you should also assess the BCS of the rest of the herd for comparison (in deer, BCS is assessed by observation in the same way that BCS of cows is assessed and it is a quick process).

what food chain information is required for the EU?

information must be provided at slaughterhouse for poultry, pigs, calves, and horses - origin of holding - withdrawal periods - no evidence of disease - no samples have been taken that would indicate pre-harvest risk

What is the appropriate navel dressing for a lamb?

iodine within 30 minutes (dipped) and some of them repeat 4 hours later. Esp. with staphylococcus dysgalactia. Part of clinical inspection - look for evidence of scours, colostrum, etc.

who is responsible for safe foodstuffs for animals?

it depends on where it comes from and if the feed is purchased or sourced by the farmers. food/water can be contaminated or have dioxin, Pb, mycotoxins, and salmonella. these can poison people. water can have pesticides, fungicides, pathogens, and environmental pathogens. bad quality silage can harbor listeria. a faulty machine leaked oil into pig feedstuff. it was distributed containing dioxins and fed to pigs. all pork was recalled in 23 countries. people got pissed AF.

should you use "target ranges" and biochems to assess TE deficiency or treatment? why or why not?

it doesn't matter if there are no clinical signs. the important thing is a return to good performance/improvement. marginal status can be subclinical - may or may not have reduction in performance at this level. vets sometimes give boluses for no reason.

what is the EU withdrawal bill? how will brexit affect food safety, the vet industry?

it means the whole EU legislation will not apply anymore post-brexit. all existing EU legislation will be copied into UK law, and then it will be changed over time. there is going to be increased responsibility by the APHA to maintain trade with EU. there is going to be a decrease in farm vets/abbatoir vets.

Which parasites are around during the year?

it varies based on the farm, but generally follows a pattern: june/july = ostertagia, haemongus Fall: tricotsrongylus, acute fluke winter: chronic fluke

what are the difficulties in food safety with the modern "food chain"

it's fragmented. the vet is responsible for part of the chain but there are a lot of different steps and opportunities for contamination.

why do we plug up dry cows with orboseal?

keep external environment away from teat

which types of farms depend most on subsidies? why are there still subsidies?

keeps them going - keeps food local and prevents food insecurity. grazing livestock, dairy, and cereals have the most subsidies from the gov't. pigs, poultry, horticulture have the least. in total it's 61% subsidised.

which breeds of dog are predisposed to obesity?

labs, goldens, shetland sheepdogs, cockers, chihuahuas, bassets, pugs, daschunds, mini schauzers

Investigation plan for high lamb mortality?

look at live lambs, dead lambs, dams, and environment.

normal mammary gland histology

look back u were poopin

Environment exam of sudden death

look for something that might poison or kill them - plants, etc Distance exam: not very useful, because the ones that would die are already dead. But maybe it could lead u in another direction if any clearly sick affected or if there seems to be more of a systemic issue. If all look normal - use time effectively

fasting state: onmivore. what is this regulated by? what are the organs doing?

low blood sugar - glucagon from pancreas: cAMP - PKA phosphorylates enzymes LIVER: glycogen broken down into glucose to fuel the body. also gluconeogenesis from glycerol (adipocytes, de-esterified triglyceride), amino acids from muscle cells. ammonia is excreted via urea cycle - more efficient in carnivores. ketogenic AAs go into CAC. ADIPOCYTES: release LCFA (or NEFAs or FFAs) into blood to use as energy. can go into CAC in muscle or liver or other tissues. ammonia from protein goes into urea cycle.

what is hyposphosphorus?

"happy downer". give calcium first and then if that doesn't work, give phosphorus. they are co-regulated via PTH. if there is too much calcium, phosphorus absorption will be downregulated. might be times when there is a lot of calcium in the feed - Ca absorption will be downregulated and then P absorption will be as well. treat: foston IV. respond well.

What are the major players/parasites of horses?

"large stronglyles" : strongulus (LI) "small strongyles:" cyathostomins (LI) Ascarids (parascaris) - SI

what does a CMT measure?

- Electrical conductivity: ion concentration of milk changes during mastitis

what are the 3 main policy/legislation bodies of the EU?

- European Commission: drafts law - european council + european parliament: confirm/veto laws, amend laws - european court of justice: intervenes with non-law abiding countries

Which parasites are adults not immune to on farms?

- Goats - Immunocompromised - Ewes shortly after/beofre lambing (PPR) - many farms give a dose of dewormers at lambing. Unsure if it's useful - Horses: cyathostomins - Liver fluke

What Toxicities cause sudden death?

- Plants: yew, oleander - Can be a result of neighbours feeding your animals, old house site, storms diagnosis: history, search of fields, PME (presence of leaves in rumen) mineral: can be supplement/vitamin toxicity, wrong type of feed. - Especially selenium, copper - Led/other poisoning - wales. Car batteries dumped into fields, old buildings, pest poisons, wrong feed

What are causes of infectious anaemia that lead to sudden death? How is it diagnosed?

- acute fascioliasis. Most often calves. Often happens when they are looking for grass so they migrate towards marshy areas. - Haemonchosis - Should be premonitory signs but we don't inspect very often. diagnosis: history (parasite control, clinical signs), pale MM, PME most useful. Liver is filled with fluke.

where do S. aureus hang out?

- adhere to skin squames, hair. median length of carriage is 11 months. - even after treatment, and "resolving" - still have it

what are notifiable diseases under the RIDDOR? (2013)

- anthrax - avian influenza - bovine tuberculosis - brucellosis - campylobacter - crypto - e. coli, VTEC, giardia

how can you prepare animals for slaughter in ways that avoid zoonotic transmission of diseases?

- avoid stress (can activate shedding of pathogens like salmonella, campylobacter) - prevent soiling of animals (stress, mixing) - assure fit for slaughter - assure fit for transport - assure animal ID

controlling zoonosis in a vet practice? how?

- barrier precautions (PPE) - good hygiene - sanitation and disinfection (equipment, facilities) - appropriate waste disposal - proper use of isolation facilities for both diseased and suspect animals - education of animal owners

what are ways that animals and humans can transmit zoonotic disease?

- carriers/infection - fomites - environmental contamination. need to SAMPLE FOR CARRIER STATUS because of the zoonotic risks.

what is the lab-based disease surveillance of APHA?

- centres spread all over the country. reduced due to cost-cutting but try to partner with people like the RVC. - there is a free carcase collection area if they are too far from the centres. farmer calls you: you sent to an invest. centre and get a postmortem done. you are essential. they are SUBSIDIZED: 89 pounds including labs on all stuff - they are concerned abt chickens so they are only 40 - they have experience vet investigation officers - independent from vet practices (not trying to replacE) ~ STANDARDISED diagnostic criteria independent of location - testing is carried out to UKAS accreditation, quality control - species expert groups who can provide advice, distribute findings across country

zoonotic risks for pregnant workers

- chlamydia psittacci - chlamydophila abortus -listeria -t. gondii - borrelia burdorferi (lyme disease) - coxella burnetti (q fever)

how do we get from carcasse to data in disease surveillance?

- collect - collate/analyse - interpret -act -assess success there are submission forms files for them to notify APHA. they go into FarmFile, which also has strict criteria for postmortem diagnoses. if a diagnosis isn't reached - it is of particular interest, could be a novel disease. that will lead to targeted surveillance if there is a targeted disease, and that will lead to free postmortem.

What are the common types of septicaemia/toxaemia lead to sudden death? How do you diagnose it?

- common usual bacterial: clostridium - Often in environment or commensals - Predisposed by mgmt factors - nutrition (clostridium), stocking density (salmonellosis), flooding (leptospirosis) - Diagnose via history (vaccination status, mgmt), clinical signs, changes in MM colour, PME.

what are stages of the pig life cycle where nutritional changes occur?

- day 0: colostrum - day 10-17: weaning (sow's milk + creep feed), .5 gk/day - if fattened: ad-lib and restricted feeding 1-2 then 2-4 kg/day - if breeding: can get fat sow/thin sow syndrome - lactating sows get 5 kg/day

how did they control Q fever in the netherlands?

- disease mad notifiable - mandatory testing/culling - mandatory vaccination - ban breeding of milking sheep and goats in farms >50 animals - waste management reccommendations - hygiene protocols

what are ways to increase calorie expenditure in the obese horse?

- don't rug a horse - clip the horse (makes it colder) - hay and water at opposite sides of field - circumferential strip grazing or any other type of dynamic feedins system

how do you assess risk of a pathogen outbreak/the damage?

- evidence on prevalence of hazard: species, regions, production system - info on biology of hazard: transmission pathways, survival in the environment, infective dose - think about consequences: severity of disease, treatment options, duration of illness - think about risk PATHWAYS / endpoint. what sequence of events could happen? EXAMPLE: west nile. can infect birds, horses, people, other vectors. those travel like tourists, migration, food, captive birds, research samples, etc. that's why they spray airplanes to kill mosquitos.

How to examine ewe and environment for lamb mortality?

- ewe BCS - Lambing environment - clean and dry, good drainage, stocking rate - Poor weather NOT a cause in itself - they are hardy. If they are well-fed, etc, they can handle weather and predators. - supervision: training/work rate more important than numbers

what are some general parlour procedures that can prevent mastitis?

- general hygiene - pre-dip? - strip/wipe teat - teats clean/dry?? put a paper towel over them just before the cluster is on - paper towels v. cloths - stimulation of udder (strip out the milk) - liner slips (if you hear a sqawking noise, correct it) - overmilking - damages the teat - post-dipping - is it sprayed on properly? - relaxed cows

what is looked at in a "distance examination"

- general info about the animals (species, breed, sex, approx) - Husbandry situation and environment e.g., housed or outside, bedding, stocking density, hygiene, food type, amt of food available - Attitude and demeanor of animals - do any appear abnormal - size, appx weight/variation in size - hair coat/skin/fleece - lameness or limb abnormalities - diarrhoea or evidence of - lesions - listen for coughing - smell: some conditions like footrot/blowfly strike

What metabolic disturbances can cause sudden death in farm animals?

- hypomagnesaemia, hypocalcaemia, ketosis, acidosis Common in cattle (dairy). Hypomag was 50% of sudden death in cattle Diagnose with bloods? - Feed changes can cause acidosis - Nutritional deficiencies or imbalances can cause acidosis, bloat, gut torsion. Can be intrinsic due to change of flora or extrinsic

how do you undergo risk analysis on a farm?

- identify hazards and assess risk (science based) - policy: implement options requires exchange of information with risk assessors, managers, stakeholders, public set priorities

what are tips for successful weight loss programmes for dogs

- meal-fed, not ad-lib - all meals carefully measured - full diet history with whole family - log of everything fed for 1 week - add exercise plan - stop begging. people can't resist - make it realistic for people: allow treats, just make guidelines - high protein makes you more full - feed less = DOESN'T WORK. must calculate what patient needs, RER. determine what is actually fed. - follow-up: make it personal, develop rapport

Why is spring such a dangerous time for parasites on farms? what are the main threats?

- new crop of young animals - weather: warming up, moist - sources: arrested larvae (cyathostomins, ostertagia), coccidia from older lambs, larvae on pasture from adult animals/over-wintered - Main threats: nematodirus bats (lambs to lamb, no ewe) type II ostertagia (young cattle), cyathostomins (young hourses, emergence of larvae) - Nematodirus: FEC doesn't help. Bulk of damage done as larvae, done in endothelium of intestines/flatten villi.

History for sudden death (lambs/cows)

- number/groups/field/ages affected - Progression of signs (if any) - vaccination/worming history - mgmt: recent treatments, changes to feeds/field, unusual weather events?

mammary tissue damage is caused by

- pathogens (toxins) - inflammation: neutrophiles, proteases/kinases - reparative responses (fibrosis)

What parasites threats/conditions are in the autumn?

- peak in pasture larval levels - Liver fluke metercercariae in snails - Animals are building up immunity - ACUTE fascioliasis: ingestion of millions of metacercariae. Young animals more likely to get acute/fatal

what are the nutritional requirements of a lactating sow?

- peak yield: 11 litres. produce more milk per kg than dairy cows - can consume 8-10 kg of feed at peak (3 wks into lactation). need feed high in energy, lysine, protein. need adequate calcium. - piglet mortality/poor growth can be a sign of poor milk production due to nutrition/disease.

how do we estimate EBV for a trait?

- performance testing: individual, sibling, pedigree, progeny - repeatability - heritability used to select towards a positive trait or away from a negative trait.

what can cause copper deficiencies? what are clinical signs?

- primary or secondary. affected by - age of animals - pasture composition and time of year (high in summer pasture) - genetic influence (esp. sheep) - molbdenum, sulphur, iron - bind to copper, make it unavailable SIGNS: - swayback - hindlimb dysfunction. terminal spinal cord not myelinated - anaemia/lethargy (lack of erythropoeisis) - abnormalities of bone/connective tissue - unusual pigmentation, lightening of hair coat (rings around the eyes) more common in calves and often treated with the propriate amount of food.

what are contributing factors to dog obesity?

- primary: imbalance between energy in, energy expenditure - excessive intake + lack of exercise - metabolic status - genetics - lifestyle CLIENT FACTORS - ad-lib feeding, schedules - multiple pets in household (one eats more/fasteR) - small childen - multiple members of family feeding AGING: energy requirements related to lean body mass. senior diets often less enerrgh dense.

how does the gov/APHA contribute to national veterinary scanning disease surveillance?

- provide mostmortem exam facilities with subsidised services - provide lab facilities for diagnostic testin ~ run advisory species expert groups (cattle, small rum., pigs, etc) ~ run an international disease monitoring team ~ run a vet. exotic, notifiable disease group

what purchasing policies for farms reduce foodborne illnesses?

- quality standards for purchases within production chain - health certificates for animals - quality certificates for feed. example: a c. bovis infection in fattened cattle from a single abbatoir. could be tracked back from a potato shipment (which lead to a different outbreak in 2014). even with intense biosecurity, if there are sources of contamination from food/other things, you can't stop that.

How does birthweight affect lamb mortality?

- related to nutrition in late gestation. Smaller ones less energy to drink, etc.

primary agents involved in lactating mastitits

- s. aureus - e.coli - strep. uberus (we don't know where it comes from) - mycoplasma: no cell wall - can't use beta-lactams on it.

which species of salmonella are zoonotic? how does it transmit?

- s. enterica typhinurium, s. enterica enderidis. - can contaminate feed. found in 1.3% of ingredients for food in UK. 12.5% in US. - eggs: can be contaminated before shell is formed from all flocks of poultry. not very common in eggs, however. decreased significantly since the 90s. there was a control program that worked very well. started with breeding flocks (vaccination, etc).

what pathogens have a faecal-oral tarnsmission pathway from farm anials?

- salmonella - campylobacter - e. coli - crypto - giardia. think petting zoos, wet markets (other countries)

how do you feed weaned gilts?

- similar to fattening pigs. - "flush" around mating - high energy feed to improve number of piglets avoid competition/stress to improve litter size during pregnancy. feed individually according to body conditions.

how should you deal with an animal with a zoonotic infection known?

- straight into the consult room - seen at end of day - disinfect b/w patients - move contagious patients on trollyes/baskets - special care in procedure areas - barrier nursing - hand hygiene

lyme disease protection and control

- tuck trousers into socks, wearing long sleeves - checking pets - dont put ur tent near bushes

what are ways to prevent/control zoonosis on a farm?

- vaccinate/worming program - avoid contaminating drinking water - routine health checks via vet - implement herd health plan - good animal husbandry/management practices - implement biosecurity (like quarantine) - good waste management - promote ppe use - esp. when working w/ sick animals and potentially infected material - control pests/vermin, educate farm workers/visitors, detect and report

what are some considerations of a high protein diet for weight loss?

- very palatable so you have to moderate amounts (calories) - don't know long-term effects: impact on liver, kidneys - don't let them go into crazy evolutionary diet territory

what are you not allowed to feed pigs in the UK? why?

- waste from kitchens/catering facilities with the exception for vegan household kitchens which don't handle any animal products - meat/meat products - milk/milk products unless form the same holding or suitably treated CAN be fed: - commercial pig feed - veg waste from wholesalers who don't handle animal products REASON: AFRICAN SWINE FEVER from contaminated food

how to monitor your horse's weight?

- weigh tape - weigh bride - tape measure: heart and belly girth. much better with bCS.

What parasites threats/conditions are in the winter?

- young animals immunity developing - Larval development halted - Liver fluke develops to adults - CHRONIC fascioliasis, in the bile ducts

who are at risks at petting zoos?

- young children (<5 year old) - elderly people - immunocompromised individuals - pregnant women golstone e. coli outbreak on farm.

What parasites threats/conditions are in the summer?

- young susceptible animals begin grazing - Larval numbers start to increase - Liver fluke eggs begin to hatch - Telodorsagia (a nematode) in lamb/goats/calves causing lack of wt. gain, parascaris (late-born foals), and cyathostomins (horses) - Subclinical effects, PGE

when should you wean a piglet? how does early weaning affect the animals?

-can't be less than 28 days unless welfare is compromised - can be weaned up to 7 days earlier if moved into specialised housings which are emptied, thoroughly cleaned/disinfected before intro of new group - organic: must be at least 40 days - weaning pigs need special weaning pellets and creep feed. can't just feed whatever you want to weaning pigs or they won't digest it. early weaning: helps thin sows recover, more litters/sow/year. however more health problems in piglets - diarrhoea. need better hygiene.

bacterial agents of SUBCLINICAL mastitis

1) CNS (coagulate-negative staphylococci) 2) Strep. uberis 3) S. aureus

what groups of cows should be profile 4x? what are some common errors?

1) EARLY LACTATION 10-20 days after calving 2) mid-lactation 100-200 days after 3) dry cows within 14 days of calving 6 cows from each group. errors: sampling cows calved more than 20 day after, failure to includes some lactation 1 cows, or immediately after a major management change (always wait 10 days), or including problem/poor cows.

how to control zoonoses in small animal medicine?

1) EARLY SUSPICION/CORRECT DIAGNOSIS - test!! make sure you inform owner the importance of testing 2) CLIENT COMMUNICATION - must provide copies of relevant clinical findings/lab results. - make sure they know the risks 3) PREVENT SPREAD - practice: surfaces, multi-injection vials - personal: staff, uniforms, owners, hands - patients: wounds, known infected, carriers

What are causes of sudden death on farm animals?

1) Infectious: septicaemia/toxaemia, anaemia 2) toxicity: plant or chemical. Plants tend to be over-reported but 3) chemical is pretty common 4) Metabolic disease 5) Nutritional 6) Other - climate, trauma, etc. climate can give farmers insurance claims lol 7) Keep an open mind. Might require re-visits, prolonged investigation

what are the 3 most important diseases in dairy cattle?

1) Mastitis 2) Lameness/Foot issues 3) Fertility

Bacterial agents of CLINICAL mastitis (4 main ones)

1) Strep. uberis 2) E. coli 3) Coagulatve-negative staphylococci 4) S. aureus

Misconceptions about anthelmintic resistance

1) There are varying levels of resistance and you need to be aware of how much different things are resistant 2) There are temporal and spatial changes in resistance - it's often one species of worm per farm. Generally the one you keep finding on postmortems. One species CAN have triple/quadruple resistance.

What are the 8 SCOPS principles?

1) Work out a control strategy with ur vet/advisor 2) Use effective quarantine strategies to prevent the importation of resistant worms in introduced sheep/goats. Take into a shed, treat with group 5 or 4, leave for 72 hours. Those drugs kill everything in the gut. If anything is left behind, the refugee on the pasture will outcompete the stragglers. 3) Test for AR on ur farm 4) Administer anthelmintics effectively. for example, benzimidazole is still hugely effective for notamidirus. Treat for the heaviest animal. You won't get toxicity. Make sure they don't spit it out. If you starve them for 24 hrs they will eat it 5) Use anthelmintics only when necessary - USE FEC before you treat!!! Not just every 3 weeks. If you DO treat, treat again 3 weeks later. 6) Select the appropriate anthelmintic for the task - don't use combinations 7) Adopt strategies to preserve susceptible worms on the farm - leave the best 10% untreated, refugia. 8) Reduce dependence on anthelmintics

how does one choose a bull for a herd?

1) assess breeding goals: what are most important? look at what your cows are lacking - fertility, lameness, scc. etc. work with vet and nutritionist. - you can do this using KPIs on your farm, honestly. triage. 2) choose a bull. would be better on a cow-by-cow basis, but that's probably too work-intensive. you can use PLI for an initial screen and check inbreeding index. - sometimes you can use sexed semen. 3) once you look up a bull, there's a lot of different traits you can look at as well as the RELIABILITY of this info.

what steps should be taken when investigating mastitis issues? (7)

1) bulk milk somatic cell count 2) records of clinical mastitis cases: can look at # of antibiotic intra-mammary treatments sold, tubes used per case. this helps if you have poor record-keeping. this can depend on if you keep treating a cow cuz it's not getting better. probably 3-4 tubes/case. 3) look for "problem cows" which are reservoirs of infection. - repeat cases of mastitis >3 cases in the same lactation - individual cell count persistently high - drug records show repeated treatment 4) check milking routines. - watch milking session for a LONG time (so that they aren't performing for you). don't piss off herdsman or tell them how to do their job - look for udder cloths (and steal it) - observe/listen. follow with a written report. 5) check 5-point plan. 6) check environment. cows, cleanliness score. are cubicles long enough? cow comfort index (proportion of cows standing one hour before milking). target <15% 7) check bactoscan. examine teat ends - damage caused by vaccuum, inversion/increased keratin. damages to sealing can make it more prone to bacteria entry

which diseases are priority for foodborne diseases in the UK?

1) campylobacter. greatest burden due to very high case numbers, severity of disease. 2) listeria - is rare but severe. 3) e. coli 4) Salmonella 5) norovirus. 3) c. perfringens.

two main causes of mastitis? which pathogens are associated with these causes?

1) contagious (strep. Agalactieae, staph. aureus) 2) environmental (E. coli, S. uberis) huge genetic diversity in terms of the strains of bacteria/pathogens and who they infect

what are your options for a problem cow?

1) culling. this is very effective, but if it's your ONLY form of control, mastitis will build back up and you will have to cull more. 2) put them in a problem group/isolation. milk separately. 3) treat. bacteriology on affected quarter, identify with CMT. appropriate/prolonged antibiotics. - CMT measures CELL count, not BACTERIA.

what is the 7-step process of herd/flock investigation according to blahblah?

1) define the problem. disease, and/or poor production. refine - whole group affected or only certain individuals? use available data such as weights, slaughter records, scanning/pd results, calving/lambing data, etc. 2) history: management practices (worming protocols, moving sheep, etc), predisposing factors, clinical signs + progression, temporal/spatial patterns, his medicine records 3) distance examination: the grass (is it long enough?), skin conditions, wool tags, fencing, water sources, etc 4) clinical examination, +/- PME. can do a limited exam on a large number of animals relatively quickly. MMs, BCS, temp, weighting, HR. something like that. it might be justified to euthanise in order to do a postmortem if one is really sick. a sample size of 1 is tricky, though. PME's can be done on the spot, might take samples for further analysis. 5) anciliary aids/further diagnostic tests: don't usually do random blood tests. collect what is appropriate and necessary. take FECs (multiple, pooled). be able to justify every test u take. 6) analysis and decision making: how can the problem be prevented/minimised? intervention or change to management required for long term prevention, but also what can i do today? full de-worming right now, come back and sort it later. - management changes: reduce stocking density, change nutrition/feeding system, not mixing groups, buying disease-free herds, quarantine of new animals - vaccines: is it justified? can it be eradicated? is it economically feasible? how to reduce predisposing factors? - worming protocols: very complex. prevent resistant populations, nutrition, etc. make sure it can be effectively used over a period of time. - evaluate trace element deficiencies and if they need to be supplemented. 7) reporting back, further monitoring. clarify, written document. he will get it wrong, and poor record keeping is always an issue. on-going contact with farmer, correct course of action in many cases. every farm needs an individual bespoke plan.

Liver fluke life cycle?

1) eggs shed into faeces (8-12 wk PPP) 2) miracidium: into snail (can be 7-8 months on snail. Keep away) 3) Cercariae: out of snail, onto vegetation 4) Metacercaria: encysts on vegetation, eaten Imm fluke migrates to liver

what is the use of submitting a postmortem to national vet disease surveillance? what does it inform?

1) endemic disease level 2) animal welfare issues 3) notifiable diseases (right now it's african swine fever (stays in ham), avian influenza, bluetongue, newcastle disease (neurological in birds), BSE from scotland) 4) novel diseases: schmallenberg (lambs) 5) zoonosis 6) chemical threat to food chain 7) antibiotic resistance 8) adverse reaction to drugs/vaccines (like bluetongue)

what are the consequences of SA obesity?

1) general anaesthetic complications - more difficult to monitor patients - airway issues 2) complicates treatment of various diseases - harder to Xray - CATS: hepatic lipidosis, development of diabetes (3.7), urethral obstruction - DOGS: pancreatisis, worsening degenerative orthopaedic disorders. - RESP: increases UA resistance, decreases functional residual lung capacity - NEUROLOGICAL: physiotherapy more difficult - ORTHOPAEDIC: excessive stress on arthritic joints, decrease mobility, higher post-op complications

what is the 2-tiered approach to pre-harvest risk management?

1) generic practices: - purchase policies/biosecurity - good farming practices, hygiene, management - feed/water - veterinary drugs 2) pathogen-specific practices and technologies - use of probiotics for campylobacter or vaccines to reduce E. coli 0157 infection/shedding - TB/Salmonella/BSE all have their own Tier 2 approaches

4 main causes of lamb mortality? How can they be prevented/treated?

1) hypothermia: make sure lamb is well fed. Can be primary or secondary (started out cold). Brown fat first 5 hrs, after that colostrum. Can bring to a warming box. If over 6 hrs old - not enough energy to maintain temp, body temp drops, comatose. Need intraperitoneal glucose injection, then feeding. 2) Watery mouth: E. Coli colonisation of the gut of newborn lambs. Can treat with soapy water enemas, mild laxatives/purgatives, oral antibiotics (early phase), oral electrolyte therapy, penicillin-type drug intramuscularly. - prevention: sort out COLOSTRUM, staff training, replacement colostrum, yoghurt?. You can use dairy cow/neighboring farm colostrum/farmer's market. You can also take from ewe's with dead lambs. Also streptomycin. 3) Dystocia: training, hygiene, lubricant, empathy. Also better ram selection and control of BCS. 4) Abortion-associated pathogens: biosecurity measures (quarantine, fencing, vaccination)

what are the three main steps of risk management in food safety?

1) identify the most cost-effective option 2) implementation 3) monitoring and follow-up. targeted at interrupting, preventing, or eliminating transmission pathways identified in the assessment. COMMUNICATION IS CRITICAL for effective risk management by clients.

extend starvation in omnivore - 2 main consequences? (or perceived starvation)

1) increase fat mobilisation (more NEFAS): a lot of them end up it the liver - fatty liver (hepatic lipidosis). happens also from eating too much fats. physically impedes bloodflow in liver. cells accumulate vacuoles of fat. 2) too much acetyl-coA: Ketosis. due to a) making more of these acids from AAs, and b) stealing CAC intermediates to make glucose (leaving with extra ketone bodies/acetyl-coA and too many fats mobilised) signs of ketosis: smell of breath, "slow cow" (depressed, nonresponsive, headpress. in cats, can lead to ketoacidosis/metabolic acidosis. also can cause pregnancy toxaemia/twin lamb.

Disease processes involving the mammary gland?

1) mastitis 2) diseases of the skin/teats 3) neoplasia 4) pathogen transmission to young - don't feed waste milk!` galactophoritis = disease of ducts.

what are the 4 different "types" or severities of mastitis?

1) peracute, potentially life-threatining - s. saureus 2) acute with or without systemic signs, can progress to chronic 3) chronic, progressive loss of secretory ability, following subclinical or acute (s. aureus) 4) Subclinical: no gross changes or inflammation. detected via SCC.

what factors decreases VFI? how? (name 5)

1) pregnancy/ inert fill: GROWING FOETUS flow rate increases but not enough to compensate. need more digestible feed to pregnant/twins. 2) Body Fat 3) Neutral-detergent fibre: increases retention time. 4) water in the plant. not water in the rumen or drunk with dry food (water holding capacity. chop up plants so they digest faster and hold less water) 5) rumen outflow rate: particle size reaching abomasum. depends on ease of feed breakdown. 6) VFAS: massive feedback loop. especially acetate/proprionate.

5 point plan for treating mastitis

1) prompt detection/treatment of cases - before milking: detect in parlour. flushes out bacteria laden milk. milk all over floor- strip cup/splashback - hygiene in parlour. one paper towel per cow, never udder cloths. wear gloves. can use pre-milking teat dips to further improve hygiene. 2) post-milking teat dipping. - teat orifice remains open for 30-40 minutes. keep cows standing after milking to allow sphincters to close (feed). - disinfect which coats teat skin/kills bacteria: iodophores, chlorine based, chlorohexidine, quats - can use a cup, a spray, or an automatic system. 3) DRY COW THERAPY - long-acting antibiotics: removes existing subclinical infections during dry period. however - antibiotic resistance. now aiming for selective dry cow therapy for those with increased SCC - teat sealant: inert substance, infused into eat canal and blocks it - prevents bacteria entering during dry period - hygiene must be excellent with PMTD. 4) Cull persistent offenders (3 or more during a lactation persistent high Individual SCC). Do not take decision lightly. 5) Regular Servicing and Maintenance of Milking Machine. want CONSTANT vacuum applied. Liner opens and closes to massage teat. Change liners - 2x/year isn't enough.

what are 4 specific strategies to managing risk?

1) risk transfer: insurance against events. 2) risk avoidance: not performing the activity that is hazardous but losing opportunities. example: switching from production to petting zoo or something of the like. 3) risk mitigation/reduction: to a level that is accepted. target levels of risk 4) risk acceptance: what is the acceptable level of risk? this is what people disagree on.

resistance to infection at the teat (physical factors)

1) teat canal: primary role in preventing entry of infection. biofilm, keeping it clean 2) smooth muscle sphincter 3) keratin plug from epithelium containing fatty acids - bactericidal, look back 4) furstenberg's Rosette: wtf is this? prevents entry? physical flushing action of milk

how do you investigate poor thrift?

1) weight gain/loss - magnitude: number of animals affected, severity, how long has it been going on - farm records, slaughterhouse records - entire herd/flock or subgroup? - nutrition adequate? difficult to get accurate information. 2) history. - repro rate/spread, time of calving/lambing, weaning - farming system, feed management - previous TE problems, supplements used - worming regimine, anthelmintics used - clinical signs, environment in general 3) environment exam. pasture, feed availability across farm 4) a. distance exam - variation in size/weight, scouring, lameness, coughing, pruritis, etc b. individual exam. careful selection of those to choose. "basic" and "full". can tek some procedures on a large number of animals relatively quikly - weigh, BCS, MMs c. postmortems - can be useful in sheep, for example. check with VLA first. consider sample size. can collect liver for TE, fluke, examing GIT for worms, lungs for resp. disease, other PM signs. trichostrongyles difficult to see 5) anciliary aids/further diagnostics. almost certainly required - consider sample size and which animals. faecal egg counts, liver/blood (TE analysis), feed analysis 6) data analysis, decision making: careful interpretation in context. if TE levels are "marginal", will there be response to supplementation? is it just that? what is the relative contribution of each?

subclinical mastitis: prevalence, clinical signs?

10-40x more prevalent than clinical mastitis. no gross inflammation or changes in milk. only way to detect: somatic (inflammatory) cell count (SCC) in milk samples. has a similar pathogenesis/aetiology just to a lower level.

You visit a farm which is rearing 200 dairy x beef breed calves. The calves are housed indoors in group pens with 20 calves in each pen and are fed an artificial milk replacer and calf pellets. The owner is concerned because a number of the 1-3 week old calves have diarrhoea and two have died. On distance examination you note that the problem seems to be restricted to 3 groups of 1-3 week old calves, and you estimate that 25 calves are scouring of which 5 look very weak.

2-3 of the weakest calves and 2-3 that are normal scouring

what is obesity defined as?

20-25% above ideal body weight (in people). degree of obesity that results in a detriment to health in animals is unknown. call it a "disease" to remove stigma and emphasize affect on organs.

Proportion of ice-free land in the planet used for grazing livestock? proportion of arable land used to produce crop for livestock?

25% used for grazing livestock. 33% used for people.

what is the target for mastitis in a herd?

30 cases/cows/year. CASES, not cows. this figure gives the incidence. we should be much lower than that, but if you're over 30 it's a problem (like a C).

what are genetic causes of embryo loss in cows?

30% of failures are due to embryo itself (probably a result of inbreeding or other genetic inviabilities) as opposed to environment.

what is the incidence of clinical mastitis?

35 cases/100 cows in SE england its 45 cases/100 cows (some might be reoccurrance)

out of the top 430 disorders in dogs, how many of them are single-gene?

4.3% of disorders, 1% of disease events. breeding in the mind of ONLY single gene disorders is really not useful.

when is BCS the most important to analyse?

6 week either side of calving. poor BCS can cause poor DMI after calving, metabolic disease, poor milk production, poor fertility. DRY cow - want BCS to remain constant. want to dry off at the same BCS that the cow should calve at (3.0). hard to lose weight when it's not milking.

are diseases more often single-gene or complex gene?

80% are complex - involve nutrition, epigenetics, neonatal environments, multiple genes.

what is the main energy source of a fed omnivore? where does it go in the body? how is it regulated?

80% of glucose taken into muscle, stored as glycogen. GLUT-4 transporters (independent) which regulate uptake when there is insulin around. 20% glucose goes into the liver - stored as glycogen or goes into the citric acid cycle (excess) via glycolysis. GLUT-2 transporter with a really high Km (only at high levels of glucose). also in the pancreas (beta-cells) - signal as insulin release. also goes into the liver for fatty acid synthesis from acetyl Co-A. insulin: deposphorylation cascade which activates glycolysis, etc. glucagon: phosphorylates enzymes, turns it off.

what is hepatic oxidation theory?

ATP levels in LIVER determine vagal stimulation. low levels stimulate the hunger center. in liver, sources are: VFA, BHBA, NEFAs. can cause negative feedback in ketotic cows/fatty liver because of high levels of ATP in the liver.

what is usually the limiting factor in poor thrift in animals?

CALORIES, not TE's. often concurrent with parasites. usually if you sort out the calories, the TE's sort themselves out too.

what are the two sources of energy in forages? how do they vary in digestibility?

Cell contents: sugars, starches, proteins, etc. 90% digestible, rapidly available. cell walls: cellulose, lignin, hemicellulose. 40-70% digestible, more slowly available by fiber-digesting bacteria.

what are the clinically relevant multidrug resistant pathogens? (humans) why is this important?

ESKAPE: - enterococcus faecium - staph. aureus - klebsiella pneumonia - acinetobacter baumanii - pseudomonas aeruginosa - enterobacter species there are possible reservoirs of hospital superbugs in dogs/pets

what is the EEC? how do vets play a role?

European Economic Community: all countries in the EU have same regulation, legislation, and standards for free trade. in this context, vets are service providers for food chains and ensure that food is SAFE.

what is the issue with the "emergency treatment" approach to farm animal vets?

Focus on individual animals: cost-benefit ration might not favour intervention, esp. sheep ~ focus on TREATMENT rather than PREVENTION. ~ focus on clinical rather than sub-clinical disease ~ no integrated approach to disease control - husbandry plays a huge role

grades of mastitis

Grade 1: milk change only - decreased yield Grade 2: acute. milk changes, udder changes, decreased yield. chronic: as above, but persistent Grade 3: as grade 2, but a systemic sick cow.

what are examples of hazards in risk analysis on a farm? what does assessing a "risk" involve?

HAZARDS: e.coli, disinfectants, poor quality silage (listeria), not monitoring water, salmonella. can be microbiological, chemical, and physical. very diverse. RISKS: PROBABILITY and CONSEQUENCES are both taken into account when assessing risk. includes food safety, animal health, animal welfare, and the environment. objective of risk analysis is to identify and evaluate hazards and prioritise them, and evaluate risk management strategies.

Most effective diagnostic tool to investigate sudden death? What should you do after? Follow-up?

HIGHLY recommended. Much more likely to get a diagnosis for sudden death with a PME. Can do on the spot diagnosis, collect samples for further analysis if there's no diagnosis. Further diagnostics as appropriate, routine part of PME. No "random" sampling of flock to "do bloods" but if you think it could be a toxicity/poisoning you can sample the dead animal and run bloods Need to be quick and decisive If it's a toxicity/poison/feeding change, it might be too late for the ones already exposed but you can prevent more.

contrast the intensive and extensive systems in terms of income changes, breed changes, disease burden changes, and demand for veterinary services

INCOME: intensive make more money per animal but extensive have lower costs. lower income in total unless large # of animals. BREED: local breeds more appropriate for intensive (can suit climate), exotics more appropriate for intensive DISEASE BURDEN: extensive breeds well adapted to local endemic diseases, more resistant. losses when intensive epidemic diseases occur are high. DEMAND FOR VETS: higher for intensive, and increase. role of vets in prevention of disease more important.

how does lignin affect DMI of cows?

LIGNIN has NDF - will reduce DMI. it's not digestible. hemicellulose is the most digestible, cellulose is less, and lignin is the least.

First two things to do with sudden death

Is it really sudden death? Could have been dead or ill for a long period of time and nobody noticed Anthrax is a whole other story, it is a cause of sudden death and it is the first thing to look at

where should you sample each TE? how many?

Lots of samples: Cu, Co. variation within flock. Few samples: Selenium in blood: Se, Co in storage site (liver): Cu, Co. liver biopsies are straightforward, you can also do at PME.

describe the two meticillin-recistant staphylococci that are the most important. where do they come from? what is their relevance?

MRSA (aureus): - human hostpitals, communities, livestocks - broad b-lactam and often also fluoroquinolone resistant - reverse zoonotic transmission: spillover from human hospitals - in the human nose, very opportunistic. causes extended lengths of stay in the hospital and treatment options are limited - if the pet has it, there is a good chance he got it from a hospital/family member. high risk of human infection - most can be treated successfully MRSP (psuedintermedius) - dog-adapted, nosocomial pathogen - increasing in frequency in usa

why is NDF important? what is ADF?

NDF (cell-walls) are the most useful in balancing rumen-healthy rations and predicting how much forage a cow can consume. single best measure of forage quality. ADF (acid-detergent fibre) are the least digestible parts - cellulose and lignin. it predicts energy content of forages.

Life cycle of the nematode?

PPP is 3 weeks. Best larval development when warm and moist (can survive freezing but not desiccation) (land on the floor, do some maturation, get eaten again)

what's the difference between scanning surveillance and targeted surveillance?

SCANNING surveillance: passive process - information generated from diagnostic testing, necropsy examinations. it's cheaper. - there are a lot of infected animals that are NOT investigated, a lot is missed. TARGETED surveillance: investigating something that is unusual via free postmortems for the species/target - BSE, TB, Anthrax, FMD, notifiable diseases - zoonotic diseases (campylobacter, salmonella, toxins, etc, novel diseases, import testing, AMR) - APHA has field officers. - provied a lot more data. more expensive but more comprehensive.

founder effect v. genetic bottleneck

When a small group of individuals contributes exclusively to the gene pool of the next generation (founder) bottleneck: a bunch of people die

what does the expression of a disease look like when it has more than 2 genes? how can we use that to our advantage?

a bell curve. that means we can apply artificial selection to reduce the frequency of that disease.

what is Food Chain Information?

a document that the farmer is responsible to provide for each animal that enters the meat chain. now fully implemented. provides info on: - producer - health status - treatments - veterinarian slaughterhouse operators must request, receive, check, and act upon food chain information. dairy farms are also inspected by animal health on milk hygiene, equipment, animals.

what water requirements do pigs have?

a lot. sows can consume up to 30 litres a day. hungry piglets can be a sign of restricted water intake - must check regularly. piglets over 2 wks of age must have permanent access to fresh drinking water.

what is a carrier pathogen?

a pathogen isolated from animal/humans without causing clinical signs of disease in the hose.

what affects milk fat?

amount of fibre in diet. if concentrates:forage ration is too high, the fat content will drop significantly. spring grass can be low in fibre. low bulk milk fat can indicate SARA, but it can be obscured by variation in groups

e. coli mastitis

acute, antimicrobial resistance. pathogenicity depends on combination, quality of properties alpha-haemolysin, CNF-1, endotoxin, pili, etc. VACCINE: just came out. lacking O-antigen. can be mulit-resistant.

Affect of trematodes (liver fluke)?

acute: liver damage. Die of acute haemorrhagic shock chronic: blood and protein loss. Ability to clot is reduced

how to PREVENT dog obesity?

adjust feeding to suit lifestyle (even after neutering, etc)

what is total mixed ration?

all the feed components (forage, concentrate, etc) mixed up into one thing. sometimes concentrate is also fed in the parlour to tempt them in. the point is to get it all fed throughout the day in a mixed way. evens out the rumen pH. ISSUES: sorting (the cow picks out the delicious things)

how do you BCS horses? what areas are emphasised?

along neck, along withers, ribs, behind shoulder, down back, and tailhead. there's a 5-point and 9-point scale. howeve,r people are so used to seeing fat horses. want to "just about" see a horse's ribs.

carnivore: major dietary inputs?

amino acids (glucogenic and ketogenic). glucogenic becomes pyruvate, ketogenic becomes acetyl CoA. some can be both.

difference b/w bacteria and bulk milk cell count. what causes high bactoscan (4)?

amt of BACTERIA in milk - should be <50,000 ml. target should be < 20k or 10k. BACTERIA =/ MASTITIS. sources: 1) mastitis 2) contamination from faeces at milking, dirty teats, wet teats, dirty hands, etc 3) milking machines are dirty - "cheese in pipes" 4) failure of refrigeration in bulk tank

what is thermostatic theory?

animals eat to maintain body temp/avoid hypothermia. however, rumen is exothermic though. the relationship is poor with the cows. for poultry: relationship is good.

treament for mastitis?

antibiotics: systemic, intramammary during lactation, or in a dry cow choice depends on: sensitivity, pharmacokinetics, availability, costs, herd history, and withdrawal time also: oxytocin, NSAID's corticosteroids, fluid therapy, calcium, dextrose

milk protein - what amt is it and what can affect it?

at 3.4%. milk protein drops after a period of inadequate energy intake. t's difficult to correct quickly.

what is the average feed conversion ratio for growers/finishers? why is that important?

average is 2.31, top 10% is 1.74. one of the most important economic and health indicators in fattening pigs.

what are zoonotic diseases in companion animal practice?

bacteria: rabies, salmonella, brucella, pasturella, leptospira MRSA (tuberculosis) Worms: tapeworms, roundworms parasites: toxoplasma, psittacosis, sarcoptic mange, termatophytosis (ringworm), cheyletielliosis (rabbits, itchy forearms)

what are examples of biological, chemical, and physical hazards in animal-derived foods?

biological: bacteria, viruses, parasites chemical: environmental contaminants, illegal substances, natural toxins (mycotoxins) physical: glass, metal, non-edible ingredients.

metabolic consequences of a ruminant in high demand?

blood sugar levels fall, too much LCFA mobilisation = fatty liver. "milking off her back" - it comes from her back fat. ketosis from CAC byproducts. if you get enough AAs in them, you can prevent ketosis by gluconeogenesis (anapleurotic). make sure your microbes are healthy. supplement with soybean. secondary ketosis: something that stops them eating. Not foodstuff. would be indicated by only 1 cow in ketosis.

what are some genetic tools to breed cows? what do most UK farmers look for?

breeding values - genetic merit of the animal. called predicted trasmitting ability (PTA) selection indexes are combinations of desirable traits. there are a large variety of traits. in the UK: breed based on 45% protein/fat, the other 55% other things. scandinavian breeds are healthy so we integrate those.

which figure indicates the PREVALENCE of mastitis?

bulk milk somatic count. proportion of quarters that are infected (usually subclinical) on the day of sampling.

what does fertility index measure?

calving interval, non-return rate at 56 days, BCS, milk yield around insemination, days to first service, and total number of serves/conception. when the FI was introduced, calving interval has decreased. however conception rates aren't changing too much.

what is the most common cause of food poisoning in the UK? where does it come from? what are some on-farm interventions? why is it so hard to eradicate?

campylobacter. comes from poultry/livestock. broiler meat main food-borne source of human campylobacteriosis. present in 65% of chicken samples. INTERVENTIONS: biosecurity (fly screens), feed/water additives that reduce risk of colonisation, vazzinaction, genetic resistance. unfortunately even with highest security, only reduced incidence by 1/3. there are other factors that need to be identified. it's ASYMPTOMATIC in poultry (carriers) which makes it difficult.

what are cattle/deer, sheep, etc most susceptible to in terms of TE deficiency?

cattle/deer: copper sheep: rare, varies among breed. cobalt most common. all species: selenium, vit. e

what are causes of hypomagnesia in cows?

causes: low Mg in the diet (fresh grass), poor feed intakes (rain), poor absorption of MG (excess K (DCAB), N (+ve), Passage rate (lush grass)) little homeostatic regulation of Mg in ruminants as opposed to calcium. deficiency is when high demand is combined w/ decreased intake.

what equines are more likeyl to be obese?

certain breeds - draught, cob, native, welsh good . "doers" ponies summer non-ridden

When is clinical mastitis most common?

dry period mastitis (subclinical) becomes much more severe in the first 50 days of calving. They can also pick it up from being housed.

What is the common clostridial vaccine protocol?

clostridial disease really shouldn't happen - this is the one thing you MUST vaccinate for in sheep. Cheap and easy and clostridium is ubiquitous. 1) ewe: sensitiser + booster 4-6 wk later, 4-6 pre-lamb again for colostrum 2) Young lamb: MDA until 12 wks 3) Weaned lambs: decide whether or not to vaccinate (length of Time to slaughter), need 2 doses 4-6 weeks apart for full protection Vaccination is very effective - so effective that the farmer DOESN'T think he has clostridium.

what TE deficiency is most commonly related to poor thrift?

cobalt deficiency most common (can't metabolise proprionate). copper can, also has diarrhoea, poor pigmentation. HOWEVER: poor thrift is often multifactorial, related to poor nutrition and/or paratisism as well.

where do dietary fats in the fed state of an omnivore go? how?

come into gut as chylomicrons, go into the tissues where the fat is extracted to be used in adiposides (esterified with glycerol to make triglycerides). excess: can be used as acetyl CoA in muscle, liver.

what are routes of zoonotic e.coli infection? what is the main reservoir?

contamination of food/water, direct contact with animals/faeces, person-to-person spread. main reservoir in UK: cattle, but other ruminants too. infected animals do NOT normally show clinical signs (CARRIERS). there was a big petting zoo e. coli outbreak that killed a bunch of old people. "RAW" milk a HUGE disease risk

what is lipostatic theory? does it apply to mammals/cows/anyone?

control of mammalian energy balance - body weight, body comp involves a hypothalamic feedback loop in which body fat reserves modulate food intake, energy expenditure. NOT effective in cows or really anyone. some species might be.

what are ways to prevent crypto? why is this important?

control: colostrum to calves, isolate sick animals, hand washing, PPE, cleaning/disinfection life-threatening to children/immunocompromised individuals, elderly. outbreaks can occur in drinking water, water treatment plants.

why are cows getting culled earlier and earlier?

cows were selected for milk yield and not any other type of robust health aspects. fertility decreased. fertility is the top reason for culling. holsteins have high potential for yield, low fertility, low health (mastitis/lameness), and a short productive life. farmers are trying to breed for healthier cows these days.

what are the causes of milk fever? how can you prevent?

demand not met by supply. prevent by low Ca in dry cow ration and High Ca in milking ration to increase absorption with DCAB, supplement magnesium. you can also drench at calving and bolus just before calving. risky cows are older, fatter, channel breeds (jersey). fatter cows will eat less and have more of a negative energy balance. older cows have less bone reserve. response: quick in kidney (but little), slow in bone (but a lot).

what are causes of poor thrift?

depends on clinical signs. IF APPETITE NORMAL AND NUTRITION IS ADEQUATE: maldigestion/malobsorption (paraticism, johnes, tumours). -if parasites: most or all the group is affected (maldigestion) - if johnes/chronic disease/tumours: only 1 or 2 animals affected at one time (malabsorption) INADEQUATE NUTRITION: under-feeding, trace element defeciency IF APPETITE NOT NORMAL: if it wont eat - parasites. appetite change not normally obvious to farmers if it CANT eat - dental disease, severe lameness. only small proportion of group affected.

why are horses obese? what are the effects of obesity?

designed to live on scrub in the summer (get fat) and then work very hard for food in the winter (lose weight). we rug them up, give them lush cow pastures, and physical inactivity. excess adiposity leads to health issues. exercise issues, abnormal reproductive performance/dystocia, mesenteric lipoma (can strangulate), laminitis, EMS, hyperlipaemia and DOD. 83% of laminitic animals are obese. changes in insulin signalling, IGF-1

what is DCAB/D? what does it achieve? how do we do it?

dietary cation/anion balance diet by making sure we feed more anions than cations. cations: Na/K anions: Cl/Sulphur analyst them in mmol/kg DM formula (Na + K) - (Cl + 2S) provides excess of anions over cations of -100/200 mEq. to decrease the pH of blood, PTH more effective. in dry cows, its is useful to alter calcium metabolism by activating PTH homeostatic processes by decreasing the pH of blood, forcing metabolic acidosis. this causes PTH to be ionised and more effective. this does a better job of regulating calcium levels. we reduce K in the diet (like giving no grass). less fresh = less K. hay, straw, and maize are better. add anions: mg chloride, mg sulphate, cacl, ammonium chloride. need to get them to drink water too. make sure they are eating enough because anionic salts are not very palatable. monitor pH and the aim for 5.5-6.6 in the urine. check several cows/week.

what are 2 types of cow feedback mechanisms for feed intake?

distension/fill: might adapt to the loading, however not the only factor. ruminants eat in meals/phases, not constantly eating. chemostatic feedback: receptors detect fullness.

how should one split dry cows?

divide into 2 groups. 1) from dry until 14 days before calving 2) from 14 days before calving up to day of calving. get them on the same feed components after they calve so they don't have to change their diet while they calve.

how would you assess if TE treatment is successful?

do a controlled trial. farmers like 25/75. then measure if your treatment is cost-effective (is the growth leading to profit that exceeds expenditure on treatment?) your job is not to improve the biochem.

how does DMI affect retention time in the rumen?

high DMI: faster in the rumen low DMI: slower in the rumen.

what is the importance of poor thrift in adults?

economic costs at key times of year. sheep: weaned, non-lactating mating: increased anoestrus length, increased number of services, decreased coneption rates, decreased ovulation rates early pregnancy: decreased placental development late pregnancy: increased risk of metabolic disease lactation: decreased milk production also welfare lol

what is cobalt? how is it important in glucose pathways? what can a deficiency lead to?

essential component of vitamin b12. important in the conversion of proprionate to glucose via B12-dependent enzymes. cobalt is combined into B12 by microbes in the rumen. deficiency: shortage of glucose, poor thrift, esp in weaned lambs. can also lead to anaemia if severe. often in the upland hills.

what is the role of copper in the body?

essential part of many enzymes. cytochrome oxidase (myelin formatoin), tyrosinase (pigmentation), other things. liver levels of Cu often deplete during the winter.

why is poor thrift in young animals important?

even a small decreases in growth rate can cost a lot of money. it's common and often a herd/flock problem, and expensive. often the problems are only recognised when they fail to reach expected weight at slaughter time.

majority of world's livestock are intensive or extensive? why?

extensive. they have low levels of inputs, limited labour inputs, and produce small amts of product per unit of land per animal. found in areas with limited potential

how do you reduce calories in the stall?

feed 1.5% BW of hay. to slow consumption: - make the holes smaller - hay bag with holes more confusing - hay bag in the middle of the stable so it's harder to get out (like a punching bag) - substitute some with straw - you can soak it, but will only reduce if INSISTING on 3 meals a day, substitute hay with chaff or unmollassed beet pulp. you can sub 1 lb of beet pulp for 1.5 lb hay.

pathogenicity factors of s. aureus

fill this in

what are farm assurance schemes?

food processor, supermarket standards. RSPCA Freedom Foods focus on welfare, Soil Association focuses on organic production. they use the legal framework as a basis and often go beyond that, responding for consumer demands.

what were daschounds bred for?

for digging into burrows/tunnels. (badger-dog). "fit" for their local environment.

what is post-digestive feedback? does this apply to cows

glucostatic - short-term. glucoreceptors sensitive to rate at which they are using glucose. low CNS glucose leads to hunger, high CNS glucose doesn't. ruminants: not glucose. ruminant CNS insensitive to changes in blood glucose. hepatic gluconeogensis from PROPRIONIC acid, don't have high blood glucose levels. proprionic acid does have a feedback mechanism. most of their glucose goes into milk.

zoonosis animals

go over beginning

anthrax

go over this. sources of infection: animals, animal products types of infection: cutaneous, inhalation, GIT, injection

describe how to determine gross margin and examples of each variable

gross margin = output - variable costs. doesn't take into account fixed cost- just measures efficiency . variable cost includes everything that changes (food, casual labour, etc). gross margin per ewe is 37 quid.

how do VFA proportions affect VFI?

higher acetate, lower feed intake. butyric acid: absorbed slower (it's bigger) in the rumen, may cause ruminal stasis. it's an issue with poorly fermented feeds

differentiate hill, upland, and lowland

hill: not a lot of grass, can only do sheep/cattle, also have BnBs. poor land, harsh climates, low stocking density. upland: a bit better, might have sheep as a component of other system. lowland: land/climate favourable to cropping. sheep one of many enterprises, might be well integrated. ideal. regardless, extensive animals will grow more slowly.

distinguish between hill, upland, and lowland breeds.

hill: scottish blackface, etc. used for breeding of upland sheep upland: cross hill and upland to make lowland lambs, finishing lambs. bluefaced leicester, chevio, radnor) lowland: texel, dorset down, etx. used for finishing, or wool (all of them)

what is dry matter intake? what is the formula for a lactating cow?

how much cows are actually eating. always measured by this basis. must know the DM content of all feeds in the diet - must be measured as estimates are often inaccurate. DMI for lactating cow: 0.025BW + .1MilkYield

what is the inbreeding index of a cow?

how much it's been inbred. the arbitrary recommendation is not to exceed 6.25%. you can check a bull and cow before you breed them. however, these aren't really that accurate.

trueperella pyogenes

idk

how has TB been controlled recently? are the measures working? how can the current measures improve?

incidence has been increasing since compulsory eradication campaign ended (1980s). costing 500 million in last 10 , intense testing regimes. testing keeps it low but can't eradicate it. testing varies according to level of risk (every 4 years minimum), e.g., scotland is TB-free but wales tested every 6 months. control measures were reviewed: need more accountability (farms find it unavoidable), badgers as a reservoir, help farmers make purchasing decisions, tighter cattle movement controls, removing infected cattle from herds, and enhanced testing. there was a badger cull.

what are anti-nutritional factors in cow feed?

lectins: in legumes. poor food utilization, impaired growth. glucosinolates: cabbage, oilseedrape. affects thyroid function. saponins: soybeans, peanuts, sugar beets, others.

how does leptin level affect VFI in cows?

leptin is produced by fat tissue. the more fat, the more leptin in circulation - can have a negative effect on feed intakes. we are not insure the role leptin plays in metabolism. this doesn't really apply very much in cows.

acute mastitis: clinical signs, microscopy

less damage to tissue, mostly local effects - oedema, fibrin exudation, neutrophilic response. altered milk quality. microscopy: initially, extensive interstitial oedema with neutrophilic infiltration of both interstitium and glandular acini - leads to vacuolation and desquamation of acinar, ductal epithalium

targets from BMSCC?

less than 100, intervention at 150, financial penalty at 200.

What are climactic causes of sudden death?

lightning, hypothermia (reasonably common in young lambs or sheep after shearing)

how do you determine the nutrient needs and energy density of a cow?

maintenance + prod. 2.5% of BW + 10% of milk yield. for OTHER adult animals: 2% of BW is a good estimate. for poultry this is significantly greater. that's about 65MJ + 5 MJ .pregnancy requirements: 40MJ at term. 1KG bodyfat is about 25MJ. to calculate energy density: you divide MJ by KG. a cow producing 30L/day needs 65+ (30*5) = 215 MJ. 2.5% bw + 10%yield = .025*650+3 = 19.25 215/19.25 = 11.2 MJ/KG. to LOSE weight: 1kg ~ 25MJ energy.

What are the affects of nematodes? how?

majority subclinical (reduced wt gain). ALL Grazing animals are affected when it's on pasture. Clinical can be diarrhoea, weight loss, death. Mechanism: reduced appetite, changes in gut structure/function (increased permeability, protein leakage), immune/inflammatory responses Protein-losing enteropathy Continuous low-level exposure of susceptible animals to infectious larvae (even with very regular de-worming) they are still going to have poor growth. It won't return them to normal.

mastitis in ewes: what are tha pathogens?

manheimia haemolytica + s. aureus = 80% of cases OUTSIDE UK: mycoplasma agalactiae

what is inbreeding depression?

many harmful recessive genes are lethal, and can cause increased embryonic deaths, stillbirths, smaller litter. those that live have lower production, lower reproductivity. this can be counteracted with hybrid vigour.

what undesirable traits are correlated with productivity of dairy cows?

mastitis, lameness, and fertility issues (Calving Interval). choose a bull with lower correlation of those values using the EBV. ones that are productive and fertile. SCC is heritable, related to mastitis. a -15% PTA is less SCC for daughters. there has been improvement recently in SCC.

what is cresty neck scoring?

measures regional adiposity. a good idea of fatness. donkeys can get really fat there until it falls over.

when do cows begin to become profitable?

mid-way through 2nd lactation. however the culling rate is 26% per year. the average age of culling is after 3.5 lactations. those cows need to recoup the loss of culling. over the past 7-8 years, cows have been living shorter lives. they can live long into their teens as a suckle herds.

what is bovine paturient paresis? what is the normal calcium homeostasis in the cow? how is it regulated?

milk fever/ hypocalcaemia. causes acute flaccid paralysis. normal in the blood 2.3-3.2 mmol/l. it's absorbed from GIT/kidney, bone and regulated by PTH (excreted during low levels of calcium which activates D3 in the kidney) and vitamin D3 and calcitonin. when they are about to calve, the homeostasis mechanisms are not good at responding efficiently. mg co-factor also required.

how has risk management of food changed in the recent years?

more focus on PREVENTATIVE medicine/pre-harvest stage as oppposed to post-harves (USA)

what are the epigenetics of diet?

mothers who are obese have increased glucose, NEFA - increased epi changes in leptin gene. possible changes to fetus and makes your babies fat. possible permanent changes: appetite control, neuroendocrine function, metabolism/energy partitioning high fat diets - HMS in humans. ALSO: sub-optimum nutrition decreases pancreatic weight, beta cells.

s. aureus mastitis - signs, habitat?

natrual habitat: skin, mucous membranes. likes damaged tissue, entry through teat canal. from subclinical to severely gangrenous mastitis (peracute) 70% are beta-lactamase +, MRSA also found. intracellular location may allow it to evatde the immune response - can cause recurrence/flare-ups/reactivation. does not always invade udder tissue - can affect sinus/internal duct

strep. uberis mastitis

natural habitat in the environment (? faeces?) - requires trauma or wound to initiate invations - no Lancefield (?) group. no vaccine (yet)

what do cows need in terms of water?

needs to be clean and COOL (the summer was hot). TDS (total dissolved solids) can measure it (not much of a problem in the UK, bigger issue with boreholes).

What are the major players/parasites of the ruminants?

nematodes: osternagia (abomasum), haemonchus, trichostronguls, nematodirus (SI) trematodes: f. Hepatica cestodes?

what is the main energy source of the steady state-ruminant? how is it used?

no post-prandial phase (always ruminating). VFAs/ketone bodies from GIT (produced via anaerobic fermentation to prevent full oxidation). acetate, proprionate, butyrate (same as the KB). used in liver/muscle like glucose in CAC. very focused on oxidative metabolism, not so much glucose metabolism. can also be used for gluconeogenesis (PROPRIONATE) as the source of blood sugar. from there, the Acetyl CoA makes LCFAs that can be mobilised to adipocytes, muscle, etc. 1/2 level of blood sugar

what can happen if the grass is too long?

no soil exposure. can starve. some people trim their grass.

what are amniotic salts? why can't we use them to induce DCAB?

not very palatable, reduce DMI. can in turn cause negative energy balance, fatty liver, metabolic problems, etc. use with G R E A T care.

What factors affect PERInatal mortality?

nutrition: ewe BCS, colostrum accumulation/colostral transfer, lamb birthweight. They very commonly don't get enough to drink, enough colostrum. Supervision - poor hygiene, naval dressing Infectious diseases, iodine deficiency Poor weather

when is forage quality the most high for extensive farming? how does this affect sheep nutrition?

nutritional value decreases midway thru growth. pasture lambs just before "flowering" of wheat for peak nutrition. to help it - rotate or trim grass. animals will lose weight in the winter. can minimise this loss through supplementation. will start to gain weight again in may for spring lambing. early lambing can cause complications.

what are ways to avoid contamination in foodstuffs for livestock?

on-farm production: record use of fertilisers, chemicals. pasture hygiene. purchased: known source, keep receipts/records. storage: safe from birds/rodents, keep it dry, keep records. water: fence off polluted water, protect from contamination (human/animal slurry, chemicals, spraying) and monitor wells.

what are store cattle/lambs?

ones that were unable to gain weight quickly enough (may not be enough grass), so they stay an extra few weeks/months

when is the cost of treatment worth it to the farmer?

only if the avoidable losses from the treatments are GREATER than the cost of the treatment. otherwise not cost-efficient.

how to dose/supplement animals with TES?

oral dosing if you want every animal to get it. even if it's in pellets - some sheep just won't feed from the bucket. can be uneven.

where are the sheep in the UK farmed?

out of 17 million, wales (60% hill), scotaland (90% hil), and england (40% hill)

what are the advantages/disadvantages of indoor and outdoor sows? what about backyard pigs?

outdoor sows: less investment in buildings however: need more feed, more labour, fewer piglets/sow/year backyard pigs: rations not balanced, fed kitchen waste, wrong feeds are sometimes given. need vet advice to avoid welfare problems.

what is the gene frequency of A=p? a=p?

p^2 + 2pq + q^2.

what is poultry "thinning"? what is it used for? what are the issues with it?

partial depopulation of poultry. introducing an excess of chicks and then thinning them near the end so that you don't exceed a biomass/space limit on your farm. essentially slaughtering in rounds. leads to increased risk of infection of campylobacter - 30%. M&S has banned thinning for their suppliers. there are financial consequences. they will also publish contamination levels on farm.

what determines rumen outflow rate?

particle size reaching omasum. depends on ease of feed breakdown by chewing/fermentation. pressure w/in rumen may have SOME effect, acidosis also has an affect.

what is the role of metabolic profiles in dairy cows? when should you perform them?

planned, regular blood tests that look at a number of metabolites. gives an objective indication of how well the cows are handling the diet. on a regular-planned basis. 1) after turnout 2) mid-late summer (assess pasture quality) 3) after housing 4) late in winter housing also after any major diet changes. wait 10 days after change before sampling. only sample healthy cows.

what are most common causes of vitamin imbalances in dogs/cats?

poor nutrition during growth phase - getting advice from breeder. nutritional secondary hyperparathyroidism: Calcium/D deficiency can lead to increased PTH. severe osteopenia, hypocalcaemia, etc. ALL MEAT DIETS - esp. in cats. come in with spinal fractures.

echinococcus granulosis - where it's from?

prevent working dogs from something hi sophie

dry cow mastitis: what are the primary agents?

primary agents: trueperella pyogenes, strep. dysgalactiae, peptostreptococcus indolicus

what changed with the new EU food hygiene regulations?

primary responsibility for food safety borne by food business operator (farmer) had basic hygiene requirements.

what is a primary v. secondary TE deficiecy?

primary: soil/plant deficiency (Co, Se, I, Cu). depends on location and plant colonisation. secondary: lack of absorption in animal (Cu). binds to Mo, S, Fe in rumen, can vary in deficiency among farms, seasons, individual animals.

what is the PLI?

profitabile lifetime index: what traits of cows contribute to profitability.

chronic mastitis: clinical signs, prognosis?

progressive loss of secretory ability following subclinical or acute infection. gland is hard/atrophic. leads to involution: temporary loss of secretory function due to obstruction (granulation tissue) and acinar stagnation and then fibrosis: permanent loss of secretory tissue due to progressive destruction. untreatable.

what to consider when cows are grazing?

quality of grass often variable, difficult to assess. common mistake to overestimate the value of grazed grass, esp. in long dry summers. other issues: frothy bloat from clover, mg deficiency. can feed "buffer" to supplement. prevents overeating of hungry cows.

Presentation of mastitis

re-watch this

in a fed omnivore, what are amino acids used for?

really versatile. you can use them for lots of different purposes (de-aminated) or just go straight into muscle protein. we eat too much protein

What should you do with dead lambs on farm?

record: twin/age/sex, etc On-farm PM useful: ZST, colostral transfer, navel ill, fractured ribs (dystocia), fat cover around kidneys, goitre, tests for toxo/EAE

which cows should you culture for bacteria?

recurrent cases, persistent infection, rise in somatic cell count. it's important - can never tell on the basis of clinical presentation. you can freeze the sample. also can do a bulk take sample. but individual quarter sample is important: cleanse udder, swab teat

what is traffic-light isolation protocol?

red: must be isolated unless clinically unstable amber: barrier nurse in WARDS/ICU, awaiting micro/virology green: patient can be nursed in wards. only after CARRIER STATUS resolved. degree of hygiene still must be there.

How to control endoparasites? Main goal

reduce #s on pasture Anthelmintics BREAK life cycle but want to minimise use "safe pasture" - alternate species/adult, long grass = dilution affect, or convert to hay/silage aftermath or crops Sell lambs/kids early to minimise # of susceptible animals

how does increased animal welfare affect food safety?

reduced stress-induced immunosuppression, reduced incidence of infectious disease on farms and reduced shedding from farm animals, reduced antibiotic use and antibiotic resistance.

Where are most of the nematodes living at any time?

refugia (grass), pasture. Small % on population. Bulk on the lower part of the grass where it is warm and moist, not dried or exposed to sunlight. Best part of the plant: 5-10 cm. the lower end has no calories and parasites , so mgmt of pasture can prevent

what is the difference betwen regulations, directives, and decisions?

regulations: binding, directly applicable laws. don't need to be approved by national parliaments. example: salmonella control/monitoring. simple, clear, direct. directives: bind the member states as regards to objectives to be achieves, which then must translate them into national legislations to meet the directives. decisions: fully binding on those to whom they are directed (country, entitiy, etc)

what is the role of iodine in sheep/cows? what are signs of an iodine deficiency?

required for synthesis of thyroid hormone - can get goitre, increased peri-natal mortality.

what notifiable diseases are "hot" right now in the UK?

right now it's african swine fever (stays in ham), avian influenza, bluetongue, newcastle disease (neurological in birds), BSE from scotland

problem mastitis cows often caused by...

s. aureus - highly resistant. persistent high counts or 3 or more cases in a lactation. can: cull put in problem herd. treat at drying off + bacteriology and see what happens.

what are "latent zoonoses"? what does that mean?

salmonella, e. coli, campylobacter: can be in perfectly healthy animals - including "super-shedders of E. coli" but can transmit diseases to people. it's not the goal to make animals healthy. the goal is to protect people.

How to help lambs get colostrum? How to check for colostrum?

same rationale as calves. Linked to ewe feeding. Husbandry important: targeting the calves that need supplementation. hungry/assisted birth/meconium stained need the most help 50 ml/kg in 2 hrs, 200 ml/kg in 24 hrs. essential. to check: pick them up and squash them. If you can get your fingers to touch - their belly is empty.

how do you select for health and welfare traits?

several traits such as calving ease, longevity, and TB resistance. the LIFESPAN index includes feet/legs, locomotion, mammary, fore udder attachment, SCC, etc. you can include more info as daughters age.

peracute mastitis: clinical signs? prognosis?

severe nerotising/gangrenous. - "toxic" form due to coliform endotoxin release or gangrenous due to s. aureus. - usually around parturition and death can occur GROSS: swollen painful hard quarter with rapid progression to gangrene (necrosis). - rapid progression to MOIST gangrene: dark-blue to black, blistering, oozing serum - death, sequestration of glandular tissue leads to sloughing - cold to touch - ventral abdominal oedema - can be comatose (toxaemia)

what is the cow comfort index?

should be 85% lying down/chewing cut 1 hr before feeding. they should spend 60% of their day lying and ruminating. assess the comfort of the cubicle.

s. agalactiae

slow, progressive, chronic. fill in

what are ways to reduce zoonoses in exotics? what are some examples?

small "furries" - often handled by hildren reptiles/fish - hygiene of tanks/equipment birds - dispersal of pathogens in faeces, during flight (psittacosis) reptile related-salmonellosis is zoonotic, same with fish tank granuloma (mycobacterium marinum_

what is water holding capacity of feed? how does it affect VFI?

soluble fiber/non-starch polysaccharides will retain water and prevent absorption by trapping it in the cell wall. this slows the passage of food, decreases feed intake. chopping the feed/decreasing fibre length will increase feed intake.

how should you safely control a horse's eating?

some horses might eat wood shavings and can cause obstructive/distension colics. if you change their bedding from straw to wood, they will eat it. grass can provide excess calories so you need to reduce grass consumption - turn out less time, strip graze, or a grazing muzzle. the muzzles are controversial make sure you add balancer.

environmental pathogens cause what type of mastitis? how? which bacteria are they?

sporadically gain entry to udder and can cause very serious mastitis (or be rapidly eliminated). if quarter infected during dry period, can persist and cause problems in early lactation. can gain entry at milking time, but housing design/management also important. cubicle design, yard management, scraping of dung, and dry cow housing also important. organisms: e. coli, strep uberis, klebsiella (woodchips), coliforms - bacillus cereus, fungi , yeasts

what is hypomagnesia? what are clinical signs/treatments? how do you prevent it?

staggers/grass tetany. signs: hyperaesthesia, ears twitching, sensitive to sound/hand clap, staggers/collapses, champing of jaws, sudden death. can have a slow onset over 3-4 days with spasmodic urination/defecation. they are dangerous because they kick a lot. chronic: few signs. just poor appetite/depressed milk yield. INCREASED HR ALWAYS. treatment: urgent. bottle Ca with Mg, Mg sulphate. give IV. animal can kick. so be careful. prevention: MgO in concentrates, mix with molasses (it's gross). bolus orally to those at risk, can also add tablets/flakes to drinking water. avoid K fertilizer/pig manure if hypomag is a problem.

what proportion of costs for sheep farming goes to a vets? what about forage and feed?

vets: 5-7%. however they can influence efficiency of feed/forage, productivity, and overall cost effectiveness. forage/feed: 30-40% for lowland, less for upland/hill

What is the EU animal Health law?

strengthens enforcement of health/safety standards for the whole agri-food change based on PREVENTION over CURE. simple, clearer rules to enable authorities to focus preventing and eradicating disease. responsibilities clarified for farmers, vets, others dealing with animals. also monitors AMR.

contagious mastitis often causes what? which organisms are involved?

subclinical infection. spread from cow to cow at milking and lives in the udder, teat skin. organisms: strep agalactiae, strep dysgalactiae, staph aureus, and strep uberis (from the environment/straw bedding, and then spreads from there) Minor pathogens: Coagulase-Negative Staphylococci (unlikely to be pathogenic)

what are clinical signs of mild, moderate, and severe bovine paturient paresis? how is it treated?

subclinical: able to stand, excitable, tremors, eat twitching, ataxia, flies. moderate: sternal recumbency, depressed, dry muzzle, cold extremities, bloat/gas in gut, no defecation, delayed/absent pupil response. "S neck" severe: reduced consciousness, lateral recumbency, unresponsive to stimuli, muscle flaccidity, reduced CO treatment: give calcium lol. often mixed with magnesium, P, Glucose. can give subcut to even out Ca levels (slower uptake). give IV slow and monitor HR. she should burp and sit up. first thing she should do is eat.

Affects of haemonchus?

sucks blood Strongylus: plug feeders - physical damage. Verminous endarteritis (goes into the arterieS)

what's an issue with self-feed silage?

system where cows feed directly from silage face. opportunities for fermentation, spoilage, moulds, and mycotoxins. tightly packed silage has an issue too.

what is a way to measure quality of silage?

take the pH and the Ammonia N. - amount of ammonia N (degraded protein) leads decreased silage DM intake consistently. - low PH is slightly correlated with intake, high pH negative relationship. these are both correlated with quality of fermentation.

what is oak poisoning?

tannins from acorns: precipitate enzymes secreted by microbial bacteria, reduce fermentation, cause GI ulcerations and are fatal.

what is genomic selection of cows?

testing a cow's DNA at birth in order to assess its various performance qualities. it saves time because you don't have to wait 5 years until its progeny grow up to determine its EBV.

how do you define selection intensity?

the difference in the mean for a trait between the total population and the population that is currently breeding. however it has to be balanced with the need for genetic diversity. selecting a breeding program just for one disease is not generally a good idea - can end up with other disorders (inbreeding)

what is hybrid vigour?

the heterozygote advantage. however it's a "one-off" hit. the F2 can lead to backcrossing, and then have the same issues as the grandparents.

what does it mean for a gene to be Identical by Descent?

the probability of an animal having two identical copies of a gene. correlated to a risk of inbreeding - removing large amounts of genetic diversity, increases proportion of recessivity, inbreeding depression. small levels of inbreeding have huge effects.

what is heritability?

the proportion of a phenotype of a disorder that we can attribute to genes. we can use these to create an EBV (estimated breeding value).

What does bulk tank SCC indicate?

the proportion of quarters that are affected. epithelial cells increase towards end of lactation and are high immediatly after calving. will die down. subclinical infection can cause prolonged mildly elevated SCC of quarte (>200), spreads at milking time. contagious organisms.

what is a risk pathway?

the sequence of events or actions that can lead to outcomes happening - can be the basis for prevention. EXAMPLE: bovine reservoir of STEC. shed in faeces, milk, water, and beef. humans can get it from direct contact, drinking/bathing, uncooked/partially cooked foods, milk.

how is hygiene practice on farms regulated? what are some things that can be done?

there are FSA guides to dairy hygiene. it's not legally required but they make recommendations to achieve the standards required by law. - staff information/training - health status of staff - maintenance, cleaning, and disinfection of equipment - pest management - waste management - animal production monitoring - general aspects that are relevant for animal welfare and health.

how does cow feed/what they actually eat differ?

they don't eat palatable things and they favour high energy/protein. they also won't eat old food. don't want to starve them into eating. also, they might be affected by bullying - trough space. make sure they all have enough space. need at least 60 cm per cow. physical condition of trough, plenty of clean water, enough space around the water trough, and the flow rate. make sure its cleaned out.

how do leptin levels change in dairy cows? how does this affect VFI?

they have a negative energy balance. despite this deficit, the metabolism is devoted to the mammary gland. this reduces plasma leptin and could increase feed intake, divert energy from non-vital functions. VFI increases sharply after calving. however they aren't making that much milk in the beginning - can eat too much.

what are the important amino acids that pigs need? vitamins?

they need 10 from the diet: lysine, methioninc, and cysteine. lysine most important. can constrain growth/productivity. vitamins: E, selenium. otherwise get mulberry heart disease. vit E can be degraded over time.

what are ketone bodies used for (non-pathologically)?

turned back into acetyl co-A and oxidised in the muscle. the brain uses them preferentially because they can't use LCFA/NEFAs. reduces need for glucose when you're fasting. SCFAS (like KBs) are soluble.

what is a milk spectroscopy machine?

visible, near-infrared, blah blah detectes fat, protein, lactose, SCC, and MUN. LDH increase as a mastitis indicator.

what is molecular genotyping used for? how are dogs categorised based on their genotype for a specific disease?

used by the kennel club. to detect SIMPLE diseases in dogs. blood/mouth swabs used for simple inherited disorders in many breeds. microchipped/tattoos. effectively reduces, eliminates undesirable disease genes. however there is very little regulation for DNA testing centres. recessive genes: will be either CLEAR, CARRIER, AFFECTED. - the issue is that the breeders will only breed clear to clear and eliminate a large amount of genetic diversity. should also breed carriers. dominant ones: clear, heterozygous affected, or homozygous affected. only breed clear to clear. you can do linkage tests but they are not very accurate.

what is an in-line SCC?

uses ATP luminescence as an indicator as the number of somatic cells in milk. connected to the milk hose below the claw

how to score cow dung?

want it to sound like one hand clapping. score 3. when pushed for higher milk yield - more concentrate - more loose faeces.

when is subclinical mastitis most common?

wat

how do you assess poor thrift?

weighting: varies with breed, age, gut-fill stage of production cycle BCS is better.

how to measure voluntary feed intake? why is it important to measure?

wet weight, dry matter, per unit of metabolic weight. all give different answers. average is a good answer, but it's usually a per kg DM intake. optimise intake for production, economics, weight control.

what can a selenium/vit. E deficiency lead to? what is its role?

white muscle disease - muscle cell necrosis. can be congenital at birth or at 2-6 weeks. sub-clinical: poor growth rates, abortions, disease susceptibility. can eventually lead to locomotor abnormalities, respiratory difficult, and death. they are thought to play an important role in immune function as well and protect agains free radicals, lipid peroxidases.

mycoplasma bovis

widespread organisms, major cause of mycoplasma mastitis. milk yield dramatically decreased. habitat: genital, respiratory tract MMs. reach uder via haematogenous spread. NO B-LACTAMS

what is listeria? how does it get into feed?

widespread pathogen in the environment. can affect cattle, sheep, and goats in contaminated silage. low silage pH will diminish growth but if the pH gets too high, it will be contaminated.

what is the key management strategy to avoid contamination of drugs into animal products?

withdrawal period - part of licensing procedure. there is a lot of changes in terms of antibiotic use. RUMA (responsible use of medicines in agriculture alliance) has guidelines.

List a yellow, white, clear, orange, and purple anthelmintic.

yellow: levimasoles white: benzimidazoles clear: macrocyclic lactones orange: amino-acenonitrile derivates Purple: spiroinoles NO resistance (yet) to purple or orange. Used for "clearing" the gut.

General signs of a parasite for growing v. Adult animals

youths: poor wt gait, Poor feed conversation ratio, +/- anaemia, Death adults: weight loss, poor BCs, reduced fertility and production. Can get immune by the time they are adults.

What are the most important internal parasites in grazing animals?

~ nematodes (all species) ~ Liver fluke ~ Coccidia ~ Lungworm

what are two ways that selection can lead to disease?

~ planned selection related to exaggerated features (brachycephaly, etc) ~ unplanned selection (deafness with piebald gene, etc)

what are genetic forces acting on breeds/populations of dog?

~ selection: natural (still happening), artificial ~ loss of genetic diversity: inbreeding, genetic drift (hardy-weinberg principle) due to making new breeds ~ immigration (out-crossing), such as the dalmation which was outcrossed with a pointer to resolve urate stones. ~ mutations