Animal Nutrittion 2

II/A/2. Feeding and Care of new born and suckling Piglets.

1) Standard date 2) Suckling piglets 0D(1.5Kg)-D28 (7-9Kg)!!!! 0-10D= Colosturm then milk 10-28 Milk ? prestarted/creep feed 3-4xfeed aday Post natal nutrition 1) *Bw* doubled during each week until 3rd w. high energy & heat, supplement. less then2% bodyfat, new born glycogen stores only keep them alive for 2hr, colostrum is imp asap (Glucose>>>>>NB Vs Fat) Colosstrum vital=ABs, antibodies dont cross plasenta, absorbed in colostrum in first 36h of life, availible 10hours before-36hours after. best quality at beginning 2) Composition of milk(sow) colostrum= high in Prot, low fat vs milk. Trypsin inhib. High P> Ca bc piglets need this first, protective factors= IG, protective C(macrophage/lymphoC) Regulatory factors= epidermal growth factor, insulin. Enz= amylase, lipase, protase(inactive), NB for milk replasers 3) NB nutrients for suckling piglets *fat*=major *E* source, emulsified by lipase(secreted pancrease). Proprionat,but, A (VFA) inhib E.coli growth! adding fat into late preg sow will increase Milk Fat and weaning weight. DO NOT overfeed preg. sow! underfeeding is less problematic. *H20*, sow milk not enought, so additional must be provided. *Iron*- piglets need iron supplement 100-200mg fe dectrain given after 3ishD (if not might destroy AB!). Fe toxicosis includes stiffness/lameness. Absorbed Mothers milk not enough. 4) Prestarter (creep feed) induced from 2weeks, Prot Rich 24% E*14MG/kg* fat sourse is dry veggetable oil similar to sow milk ensurieng better absorption also contains extra flavour. Fed by scattering it on the floor so piglets can recognise it and eat aroun 1kg during sucking period, good but expensive! Creep feed=prestarter, on ground eat 1kg during suckling period *CP=24%* *DE* (MJ/Kg) 14MJ/Kg Energy stays the same: CP Fat, lysine, ca&P decrease. Lysin=NB= add as it limiting aa w optimize growth. 0Hour 12H 2Weeks Prot 60 49 30 Fat 20 35 40 Lactose 8 16 2 Vit E/selenium deficiency= retaine placenta, Se=pangrease/fibrosis.

II/A/9. Digestive Physiology of Horse.

1) Digestive characteristics: Horse has highest CF digestion ability of all monogastics. Adapted to frazing choosing grasses highest in h20, h20 sol. proteins & structural carbs but low in starch. During domestication increase amount of cereals were fed so the EQ had to adapt, metabolism 3-4x slower then RU bc more intesive chewing, EQ needs long period FI. Eq are ceacal & colonic fermenters. 2) components involved in EQ digestive system: 1) Saliva - 40L/D depending on feedstuff, no digestiv enz. HCO3 content moistens feed & buffers the prox part of the stomach. 2) Oesophagus: Acute angle, the spincter does not relax inhibiting vomiting & erucation leading to Colic & stomach rupture. pH5 3) Stomach: small capacity, 8-10L, 9% of GI capacity, Dos not reach abdominal wall. Protein digestion limited bc short transition time & small size, ingesta remainsin stomach for 2-6H then move on the duodenum microbial fermentation of readily vailible carbs producers, lactate; absorbed in SI. Prox part= pH5 & pylorus=2.5 bc HCL secretion. ingested h20 flows along greater curvuture to avoid high prod of gastric J. 3) Sm Intestine Carbs plit into glucose&absorbed. A-amylase in pancreatic juice only 5%, most carbs passed to Li. DIetary proteins are partyly hydrolyzed and aas are absorbed/used 3x stomach. NPN are absorbed and transported to liver. Fat; no GB, cont. secr. of bile resulting in good digestible & increase tolarance. Most minerals & vit exept P are absorbed in SI, P=colon. 4) Prececal & preileal digestion of starch: Source of starch& degree dependent.of Cereal. Oat>barly>whole (ground has highest dg) 5) Cecum; 16% of digestive tractm crucial role in fiber digestion. 6) Large intestine Microflora & fauna contents in the LI is simmilat to Rabbits, Lactobacilli/streptacoccus/bacteroides & protozoa (ciliates). Dietary carbs (cellulose) & prececal digested starch are fermented in VFA & absorbed as E. Rapid Fermentation of starch= increase Heat/sweatting, barly is not rapidly fermented as corn. Excess amount reach the hind gut then Lactic A is prod, lowering the pH6. To avoid disorders 16-18% CF should b fed (laminitis&diarrhea). Proteolytic enz=>protein breakdown =>aa & nH3 most which will b used for microbial protein synthesis but some aas are absorbed. Excess NH3 from NPN is absorbed(transformed in liver)Urea=>excreted as urine or reenters ileum as NPN to continue the cycle. NPN supplement is prohibited incase of NH3 toxicosis. avoid startch overload & excess fermentation, EQ should b given 3meals/day & conc. should follow forages. hay 1st limits fermentation. Oat 1st results in whole starch content fermenration.

II/A/21. Feeding and Nutrition of Beef Heifers.

1) Lactation of the beef heifers is only meant to cover the need of the calk, calf rearing is much longer than dry cattle. 2) table: age weightKg ADG Notes birth 50 900-120g pre-weaning stag 7Month 200 500-700g weaning 14M 300 400 mating 24M 480 250g calving/suckling 3) Four dif nutritional preiods used: 1- Pre-weaning, 0-7Months )00-1200g Goal= great devel=> wean ASAP conc are given from week3 to increase propionate:puberty is reached earlier w/conc (LH increase). Quality Hay=>Increase Acetic A. Also in US:GH may b implanted 2-3 months 2- Weaning to mating 7-14 m, ADG... its 180-270 kgm if under 180kg she will not b a good mother! High quality feed good w dg &BV-forages, grain, corn silage.. 60-70%adults BW should b reached by mating time. <flushing takes place 2 weeks b4 mating:Increase E:P, B-carot&vit A to increase # of ovulated eff (Increase fertility rate). Matin of beefheifers is done 3-4 weeks earlier then dairy cows. 3 Mating & calfing:14-24 m, ADG 400g BW should be 85-90% adults. 1 oestrust is norm skipped, calving is 10 months later at 24months. Heifers needs extraEnergy as shestil needs to gain weight (400g/day) besides the E needs for preggo. Good conditions eses calvings& re-breeding. NEm+NEg ? E for preggo 4 Suckling adg 250mother still need to gain weight, so supply should cover this (250g/d) in addition to lactation E. NEm+NEG + excess energy for lactation, NEg is uced until 4th lactation when the mother is now an adult. Nutritional requir of BEEF breeding heifers & cows. 1. maintanance Energy. 0.322xW^0.75NEm Pregnancy:Tranformation from ME=>NE is only 13% in preggos, NEmdep on birth weigh & Time of Preggo 2. Lactation Energy depends on fat milk content 3. Prote 2systems; a-factorial calculation(usa) give CP by calculation input&output(beef). b-MP system; give value; MPe&MPn use the lower one (dary) 4.May be benegicial to give vit A injection 2xYear Condition scoring of beef: 1-Nebraske system: touch ribs 2 check fat cover (from 1-9) 5 is best, 6,autom)=beef 2-Scottish system used fairy cows, beck &mtail region is evaluater (1-5...3best) Feedstuf=> must b ecconomical, chep is bettter 50/50% grazing&hay, Strawes depend on time of cutting, earlier are similar to hay. No NPN source (bc constant E deficit, mictobes dont get enough energy to build in urea). Beet pulp not in frozen form. Silage in combination; corn stalk & diluted molassess good DM content & cheap Calf nursery: Concentration onluy in high deman; exp used in calving & flushing Minerals: P (As lib) & salt in licking stones, dopends on soil type, hungary is low. Vet B-carotene& vit A better in foor tather then inj. Proteinc souce=Alfaalte; 1-2kg carrots or alfalfa before mating

II/C/8. The most important metabolic Troubles of periparturient Dairy Cow, and their Prevention.

High producing dary cown are most susceptible to metabolic diseases during the periparturiens period. In cattle these diseases are acute, temporary but potentially fatal deficiencies Milk fever- hypomagneseamis-ketosis-fat cow syndromes Milk fever: 1-24H after calving: high ca(bc milk production) , low PTH, hihg P. positive correlation w/age& milk production as Ca utilization decreases by 205 IN OLDER COWNS, & pth_R ON BONES DIMINISH. sYMPTOPMS: Early= decrease appetite, git becomes inactive, full, ears &muzzel cold. Later=cant stand, head turned to side possibly due to other sieases like reteined placenta. Ca is requird for the release of Ach @ neuroM. junction, animals experience M. weakness=> cows befome 2 week 2 stant=>comatose Cause: *clasical*: Ca rich dies at dry, downregulates PTH, when prod starts again, Ca cant be mobilized from bones quick enough *Atypical*: large P is given counter balance the high Ca,=> decrease Ca absorption by inhib :1.25DHCC. *Cation-anion* balance of daily rotaion: feeding a cationic diet during dry period increases chances of milk fever as PTH response decreases. Anion diets decrease the chance of High blood Ca & PTH responsiveness Prevention: Cover maintenence & gestation only, last 2weesc before calcing decrease Ca intake @achieve PTH. recomented @ dryperions *6.1gCa* & *4.2gP/10kgbw* Hypomagnesemia =grass tetany, & reduced Mg in CSF <0.1mg/dl=> hyperexcitability, M.spasms, convulsion, respiratory distess, collaps/death. Caused= Decrease levels in spring grass, oftenoccurs w decrease Ca. Absorption of Mg is cegreasedd bc less NA or 2hihg P/K. prevention: licking stones, Mg supplement/bolus 3mg/kgBw, lactations=120/kg milk Fatty cow syndrom: often in fat cows fet 2 fatty food + snutritional stress during last 2 months. after calving lose appetite, grow weak, weak puls, fast...sternal recumbancy occur. often see excess nasal discharge& rapid breathing w grunning. a week after 1st signs the cow comatosies & dies! prevent by propper feedng & treatment w/anabolic sterioids & glucose fluids + electrolites IV. Displacement obomasum inc chance if fed high-concentrate low forage diets. & those only fed finely chopped forage grasses. =mild 2ndary ketosis, prewented w proper treatment Downer syndrom Hypocalcemic parturient paresis, its fatal. M.necrosis nerve damage of hinds, nepatic myocardial degredation Dystocia: difficulty calcing bc obesity, tetosis & milk fever. prevented w proper feeding, txus assustece during parturation chronic lactacidosis: high CC lactic A. anorexia, dec milk prod.. tc: buffers. mastaits/=low se, VITA!, E metritis:= ketosis Low VitE. B-carotene def= sterility, oestrus prob, 300mg/cow/day

II/B/6. Feeding and Nutrition of Chicken Hybrids kept for Egg Production. II. Layers (Commercial Hens) laying hen period

Laying hens are thos ekect for market egg production, begins at 18week ends week 75. where each egg will produce around *300eggs*, =3%Bw (60g), after 75W they are sloughters or cept for nd laying (dec egg prod) Breeds used for hybrids: 1) Leghorn= white eggs <2kgBW, danger of being obese as fed Ad libitum 2)Leghorn?rhodeisland/newhampshire cross=Brown eggs, medi, controller FI. ***Level of egg production: expressed at % week 18; 5% (100birda=5eggs) 20 W=10% (1.7Kg) 21-23W = 50-60% 24-26W=95% *peack* Its impassible to reach 100% takes 26hours to mae 1 egg & they dont produce after 4pm. they always 2h later then the prev day, after 4pm they take a break day and start the week again (8am-4pm, break->8am) 65weeks75% mintained until end ofleying period. Nutrion of laying hes - FI is regulated by h20 suppply, if intake decrease then= poor /sick herd! 3diets bc changes in rew: Pre-Layer(18-22weks), Layer1 (23-64W), Layer2(56-75weks) Nutrition - *CP%* - 16% for prelayer, then increase: 18% but decres 16% (bc layer 2=>produce less eggs) -*ME* *MJ/Kg* Roughly at 12MJ/Kg: covered by careal grains - *P:E* g/KG: Highest in Layer 1, lower vs broilers as requres less. - *Lysine* = 6.4G/Kg less then broilers as used for meat production - *Ca* Prelayer:18g/kg-> layer1:36g/kg->layer2:37g/Kg (higher Layer2 bc eggs larger, & reserves are empty, supplement w grit) - *P* g/Kg= stays at 4 Feeding comercial hens: - Ad-lib: feed mash to limit intake -Grits: limestone particles, Ca supplements, 2.5x actual requirements mst b given, FI decrease if 2much. -Efficiency: 2-2.1Kg/kg of eggs=> layer feed contains less energy than broiler, very efficient Lighting program: - 18-21weeks: gradually increase from 8h/day @ 10 LUX to provoke sexual maturity (which is done by icreasing 1H/weeks= -22W: 12H/d @ 20Lux -24W 14H/d @20LUX 85% egg production: 16Hr/d- Keep max light to ensure max prod.

II/A/14. Applied Digestive Physiology of Ruminants. II. Degradation and Synthesis of N containing Substances.

Nitrogen degradation & metabolism. CP= total N(measured with the kjelfahlmethods)x6.25 TN true protein (AA-UDP/RDP) NPN(urea) common in meat producing animals, never in dary as their microbes are saturated & cannot produce more NH3 (energy def) Protein defradation: TP (bact.Protease)->Peptides (peptidase)-> AA(deaminase)-> NH3+VFA+CO2. 2NH3=Urea is convertd to NH3 w/urease tis is the most important starting &end point prod. Rumen diagram; Draw circle CP= NPN->NH3->M.P CP->TP->UDP-> => RDP(rumenDegra.Prot)-how much of the 100%is rumen degradable? 1) High- 70-90% of feed protein= degraded in rumen only 20%(UDP) reaches the obomasum=not enough (wheat, barley, sunflower meal) 2) Med; 50-70% feed protein is degraded in ruen (corn/soybean meal/grass) 3)Low is 20-40% animal producs like meat/fish meal banned in EU (70% will reach the obomasum, good dor dairy cows as microbial protein is not enought to cover hight protein demand) The longer feed spends in rumen the less UDP occurs & digestion increases. How to increase UDP of feedstf? -Heat treatment= lowers RDP but we have to make sure it can b degraded in the intestines. -Formldehyde treatment= strong connection bt aldehyde & free Amino group of prot allowing it to b degraded in the SI. -Maillard reaction= connection bw carbs&prot in rumen allowing degradation in the SI (calkedsy pass(Soy bean as starting material) common feed additive in high yield.). -Capping= methionine (limiting AA is High yielding cow), microbial protein does not have neough of it. Protec it by capping ith a lipid layer allowing it to b broken down in the SI by lipase. Connection bw liberation of Ammonia & E in Rumen. - If ammonia is liberated quicker than energy this leads to: Graph.; Ammonia excess-cannot be fixed by bacteria not enough E so it is absoredas N-waste. E-excess-npt enough NH3, not enough NH3 to b Built in Add Molasses to brung up E. Levels: UFP-UFerm..Porential: calc from the TDN & Dg (degradeble prot) #Urea added 2 1kgDM= Depends on P:E >0; urea ma b added, value shows how much in gr =0: No need for Ureas; <0=Do NOT give urea MPN<MPE=E is in excess so give Urea MPN>MPE = N excess, DO NOT give Urea (dary cows) UREA supplement: 20-30g/100kgBW/day. UFP= ((1.044xTDN-do)/2.8)

II/B/3. Digestive Physiology of Poultries and its Nutritional Consequences.

Use chicken when it comes o basic feeding req of other domestic avian sp. except pifeons: the values are opposite for them: Hybrids: used for the prod of market eggg/meat, they are breas & cross bred for their traits resulting in higher prod levels than their parents. Purebreds are only used for prod & breedng eggs. Pure breeds : those used for producing hybrids are 3 groups= Ligh, mean & heavy breed. Bw & egg prod are negatively correlated!!! GI tract poulty, body lengeth:gi lentth= 1:5-6 1) Beak: Ø teech, rigid tongou, ducts not adapted to seed, geese are adapted to grazing. Poultry- originally seed eaters, they prefer feed similar to seeds: 1) Mash(brown meal)=used to decrease FI!! 2)pellets (ground feed+molasses&pressurised)=larger. 3)Crumbles(made from pellets)=size, btw massh/pellerts Since FI dosnt depend on E content bu phys form, we incrase or decrease. The FI by changing form & not E. content. Aso colume of feed depends on form, so increase FI, we can give more conc.feed 2)Saliva: low #(10-30ml w/MYLASE&INACTIVE LIPASE)!!! 3)Oesophagus: flexible, part makes food softer & lubricates. 4) Crop (enlargement of oesophagus in duck/goose) Storage place, small in small birsd so they need more frequently meals. Digestion;not excessive, main dg is in SI. Facilitates prervation+ moistens: pre-soakes/softening, Pigeons form crop milk from ep C. for young! 5) Gizzard: grinds feed into smaller particles due to lack of teech (m. part)= grit is given in feed to help mastication, grit can b normal stone 6) Proventiculus= secreats HCL & pepsinogen when feed is detected. 7) SI= Very short, narrow, villi/microv.. Ø lacteals, cerial grain need to cover E (10-15%CP) and Legume seeds protein. Nutritional conc of narrow int= B-glycans(NSP ant fact of barly) has high vistosity, so bind humidity in narrow SI and decrease digestion of valuable nutrients?!?! 8) Liver: no b-galactase so no digestion of lctose, degraded by bact fermentation 9) caecum: doubble but small 10% feed reach caecum=low digestib of fibers (2-3%) and some fibers needed to increase peristalsis, but 2much decrease diggestion and increase cecal loss. 10) Cloaca= Urine and facese together so ME is needed. Poultry are strong animals w good production, in order for the production tto increase every year, the feed needs to be good quality! Groups of feed in poulty diets: E surce= 60-70% if feed mis: cerial grains = cerial grain (CP10-15%) need 23.5% in started diet. Protein source= 30-40% of feed mix: Legume seeds (CP20-40%) and extraced oilseed meals (35-50%CP) supplements,: feedstuf dont contain enough minerals= Vit/minerals/AAs (oil n seeds= if 2low Linolenic Acid (omega 6) groth decreae, or skin problems!! NB factors feedstuf used in poultry: 1) Cerasl: list ifferent specifications of from feedstuf (*Corn/Wheat/Barley/oat)* Legumes seeds (*Field* *pear,horseBran,Lupin&SoyB*) Extra meals (*soyBeanMeals/extSunflowerMeal/ExtRapseSeedMeal*) Diluted E Density (*WheatBran&Alfaalfa*meal)

Pigs stadard data Definitions Weaning: Include this to ANY of the pig topics!!! + draw the Nutritional life cycle (0day born, 28d=weaning. etc...) Birth weight? colostrum weaned etc

*Weaning* = a big adjustment in social, thermal, and physical env and also huge change in diet form & composition days feed/notes 0 Birth: 1.5kg 0-3 colostrum 0-10 mothers milk 10-28 mothers milk & pre-started (creep feed) 28-42 pre-started & started (weaning =2-70D, 7-9kg) 42 beginning of started diet 70-90 piglet diet, ad-libitum 90 end of piglet period -30 kg -F1=1.1.2kg/d - Puberty: 6 - 8 months - Estrus length: 19 - 21 day - Eggs ovulated per estrus: 10 - 20 - Gestation length: 3 months, 3 weeks, 3 days - Lactation length: 21 - 42 days - First estrus post weaning: 3 - 7 days - Average litters per year: 1.7 - 2.5 - Weaning age: 3 - 4 weeks - Dry matter consumed per day: 2 - 3% of body weight 44 teeth+ including 3 incisors and 1 canine in both the lower and the upper jaw. 3143 3143 gi length = 14x the body length

II/C/3. The Most Important Metabolic Troubles of Goat.

1) Abortion (def VitA, Copper;Iodine) stress abortion=> decrease glycogen levels aroun 90-110 D, oesopgagenous effect of sterioids produced by kid Habitual abortion: hormonal imbalance=Zbc death of foetus 2) Acute EnteroToxaemina: (High cc= Lactate toxic) after birthd= bc C. Perfuringer C/D, Rumen =pH4.8=lactic Acid toxicosis 3) Ketosis (def E. Intake, glucose demand vs Na-Proprionate+ prop.glycol 600mg/ml) high ninEsterifiedFattyAcids 4) Parturient paresis: basically the same as milk feaver, like in Dairy C, less common 5) Poshtitis (overfeeding proteins) Urea cc Uring HIGH bc HIGH PROT Diet= corynebacterum renale=inflam preputum 6) Toxic plants: goats normally resistnat, tolerate TANNIN! 7)Urea toxicosis Lethal dose 0.44g/kgBW 8) Uroluthiasis 8increas grain, CaPosphte struvite) Bucks who ingest high levels P and low Ca+K diet treat w KCl mixed into feed to acidify urine

II/C/1. The Most Important Metabolic Troubles of Poultry.

1) Acutey Death Syndrom: Chicken(C) + Turkey (T) Acid-Base distrurbance=increase Plasma lactate(bas an extrarenal buffer 2 combas the alkalosis, but) Increase ein blood latctat damages the cardiac system=Acute Renal syndrom. Mainly males 3-4W old chickent Caused= Easily fermented carbs, Lactate acidosis (bc heatstress/ionophore coccidostatics) =sudden death bc breakdown of cardiac tissue&circulation. Solution: Day long feed restriction; 10-15% less at 20D old! 2) Aortic Rupture of Turkey (T) Damage 2 Vessel wall. effecting 12-16W, Mostly Males Caused: 2 high protein & fat levels in feed at 1st 3 months. Øenough copper.= sudden death 3) Early motility: 1day old chicken (C) cause: Microelement deciciencis&vit from parents supply of yold. 4) Ascitic syndrom: (C) High protein synthesis bc rapid growth, needs mroe O2 whihch it cant fet=> high Serum-containing liquid enters into abdominal cavity. Right ventricle of hears is enlarges=R. sided heartfaulure? acitis (body trying 2 meet O2 demends=>pulmonary hypertension) Broylers, maily males causes (poolry oxygenated tissue bc): High protein secretion, good feed convertion=rapid growth :( 5) Cage layer fatigue (C) Egg production & Ca levels meintained by excess ASH content of bones=>spontanouth fractures(osteoperosis=>crippled unable to stant Layers in battery cages Cause: disorder og CA metabolism (@peak egg production) needs are met but mobilized from bones=>Osteoperosis. Solution= Ca supplement?extra ascorbic acid intake 6)Goose stress lameness syndrome: (G) Dont produce enough endogenous Vit C by Kidneys=> relative deficincy. 1D old&growing gese cause: multiple stressors=>over pop, heat/wind/cold: Fatty inferter in fibroblast of collagen fibers! Solution=decrease stressors! 7) Fibre Deficiency geese: 2 little fresh grass& 2much commercial feed (=ish 6%CF) geese needs 12!!! caecum inflamation, bedding, plasma in lumen. Solution= give more 8)Hind Gut acidosis: Layers fed 2much concentrates! Process: accumulation of LacticA. bc hind gut of lauers when they are exposed 2 new single cereals (corn/wheat/ry/barley) Solution= let them adopt 2 new feds & mroe concentrates slowly!! 9) Fatty liver &kidney disease: young chickens: bc Biotin&choline def=> increase Fatty Liver&kidneys, die in sitting position. Solution= give choline + biotin in drinking water 10) Skelletal disorder: Intensive growing broilers & torkeys. Rickets, juvinile ostepporasis & tibial torson/tibial dyschondroplasia. caused by genetic disposition of 2 hight growth rate 1 or 2 lack of nutrients & ant factors 11) Osmotic diarrhea: diet w/high salt! associated w NonStarchPolysaccharides (NSP). increase luminal digestion

II/B/7. Feeding and Nutrition of Turkey Hybrids.

1) Charecteristics: Use either whole bird (broilers) or valuable glands (giant) for food. mostrly year around. Healthy mean less then 1%fat Female broilers. growrate until 18weeks, andmaes 24 weeks. Sexual dimorphism: femalsa 1/2size males. Main companies: British united Turky UK, Hybrid turkys inc canada. 1day old=60g. Type of fattening (not genotype) can either b Heave (M&F) or Semi heavy(Only M). 2) Cycle&growth Male: 22weeks=25kg=sloughter Femal: 18W=12Kg=Sloughter Measuer breast weight 4 groth intensity *35%of* carcase Feed efficiency: 3Kgfeed/kgBW gain (Broliers=2), good as it is only for 6month (76kgfeed) daily weigh gain *150-160g*best of all *poultry* 3) Feedung gaint/heavy turkeys: dont produce more fat w age, prod in diet decreast, FI increase. E needs increase w/age, as maintenence needs hig w growth, not enough E will Increase FI. Goal is to produce valuable bodyparts for human consumption. Giant turkeys=90% of turky mean on market, kept for longer perisods. Giant turky =Ø a hybrid but a way of reading. - Female giant turky (Økept after 12kg bc eat more, produce less. switch 2 less nutritionous diet than maes as feed efficiency decrease) - Males: more ecconomical up2 24w. Practical feeding: 1st crumblen then pellets, NO mash as we want to increase BW. Color of started diet is red, able to be seen by chicks, normally yellow. Younger chicks seperated into smaller houseing & fed ad-lib to find feed housen on deeper litter. artifishial lighting(24h=>14-16H/D@5LUX). Diet&Nutrition: 6 phase feedings, starter 1/2, grower 1/2, fattening & finisher Male female Starter 1 0-4w 0-4w start 2 5-8w 5-8w grower 1 9-12 9-11 grower 2 13-16 12-15w fattener 17-20W 16-18w Finisher 20-24 :( Nutrition: 1- *CP* higher then broyler, turky only birds needing high CP. Decrease from 28-15% 2- *ME* MJ/Kg: start low, becomes higher at end bc body size. cant b covered by cereas alon, oilseed meals should b used 12.2->14MJ/Kg 2 *LYSINE* Much higher in Broylers, needed for meat production, highest in poultry. 17g/kg=>8g/kg *Met-Cys* decr throughtour but needed for balanced diet *OMEGA6* dec slight higher then other birds tho *Ca* needd for bones, 14=>8g/kg *P* dec by half not covered by grains alone. *VitD3* NB in Turky bc *FAST* *growth'!*

II/A/4. Practical Piglet Weaning Systems

1) Definition: Weaning 2) Types Age week Solid feed cons% traditi sys 6W or more= 70-80 recent/usual 4-5 (24-35d) 50-60 segrated earlyW 2 very little 3) segrated early weaning: Swe: 4 phases -dev on assumption that disease transmission from sow to piglets during the 1st 3 weeks is minimal when passive immmunity (ABincrease) is at its highest (2weeks).& increase growth rate. Increase prot, lysine in starter diet. -10days followe by the 3phase started system, also the sow returns to oestrusquicker. 4) basic essentials: minimise stress & Good feeding rate 5) Advantages & disadv of early weaning. + = disease controll, uniform growth, productivity - = delay productivity (sow), § & competent staff 6) Maajor risk factors predisposing to post weaninf scour: pre-weaning scour. Contaminated feed &/or h20 7) factors limiting post weaning growth: Decrease of digestive enzymed & decrease feed intake/h20. Reduced absorption capacity bc changes in cili=> decreaced acid secreating ability. 8) CHanges occuring at weaning= stress!! - abrupt removal of sow/piglets from ursing pen - synchronized feeding period vs whenever piglet want -liqquid feed 2 dry, H20 intake drinker Ømilk, pigs removed & sorted 9)see flashcard w graphs

II/A/4. Practical Piglet Weaning Systems.

1) Definition: Weaning is a big adjustment in social, thermal, and physical env and also huge change in diet form & composition. 2) Types Age week Solid feed cons% traditi sys 6 or more 70-80% recent sys(usual) 4-5 (24-35d) 50-60 segrated early wean 2 very little 3) segrated early weaning: Swe: 4 phases -dev on assumption that disease transmission from sow to piglets during the 1st 3 weeks is minimal when passive iemmmunity (ABincrease) is at its highest (2weeks).& increase growth rate. Increase prot, lysine in starter diet. -10days followe by the 3phase started system, also the sow returns to oestrusquicker. 4) basic essentials: minimise stress from social/env aspects. good env=comfy zone/temperat. adequet gtoup size (10-20)&flooring. Good feeding rate (tase,drinkers, feed little&often) 5) Advantages & disadv of early weaning. + = Better disease controll, uniform piglet growth, & bettter sow productivity bc shorter lactation - = potential delay in sow productivity, expensive & vompetent staff needed! 6) Maajor risk factors predisposing to post weaning scour: pre-weaning scour (diarreah) improper nursing conditions & sanitation. Poor ventilation (diets not mach digestive ability). Contaminated feed &/or h20 7) factors limiting post weaning growth: Decrease of digestive enzymed & decrease feed intake/h20. Reduced absorption capacity bc changes in vili=> decreaced acid secreating ability.

II/A/7. Feeding and Nutrition of Pregnant Sows.

1) Gastration: @ 3 months, 3 weeks, 3 days (114d) the sow is inseminated wen shes 210 (310kg) . she ways 180 kg at parturation. BCS=3, backfat 18-20mm. sows only gain 59kg(20kg piglets) @ first farrowing as she still growing. 2) Goal: to Optimize Conditions & reproduction 3) Flushing: Occurst 14 days before insemination, if BC i not ideal then we waif for next oestrus. 4) Feedig preg Sow: 1 type of feed: DE=14MJ/kg, CP14% Lysine0.65% Days Amount food Notes BCS 0-3 1.8-2.3kg/D Decr Fi=dec*T=Dec ebryo resorption maintenance (E=13.5 P=16%) 3-30 1.8-2.3kg/D Backfat min18mm, if 2thin give 3kg. Incr BC 30-90 1.8-2.3Kg/D Maintaince 90-114 2.7-3.5 100D+ Incr E fpr parturation avoid ketosis Intensive foetus growth You must not overfeed a sow as if the animal is too fat then more leptin will b produced decr appetite, if she eats less parturation then she wont produce enough milk. at parturation give laxatives/liquid feed to avoid obstipation and ad lib drinking. factors influencing litter size Ovulation rate: morn 10-20 eggs Fertilization rate, embryo survival, piglets born and weaned 12-16B/9-13W) litters/sow/Year: 2-2.5 Prenatal nutrition&develipment aas across the placenta, fat is not effectivly used by foetuses, mother provides AAs glucose vitamis & minerals to foetus. H20 soluble nutritiens are transformed faster than fat soluble, location in the uterine orn influences the bw of nuewborn. How to Increase producation: Increase efficiency in insemination, increase no of ovulatied eggs (oestrus #) decrease embryo loss by protecting against heat.

II/A/19. Feeding and Nutrition of Dairy Cows in the different Phases of Lactation.

1) Metabolism&regulation of milk Prod -Homeostasis= maint of physolog. balance & dist of nutr -homeorthesis= equal metabolig change @tissue lever; redist of nutrients During lactation= GH regul, incre Milk prod&lipolytic activity mobilising fat stores. 5nb Phases (3lactat/2dry) Phases: 1- Early lactation (0-70D pp) Rapid incre milk prod@6-8Weeks FI does not keep up with demands, E balance, Bw loss (50kg)=> kitosis &Milk fever bc catabolism of tissues. Aim: manintain &get cow ready for AL (incr conc 0.5ish/d=> increase nutrients minimises acidosis CF= 18-23%DM=>optimal Acetate4 milk fat. Prote=20%DM (ex soybean) stimulates FI. Increas FI by= adding fats, decr stress, haiving constant acces to food. . Norm 40% forage, 60% conc. (2hight grain can lead 2 kitosis) 2- Peak DM intake:70-140D Aim= prolog Milk prod high as long as poss, reach DM intake peak & prevent loosing BW (Grain intake can reach but nor exceed *2.5%BW*!. Give QUOLiTY forage. AL is carried out at Day 85 if optimum conditions is reached. Increase VFA= Increas Avetate=Increase Milkfat! 50%foreges & 50%conce should beefed www23- Mid late lactation 140-305 CF should b close to *23%DM* Lactating cows need ledd feed to replace 1Kg of lost tissue than dry cows. 40%con& 69%forages. young cows req extra nutrient for growth 1st lactation=+20% maint & 2nd=+10%

II/A/11. Feeding and Nutrition of Working Horse and Stallion.

1) Nutit requirement for maintenence: DMI - 1.5-2%BW (low due to the low capacity of stomach) DE: depends on BW-> 600kg (35-70MJ) CP: DCP->0.5g/kgbw CP is used in practise CF: Min 16-18%DM Ca:P 20g/day & 15g/d, for foals its 1.5:1 & adults 4:1 (max) H20: 2L/1kgDM 2)Breeding stallion nutrition fed maintenance until 2w b4 mating, supplu hih AA, vit, minerals(hig sperm) low starch + high fat prevents stomach overload and increase E. Max 2.2-2.5kg/100kg (10-15kg day) give Vit A,C,E, & max 0.75 kg concentray /100kgbw 3) Feed according to immediate needs & reserves for future events over/under conditioning worsens the performance. resting must b considered; prevent myoglobinurie on rest day, you must talk, high forage and low concentratates. estimating is dificult done by dividing EQ into 33 groups (depending on work intensity) a- Light work- 1-3 hours/d (pleasure +25% maintence DE (P 25% 60g) b- moderate 3-5h/d (jumping) +50% maintence DE (P 50%, 120g) c- hard work 5-8H daily (race/polo) +100% maintence (P + 80% 300g). protein - 9.5 x DE (700G/Eq, similar to maintenence as the working has no efect on the req (+25%, +50%, +80%) H20 & NaCl - NaCl (60g (light), 120 g(mod) & 300g (hard). H20 primary mechanism to avoid excss body heat VIP. 4) General hobby Eq- need supply for maintenance no need for conc. 5kg meadow hay, 1Kg alfaalfa. 0.5kgmolasses & straw to demand. 5) Race Eq need extra E. for work, ration is NB, small # fed frequently. 6kg Hay, 8kg grass, 5Kg conc+vit/minerals.

II/C/2. The Most Important Metabolic Troubles of Sheep.

1) Rumen flautulence: cause= eating 2much Legume protein §(rich ex:alfaalfa) 2)vit E & Selenium deficiencies= White M. Disease Preggo ewes fed a diet porr in E/sel.=lamb gets WMD! hyaline degredation followed by coaculation necrosis ? calciffication= Zenker treatmen: Sel/vit Ee for ewes or 1D old lambs WMD= CUTE & CHRONIC forms 2nd photosensitivity: Acute= cobalt def=>vit B12 def (7-10D)= IM inj Chron= prop metabolism in liver disrupted=Inc propionate VFA 4-6 W results: Acute= Eyelips/lip infla, oedema, lacrimation (increast tears) chronic= aemia, weigjgloss, decreas growth & albumin 3) thiamine Deficiency: 3-4months old fatteing lambs Cause= high levels of conce qw/o transition time/antimetabolite in Hay. Thiamine is produced by bacto in rumen, thiaminase (also prob in rumen) proliferates & deactivated thiamine Symptomps= 1st 2-5D excitation laying down &holding heat upwarsds (stargazing) thiamin def dec E availibility to brain=>brain degeeration treat: Thiamine injection, only if done early enough Spring time> morbidity 40% mortality 15% 4)Enterotoxaemia of fattening lambs-Pulpy Kidney Disease: (over eating: ehigh grain ratio) sucking lambs, lambs on milk replacers, fattening on high conce dien Symptomps= pulpu kidney disease, toxins in ruminal fluid results= sudden death by Clostridiup Perfringes D 5) Copper deficinecey: copper toxicosis 2750mg/kg DM, icterus. decrease wool quality, anaemia 6) pregnancy toxicosis in Ewes (sheep Ketosis) decreast concentration in diet, energy supplied by got at stores=> ketosis also by late preggo. results: yellow liver w/rounded edges 6) New borne lambs starvation: Big colostrum requirement (210-289ml/kgBW): decrease intake=>HypoGlycemia & immune incompetence 7) urolithiasis: Rupure of bladder=>urin in abdomen. In Castrated Rams/fattening rams on high conc diets (high Ca, P, Mg &K) Smptomps= sedimentation of minerals in the urine precvent by decreasing P content in Urine! 8) Urea toxicosis: Giving NPN w/O transition period treat w vinegar diluted 10-20x 9) Milk Fever: classical =high Ca2+ , Aclassical=High P between 1-24 H after lambin, bc High Ca demand of milk production. Symptomps: early: decrease appetide, comatosis & weakness, ears / muzzel cold, later: cant stant! cause= typical= Ca rich diet during dry period, down regulates PTH when lactation starts, the PTH is not able to regulate stores Prevention= regulater Ca & P in dry period should only cover meintenence

II/A/2. Feeding and Care of new born and suckling Piglets.

1) Standard date 2) Weaning Fat prestarter/14 starter piglet diet CP% 24 21 18 DE (MJ/Kg) 14 Energy stays the same: CP Fat, lysine, ca&P decrease. Lysin=NB= addotove as t limiting aa w optimize growth. Post natal nutrition 1) Characteristics: body wightx2 per week gain until 3rd. Decrease 2% bodyfat. Colosstrum vital 2) Composition of milk(sow) colostrum protective factors= Regulatory factors Enz 3) NB nutrients for suckling piglets fat Proprionat(VFA) H20, Iron 4) Prestarter (creep feed) Vit E/selenium deficiency

II/A/3. Digestion physiological Background of Piglet Weaning.

1) Standatrd info 0-28D=sucking 28-70= Weaning! pre-starter (D28-42D) & Starter (42-70) diet: E stays 14MJ/kg CP/fat/Ca&P/Lysine decrease Weaning= Big adjustment in social, thermal and physical enviroments & change in diet farm/campos 3) *Synchronised**feeding* period instead of ad-libitum. removam of Sow from farrowing pen, liquid feed=dryfeed. *H20* intake from *drinking* *notOnly* from *milk*. if piglets are moved, mixed and sortedd adding stressors, houiseing change= no mother, temperatura, humidity, less stressful if mother is moved instead of piglets and diet is maintained till piglets adapt. 4) development of GI system- reasoning in favour of weaning 28days *Villi*- longer in suckling pigs=>decrease after weaning, *crypts* deepen= new endothelC & IGgs production=>*slower* *growth*. Increase pH (intestines) @ weanin, then decrease (high pH allows E.coli to grow), HCL has not yet reched adult lever, allowing 10 days for transition, feed carefully small amounts avoiding E.coli overgrowth. Stomach is *hypochloric* *@weaning*! 1st 2 D they will not eat, then over eating , then overeat=increase E.coli=> >Diarr Difference in pH due to restricted/ad-libitum feed (previous topic). *Trypsin/chemotrypsin/pepsin* activ decrease @ weaning= indigestion. *Lactobacillus*: Weaning feed must have milk suggar to keep lactobacillus high& E.col low! VFA decrease during weaning to act as inhibitors of unwanted microbial growth. production of enz for milk degradation decrease ad enz for solis increase. 5) piglets immunity at birth *passive* immunity system is high, active is low but gradually shift, @3weeks both low=easy for E.coli. @5weeks active system increases making it better weaing time. 6) Milk production: *peack@2-4w* of lactation, weaning earlier is ecconomical question. 7) post weaning fertility Suckling inhib, ovulation, # oflicular ovulations high after parturation, but decrease drastically after 1st W. hightest at 28 days after parturation (weaning time) 8) Labour competence - earlier weaning is more diff. staff attirude should be considered Early weanign types: -recent system= D28 old: consume 20-30%solid feed - SegratedEearyWeaning. 2W age; consume V.little solid Phase feeding (4 swine production meeting nutriten need of growing pigs) =/<21 - 4 phase =>28 - 3 phase 1: milk replase=23% protein 2: Pre-started 21%p 3:started: 19%P 4: Waning 19%P 9) earlier weaning - more critical & expensive, but piglets dont eat alot. , more uniform piglet grwoth, better sow prod. bad= delayed fertility sows, specialfacilitied, expensive diets, labor force 10) Limiting factors of post warning growth piglets - Øenough digest enz -reduced absorption capacity -inadequate acid secreating ability -not tough to eat the food onthe ground 15D and 45 kg feed*!* ?!? Nursery diets: formulated to achiece, early return to food intake, reduce risk of bacto growth induce rapid grain despite limited intake=mimimise digestive upset. Muse be economicll feasible, Diets unmatched to digestive ability will predispose piglets to scour (diarrhea) newly weaned pigledts should b fed 4-6x D, never overfeed, make feed easily availible on rubber mats, keep fresh and have constant h20 supply

II/A/3. Digestion physiological Background of Piglet Weaning.

1) Standatrd info Tendency of pre-starter & piglet diet: Energy stays at 14MJ/kg CP/fat/Ca&P/Lysine decrease Weaning 3)changes Synchronised feeding period instead of ad-libitum. removam of Sow. H20 intake sorted/stressors, houiseing change. Moving piglet vs mother 4) development of GI system- reasoning in favour of weaning 28days Villi- longer in suckling, crypts deepen= new endothelC & IGgs production=slower growth. Increase in Ph weanin, decrease HCL, 10 days for transition, E.coli overgrowth. Stomach is hypochloric at weaning! 1st 2 D they will not eat, pH due to restricted/ad-libitum feed (previous topic). Trypsin, chemotrypsin & pepsin activ decrease @ weaning= indigestion. Lactobacillus: VFA 5) piglets immunity 3 vs 5 weeks 6) Milk production: peack 7) post weaning fertility Suckling inhib, ovulation, 8) Labourr competence 9) feed coast: . 10) limiting factoers of poswt weaning groth piglets (4) Add: Nursery diets: formulated to achiece, 4-6x D, never overfeed, make feed easily availible on rubber mats, keep fresh and have constant h20 supply

II/A/6. Feeding and Nutrition of Replacement Breeding Gilts.

1) def: Breeding gilts are future breeding animals, aim is optimise reproductin & isometric growth 2) 4 stages of Sow Nutrition 1. Replacement gilt 2. Gestation sow (13.5/12.5), 3. lactating sow (18/14.2), 4. emty Sow 3) goal: Optimise production. Help egg production/ovulation. Increase live piglets & weaned piglets/weight. Ensure good results of next preg. 4) Selection: @90 D farmer select: Fattening(Allosteric growth) /breeding (Isometric). Replacement gilts: are 90D old (30kg) when they undergo their 1st preseselection & tak out of grouping units. @140D (90kg) 2nd preselection & 190D they undergo puberty & are inseminated after the 2/3rd heat (210D-130kg:16-20mm back fat) BoduConditionScore 3. Larger sows produce larger litters. Diet nutrients stay the same throughout period: *CP=13.5* *DE=14MJ/kg* 5) Feeding strategis for replacement Gilt. 1- Genetically lean animals (*CP=13-14*. 0.70) Increase Muscle from prot, we want fat not M. ideal: 18-20mm thin bk fat. Feed Increase Energy, minerals n Vit 2- Industrial average, deacrease lean potential: Decreas Prot, increase fat=> 2 prevent fat deposition >32 mm at mating. Decrease Energy in feed to increase Proteins, miner & vit. 6) Gilt condition - improve lifetime performance shoul be: mature w good fat (220-230D, 140kg), Back fat 18-20mm at P2(reasmost edge of last rib). Mating at 2nd/3rd Oestrus, dep. on condition 7) Flushing, short period 2weeks, b4 fertilization where FeedIntake (Fi) is doublled to high ovulation rate and litter size: Oestrus cycle= 19-21 d. Must return to Normal restricted feeding after 2weeks!!!, good to keep older & younger Sows together bc passive immunity, increase pathogent int.

II/A/1. Digestive Physiology of Pig, Change of Enzyme Activity from Birth till the 6 th week of Age, and its practical Importance.

1) standard date 2)Salivary gl- 3 2)stomach Type, 3 pards: cardia(w/espophageal part & glandular part), Fundic (glands) region & Antrum with different enzyme secreting cells. 3) Intestines: *Duodenum* *Pancreas* (trypsin=>prot, amylase=>stach, lipase)+ liver & GB *Jejenum*=digestion&absorption *Ileum* Large Intestines: Ceacum Colon. 4) Lowers the pH of mothers milk= Lactobacilli-> ferments lactose-> endoproduct-> lactic Acid. 5) how the feeding influene pH: Fed resctictely, fed contations ad lebitum ad lib after restricted/red ad lebidum past feed deprivation: 6) Conclusion: Diet of young piglets should b constructed in accordance w enz. activity. as age increase, the product of milk degradation enz decrease (lactase) but enx for solid feed increase (amylase)

II/C/11. Control of Mineral Status in Cattle Herds by the use of HACCP.

1st Check major problems, then mineral status. After this determine whats really needad & not meeded in the cow diet according to safty margins & prevention. Shoul db economical & interactions shoul db considered, then; 1. Natural factors should be considered ● Knowledge about soil, pH of soil ● Mn is good in acidic soil and decreased in alkaline pH ● Zn is decreased in sandy soil ● Cu and Mn is decreased by riversides - Field soil → increased pH → increased Cu → Zn deficiency n Mn 2. Secondary deficiency due to interaction between minerals ● Ca → decrease Zn+Mg+P ● Fe → decrease P ● S+Mo <→ Cu decrese ● K → decrease Mg (grass tetany) phytic acit-> P & Oxalate->ca 3. Combinations of plants to avoid ● Alfalfa + grass → Ca:P ratio ● Rapeseed → Cu, S ● Sunflower → Cu 1. Improve mineral compostion by selected fertilizers - k-p or N fertilizers (have different Mn absorption= - add chalk lime to the soil 2!!! Orientation w lab analysis: Hazard Analysis & Critical Control Points of mineral status (HACCP) - evaluate of living microorgs by; blood, uringe, hair&saliva, enzyme activity, Total balance; intake, Urine(P) & Milk (I) & feaces (Ma-Mn)

II/A/5. Feeding and Nutrition of Fattening Pigs from the Onset of Fattening till Slaughter.

Age-D BWKg Period Diet suckilng 0-28 1.5-10 birth-weaning milk-prestarter starter pig 28-70 10-20 inbreading uni w/other pigs prestart+starter feedr pi 70-90 20-30 --II--- Piglet diet Grower 1 90-110 30-60 Fattening unit grower1 ----II--- 110-140 60-70 --II-- Gr2 --II-- 140-160 79-90 --II-- gr3 finishing 160-180 90-110 Slaughter finishing 2) Trends of grower 1-3 diet and finishers *CP* *20%* and grad decrease. *E* *14MJ/kg* stays the same! 3) concepts in starter diets formulation Get pig used to the cheapest diets quickly corn based, new born pigs have decreased energy,max intake is NB. 90Days old farmer decides wether pig for breeding or fattening bc allometric (fattening) or isometric (breeding) growth. Isometric is proportinal gorwth or organs 4) Goal of fattening M. building not fattening to achive the genetic potential of the pig economiclly. - Pork -16 weeks: 60-75 kg (112 days) - Bacon - 22weeks:80kg (154 D) - Heavy hog - 26 W: 90-120 (182D) pigs undergo many physiological changes to better suit their diet to absorb & break down complex carbs, proteins & fat. changes on the basis for feeding recommendations for growing & finishing pigs. 5) Requirements: A- Energy: *DE* (needs to cover Maintenece &growth). *Maintenece=0.477xw^0.75* Gain 1kg fat needs 55.7MJ DE, 1kg Prot=45.7MJ DE. E from carbs, fat, oils, avoid prot. during summer fat is more economical=decrease heat prod and winter more fiber is economical =increase heat prod! B- *Proteins&AAs* good amount&quality f proteins throught life quality determined by Biolog.Value (absorbed prot from food, incorp into prot< in body). *Digestability=breakdown* of prot=aa. BV= %aa build into new prob- Soybean has good prot (45%) but only 40-50% can b used due to anti nutritat subs. Limiting aa=lysine C- P:E ration gProteins/MJ E *14g* needed in beg, *12g* when pigs 50 kg. Idealy have enough energy needed for in-builfing protein. Nonideal= E>P-fat inbuilding / E<P:proteins are burned to fat D- Fat NB E source, minimum *3%present* 2 avoid deficiency and absorbed fat sol vitamines/essential FA. Essential FA= *Linoleic* acid, 2much is excreated w Ca/P soapy E- Fiber= *4-5%* F- Nutritent: 20-60kg:4Liter/day 6) Growing-<finishing recomendat. Ad lib often fed until 50Kg, after this its bult in fat. Give optimal amount of feed=increase BW and Decrease Bw intake% Always use phase feeding according to phases of life 2phases are used in fattening persiod over 5days. 7) Growth promotors CuSo4 flavouring, Organic acids (acetic A. gives better tast) Enx, Probiotics&prebiotics

II/A/8. Feeding and Nutrition of Lactating Sows.

Aim: Maximize the voluntairy FI of sows to maximise milk prod& minimise Bw loss 2) General Lactation starts at parturatio & lasts for 28D til weaning it requires high E. If Energy is not met the sow will use up personal fat & M. supplies decrease condition. Since the requirement is voluntairy feed intal the sow will lose some BW, but hopefully less then 10kg.larger litter require more E. Sow will weight 160kg at farrowing by weaning shell lose 4mm back fat & 10kg Heat, humdity, floor type,, water, feeder & litter size all influence voluntary feed intale.. Nutrition of lactating sows: 18-19% DM should be protein they have high demand. 1st 2 weeks of lactation will not b affected the weaning weight of piglets as lactation covers need but later lactation does. the higher the feed intake the better: 1) <Option 1:ad libitum from Day 1, 2) Option 2: Gradual increase until ad lib (1.8kg on day 1, 1kg increase til day 6, then ad lib til weaning 5kg a day). option 2 better as ad lib from D1 could lead to decrease appetite & low milk production. Increase # of litters means increased size so se needs more food. After lactation period (28D) sow has 3-7D rest period (3.5 kg/D9 then heat occurs & insemination occurs once again. Illnesses: Agalactia, Mastitis (milk feaver:normally caused by bacto treated broad spectrum AB). Decreased nutrient intake usually during lid-late lactation. Constipation- better to prevent rather then trea, prevent by supplying MG a week before farrowin. exercise is best treatment.

II/C/6. Clinical Dietetics of Beef Cattle.

BROWN SLUG HUH Bloat= 2much immature legum eintake (alfalafa/clover)=>leaf toteins. Inhib regurgitation, treat w/polazalene (liquid molases) max 35%lumes Rickets = High grai=>breakdon the heel bone & achillis=lameness, urgent sloughter! Prevention:give calcium/vitD Others: Phytoestrogenm, photosensibility poisonour planst washy pasture: high water content in early spring =watery feaced, early spring, prevent feeding by giving hay in the morning=>graduately adjest to lush pastures Nitrate-N toxicosis:= N-fertilization, liquid manure, Sorgum (=Nitrate accumulating plant). Nitrate-nitrite conversion ocurs in rumen=> MethHemoglobinemia (Øcarry O2) Ensiling forages, prevent by=> mixing low nutrat foraves to avoid NPN Sand= less serious then in Eq, decreas appetite, prevent by addign hay & straw Lactacidosis: Ingreat grain pH<6: => Damage rumen epithlis, f.necrophorium causes laminitis & liver absesses Urolithiasis= High grain=struve=bc high levels of silica from sour grasses, prevention by acidifiers of urine, increase water intake and provide good quality alfaalfa hay. Grass tetany= spring grain forages&grasses in lush growth stage, treat with MgSO4 Hardware diseases= metal wire/nails in reticulum injures lining. prevent by puttign strong magnet in in feed processing equiptment, Urea: toxicosis= NH3 toxicosis; 0.3-0.8g urea/kg bw= if given 2high NPN with lack of availible energy. treat 20-40L cold water + 4L diluted vinegal HYdrocyanic acid, => => HNC=>respir failure/death

II/C/7. The Most Important Metabolic Troubles of Calves.

Bload: -occur bc overgrowth in bacteria in the obomasum dev forstomach (E.coli/C.Perferinges)=>gass production Cases= diluted milk replacers, low fiber inhibition of eosophageal <groove relex: normally gass is released but w foam proces inhibited Richets,soft Bones due 2 Ca/P deciiency/vitD bent, twisted lefs, humpback swallen joints Mg Deficiency: Coma in calves fed on milk replacers= decrease mg in milk replacesrs=srargazing/dull sight, ear hanging/hypersensitivity Zinc def. 1 & 2 (Mo & S inhibits absorption)= Get anaemia, osteoperosis, still fait, depigmentation of hair Manganese deficiency common on sligly alkaline soils, addecte Males>>F swollen joints, MN used for catrukage production Vit A Def levin in blood depends on mothers supply during dry period, symptomps: night blindness, damage N.Opticus pnemonia diarreah VitE/Selen Def protects against free radicals, decrease accumulation of peroxidase & damaged c.walls. aswell as Whide Muscle Diease (effect skelletal M.) Thiamine dec: anorexia, leg weakness, uncoordinated movements, arrythmia & irreg breathing

II/B/4. Feeding and Nutrition of Broiler Chicks.

Broiler= hybrind for meat production- Male cornish white ? female pluth rock Basic info: Hatch weight= 40g, BW slaughet=2kg (50x heavier) Leng of fattening=35-40D (v shrot, more conomica) growth capacity: V.intense) Body composition @ hatcing inbuild 4x more prot vs fat, later only 2x(DMcontent) Fat in building= More E requirements vs Prot in ulding mroe expensive, in poudty, fat is stored in the abdomen not in tissue=> loss, decreased growth w/age but fat inbuilding increase whereance the early, earlier in girls. Feed efficicy= *Kg feed need for 1kg weigh gain = *1.7-1.9Kg/KG* worsens w age since maintainnce req for 1kg BW increase due to fat in-building. Dressing%: %lean withg that is carcass, higher the beter (68%norm) In feeding broler chicks we mus use multiple step diets (phase feeding) Due to biological changes. Amount of phases change in contries, but normally 2-4stages using 3-5D transition *0-10D*=Starter Diet(*crumberls*) CP=23.5% rotein in-building is hight ME=12.6MJ/Kg *11-24D*=grower diet(Pellets*) 25=sloughter(-40d)-finished diet, pellets. CP=20%(decrease bc protein in-building decrease-give legumes) ME=13.6MJ/KG (increase bc incre fat in-building increase maintenence- Cereals) P:E=14.7g/MJ decrease E=Decres FI= Decrease Nutrients Nutrients requrements: 1)Lysine g/kg= 1st limiting factors (met/cyst) 2nd but feather prod isnt impor. Decrease form 14->8.5g/kg= M. production, artifisial supply needed 2)Meg:cys g/kg= decrease 10->8.5 used in feather production. 3) Linoleic acid= decrease 1.3->1 corn can cover this req aline. 4) Ca g/kg= 10->8.5 5)P alwasy suppleentat as 50% od grain: phytic acid binds P. & chickens have low phytase activity= 5->4 6) NACL stays at ->0.. to little decreae FI. All salt is not absorbes=excreated uris if enough h2o=ok 7) h20: influence grately: normall 2L/kgDM general facts about feeding: E upplemtnsation - full fat meals are used. Ad-lib in boilers to make FI & genetic capacity Housing & artificial light (artif heat+ deep litter) sex detependent rearing= after 3rd week: female dec more fat, less M from slower. Males should b slaughters later & fed/reared diffferently, many farms keep them 2gether. Alternative rearing= Free range= sesonal prod. and sloughtering (bad for market) lower growth intensity so no need to intesive hybrids. Sloughter later low nutrition requirements: # animals proteins used

II/C/19. Dietetics of Congestive Heart Failure in Cats and Dogs.

CHF: development & pathological= caused by weakning of Heart M. plasma leaks into abdomen & thoracis cavity leading to difficulty in breathing Low BP=> poor renal perfusion=> increase rennin/angiotensin/aldosterone=> Na/h20 retentin=> increased BP/load 2 clinical findings Left pulmondary congestion/iedena/ascitis & hydrothorax 3. Dietary treatment & control: Low Na(decrease 0.25%DM) decrease palatability, many small meals, warming hel(tuna/garlic supplement?!?) decrease salt (avoid chese, bread, processed meat, carrots, heart/liver pet treats..)(low in salt= beef, rabbit,chicken, egg yolk, oatmeal...rice paste) Na-hypertension low Protein just if CRF simulatniously

II/A/25. Types of Dog and Cat Foods.

CP=18-20%K9, 23-26%Fel (indor need lower) NEm-ME (Based on metabolic weight x factor) in K9 x2 preg & x3 for lactation. *P* *K9=23*, *Fel=28* fat- min 9-15% essential FA inc: linoleic linolenic and arachidonic acid. *F* *K9=55*, *fel=9* Fel Ø tolerate cabs!! Age Protein gat puppy 28 17 adult 18 9-15 perform 23 20 racing 33 50 lactation 28 17 Tpes of feed= Bases on moist contend, cannes (>14%moisture) dry(<14mois) 1) K9 feed= Bases acording to size (s/m/L), Age(young/adult/senior), Condition(strive/allergy/obesity) 2)Fel= Acording to breed(pufa for persian, large kibbled for maincoons 2chew), Prescription dies; Struvite, obese (low fat, energy & high fiber/protein) 3) Acana diet: Canadian feed which contain protein sounce from different animals (80%) & proteins from fruit and veggetables but Ø cereals. 4) Dont feed exclusively all mean diets bc Ca deficiency&rubber jaw, prevent this by giving bones wih meat or Ca supplements. Low Ca0>Increa PTH=> ca from bone goes to blorrs= rubber jaw! Feeding raw food: 1- Raw meat: bad as it contains parasites, bacto, viruses. 2- ras fih= bad bc Thiaminase besides the paresites, untreated means death. 3- raw egg: Causes biotin def due to aidin, loss of hair and depigmentation 4- barg - biologu apporp raw food (raw + bones for cats + minerals) improving hairs coar: Omega 3, biotin(tolk) pathothenic acid. Øchocolate/coffee. h2o shoudl be give ad-lib, cats dont normally drink enough, more salt scould b given to stimulater drinking, kibbels. Yorkie:flaky to promote oral hygene, Golden Retriver=hole in the middle to slow down FI, Maincoon= larger promote chewing. GrateDane= high E, 2 meals to prevent overloading, E=18MJ/kg beagel=ease gains weight, size,shape of kibble slows, E=15MJ/Kg

II/C/18. Dietetics of Dog and Cat with Diabetes.

Diabetes mellitus ● Type 1: Insulin dependent (IDDM) . → destruction of the insulin producing B islets in the pancreas. → give insulin injection. ● Type 2: (Associated with obesity, reduction of insulin receptor sites) NIDDM. → Don't have to give insulin since the receptors are not sensitive. → Only in the very severe cases have to give insulin. → 1st NB= reduction KG! ● Type 3: (Abnormal glucose tolerance, CrIII) → The blood level will be much higher. → More or less organic chrominum (part of GTF) moderate the sensitivity of the insulin receptors which might help. Main clinical signs: Ti= catarhacta and Polyneuro-pathy -hypersensitivty. Insuline types 1) amorph insulin= in the am, quick abs, before feed 2) Chrystalline insuline: eve, long effect, gond geive if animal dont eat=hypoglycemia! Feed what: ● Low fat less than 10% DM, Not high in fat since it can produce ketone bodies so not given. ● Moderate protein (25-30 %, with high BV) high level of complex carbs (ex Rice)= 50% DM w/low Glycimic indes, so insuline demands stay low as glucose rel, is slow. -High fiber (10-30%DM!!) to decrease rate of absorption, oats & bran Daily routine: 1) measuer insuline, 174th Amorph insulin +food. 2)1pm= food + 1/4 crystalline insuline 3) 5pm, measuere, 1/4 crystaline insuline + food 4)9pm, food + 1/4 crystalline insuline *control by measuring glucose levels in urine or blood 2 correct insuline dose* Hyperlipidaemia • Lipidemy in fasting (endocrine disorder) Hereditary problem = fasting. • give Low fat, high fiber Puerperal eclampsy ● In bitches with large litters (Ca low in blood) Cf. with milk of dairy cow. ● Calcium borogluconate (iv) *small bitches with high lactation rate cant eat enough to cover the big lactation - low in Mg and P → eclampsia.* + retard (crystalline) insulin SC

II/B/10. Production of Ducks' Liver.

Duck liver production is a growing industry, duck liver almost same wuality as goode liver and is gettign better. easier to produce bc good reproduction performance on males are sued 2types of duck: *Muscovy* & *moulard* duck Physiological basis of force feeding:fat is stored in SC then migrate to Liver: Feed high in carbs (corn-E) is fed=> converted to tryglicerides in liver=> leaves liver as VLDL, but since its transport <trygluyceride production=>fattyLiver! 2get extra large livers must feed extra high E. supply and low trasport capacity Phsiological basis of force feeding: -breed & geneotyp(hybrid) -sex(M) as females have smaller livers & larger vessels (not palpeable) -Levers of lipotropes (meth+choline) for poor transport capability. -Maintain flecible levels in liver celle= increase regeneration) for low levels of fat loss @ roasting. Younger the animal the better-liver size before forcefeeding Feeding of duck for liver porduction 0-7W=like roasting ducks 8-11W= preparation for force feeding (16-17%CP). since DUcks have no crop, need to increase size of oesophagus & prep the liver for hight fat intake&storage. 1 meal/day(overeating as they know they get 1meal)=enlargement of oesophagus so not ad-lib Forcefeeding *muscovy* duck: onset 12w of age, BW=increase 4.5KG, Leth of force feeding=2W. Fed twice a day. during this period 6-7kg corn is given & liver will get up to 450g. lipid loss when rasting=30%(worse liver quality) *Moulard* duck: starts 12-13W, Bw mroe then 4kg. Lenth 12-13, fre is 2xDay. 11-12kg corn/duck over the period. Liver weight is 650g, close 2 geese, and roasting loss=15% Mehotds for force feeding: Corn grains(high E) used in natural form (conc.E) but air is precent under the shell so duck cant eat as much. *SoftMash*(ground &h2O) 2much water will fill the stomach =>Decrease in FI. Corn grains & soft mash is better, but all 3 have positive n negs Keeping ducks indivitiual cages: fed by machine+-automated & not indivituals. <Feed 2xDay, 230g/d increasing to 450g/d towards end

II/C/20. Dietetics of Pancreas Diseases in Cats and Dogs.

Exocrine pancreatic insufficiency (malabsorption) - decrease or no pancreaseic enz: either congenital or chronic pancreatitis (sheapards)=> rapid kg loss, &M. atropy & poor hair coat. Chronic diarrhea w/light yellow/clay-colored stood. treatment= easy but expensive&lifelong: enzyme replacements, lipase&trypsin. alter diet: highly digestible food, low fat, lots of water!!, vitamine supplements=>fat souluble (E/D/K/A/B12) Acute pancreatitis=> Infect, metabolic disorder, hyperlipidemia/hypercalacemia/obesity/trauma shock. Øcommon in fel Signs=> painfull distended abdomen, decreas FI, depress, deh/vomis/diarr. Severe=>arrhytmias & sepsis. treatent=Nothing rally for 3-5 days traditional, if severe vomis, treat begins by decrease FI, Water + oral drugs for 24H. Give easily digestible meals (high carbs, low far 3-5/d, gradu & treats, Liver: affects only 2% population: decrease load on liver & restore function. Nh3 traps (lactulose: binds nh3 excreated in faeces, if not absorbed goes 2 liver (overwork). In comercial feed (dry sugar pulp), home made(boiled carrow). Hig BV protein low amount. Increased B vitamine high E from carbs 2 spare protein Badlingon terriers Copper storage disease: mutation/wilsons disease. Accumulation of Cu in liver=>slow hepatopathy bc decrease metallothionin. low Cu diet binding coumpounds in feed, S=> antagonist! DIet= Zn, bc competatic antagonist of copper!!! Gastric dilatation and volvulus (GDV)

II/C/4. The Most Important Nutritional Troubles of Rabbit.

Fibre: Cars either Readily availible (suggar/starch) or Structural (cellulose). 2much readily availible increase chances of enterotoxaemia bd carb overload in hind gut (structural fibers help by preventing diarrhea & maintaning growth peristalsis (lignin) & absorption of toxins (pectin) as well as feeling full and good microbes. Fiber Deficiency syndrom: Fermenteation dysbbiosis,= carb overload in HindGut (bad bacto ex C.Perferinges favors) Fur cheinew Sacromycosis: gass production in Hind gut Fiber overfeeding leads to obstipation Alkaline value of feed & feed mixture AV=bicarbonate quantiry=HCL amount able to set pH of 1KG feed to 3. 2 alkaline diet=> bicarbonate OD(BLOOD)=> Increase in pH in Cecum (normal is 6)=> diarrhea & death bc bacteria multiplication Prevent Diarrhea= Acetic acid added to water (binds NH3 in GI)Lactic A has no effect Mycotoxicosis: 1) T2 toxin: Produced by Fusarium -most common damage brain tissue, kills LC, prominent in sleep, Excreted in milk& ccotrophi feaces recicle. 2) Alfatoxin: Produced by Aspergilus baeris (intake of Small amounts =>chronic Alfatox. in growing rabbits=> Decrease in FI, Decrease in weight gain & fur chewing ? Splenomegalia 3) Citirin: Produced by Aspergillys&penicillin => diarrhea neprosis PO Antibacteris: broad spectrum AB PO destroy G+ anaerobic population causing dysbacteriosis this lowers VFA produceion and is atibiotical effect, overgrowth of pathoges, causes ZENKERSNECROSIS!!

II/B/2. Practical Feeding and Nutrition of Rabbit.

For practially four rabit catagories: 1- Adult non producing (buck, non preg, doe, culling breeding animal=high DMI 2- Pregnant lab animals = Low CF 3- growing reabbits=CP high 4- preg & lactating (simulatnously)=110-300g Milk/day= Increase EE. Rabbit milk is 3x more conc then cow milk. Lab animals=ct 2 as they need extra E for tests. 1- E supply voluntary FI dependends on E cfeed content DE, in MJSE/KG (air dry feed) =average *DE=0.9-1MJ*, Lactating needs more= up2 1.5MJ in peack day*15-20* Request essentail Fa(*omega3/6* & *Arachidonic* A)- *2-4%* 2- Fibre requirements Bad fibre digestion but high fibre req bc large GI tract which needs stimulants, , *CF=12-15%* increase trasit speed, decrease nutrient diges=diarr. 3- Prot/AA *P=12\5-23%* CP high, as it stim milk prod, Low CP(under16%=> dec weaning weight). Deficiency or imbalance decrease FI! 4- Minerals&Vitamines P/Ca needs 4 growint rabbit=ower then those Lactating. Ca regulation on excretion lecel in urine. Phase 1/3 have least Ca&P rew & phase4=highest Ca&P req *Na=Need* more Na then other monogastrics due to *largeGI* VitK/B= enough in ingested by caecotrophy maintancens Feeding practice: Alwys Pellets : Ømeak form Techneques& amount of ratio: -Back yard keeping; cereals, roughage & wheat bran -Sm breededs: Commercial pellets & natural ing Intesive reprod. cycle= Ad Lib(not bucs) -Semi intense breeding= Restricted from weaning til next kindlin. Growing broliler rabbits=> alwasy d Lib. NB rabbit feedstuf: Oat=amont not limited, enterie cereal ration can consists of oats, barley is good replacement What= stach content more digestible vs corn 10-40%, Corn high fac accumulation. Antibiotics cayse Dysbacterioses= DONT GIVE!

II/C/5. Clinical Dietetics of Horse.

Genera facts about Eq GIT - FI small quantities but frequent (3-10l) best w/5 meals a day Caecum &coloc fermenter herbivores (loooose attahed, when any abnorm movement can cause cholic! Øvomic, sensitive to peritoneum, surgeries on abdomen must b done in more sterim conditions (even more then HUMAN!!) prohobited subsb: GlucosInolate (found in rapseed causes colis 3g/kg) Gossypol (cotton seeeds)= anti VitE, binds Fe= anemia (60mg/kgBW) Broad spectrum Antibiotics PO ex: ampicillin (destory G+ & G-=dysbacteriosis=death) NPN=> urea must never enter ceacum(even if protected urea is given)= acute toxicosis Ionophores=> same as AB in chickens Controll of ration balance & digestibility 1) Control of Ration Balance BW BCS(0-4) optimal =2 in EQ Appetite, age, work, reproductive status temperatir and relative humidity (Eq dont liek humidity!) Illness (fever= increase Energy req), feeding techniqeus:grazyng/nor 2) controll of digestion: Feed practicle (size in feaces, sand & sol in faces=> can cause colic Digestion (Mn) Absorptive cappacity (Glucose, lactose, xilose =all PO) Pancrease exocrine functions (givng starch PO) Metabolic profile HACCP) what & where? What to check where is it water blood:hematocrib&prot protein blood ures ca,K,Na urine Fe blood hb cu,zn,se Hair, blood & liver enz Diets of special pathological states 1) orphan foals: *600mlDairy* milk- 3g suggar & *400mlH2O* first 4liters, then 9/10/d, give every 2-3H + 2-3 raw eggs a day (increase vit B&good prot) 2) old Eq ?20-30Y Vit C increae AB response. CP=12-16%, lover fiber digestion bc dont checw/salivate=can chocke. give easier masticated/palatable diwet w/high protein(soybean) Ca:P 1.5:1 3)athletic EQ: 4) Hypophagia: ANorexia: insufficient voluntary feed intake, vitB helpful: nutrition support by encouraging to eat,useually its bc disease 5)Fever/trauma/burn/sepsis=> low FI=> give small amounth but frequently (14-16%CP/7-10%Fat) 6) Hoof defect==>Biotin supplements helpfull! Developmental orthopeasic disease: foals is reared more intesnsly; predisposed to DOD, make sure to rear foal in Moderate! Dig. Trouble*** bc(sonsequenses of domestication,antinutrition, anatomy: 1)diarrhea, constipation, maldigestion, malabsorption 2) post op period, 3)dysbaiosis/trouble in passage 4)intake of soil&sand 5)gut tourson Localisation of Colic: Clinical signs=nervously watching abdomen, abnormal leg movements, fallin, rolling over, eater dirt. 1) Obstruction=>colon; 2much oats,barn,long hay feeding: removal by rectal exam 2)Obstipation=>*Cecum&colon*=2much long old hay 3) *fermentation* failure=>stomach(microbes), caecum(2much cc) &colon(2much prot not enough fiber)

II/B/9. Feeding and Nutrition of Roasting Ducks.

Goal&Characteristics: 4 meat production(rosting duck similar to broiler chicks) liver feathers, eggs for breeding, not keptas intensively as broylers! fattening= 45-49D (7W), Hybrids5-6W Day old=50-55g=BW@ sloughter3-3.2kg (60xBW at hatching) after 7th week:growing slows down, more fat buils & 2high maintenance. Feed efficiancy: 2.6-2.8kg/KGBW (not asgood as broylers) General factors of rearing: 1-Beak adapted 2 water life=efficiency is poor as they filter feed. 2-Physical form of feed: Lower energy density of feed: (Mash=>high wastage but can b wet/still not good. Crumbels=newly hatched. Pellets=stillsome loss. 3- Øcrop , flexible oesophagus=Østorage need to eat/dring contin (intake daily=BWish=compared w broilers its doubble) 4- gritts & gravel is needed for machanical digestion and Ca needs 5- Maintenance req are very high they are very active birds 6- h20:3-5L/KgDM(as they also bade in water). 7_fat building(4-5weeks)subcut proportion increase by age to tolerate water?!?! 3stage diet:feeding libitumpellers=>we want them to grow asap 1-starter:0-14D, 2-Grovers:15-42D, 3-Finisher:43-49D Nutrients: *CP* 210>16 =Decrease, bc protein inbuilding decreasw w/age *ME* mJ/Kg: 12=>12.9, high E when prot in low, more fat is build in(high active) *Ca* 9=>8g/KG used for boe dev. *Lysine* 10=>7.5 ,req less protein so less lysine 2 Hoursing: semi intensive: take advantage of seasones, cheaper to keep outsoors in summers, post rearing=dry methoth, ØH2= sloughter on 19th day, less expensive Intesnsive: Closed confirments, market need meat throught the year, artificial ligher.

II/A/24. Digestive Physiology of Healthy Dogs and Cats, Nutrient Requirements.

Growth breed dependent, larger dogs steeper curve (large amture 24m, smaller 8m) Sexually mature 4-18M females, some breeds cycle every 4 months, preggo 63D, 6pups/litter. Birthwaith= 100-750g Fel Little variation in gorwth curve, males around 4kg fel3kg. puberty 9-10 month, 63 days gestation, birth 90-120g Digestive physiology&anatomy Mouth: teetch 42K9, 30Fel), Ødigestive enz in saliva, dogs have few, (vertical chewing) Stomach:(monogastic) fe-45-100ml, K9500-3L capacity. Simile type makes up 60-70%git. High pepsin & HCL content, low pH(2.) & good protein dg. Smll intestine: Short 3-6x body length, 3-4=fel, 5-6=k9. Øprobln bc fat & protein dig in stomach is enough, they digest chyme from stomach & absorb nutrients. packed w/villi to increase absorp, microflora move enterocytes from cryps to villy& unto the content where they liberate disaccharidases & peptidases. *Produce vilikinin inducing cilli action=lactate is produced in young animals. Large intestine-short&simpe, absorp h20 & electrolyes, store water, low microbial fermentation Digestion: Startch-low salica amylase=k9, (Øfel), bigest by pancreatic amylast in SI. Fat-digested in stomach & SI w lipase & bile. Protein- stomach w/pepsin&HCL in SIw/trypsin!!! Retention time= 13H for fel(better dg), 22h k9 General= k9 liver can detoxify vit N., fel dont have carotenase enz. kidnes produce bad smelling concentrated urine. pancrease produce pancreases like trypsin &lipase, trypsin is most NB, low in newborne but rapid increase. Lipase is higher in pups but lower in kittent vs adults. Special concers Fel/k9 nutrition 1: differences: K9=partially omnivores, adapted to human diet. Fel=abligated carnicores=rewure animals tissued for aa, no startch digestion! 2: Eating habbits K9=large wualitied once a day, overeat, obese, regulate intake by vold not energy, learn sloly n forget quickly fel=smaller qantities more frquently reg by E value, proteins & vit. difficult to change diat, learn fast, forget slow. Nutrients requirements 1) E for Maintenace= -12-14MJ/kgDM fel&K9 K9= sice varies use BW, E=552W^0.75 increase of pregnancy, increase to 1.2-2x withg increase last 3weeks. do 2 stomach compression, feedmaybe times a day in small amunts in lactation increase x3. Fel=more similir in size, k to use BW=336W(21 for indoor fel), fel fetal frowth is gradual not exponential. 2) Prot &AA; increase leverls needed & tolerated, P:E NB! K9=18-22%CP, Fel=23-256%CP Essentual AA: Arginine(4 urea cycle), Taurine (NB FEL>nbK9 for supplement!). Sulphur containing AA; met, cystine&taurine: high lecels NB Fel!. Niacin NB , bc no enz to convert tryptophan to Niacin. 3)Fat&essential FA requiremnet. req. k9(9-10%DM) Fel(20-30%DM ess, omaga 3&6) Essent FA= Linoleic acit and linolenic (Omega3(6) arachidonic acid, essential FA def is not common but my happen when feeding badly formulated rancid diets. 4)Carbh: Milksuggars in Milk for kittens/pups = 20%ME in milk!!! Adult ats eat luttle carbs, dogs tolerate carbs better but should b coocked b4 feeding, raw cause diarrhea.

II/C/12. Physiological and Biochemical Basics of Special Cat Metabolic Disorders and Deficiency Syndromes, their Prevention and Treatment.

High protein need of cats, taurin is essential! When plant protein is in the diet the argininge is much lower than in animal protein so then extra supplementation is needed for excretion of urea from the animal. High protein requirements because the bloodsugar is formed from GNG and the enzymes(glucokinase) is always high as proteins produced AA and Energy meaning preoteis are utmost importatn carbs are not. virtually the same amino acids are essential for all animal species: ● Arginine, phenylalidine, methine, hisztidine, lyzine, leucine, isoleucine, valine, methionine, threonine, tryptophan and valine Protein req. is very high 28 % in adult diet (same as in turkey) 5) Digestion of Carbs: ● Cats do not produce amylase in their saliva (unlike K9)=low carbh splitting activity.. ● The starch levels in commercial cat foods (up to 35% of thefood dry matter) are well-tolerated. 6) Unique Energy and Glucose Metabolism of Cats ● In cats gluconeogenesis is always active (unlike k9) produce adequate amounts of blood glucose by gluconeogenesis, therefore, carbohydrates are not considered to be essential dietary nutrients. ● Cats use hexokinase, dogs use glucokinase to metabolize glucose ● Hexokinase works at a slower rate than glucokinase=> can't use glucose in high levels=> cats fructokinase activity is low=sugars in different forms should be avoided. Can´t use sugars - its toxic for the cats because sugar contains one molecule glucose and one fructose and since cats cant use glucose its toxic! 7) AA def - sulf containing AA= high need (Cyst+Met) - *19%* *animal* *protein* is needed to meet the requrements of the growing kitten!!! -Taurin= NB (througth meat=essential) roles in - bile acid conjugation (BA toxicosis) - retinal function, - myocardium function and - reproductive performance normally procuced from methionine+cystine (2pathway) 1 produce pyruvate, other taurine. Arginine NB 4 Urea cycle: ●Deficiency => hyperammonemia (ataxia, vomid/coma) ● Two felid mucosal enzymes involved in „de novo" ornithine synthesis, so need addition of, ornithine 2 help prevent hyperammonaemie (● pyrolline-5- carboxylate synthase ● ornithine aminotransferase) ● Ornithine addition to arginine free diets of cats can prevent hyperammonemia ● Ornithine does not prevent the weight loss= Clinical signs can be seen in 3 hours so will die within 1-2 days or faster. Amino Acid Intolerance ● Excess methionine causes depression in kittens (2% additional methionine). ● With 3% methionine, some cats completely rejected the diet. ● Cats are less tolerant to glutamic acid than the rats. (Difference: Glutamic acid contain 1 NH2 group and glutamate contains 2 NH2 groups) ● Above 6% glutamate in the diet causes sporadic emesis (vomiting) and thiamine deficiency in kittens. . Vitamin A ● Cats cannot convert B-carotene to vitamin A (as dogs) ● need 2 b provided in the diet to prevent a deficiency that can result in skin, eye and reproductive changes. ● Vitamin A toxicity is not commonly observed in cats but may occur if cats are fed beef liver in which appreciable vitamin A is stored. Vitamin D synthesis in Cats Cats are not able to synthetize vit D ◊ they need supplement in the diet. def=> parakeratosis & OD (demineralisation of bones) Niacin Synthesis concerted from Tryptophan (fel can not convert niain. Tryptopan is therefore concerted 2 NicotinicA / Accoa. give fishoil/yeast (so Ø blue tongue/weakness)

II/A/23. Beef Fattening Systems (types, slaughter weights and ages, common feedstuffs used). The UFP Value.

In beef cattle, fattening begins at weaning (6-7months), ends@sloughter Fattening of beef: 1) Energy req: Give NEm&NEg Transformation efficiency (k)=NE/ME. NEm is dependent on metabilic size of animal & NEg depends on genotype/sex. 2)Cattle should gain bw 1.2-1.5Kg/D. 3)1kg gain needs 26MG NEg. 4)Env factors influences Temperature (15-25, all E goes to KG gain.) Voluntaty intace (high Tems, low FI w/30% decrease production & decreas Tem body used Energy for heat production. Availible nutriend (decrease 30' transiti time is quicker, no time for absorbtion) 5)Prot req is same for Heifers & cows, by pass prot dont need consideration Compensatory gorwth: Capacity of growing animals to ake up for lost genetic potential for poor feeding periods. Cand b used in breeding animals as diff tissues in the body have diff optimal time frame of Development, if missed cannot b replaced!!!! Thi is due to nutritional memory; ANimals adjust to begin economical, maintenance req decrease. Feedstuf of Beef Cattle: cheaper=better-same in previous topics! Feeding methods: 1- Calf fattening; 2-6M old. Milk cows=80-120kg. White M. Calfs=180--200kg(used in italian markets). Artificial anaemia is induced, fed on milk replacers/milk & keps on ruber floors. 2- Baby beef: 6months old (NO SC fat)= Small fram breeds like aberdeen angurs:350-400kg 3-Young bull fattening:16-18months old (Large breeds like limousine=550-600kg.=Diet based on forage & low quality feed (1.1-1.4ADG) 4-Intenside young bull=12-13M old.=Live in chronic state of lactacideamis->600kg. Diet based on Concentrate 1.5-1.6ADG 5- Young heifers fattening (1-2yearsOld) Sloughter @lower weight as they build fat ealy on 400-500kg. Fed on good quality silage. 6- steers 3years old= neutered do decrease growth rate=600-650kg. Only US, 2grazing periods w compensatory growth. 7- Improving old dary cows after first AL. Diet based on concentrates. extrafees given to enhance quality & marbling of meat. UFP-Urea fermentation capacity= Shows the amounth of urea (grams) which can b dded, +ve/-ve/0 balance depends on the protein digestibility and availile E. Degrees: 1 UFP of 0= Availible E is enough for micribes 2 utelize N content of feed, Urea supplementation nor needed (*E(FOM)=RDP*) 2?ve UFP#= mroe E in feeds then microbes need to utelize N-content= Urea supplement is POSSIBLE*E(FOM)>RDP* 3 -ve UFP#= Less energy then microbes need for utilization of N, Ureas ffermentation is forbidden *E(FOM)<RDP* the smaller UFP the hither urea cc in blood+milk.

II/C/10. Herd and individual Diagnosis Based on Milk and Urinary Keton Bodies in Dairy Cattle. Ketonuric Index.

Ketone bodies - Not enough glucose=> gluconeogenesis(GNG) =>ketone bodies (KB) Produced - Ketone bodies in milk indicated E. deficiet (causing fat mobilisation): decreased milk & fertility - We measure KB in milk to detect subclinical ketosis - Normal: < 0,4 mmol/L - High: >2 - Moderate: 1,1-1,2 - Urine KB: normally metabolic products derived from excess AcCoA (lack of oxalate can not go tin citrate cycle)! Primary ketosis = Type 1 = starvation - Realtive energy deficit - Typical between *3-6th* week of lactation - Not ??? just decrease milk productiopn/mastitis ketosis, retained placnta Secondary ketosis - Other disease=> ketosis - Fatty liver syndrome without ketosis, Ex: overfeeding DP Ketonuric index - Practical indicator to evaluate E-balance of dairy cows - Energy deficiency=> kenonuria - Formula: 10 * Y (+/- 2), where - +/-means nr of days after calving - Y = severity of kenonuria detected by reagent strips - *Ktonuric* Index= summarised time of appearance and severity - Evalutaion: - 0-19: kenonuria easily recovered, generally no consequences - 20-29: medium degree dangerous kenonuria - 30-39: increased degree of danger - >40: extremely dangerous and life threatening.

II/B/5. Feeding and Nutrition of Chicken Hybrids kept for Egg Production. I. Pullets.

Layer hens are more complicated that broylers; 2phase= Layers & pullets, laayers hes Length of rearing= 17W(1.5kgbc) 1- 0-3Weeks= ad-libb stater diet as mash, less favoritble 2- 4-9weeks: controll feeding & BW(dalayed sexual maturitu ttil 18th week, must check bw every week. if 2low= change to pallets (increase FI) or increase nutriten density only, If 2high give sam eamount but dont increase agorting to age until weight & age correlate 3- 9weeks: should have reached 700gBW (if good weihgt switch to grower diet), if not switch to frower diet later as starter diet is more concetrated. 4- 17weeks: pullet readin is over, house where egg lauing will start, now layer hen Nd 2 regulare sexual maturity as if they reach it 2 early1 (incre nutrients) then pullets will start laying eggs that are 2 small & not valuable. Acceleration of sexual maturity will also result in shorter laying perios=> *fatty* *LIVE!* Nutrients requirements: 1- CP% decrease proteins= decrease growth rate (starter Decrease 17%0>15¤ Lower then broiler. - MP MH7Kg (Stay at *11.7MJ/Kg*) reminds constant, dont consider fat, only protein. needs covered by seeds -P:E g/MJ= starter decrese 14.5=>12.8g/MJ lower than broler -*Lysine* g/Kg (8.5->6g/kg, lower vs broyler *Met+Cystein* G7Kg 6->5g/kg, 1st limiting factor, muscle deelopment not importants *LinoleicAcid* 1% *Ca* g/Kg= 9->8g/Kg High Xa=early egg prod *P* 4-> *NaCl stays at 0.3 Fibre: Max 4.5% Ligh programe: ore significant in pullets then broilers If light hourse are not manipulaters, egg prod could begin as in the wild. 0-3D (summer):24H/day @ 20LUX 4-21D (automn):reduce hours gradually to 8h/dau & 10LUX 21d-17Weeks winter (hours day 18W->housing (spring)

II/A/15. Applied Digestive Physiology of Ruminants. III. Degradation and Synthesis of Fats, Fat supplementation.

Lipid degredation in Rumen. EE of <feedstuf of ruminal feedstuff is normally low, around 2-2.5% Lipid (hydrolusis by bacterial lipase)=>glycerol & galactose or FFA Glycerol & Galactose are then converte to VFA. FFA are normally unsaturated & become saturated in the rumen bc high H+ linoleic Acid (corn) is converted to stearic acid (satturdated) Lipid degredation depends on: Melting point: low *T= saturated in the rumen. Hig *T=bypass to obomasum SI. Lipid metabolism in high yuilding cows. - When more energy is needed in dairy cows we can: 1)feed more concentrates, BUT high saliva=dec chewing=decrease saliva=decrease pH in rumen (carb degredation will be so quick that the amont of VFA increase too much & cant b used by cow so goes to wase metabolic acidosis. 2) Feed more fats (5-8%DM) (but fats of plant origion= low melting point so will dissolve & surround fiber in the rumen leading to decreased cellolytic bacterial activity of fibers and decrease Acetic activitiy=>Less milk fat! Solution!= Decrease the solubilitu of lipids. 1- Hyfrogenated ouls & calcium/P salts of FA (often used) 2) Capping similar to methionine->oil surrounded by a protected protein then degraded in the obomasum (§Ø used)

II/A/17. Feeding and Nutrition of Dairy Calves.

Main difference bw Dairy & Beef calves= since beef cattle, the main producs is the calf, the milk of the mother is used to read the calf so they stay together, Dairy colves on the otehr hand are sepperated & fed w milk replacers. Table Age weight KG Newborne 45-50 80-90 D 80-100 weaning @110kg 5-6Month 200kg Heifer diet starts (0.5kg hay& 1kg Conc) 15-16 Months 400kg - 1st indemination 24-25M 1st parturation 3) Functinal monogastics- Ruminal devel Rumenoreticulum:abomasum ration 1st month = 1:0.5 2nd M= 2:1.5 3rdM= 3:4.5 Obomasum most NB in newborne but decreases importance w age. Ruminal dev & rumien fermetatio -VFA production: As calf grows, VFA prod increase which increase rumen sice - microorg: mostly bacto (solid feed is given at 2weeks to establish the ruminal flora and fauna. -Papillae dev. Increase absorption SA, hy fibre triggers devel. Development of Enz. Competnace -Protein digestion; milk protein (casein degraded in intestine by pro-renin 2 rening; requires pH 4.5 & Ca fr fermentation of Casein -Milk fat digestion is done by Lipase-Main E. sounce -Carb digestion = lactose digestion, by lactase, nlu lactose can b digested for now, Maltase & saccharase after 3 weeks. Oseåhageal groove reflex: Convays milk directrly into obomasum; requires body temb to work and compounds like CuSO4 + CaCO3 + age + microflorence. Inhibited by excitation=> no closure=> bacterial fermentationof feed=Z chronic bloat. 2Main feeding systems; Traditional (mostly Beef) or Liquid/artificial (dairy) 1) 1st 7 days Colostrum: 1st 7 days colostrum: Provides Immunoglobulins (6%) higher prot, vit, Mg (0.04%) & fat content vs Milk. Within 2h calf must drink 2L colostrum Mg in colustrum increase peristalsis & fecal movement, By the end of 1st week, Calf would have drunk 35L. 2) 2nd week ->90D - Traditional system: direct suckling, less economical & increase chance of infection - Liquid/artifision system: Advantafes; better milk production, less udder injusry, whole milk & milk fat saved and sold for humans, possibility of early weaning, well balanced nutritent supply. Calved protected from maternal infections Types of artificial feeding: a- Whole milk & milk powers + h20 if price is low b- Skimmed Milk&powder + fat suppple + h20 c- milk replacer=skimmed M. podr+ whey+soyprotein+fat+vit&minerals d- protein suplm+fat suplm = normally from soybean =easily digested & high veg protein e- Acidified milk replacers=like milk replacer but w extra proprionic A 2 hid pro-renning 2 rening Milk replacer= CP20%, EE15%, + h20!!! How much 2 give: 1month=6L/day, 2nd month8L/d, 3rd M 3-4L D <Tradition to fermentabkle feeds, should b done gradually whilst decreasing milk replacer over 10 days. From day 10, add calf hay, ad lib & cc for growth from 2nd weeek add starter pellets & high quality meadow hay ad-lib, started is § in CP (18%) & medow hay is § in CP (16%), Low CF (20%) after 4 weeks high cc intake, water ad lib as it increas FI water req. 1 month: 10L 2nd15l weaning early is done 50D normally 90d/100kg Mist NB factor= dry feed consumption when it eats 0.6kg hay & 0.8-1.2kg cc, its ok to wean. after weaningthe quality of cc is VIP, due to the diffe req. of AAs and vit B!! See figure in folder!!

II/A/16. Compounds Having Advantageous Effects on Rumen Function and Metabolism.

Mostly come in the farm of feed additives: 1) Yeast: Increase bacteria viability + more stable pH - Aspergillus= Hin feed intake & high milk prod as well as milk fat -Dose: 5g/day (dairy) & 4g/dBeef -O2 removers making the rumen more anaerobic, increase cellolutic bacto; Increas Acetate prod & milk fat. Increase Lactating utiizing bacto, decreas Lactic acid in the rumber stabilizing the pH. Udeshigh high yeald dary cattle after parturation as rumen fermentation sub-optimal through the increas in microbial protein sythesis, 2) Buffers: True Buffers= Sodium bicarbonate, feeding more concentrates decreas ruminal pH so Buffers shoul b added. Natural buffers:- Saliva (maintain pH 6.2-6.8) 150-200g/day Niacin(Vit B3) Synthesised from tryptopan, decrease cholesterol. Bacto can syntheize Niacin, but its below demand post parturent, give 6g/d for 2-3weeks before and after calving!!!! acts as cofactor in intermediate metabl (Nad/NADDPP-retox potential). Protects again Fatty Liver & Ketosis in Darycattle!!!! Cation-Anion Balance. Prevents Milk feaver in the last 2weeks b4 parturation, this value shold b negative -50--150= Acidic circumstance. Acidosis promotes Ca metabilisation from boenes. Give Acid dien-> NH4Cl. DO NOT GIVE Alfa alfa!!!! Glucogenic compounds Increase B. Glucose eases the E. deficiency caust by Milk lactose. also uced for Ketosis treatment! After birth - cow- 4kg glucose (glucose+ prop.glycol)

II/C/13. Endocrinology, Genetics and Nutritional Management of Obesity (Dogs, Cats).

Obesity types= Physiological (Migrant birde/hibernation) & pathological -- can be; *Hypertrophig* Or *Hyperplastic* (cellularity). # of Fat cells increase @ foal devel & growth; adipocytes stop proliferation @puberty. - Eat 2much=>Inc size=>incre leptin pro=>hypothalamus stim=> FI inhibition by NeuroPepticeY. Leptine inhib NPY=> decrese FI NPY =responsible for inducint FI inhibiting satiety (feeling full). Obesity causes E input>>> E output factorts include: - inadequate satiery signals (ob:ob/Leptin/NPY & Ghrelin. -Diet Body ecpenditure E (excercise) & nutering T4/T3=> basal metabolic rate. *Ghrelin* SHort time control prod @stomach, induce FI by produc when empty, stops prod when full) *Le+tin= long time controm, prod by adipose, eat when fat storage reach low, less lepting produced when far storage is high. *Both act on Hypotalamus*! Nutritional managment: = Main danger of slimming diets is: fatty liver 1) owners complaince, 2) cyclic periodis designs (Bw will cont decrease) A)60% for 3 weeks,=>b)100% 3 W=> 60%3W=>100%2weeks..continue a) 60% of maintenance given w important vit&minerals b) 100% of maintenance given In 6 weeks set, fat & starch (barley) are lowered & protein & excercise are Increases 3)Degree of obesity by using FelineBodyMassIndex) & BCS. Diet foods: Hills:eight controll&obesi, or Royal canine obesity&obesity?diabetes Different diagnosis: -Preggo, ascitis, constipation, cushings, tumore, hypothyroidism -Vit A=> Leptin increase, long chain FA 2 mitocondrie -L-Carnitine(by lysine)=> carries long Chain FA 2 mitochondir burinning long chain FA -Organo tricalent chromium(glucose tolarance factor)=> Fatburner to increase Insuline deficienc.

II/C/15. Dietetics of Dog and Cat with Renal Failure.

Renal failure can be chronic or acute, but the acute is generally not detected until it is too late. Signs do not usually show until 75% of the kidney function is lost= irreversible leasions in kidney/renal function decrease. 2) CRF treatment 4 classes: 1(in blood) 3-4 (show clinical signs) a) Dietary treatment (3,4) decrease load on kidneys by providing a low protein diet (with HIgh quality bc easier for kidneys), replace the water soluble vitamins and Ca, and prevent P accumulation (if 2high=> kidneys ca not excrete it=> accumulate, increas PTH=> Ca mobilisation from bines decreast.=rubber jaw, alopecua). omega 3 FA supplementation, antioxidants & vit E. Normal protein K9= *14-16%* (nor 18-22%) Fel= *18-20%* (Nor 30-35%) classical treatment is done w:; NAHCO3 2 treat acidosis, give EPO inj Chronice glomerulonnephritis: inflam nephrons - persistent prteinuria=> hypoalbuminaemia=> ascitis/hypothorax. Caused by FeLV, septicemia, heart worm. treat: dec Prot (increas BV & dec Na to decrease pressur on kidneys) Increase serum albumin. Food: Hils & royal K9: Chroninc Renal failure diets

II/A/10. Nutrient Requirements of Horse.

Requirements of the average Eq: 1- DMI - 1.5-3% BW, low bc sm stomach content 8-10kg 2- DE (MJ/kg) depends on BW (several equations are availible, 1fr a Eqdec 600 kg& one more, normalaround 70MJ DE/day 3- Prot/AA- Officially we use DCP-0.6g/kgbw; but CP is oftern used aswell (*9.5xDE*). Optimal P:E is 5g/MJ 4- CF- 16-18% minimum to avoid diarrhea&digestive disorders 5- Ca2+ & P (g/day): Ca=20g/d (4g/100kg) & P-15g/d (3g/100kg). Ca:P should b 1.5:1 (adults 4:1 foals 1.5:1) 6- H20&Nacl- 2L/DM (5L/100KgBW (20L/d). NaCL suppl. (b/c levels are below the req in most feeds, lose a lot in sweat. 7- Feed for EQ to satisfy reqirements which generally a basal diet w/added concentrate. Roughages are used for the undisturbed running of the digestive process, to high fibers will result in decr FL, decrease stomach filling, decrease pH in SI (carbs). Concentrates are used to cover E required, too high will result in Colic&digestive troubles. 8) A- Appropriate drinking H2= & source. B- Forages (hay,haylage/silage/straw/grass/pasture). *pasture* 22-25% DM consume 50kg/d, tomothy s best but blue grass is used. Sudan grass should never be fed when its growing bc prussic acid, which is destroyed when making hay, causes cystitis- constant urination. *Hays* (meadow hay/legume hay/alpaalfa - 9-10MJDE/kgDM. Alfaalfa high in Ca & protein w high nutritative value, given to EQ that need more P & E (late preg, early lact stallions foals b4 wearing), BUT high proteins=growth rate=> dev orthopaedic disease, increase Ca could lead to kidney stones=> increase int. work leads to increas sweating High levels of ammonia also lead to liver damage. Silage: 10kg/d silage w low acid content is especially good for working Eq. Straw = High CF (40%) low proteins-5%, lowed 5mj/KGDM, Low nutrive value so used as bedding. 9) Concentrates; Improve body condition-max 0.5% BW Oat grain - crushe for young or old Eq Barley Grains - to prevent starch verload in intestines Rye grain - improves reproductive performance of stallions. Suggar beat pulp high E. Corn- high prececal digestibiligy of corn, high heat. 10) supplementation:Fiber, wheat bran: up to 4kg to prevent obstipation during colic. Fat- to high E content, veggetable oils, no more that 1g/kgbw over 3meals, mix in. Treats - dried brewers grain - replaces 40% of oats, sugar beet pulp (stomach swelling) molasses, fruid & veg. Protein:supplemented when needed, preg. early lactation, low legume pastures. NaCl for working EQ, Cu, Zu, Mn provent DOD , Laminitis due to acidosis.

II/C/17. Nutritional Lameness and Skin Diseases (Dogs, Cats).

The approach to the dermatological case: 1. Complete clinical and dietary history 2. Complete physical examination 3. Detailed examination of the skin and its appendages Skin symptoms: ● Primary: Macula, Papule - Nodule - Tumour, Wheals, Vesicles, Pustule ● Secondary: Scales (squamous), Crust, Lichenification, Altered pigmet. Dermatoses are divided into pruritic and non-pruritic dermatosis (differential diag.) 1) most commin causes of pruritic dermatosis (hypersensitivity 2 food!!!): ● Ectoparasites (Fleas,mange, Pediculosis) ● Bacterial infections (Pyotraumatic dermatitis, Superficial folliculitis) 2) The most commin causes of non - pruritic dermatosis: ● Ectoparasites (Demodicosis) ● Endocrinopathies (Hypothyroidism, hyperadrenocorticism) ●Dermatophytosis ● Deep pyoderma NB nutrients to reduce skin problems: 1) Protein ● Deficiencies changes hair and skin: abnormal keratinisation/depigmentation ● Skin=> greasy and susceptible for secondary bacterial infections Minerals: Zinc deficiency: a) Zn responsive dermatitis: treat w/zinc sulphate orally 2xD (clinical signs=alopecia, scaling, crusting of mouth, chich eys ears.. b) Zn permissive dermatitis (overfeeding Ca not enough Zn) in Bull teriers acrodermatosis (lethal, average survival=7month) c) Iodine in pups = goitre, hairloss, low metabolic rate Vit A def: (needed for MM& keratinisation. symptomps= greasy fat like material secreted on skin surfave:parakeratosis) Hypervitaminoses A(fel) Associated w/beef liver feeding (bc hihg Vit a) Signs= poor coat, painfull grooming, lameness skeletar changes, exososes, cervical&thoracis vertrae & FL. Vit e(SE) fel: Yellow fat disease or Pansteatitis in cats (ferret, mink as well) ● High levels of PUFA with low levels of vitamin E (when diets containing excessive amounts of canned red tuna or cod liver oil are fed), leading to the deposition of ceroid pigment in adipose tissue with fat cell necrosis and subsequent inflammation ● Clinical signs: anorexia, depression, general tenderness: cry at palpation, subcutaneous fat may be lumpy on palpation. Treatment: dietary correction: remove rancid food Essential fatty acid deficiency ● Component of cell membranes (phospholipids), maintain healthy epithelium ● Omega 6: linoleic in dogs, linoleic + arachidonic in cats -roughend greasy goat, hyperplasia/hyperkeratosis. _treat w suplement (fish oil) Thiamine (B1) Kittes: raw fish thiaminase, overcooked meat/canne foood.=>anorex/vomit. Inj=immitiate recovery Biotin: see symetric alopesia Hypersensitivity: foll allergies, itching, skin problems, mostly allergies 2; beef, pork, chicked, dayr, cerals in k9, fish/egg/soy in fel for fel use lamb for prot& barley for energy K9= fish for protein & potato for energy Nutritional lameness: vitamine D...Ca mobilisation

II/A/20. Feeding and Nutrition of Dairy Cows in the dry Period.

There are 3 lactation periods & 2 dry periods in Dary cows Phases: 1 Dry period: 60-14 days b4 calving & 305-350 apost partum. Aim= 2 minimiza metabolic prob. dring the next lactation & maxim yild. Udder regeneration begins, nutriens req. for body maint & foetel growth are meet= a- *DMI=2%BW* = Can b lower then 2 only when high E is fed(corn silage) to avoid over conditioning aka *grass* hay is best, E sure 2 meet other req. b- *CP=Min.12%DM* c- *CF34%DM* feed roughages. d-Avoid 2much Ca/P bc might=Milk fever (*Ca=60-80g* P=30-40g*) e- Avoid fat deposition - Acidic is given to incr Ca mobilisation & decr fat cow syndrom *NEli Higher during dry hase du to growing foetus* 2 Transition phase 350-364D pp anabolic phase aim= 2 *Prepare* rumen for High CC Diet in lactation period 1 for foetus growth some grain, if never feb before, should freshening to prepare bacterial=DMI increases. High conc. changes Rumeb bacto 2 a mixed population & conc dg increase FI=ish4kg a- *CP=IncreasteTo15%DM*- feed some UDP could b benefisial b- *CF=decreaseto20%DM* - NDF=best fiber source for the rumen, not as much required. c- *Ca=DecreToPrevent*MILKFEVER* & udder oedema. d- Limit fat to 12kg: IncreaseFIlower DM intake

II/C/9. Measurement of the Milk Urea Level (Importance in herd health, use in the practice).

Urea: produced from NH3 in kidneys & liver to decrease NH3 toxicosis NH3 is produced during tissue breakdown. NB Urea: A)important indocator if E:P ratio (balance) b) urea is excreted in urine/milk as normal NPN optimal urea in milk=3.5mmol/L. Diagram: Nh3=> MPM or MPE. Cells(AC.a=>milk + bodyfat amylas=>propr.A=>E source GNG=>glucose -Incr prot intace=>increase milk urea lev -inc E. intace=> microbial prot porid inc=> B.Urea dec - Inc H20 intake => b.urea levels Decrease. - Decrease H2O=> increase Urea levels - UDP = 10% _> small intestine _> digested& absorbed - RDP = 90%-> catabolised to NH3 ->resynthetised by microorganisms UFP = ((1,044 * TDN) - dg) / 2,8 - Positive: E>P = give urea - Negative: E<P= do not give urea - Zero: E=P = do not give anything E content should b parallel w/N-release:=> optimal as there is bothe E + N availible for microorganism N-surplus: - feeding costs: E-loss as well because production of urea takes energy - liver damage fertility disorders - urea in milk - pollution (environment) Milk analysis: - used as indicator for diet unbalance and subclinical diseases. Milk/urea test gives info about E:P supply 1. direct: urea + reagent = colour transformation 2. indirect: urea + uearse = NH3 + CO2 3. Measure NH3 by Kieldahl methos Factors influencing milk urea concentration 1) Cow: - Stage of nutrition - Breed - Maturity - Health - Body weight 2) Environment: - Winter &lt; summer - Housing 3) Sample cllection - Morning &lt; afternoon - Whole milk &lt; skim milk Others: Fatty acids, GNG, Ketone bodies, acetoacetate, B-hydroxybutyrate acetone...

II/C/16. Dietary Management of Urolithiasis in Cats and Dogs.

Urolits ● Mg-ammonium-phosphate! Most NB cat urinary stone= struvit crystals (2/3 cases =coffin stones). ● Ca-oxalate - small and very sharp like a star crystals ● Ca-carbonate, Ca-carbonate, Feline Lower Urinary Tract Disease (FLUTD)= 10% of population: ● struvite (Magnesium ammonium phosphate)=> urethral plug. 2/3 - Ca-oxalate & carbonate effects 1/3 cases ● Feeding diets that result in acidic/urine PH (pH less than 6 will desolve the stone), enhance urine volume and reduce magnesium intake. Spcial dieds: Hills W/Calculolytic=> low prot, ca & mg give sulphonamide antibiotics which might lead to secondary infection: sulfonamid-, => antibiotic treatment - doxycycline is the best for urinary infections. Canine urolithiasis (2% of population) ● struvit=> female=>alkaline ● Oxalate=> males=>acidic urine ● cystine ● urate, Males (danger Dalmatian (produce uric acid at the end not allanotoin (no uricase!) ● silicale (similar to cattle) Treatment: Sulfonamides/AB treatment earli to prevent inf. smae treatments as fel

II/A/22. Feeding and Nutrition of Beef Cows.

Voluntary feed intoke depends onmetabolic BW (bulls adds 5-10%) involved 4 periods, diagram: Feb (calving) May (AL) June-Pct(1st calf) Nor-san (calving2) Take the 3rd period(mid preg) nutritione values as 100%& add protein/E requirements as & depends on the phase: All numbers are lower then in Dary cows! 1st phare- +50% E & 60%Protein 2nd phase- +20%E & 30%P 4th phase- +20%E & 15%P (for exponential foetal growth) Life&feeding P1- Calving to mating: 2 years old if 1st time (last calving 80d) ex Feb 15th-05May. Øovulation during this period, suckling calff & cow is the fresh stage (needs most nutriten for sucling). Nutritional weigh of cow determines weaning withe; NEm=150%/P=160% 70:30 concentrate:roughage p2- Mating to weaning: around 120D til weaning of 1st calk (80->205D). Cow is preggo w/2nd calf & finishing1st weaning. 120%NEm &130%protin. 50:50-concentrate:roughage p3- Dry period: mid preggo (from weaning 110D-til just before calving). Energy for preggo is low, only maintenence level requires NEm100%. 1st stage of dry period is long so no suckling no milk production. 30:70concen:roughage p4-DryperiodCalving. Extra E needed to prepare for calging (opposite in dary cows, beef cows was lactatins & preggo @same time). 2nd stage of dry period is shorter, foestus grows fast! NEm=120% & P=115% Nutrient requirement of beef breading heifers & cows: Maintenence E= NEm & NEg, ME=>NE 13% in preggo, depeds on BW/time. Lactation energy depends on MilkFat. Energy 2-3W b4 breeding we can increase E & CP for flushing. 2Prot systems (fractional & MP). DMI=Beef cattle>Beef cown by around 10%. BCS n3braske system Feedstuf: Grazing&Hay. Straws depend on the cutting time, earlyer they are more like Hays(in nutrient). NPN is rare, Silage in combination w molases is cheap&good DM content. Conce only in calf nursery according to the demer. Carotene, mineral DN citamin A Inj

II/A/18. Feeding and Nutrition of Dairy Heifers.

When the calf is 5 - 6 months old (200 kg), the nutrition of heifers start. Want the maximal lactation according to genetic and env conditions. goal = healthy and genetically good adults. If female calves get too low energy supply (-20%), their ovaries will not develop properly and therefore no ovulation later. Male calves given 20% less energy,=> no spermatogenesis. Age Weight Kg Notes Birth 50-Isometric growth 3month 110-allom gr weaning 6M 200-allom.g becomes Heifer 9M 280 kg-allomet gr Puberty 15m 350-isom gr 1st insemintat BCS3.5 24thM 400 1st calving Sexually maturity Puberty= time when the heifer has her first ovulation. first ovulation, she should have heat periods every 21 days. The age at which heifers have their first heat or reach puberty determines when the heifer is bred the first time, delays=>late breeding&calving. Optimal age 9 to 10 months of age, then inseminated at 13-15months to calve at 24month. Correlates w body fat% not age, leptin has an NC influence, underfeding => late puberty. Overfeeding=>fatty reprod Organs=>inhibic cycle. Growht stages: 1. Isometric until 90D(100kg), danger of fat deposition, GH & mammary parachumal DNA decrease. 2) Allometric from 900> puberty, readu in terms of body form (critical period for udder devel. during this per.udder growth is 3.5x that of other systems, if you overfeed in this period, then parancyma is replaced w fat, decrease milk production &GH. 3) Isometric growth until 1st calving-temporary periods of rapid growth are acceptable, if 2fat then longevity decrease & parturation diffic. occur. Rearing intensity- Heifers skinny cows will not develop enough until the time they are needed - too fat cows will have fatty reproductive organs, which inhibit the perfect reproduction cycle - body weight, wither weight and body length is positively correlated - Result of the BCS: o 1: goat type - skinny o 2: medium - BW < or = 500 kg o 3: small framed - fat types Long time= 500g ADG inseminated @18 months, changing=200-900ADG. Moderate=700gADG insemination @15Months. Intensive=800gADGinsemin@13-14m. Very intence=1kgADG,insamin@12m Recomented *ADG=700g* inseminated @15M, increase mulk yeals and is economical. mode +15% mainenence 1) arguments 4 more intensive rearing=better 1st lactation, less need for replacements heifers 2)argument against more intensive=shorter lifespan, diff calfing. Nutritiont requirements depends on foal & heifers state -Generally; E= NEm & NEg around 25MJ/kgDM ROughtage increase VFA (Acetate) & small mount of conc. Supply Vitamin A,B-carotene, MG, Zn, Cu improves fertility!!! o *NEm* = 0.3514 x W0.75 = 23 - 24 MJ/kg DM o *NEg*: 26.8 MJ/kg DM o CP: 10 - 11% (low because the ovaries are extremely sensitive to NH3) o CF: 6% (minimum) - Controling intensity of growth: NEm & NEg Protein requrements (microbial rotein) E:Protein ration ? we use Urea will increase =>NH3 toxicosis

II/B/8 Feeding and Nutrition of Breeding Turkeys (Flock Replacement Turkeys + Layers).

flock replacement turkey: from hatching=> egg production -Reach sexually maturity later vs chickens @rearig period we must change the period many times: *0-4W-starterDiet* (ad lib but controolled (isometric) *5-8W=>grower1*:controlled *9-12WGrower2*:Controlled *13-16W=>grower* *3*:Controlled. *17-29W=Rearer:controlled!* From week 24-29: we need to improve Body conditions, special for torkeys, if at week 24, the BW is 2high and we need to Decreease ADG but nor stop growth altogether. Controlled diet: Controlled by nutrient density not Quantity! - Check BW/week:Normal=stick 2 plan, 2heavy:Alter diet for next time. if 2light:switch later. -layers have loower nutrition density than fatttened turkeys, *ad-Libitum* as we want *isometricGrowth*,Øintensive &restrict nutritent densitry to delay egg prod. Light programme is inportant,should follow seasons! Nutritent requirements: *CP%* = 26=>13.5 (decrease= dalay onset of egg prod. *ME* MJ/kg= 11.5mj/kg until rearer diet then increat= 13mg/kg as they req more maintenance. *Ca* 150>8g: only for bone/growth dev *Ca:P* decr *NaCl* 0.3% feeding layer turkey: Layer turkeys have 20.24W long laying pariod (much shorter vs hens) Laying period: 30-w= layer 1 diet 34W= peak production, 70-80% bw 30-36 wks we mas FI 40W:layer2 diet, lower prod-restricted mash 50-54w:sloughter egg prod: 100-120eggs/bird= lower then hens, valuable due to long laying period. 80-90g/egg.80_>90g by the end nutrition in laying turkeys: CP% 16.5=>15% ME: increase: 11.8=>12MJ/kg ca: increase: 25=>28g bc increase egg size & depletioed stores P:3.5->g Layer 1= use pellets bc high egg production, FI is not enough w mash layer2= mash bc increase production, if fed pellets they become less fat &lay less

II/C/14. Special Diets for Senior Dogs and Cats.

general basis of aging is given by telomere-hypothesis, in which the cells have imited capability of multiplying beofer apoptosis. Aging: slo performance of vital functions, immune&neuroendocrine system troubles, decrease lean body mas & decre ability to heal injury Considered old @ small > 11.5 years Giant> 7.5 Fel > 11 years Persian&siamese=9-10Y Nutrition: ME: high in K9 low=Fel. Lower in senior K9 vs young k9. Protein: need proteinw with High BV & digestbility (bc low liver&kidney function) in older fel Fibers: K9 needs 3-5% to prevent constipation (wheat bran) Low Na/P incase of renal insufficiency. Omega 3 & FA should b high to prevent SM spasms/inflamation L-carnitine (c)& taurine (fe)=> improve M. Capacity(heart M.) food 2 use today - Hill's senior +7 ● Hill's senior light ● Hill's b/d (can also use k/d for kidney failure, but this has restricted protein, P and K)

II/B/11. Feeding and Nutrition of Breeding Ducks (Duckling Breeders + Laying Ducks).

kept for producing rosted ducks: Onset of egg production is *28weeks* - lasts 220 D (7months). 130-150 egge produced, 75-80g intensice system: 300D:250eggs 2phase breeding birda: 1-rearing: 0-28W: more expensive in ducks then pullet as its longer 2-Laying period:28W=>end prod(7months) Rearing: Pre- or past-rearing 4 duck brreeders (traditional system) 1-PreRearing: 0-18D kept in heated building due 2 size (50g) 2-post rearing: 18D=>27W. 0-7W fast growing, seletion suiteable for breeders (3-3.2kg). from 7Wgrowth decrease as more fat is build vs M. Ducks are still very similat to netral form so they are reared acording to season. A) 0D=hatching june 10 (50G) B) 7W=fed like roasting ducks(3diets) they are selected for reeding/sloughter like roasting ducks, like rosting ducks 80% of growth capacity is lost after 7thW. C) 8-25W:feeddrearer pellets: low nutritent dencity as we dont want to inbild fat FI=150-180g/D. BWgain:600-800G(period) increae gain then they become fat and start agging earlier. d) 25W-2nd selection for breeding suitibility then housing (bw4kg) E)26W: start lauer dies= *High* nut dencity, Ad-Lib & in pellet form 27W: reach sexual maturity 28W:egging starts (january or 2nd year) laying period starts after this light program: Natural light in traditional breeding systems, acorigng to season (decrease in aurom, then increase). Intensive systems=artifisial light is uced:18H/d=Increase egg production. Laying period: 7Months, 130-150eggs, longer rearing, shorter period vs Chicken. Lighting hours are increasing as doesn the production of eggs.. at the end of the period: ducks can b sloughtered after fattening, BWincrease by corn ad-libidum. OR go in2 2nd laying period: 90% of 1st, let our of houseing into fields until november, next period starts in january. depends on the economical factors for the farmer. Nutritioent requirements: rearer & layer diets: *Cp* 14.5_>17% = increase *ME* Slight increase: 11->11.5MJ/KG Both diets are given in pelleted form, nutrients density is lower (cereal grain preventsing ducts to start earlier. Intensive program: artifishia light; always 18h/d onlu the intensity increases. Production increasing so longer egging period, more expensive vs traditional method.

II/A/12. Feeding and nutrition of Mare and Foal.

maintenence requirements 1) DM 1.5-2%Bw 2) De: Depnds on Bw= <or> 600kg norm (35-70MJ/KG) 3) CP: DCP 0.6g/kgbw but CP is also use in practive 9.5xDE g/d 4) Ca:P=20g/d &15g/d 5) h20 2L/kgDM, 6) CF; 16-18% DM Breeding mares: Seasonal polyestrus - consecutive oestrus cycle w/highest conception in may flushing DE+ 10-20% vit A,E,B-carotene improve implantation & fertilisation of eggs, same conceps as in sow but goal is to increase no ovulation. Optimum body condition should b kept throughoug the year, Robs cant b seen but can b felt, hipcones cannot b felt, small fat deposits should b present around the neck, shoulders/whithers. BCS should b 3, over/underconditioning causes foaling difficulties. Pregnant mare: Gestation 330-360D & foarl wight 50kg. DE: Foal grows slowly, in the 1st 8months so maintenance is enough after the 9th increase. 9-11months 9(+10%)/ 10(+15%) / 11(+20%) CP-(g/day) 10.5xDE(750g/d) Protein require is much higher in late pregnancy so feedalphaalpha, Feed intake: fisrt 8months good quality forage covers req. 9-11months increase conc & decrea/forage, amount of food stays the same throught! Feeding the Lactating Mare: milk yield: 12-18kg/d, peacks around 2nd month. Equivalent to 3%BW for the 1st 2months & 2% for the 4th to the 6th month. Contents of milk:less E, fat, DM, Prot, more lactose than cows milk, Less E req. FI intake should increase, 2-3KG in early lactation &2-2.5kg in late Nutritional req; a- for E: DEm & DEl we need to know the BW& milk yield. b- DEl=3.3MJ DE/kg milk & DEm=<600kg is 5.9+ 0.13BW c- Protein; 12xDE in last 3months (1-2kg forages & 1-2kg conc) d- 11xDE in Last 3months (1-2kg forages & 0.5-1.5kg conc) e- Lysine is lactatin mare is vip, often not met by rations, you musc give 3g/kg milk can supplied by green grass, soybean meal or direct lysine additive. H20=4-6L/kgDM Feeding the foal - 5kg but doubles in 2weeks Colodtrum Ig. Suckling frequency; 100x/day @ beginning, 30-40x/day later on. Creep food- 2-3weeks old, start w/simple cereals & platels. Age in month is the same as oats in liters. gradually increase forages for microflora in hindgut, but dont feed tomuch alfa alfa due to DOD. Weaning @5-6 months, 40-45% adut BW, 1kg conc can b given (5L oats+2.5kghay) DE Requirement: DEm+DEg is needed, depeds on the actual mature BW CP: Weaning (DEx 12), 1year old(DEx11), 2years old (DEx10) Developmental orthopaedic disese-DOD; The foal shoud reach 60% adult BW in 12 months, more intesidve growth risks DOD

II/A/13. Applied Digestive Physiology of Ruminants. I. Fermentation of Carbohydrates.

pH of rumen - 6.2 - 6.8 - Maintained by saliva; buffering mechanism (pH 7.2-8.5) pH of the concentrates will increase o real buffers: HCO3 - and HPO4 Carbs are structural or non-structural: o structural=hay,&roughage (cellulose, hemicellulose&pectin) o non-structural=cereals (starch&sucrose). Degradation method; vfa + co2+h2 = methane & E loss. - 200 different bacteria (cellolutic &amylolotoc) found in the ruminal fluid, they produce enz which degrade polysacch into pyruvic acid=>(intracellular enx) form VFA, co2, H2 & methana. Acetic Acid(from cellulose-roughages/hay) propionic acid (from concentrates) & butyric acid. During the breakdown of simple sugars, ATP is produced which is important for protein synthesis later on (1glucose=2pyruvate;2 Acetate, 2 Prop, & 1Buter). VFA: 3-4 kg produced by a single cow/day. 70Ruminal ATP originates from VFA. a-AceticA; AcCOA= fat (milk/body fat)&Keone bodies (in high yealds=ketosis). b-ProprionicA; E sourse, no E. Loss, play a role in GNG to prod flucose. c-Butyric acis; E. sourse main source KetoneB. Acetic A. NB for milk fat production (better with more hay) When increasing roughtage, amylolytic bacto low. lower proprionic acid& cellulytic bacto increase (more acetic A.) Beef: if proprionate is lov E. will b low leading to a low protein content of milk Dairy:if acetate is low then milk fat content of milk will b low.

II/A/1. Digestive Physiology of Pig, Change of Enzyme Activity from Birth till the 6 th week of Age, and its practical Importance.

1) standard date (Pig standard date:weight, days nutrit...) physiology: 2)Salivary gl (mandib, sublingual and parotid) produce and secreat *Amylase*= hydrolyses *starch* to *maltose*. 2)stomach (simple): ph 2-4.5, 5liters simpel muscular stomach, 3 pards: *cardia*(w/espophageal part & glandular part), *Fundic* (glands) region & pyloric. Esophagus area not secreat dig.enzymes=where ulcers often form! Caridia= mucus is secreted and mixed. food passes into the fundic region which is the 1st major portion of the stomach that begins the digestive process. *Antrum* contain *G-cels* which produce *Gastrin*. -> stimulate *Parietal* C which secreted HCL. -> (if pH is lower then. decr. pH of 1.5 to 2.5=> kills ingested bacto) stim *ChiefC* to produce *pepsin*(from pepsinogen by being broken down by HCL p). *chiefcells also produce Rennin which actss as a protelytic enzyme* *pyloric* region= responsible for secreting mucus to *line* the digestive membranes to *prevent* *damage* from the low pH digesta as it passes to the small intestine However, if pH is *low=immunoglob* will b *destroyed*. 3) Change in Enz activity 0-6th week *Piglers* Have *achlorhydric* @ birth=> able to take up *Maternal* *Immunoglobuling*, (if they have Chlorhydric as in adults=>IG from colostrum would b denatured/Øeffect). Rennin is needed first 14 days. after 3rd w more HCL produced=> Incres pepsin activ, Ig cant cross plasente= *NB* *Colostrum* In colostrum also trypsin inhibitors 2 prevent trypsin of SI 2 gigest teh IG (Proteins) -Changes in Hydrolases (stomach) trypsin inhib present in colostom to protect IGs. Lipase gradually incgreast, low@birth, amylase<lipase@birth 4) Intestines: 3parts *Duodenum* digestion w/peptide hormons and ducts from the pancreas/liver (gall bladder). Brunner gl.secretion (*alkaline* lubricant) protect from acid content. pancreas (ENdo&EXOCRINE) is responsible for secretion of insulin and glucagon in response to high/low glucose levels in the body + it has exocrine functions of secreting digestive enzymes & *sodium* *bicarbonate*=> hydrolyse *proteins, fats,&CarbS* in the chyme. *Pancreas* (help digestion of chyme and the prevention of cell damage due to pH. ) = trypsine (chemotrypsin&carboxypeptidas)=> Digest proteins, Amylase=carbs/Starch, Lipase=lipids Intestinal mucose=sacharase, maltrase, enterokinase (LACTASE&MALTACE 4 CARBS, DIPEPTIDASE FOR PEPTIDE). Liver produce and store bile in GB=>activated to BileAcids helps dig/absorp of fat and fat sol-vitamines & acids pancreatic lipase in small intest. BS helps absorption of cholesterol (which take place in lower SI. *Jejenum*=digestion&absorption *Ileum* absorption @ brushborder aka intestingal mucosa. Amino acids & simple sugars released into the brush border membrane are absorbed into the microvilli first, then into the villi, and then pass into the *circulatory system=>portal vein=>liver*. Fats *absorbed=>lymphatic ysten*=> general circulation via thoracis duct. Large Intestines: Ceacum, blind end section where material cant pass, 2nd part connected 2 Colon. Main function *LI=H20absorption* *no* *enzymatic* digestion occurs. However, limited *microbial* enzymes activity does occur in the large intestine, which forms *VFAs*. B-vitamins are synthesised. Lactate produced to lower pH for lactobacilli Transitiontime: min 18h max 100. 5) Lowers the pH of mothers milk= Lactobacilli-> ferments lactose-> endoproduct-> lactic Acid. 6) how the feeding influene pH: a- fed restrictely(small portions, several times)=Lowers the pH of mothers milk and inhib bacto groth stomach. b- fed contin *ad lebitum* ->they eat as much as they want 1/2 stomach pH7 / other 1/2 pH 3 =low enough pH to inhibig growth in 1part of stomach. c- ad lib after restricted feeding: phish=bacto overgroth, occurs when pigs change normal feed. c- fed ad lebium past feed deprivation (1st day they eat nothing, 2nd eat 2much) 7) Conclusion: Diet of young piglets should b constructed in accordance w enz. activity. as age increase, the product of milk degradation enz decrease (lactase) but enx for solid feed increase (amylase)

II/B/1. Biology and Digestive Physiology of Rabbit.

Facts: Hares live above ground, rabits below. Hare skull smaller, no cross breedding, dif # chromasomes. Rabits are altrical-dont move after birth, hares=precocial(move). Newborne rabbits=60g, hairless&closed eyes, Hares=open eyes&move, hares actide at day, rabbits night. Biology of rabbits: Maintainance higher for producers vs lab rabbits, CF is very high!! to maintain gut system (13%DM, 3x of pig!). Ca reg NB= as they excrete ca in crystals in urine. H20 req is low, around 2xDM intake. NB food is chwewed to wear down the incissors (Øgive meals form)!!. Oats>Barley>wheat (low amount low amylase activity)>alfalada meal>dried beet pulp (prefference) Rabbits have as lib feeding, DMI is determined by actuall Energy need, when low E the volutnaty DMI increase (dosnt work for animal is young, eats anti nut subst=>increase Temperat 17*) Caecotrophy: 3 factors related: - stim of rectal machanoreceptors, ID of smell of soft faces & inner motive driven by *blood* *hormone* levels. - re-ingested caecal content improves nutritent utelization - soft faces lower DM then Hard, but higher CP & EE., swallowed w/o chewing to protect bacto. Anatomy&disgestive physiology: 1: Teeth - 4 incicors on upper jaw, 2 lower (tot 28) 2: Stomach- 36% & cecum 43% bth largest in all monogastric animals, they havve disseminated pancrease. 3: Rabbits are hind gut digesters- *cecum* *fermentable* animals (ex Eq=cecum&colon) 4: pH change in GIT Stom(2)0>SI (6.7)->Caecum(5-6) -> co(6.5) Cecum: contains GALT-gut acces Lymphoid tissue. No E.colu, bacteroides are more common bacto. Fibre is digested by bact=>VFA then absorbed (A:B:P=10:3:1). c Degredation of Prot: start @stomach w Pepsin&HCL comples, SI by trypsin&chemotrypsin, Aminopeptidase in the intestinal wall then cpmplete the digestion. Proteind/digestive enz residue is then pass to the caecum to be used by bacteri. Lipid diges/Abs= By pancreatic lipase, BileSalts etc,,,70% of rabit bile is biliverdin as bilirubin is low carbs digestion= Readaly availible carbs like starch/sugar are digester&absorbed as *Glucose,fructose,Galactose.* Digestive torybles: Feeding enough fiber, preventing diarrhea & maintain growth & decrease fur chewint. pectin(apples) absorbs toxins. Cellulose(hay) prod VFA- Acetacte provides E & lowers pH. Linin(old day) is pacemaker& increase Peristltic movement in intestin! Reccomentsed feeds: 15%ADF, >25% decrease waith gain, <12%causes enlarges colon 12%CF 12% ingestible fibers