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Dis of Food Anim

by: Sophia Reilly

Dis of Food Anim PATB 4110

Sophia Reilly
GPA 3.77


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This 109 page Class Notes was uploaded by Sophia Reilly on Tuesday October 27, 2015. The Class Notes belongs to PATB 4110 at University of Wyoming taught by Staff in Fall. Since its upload, it has received 39 views. For similar materials see /class/230326/patb-4110-university-of-wyoming in Pathology at University of Wyoming.


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Date Created: 10/27/15
2132009 Enteric Disease of Swine Shannon Swis t DVM MS Gastric ulceiation Causes of diarrhea in swine Gastrointestinal System Gastric Ulceration contributinglactors 7 Feed smallteedpamtlesrzepellenngteedsdrerswnrgnlevels o unsaturatedtarslownoernrgnenergvdrers 7 issuesrnarleadrornegularteedmg patterns 7 neurnoma prgswsevereg srntulteranonareaazmore ilkeivmhlghiungdlsease neuronemarleaatarrrssuarueamsoanemmremr lnlzvtwvzm misz in lzspbnnm mienan m om vziziszs nmmmesorm vztzpmvs mi pivlzlii tziis Mommithmnuziszs m sztvztlwli tr ss ltransponanon twemnwdlng Pigs often found dead entremeiv ale 7 smss seveegasrntulteranonwnemonnageomelena 7 Vlgs dretmm exsangumanon Gastric Ulceration Age w indicator of the c Swine Diarrhea Facts at hich pig affected wdiarrhea is an ause Diagnosis can be made easier Vaccination i 7 Have pigs been previously exposed to infectious agents insidious onset slow spread a gradual increase in severity over ime Explosive onset of diarrhea is rapid spread 7 Usually associated wvirus 2132009 Signs of Diarrhea in Swine Signs associated wdisease of Small intestine Vomiting melena pooriy digested leces buiky yoluminousleces amp carbonEmu Eioody lecesgross mucus onleces smaii lrequent delecation amptenesmus M39Vomlllng Ba by Pig Diarrhea Noninfectious contributing factors Effective environmental temperature lower critical temp llcnetemp beiow wnicn pig must u y temp se extra energy to maintain bod F Avaliablilty olmlik e M k Pravl esantlhn les a energyta maintain hDWtemD Age and Cause Days after birth 12 days Ecoli hypoglycemia Clostridium 57 days Coccidia 1 week TGE rotavirus swine dysentery Salmonella Erysipelas 3 weeks May see E coli again associated wagalactia Agaiamariark afar panrmlikaftarhlrth Major Causes of Diarrhea in Swine Suckling unweaned Clostridium perrringenstype A m Clostridium errrinenstype c E coli l D 3 a E 3 2 m Transmissible gastroenteritis TGE Rotavirus Coccidia Hypoglycemia Emaciation amp Dehydration 2132009 Poord oe rs Abdominal Distention amp Pain Clostridium perfringens Type A amp C Low morbidity often biggest healthiest piglets affected High mortality l1ou al ofacule cases chronic infection higher sirvival Other s39gns paddling prostration rv0miling chronic formremacialion rough hair coat Diarrhea is watery yellow to bloody Spread of infection is slow often seen after addition ofnew pigs Clostridium difficile Morbidity 10790 Mortality upto 50 usually 20 Sudden death w no signs dyspnea mild abdominal distention St scrotal edema Diarrhea pasty yellow to walew Associated wantibiotic treatment at birth 2132009 Colibacillosis E coli Morbidity is variable entire iitter affected but nearby iitters normai Mortality is variable Occurs anytime of year esp winterwcniiied pigiets is summer wagaiac a Dehydration pasty peritoneum tail may necrose Diarrneayeiiowis wnite watery wgas a fetid odor Litters ofgi im often worse than those of sows often associated wpoor management dirty environmentamp su ooptimal temp Tra nsmissible Gastroenteritis TGE 39 Cause coronavirus 39 Morbidity ifenzootic 10750 mortality 010 Morbidity amp mortality ifepizootic 100 Vomiting dehydmtion Diarrhea yellowawhite watery distinct odor Epizooticasows sick quick spread to other pigs Associated with addition of new pigs large farms and continual farrowing operations Rotavirus Morbidity variable up to 75 low mortality 510 Gaunt rough hair coat e vomiting Diarrhea wate iy pasty wyeiiow curdalike material Coccidiosis Morbidity is variable up to 75 mortality low Infection peaks in August St September Gaunt rough hair coat low weight at weaning 39 Diarrhea Va riable Pasty to profuse watery yellowgray lat fetid or pigs w sneep peiiet feces Associated with solid floors 2132009 Major Causes of Diarrhea in Swine Nursery weaned Hemoiytic E coii Saimoneiia septicemia mueonernorrnagie diarrnea Coccidia TGE Rotavirus Major Causes of Diarrhea in Swine LawsoniaRelated Enteropathies GrowFinisher CauseLawsoniaintraceiiuiaris i trace u a m i Lawsonia areiated enteropatnies r ri ii i Proiiferative enteropatnies iiei s e Gruup of some amp enrunie eunditiunswWide variety of eiinieai signsbut iuukthe same at necrupw meaning with mumsaaithesmaii intesineaeaian Diarrnea may be bioody or not Morbidity 2074096 rnortaiity variabie up to 70 esp nernorrnagie form Weig t oss anernia wnernorrnagie form Antibiotics Vaccine sairnoneiia Swine dysentery wnipworrns rT6E Swine Dysentery Cause Brachvspira hyodysenteriae spirochete Acute to chronic contagiousinfeclion ofcolon Morbidity 90 mortality 30 Weight loss dehydration abdominal pain Diarrhea mucohem orrhagic Causes signi cant 55 loses associated wmortality decreased growth rate poor feed conversion amp treatment Antibiotics vaccinesineffeclive 2132009 How Can You Diagnosis Diarrhea in Pigs Ectoparasites as vectors Ectoparasites as vectors Maxqmtaex Hurse Virus WNV xrus WEE EEE VEE vm A was Castude Tapewmns 11de Sheep Virus Bluetungue Fhes Nematude Summer sures habmnema MG Bantamquot mama Virus 51A Bacterium Tick Cattle Bacterium Fuuthlls abumun u mm Fhes Bacterium Anaplasmusxs Baetennm ka eye w m Stephanu lanasxs Horse and deer ies Bot les Large Multiple Species 5227th adu D Females unly has n nesnutblte maybuther 7 External msecmaeanugs 7 Inumal andspectnxn amhzlmmhcs meme arvaernutpussxble Aams7ay repellents Stable ies 130m males and females 3 spams ummauae Around premises 7 39 Summer sores habronemiasis Painful bites Soggy haymanure hay ransmit Seasun Hypersensitivity cumpunent Abe t at quot msm hen 7 EIA ae depuslted m Wuunds 7 Habmnema ESP eyes cunjuneuva male Identify and comml genitalia mm limbs breeding Sims Prevent 7 xver mecn Insect pellmts Treatment 7 vetennanzn icx 1mm ingh NOSeeU1nS Culicoides amp sand ies Need aquatic habitats Allergic reactions in orses Mosquitoes C ulicoides hypersens1t1v1ty Wet sites 39 Only females feed 39 Still water 39 6 7 7 days to complete life cycle 39 Day or night feeders 39 Variable year to year depending on moisture Sweetitch Individual horses Acute hypersensitivity Familial Springsummer Regressesin fallWinter Tailrurnp backWithers 39 Manyspecies 39 Diseases 7 EEE 7 VEE Mosquito control Control large wet breeding sites 7 Pest control districts Keep water containers to minimum 7 Empty troughs every 73 days Bacillus lhuringensis BT dunks Screen water containers Stable horses dawn and dusk Insect zappers relatively ineffective 39 1 Topic sprays for horses T opical antim osquito products Pyrethrins chrysanthernurn extract 7 Effeetrve shun durauun Pyrethroids synthetic 7 Law tuxmty lungerdastrng than pyretnnns 7 p n and eyperrnetnnn Plant extracts 7 Citxunella eucalyptus pennyruyal eedar geraniul ete EET 7 Nuw EPA appruved furhurses 7 Licensed vetennanans 7 Repellent unly 7 nutrnseeuerda1 Ticks winter Vs summer Some have multiple hosts depending on stage Dermatitis Transmission Tuprealsysternre aeanudes Blow ies and esh ies 60 species Cadavers and wounds Eggsin rnoistwool open wounds or break in e s 39 SHEEP rare in cattle or horses Painful r can be fatal doc ng an insecticide treatments Treat with insecticide applications Screwworm qurld species Infantslivewarmbluudedspecies Infeets peup e open wuunds and neamny trssue Eradicated in US Esp newbums mgr munality when untreated Let in enea Cuntxulled by stenlernalerelease epurtabletu USDA FerrudierneursiunstuUsA cattle A Attack all ages esp Head neck shoulders and rurn Irritate skin Control in fall 4 Pouron formulauons7 treat twice 3 weeks apart Mange mites Nowuncommon Burrow in skin Transmission by 7 Direct contact 7 Fornites tack etc Iverrnectin Decontarnanate stables and grooming equipment Warbles Cattle grubs Hypoderma 39 Beelike 39 Cattle and bison 39 Common andnorthem grubs 39 Eggs laid on hair 39 Annoyance 39 Hide and tissue damage 39 Allergic reactions Keds Melophagus ovinus 39 Blood sucking Entire life on sheep Winterspring Damage eece Shearinginsecticide NOT major disease vector 7 Vertebral column 39 Emergein spring 39 Systemic insecticides pour on 39 Avermectins Horn ies Blood suckers 39 Eggs in fresh manure lt10 min 39 Consume 10111 blood daily 7 3000cow30 rnlday 39 Rapid life cycle 10 days 39 Strong yers 39 Live on cattle z E E 8 39 Insecticidal ear tags 39 Dragging pastures to break up feces Acute hypersensitivity reactions in horse Nasal bots 39 Occurs When female y lays batches of newly hatched larvae in sheep or goat s nostrils 39 6month life cycle N2 generations per year Symptoms sneezing coughing jerkymovements of head 39 Bacterial rhinitis and reduced performance 39 Treat With iverrnectin drench External parasites cattle D e MW WWW Pmnm 5mm o Dmmum Qummn RegulatzdhyUSDA MW Wm Mm mm External parasites horses DI Eiungmidgzs Cubconts Fm Amvymce Repellzm mm mm ham qunds hnxse deer External parasites sheep Agenus M m mm g g a mme m Meloptmgus new an owns Elaadsuckmg mm Lm 9mm 1mm mam WW Flymnke 1mm mmmg Major insecticide classes Butzmcals Pyle39hnnfaxmly mugs Pyre39hxmd may 5 Organu hus hates TxguWan nm Sprays Carbzmates mugs 0an same Taxicl Fumamdes Ammaz Liceticks m m hmses DDT derivatives Methuxychlm Gastrointestinal disease in horses Equine digestive tract 1 Diseases ofFood Animals and Horses PATB 4110 Equine intestinal tract Relatively small gastric volume 0 Inability to vomit or eructate due to strong cardiac sphincter 0 Hindgut fermentation o Secretesabsorbs ECFV every 24hours 0 Blood supplyi mostly ant mesenteric artery 0 Susceptibility to gastric ulceration rx V 0 Thin intestinal wall relative to other species 0 Catastrophic effects of peritonitis 0 Prone to laminitis 0 Predisposed to n Displacemententrapment n edu ed gutmou39lityr ileus o Tympany 0 Sensitive to endotoxin 0 Constriction points esp in large bowel Endotoxernia MEAL y J Major complication of equine Gramnegative bacterial diseases E coli and salmonellosis Triggers multiple chemical cascades mediating inflammation Counteracted by Treat shock Ieplace uids Antibiotics neutralize bacmna ooo Contml excessive in ammatory reaction an rinflammatory gents Signs of laminitis m 0 LAMENESS7 esp offorelimbs 0 If moderately severe reluctant to walk turn or trot 0 lfsevere reluctant to move or stand 0 Acute episode 1 7 3 days Treating and avoiding laminitis A Disease of oral cavity and esophagus n Avoid predisposing factors eg an upsets esp grain overload obesity foot angle Reduce pain Reduce inflammati Mechanically supp hoof wall Minimize tension due to DDF eg heel wedging on orting 3rd phalanx typically trimming Difficulty eah39ng or swallowing en pro lems Oral ulcers 7 foreign bodies and vSv Strangles gn body cholte sm Fm39ei Bomli Colic n V Acute episodic intrarabduminal pain Usually groblems in large or small intestine Occasionally problems with kidney bladder uterus cervix 39 39 e infra abdominal hemorrhag Low pain threshold colic Horses evolved eating grass 15 e 18 hrdayyet we often short change em o Rislt nionlic proponiunal to amount nigraiu in diet Sensitive to dietary changes viscera poorly anchored displacements Hindgut fermenters sensitive to effects of antibiotic overuse and dietary upset lnabilityto eructate Small gastric volume relative to size ofGlr Tendency to ru ure 9 importance ninasngasnic tube use Surgery expensive technically dif cult 5 SJDKsurge39ry Pain in colic n Mild to moderate Moderate to severe Intermittent impaction Colonic displacement Constant c Strang a 39ng obstruetion Pending calms 3 Mechanical obstruetion Dami u RD d r Salmonella e um WD n39n5aSC31ld5 Cecal or ileal or bi ng abdomen Stretching t ugh urinating Repetitive lying down and risin Rolling especiallyviolent Dogsitting Lying onbaclt Recognizing colic n Dealing with colic n V V 0 Remove food and water 39 Lank of appetite 300mm 0 Notify veterinarian Putting mouthto waterwithout drinking Provider Lack ofbowel movements Reducedabsent diges veswnds o Behavioral signs pamng lacking rolling depression Sweating 0 Respiratory rate breathing Rapid respiration andor ared nostrils 0 Pulse Elevated heart rate and pulse Depression 0 Color of mucous membranes Cool extremities o Capillary re ll o Rectal temperature o Digestive noises or lack thereof Avoiding colic Treating COllC A V V I Stick with daily feed routine Good quality roughagebased dial 0 Depends on SEVERITY CAUSE and whether or d not SURGERY is needed Do notbolt fee D o Nonsurgical n aw 0 Pain relief eg Banamine A osslble daily exercise 0 Sedagves egwxylaz e g id excess rain 0 Lubricants and laxatives Attention to dental hea th 0 IVfluids Make dietary changes GRADUALLY Aquot b d es 0 endot mn 39 D9 Bad 9 gm Failure of analgesics to confer reliefis an indication that observe mares pre and postpartum surgery maybe required Lock up grains and chemicals Surgely and colic n V o The sooner the better r o If within 8 hours of onset 77 survive surgery 7 39 39 V o If 12 houts 45 survival Most deaths uysqaost si t y About 70 deaths within 190 days Geherully horse out of th 0 Problems due to o Wound infections 0 Enclotoxemia o Lleus o Perit39ionitis c Catheterassociated jugular thromboembolism 0 Consider oirl to a center that has a successfu trac record of dealing with colic al sand impaction Assessing colic Mucous rncrnbranc color and capillary rciill COLOR Pmk goodpertusion Blue puurperfusmn dueto shock CAFILLARY FERFUSION lt15 seeundsguud gt2 seconds less guud Self Still Palpau39on twisted ordisplaced bowel IHRgt60 0 meglumine Bana large amounts otnasogastric tube re ux ml Surgery needed Types of enteric colic V A Intestinal dysfunction lmpactions 2 Tympanygas co c induced trauma pain 2 min following IV unixin mine 01h spasms paralysis ruptures grain overload metabolic disease Displacement with vascular oompromise o Displacements torsions ber 39 Enteritis andor ulceration Salmonellosis parasites toxicities duodenitis anterior jejunitis Grain Alerload V Gastric rupture n V Alt Excess ive amount of grain spp 1 lactic acid Gramrnega ve bacteria endotoxins in cecum gt circulation 39niti ered blood ow lami n 5 n of colic cases High mortality Cause r primary idiopathic 0 Secondary obstruction Stomach contents free in abdominal cavity Colic in neonatal foals n Equine gastric ulcer syndrome V Endoscopy makes this fashionable diagnosis Developmental anomalies 50 ofhealthy foals lt90 days have gastric ulcers Absent 0 narrow bowel segm 410 racing horses have gastric ulcers r Lethal Whlte foal syndrome oyeroematrng ost are asymptomauc Inmssuscep onVolvulus 39 m o o Reduced performance Clostridial enteritis purple gutquot o cane o Teeth gxmding andsrlrvataon Retained mecomum htmvmnwm o o DiarrheaWham o Gmuchy Mostly nonglandular area El Gastroduodenal ulcers in foals C0 tmllmg EGUS ulceratioe duodenitis 3 f V J rntensrye fuahng operauans Mainmin on pasture as much as possible May emu asouthrealrs lfsmll confined e freeechoice alfalfa 39 m Limit grain and excessive t in diet Refusal to nurse I Ifaffected 1 22quot de o Anusleer medication Gastl oGard 39 Chm mm s uror ngtath grindingoolrc r EXpEnuve esday Donne e sinunl raunmg wgmm o Various histamine type 2 tram blockers such as Tagamel or Treatmntvnth anti a a inflammatory drugs 7 bloclung HCl secreuon and o Pelleled antands egNegh Lox may mung NSAID duoderlitis in a foal Enterolithiasis Entem gquith stone V Reglonal dlsease persistent or recurrent low grade Lodges in small colon and de exu Factors o Arabian bxeed r High dietaryintrlee oimagnesnrmsrlts r Alfalfa diet r nintmothex nidu n i1 Good surglcal prognosls one year postesurgery collc re rope eta lfdetected before rupture gtgo96 Feed impactions of large intes ne V 0 Common 0 Mildmoderate intermittent pain 0 Impacted feed anterior to pelvic exure 0 Factors roughage poor teeth dehydration parasites abrupt restriction ofexercise lareg concentrate post surgery complication Treatment 0 Medical in most7 95 survival 0 Surgical in some 7 60 survival Clostridial diseases in horses Purple gut 0 Closn39idiumpw 39ingens 0 Type A and C 0 Acute 0 lt3 months age 0 Severe 0 Colic 0 Found deadH 0 Death rate 50 Diarrhea in foals n v Clostridin di icile 0 Variable syndromes 0 Environmental o No blood passed 0 A and B toxins 0 GI torsionintussusception Lnor Major or common Foal heat 0 Purple gut M Overfeeding Eating dirt sand feces 0 Rotavirus Salmonella older foals 539 vulgarS R e 39 Tyzzer s disease Streptococcal infection Cryptosporl39dlum spp Foal heat diarrhea r 5 7 14 day old foals 0 Generally In ld U 0 Bright alert foal with mild diarrhea o Caus o Coprophagy r Nuh itional change Rotaviral diarrhea A St139orl ylol39des wester39l39 infection Esirogenrinduced change in mare s milk U Foals o In 30 r 40 of lt3 month foals with diarrhea 0 Watery diarrhea 1 7 5 days o Rotavirus other agents 0 lnapparent inlection or adults common Crowdin 0 Hardy virus 0 Type A serotype others Commercialvaccine 0 Safe relatively effective a Vaccinate pregnantmares IM Clinicallysigni cant diarrhea adult horses 0 Major 0 Salmonellosis 0 PHF 0 Cyathostomes 0 Clostridial 0 Antibioticinduced 0 NSAIDinduced 0 UNIQVOWN U Minor 0 Malabsorptio i ranulomatous o Neoplasia 0 Heavy metal toxicity 39 Peritonitis 0 Stress Potomac horse fever PHF A V Seasonal Rparlan areas n ll bats and uke us antlgenlc stralns gtu E 8 a r Con rm serology PCR AV able o E ostiveness 5010 Dlarrheam 75 ofcllmcally affected Subclmlcal mfectlon common Moderatesevere dlarr e Collcmay e presen a and 1ammitls Compllcate l Responslve to oxytetracyc me Fatallty 30 Salmonellosis n Dealing with salmonellosis n J J ost commonly con rmed cause oflnfectlous dlarrhea in horses Strarns VARY m pathogemclty asymptomatrc horses transrently ally clear themselves of lnfectl es well m envrronrnent mfected n 1 e 10 Horses usu U lqultous rsurvlv kofseptlcerma t t a odhorses nasacm1ri ll t Horses aggxeuivalyueatad with antinliuolrial agenufoxwlic Biosecun y S a Medical tr Sueswd h o Some owners El aspect when s Acute profuse dsarrhea wrth fever s colsc egregale horses with con rmed salmoneuosrs 39 r Healthy Infected horses 7 small 115k 0 HEALTHY horses a clean areas wnh fecal contanunanon o Resmcl access to horses wnh dsarrhea Flulds and annhroucs Detectron l Repealed culture may be needed Colitis x n Strongylus vulga ris n u V Severe acute generally ml colitis ofadults horses Probably several diseases Salmonellosls Severe PHF Some porsornngs Clostndmm dtmctle Closzndmm perfrmgens mgestlon of ntectlve larvae L3 Mlgrauon oflarvae esse s oflower 51 and LI e l Cramal mesente reembollsm and cornolrcatrons T rom Long prepatentperr Contml n V Cyatho stomiasis n Anthelminlics ivermeclin or moxideclin Clean bedding in stalls Keep age groups segregated esp foals Rotate access to clean paslur s Take home A Easter and better to avotd than treat 001K Entertc dtsease in horses dtfferent a Fentomus more se Sus oe39puble to endotoxemta ls nsk nous Lamtmt Cost tt surgeryneeded Owners need to work wtth vetennanan to deetde what the level of tnterventton needs to be V Small stron yl s Suddensxmultaneous release Typteany winter 11 thnft St 5 a Dtarrhea Ventral abdomtnal edema odv condttton Treatment wermectm Diarrhea in cattle and sheep Diseases of food animals and horses February 4 2008 Enteritis in ammation of SI Colitis in ammation of colon T yphlitis in ammation of cecum Failure to resorb diarrhea q Feces Rotavirus LOSS OF ABSORBTIVE Coronavirus Urine SURFACE Cryptosporidiosis Johne s disease What happens in diarrhea Early Advanced 0 391 Volume feces Dehydration 1 Water loss 39 f Loss of electrolytes 7 Sunken eyes 7 Tented skin 7 Weakness 7 1 Temperature 7 1 pH acidosis 7 4 glucose 7 Electrolyte disturbances 7 Shock and death HOMEOSTASIS Body uids 60 body weight 0 Blood 5 25 0 Tissue 15 0 Cells 40 Feces Urine Increased secretion or leakage diarrhea 11 q Feces EnterotoxigenicE coli 1 secretion T Salmonella Urine 2 Tissue dam age Purplegut enteritis Coccidiosis Forms of diarrhea I Decreased absorption of uid I Increased secretion of uid Reduced transit rm a eg peritoni is Osmotic overlo d r eg carbohydrate overload Increased hydaulic pressure a eg brisket Assessing diarrhea on calves Mild 5 Bright Moderate 7Io Cold alert 4 3 Severe gt7 7 12 Flat out What to assess I Dehydrationskin tentng I Eyes I Type of stool 7 blood Vs watery I Alertness I Temperature of limbs and mouth I Reduced or NO urine output ying gt2Io 7 Individual calves at out and in shock It s not the cold it s the damp It s not the bullet it s the hole It s notjust DEHYDRATION it s the acidosis and electrolyte imbalance Diarrhea syndromes in calves Major I E call I Rota and coronavirus I Cryptosporidiosis I Salmonellosis I Coccidiosis OFTEN OCCUR TOGETHER Calves need 10 BW as uid daily Other causes of diarrhea I Johne s disease I Parasitic gastroenteritis I Coronavirus in adult cattle Winter dysentery I Miscellaneous iPoisonings E coli diarrhea Noninvasive minimally destructive 7 Enterutuxigen 7 K99 in ealves andlambs 7 Adhere to gut lining 7 Cause hypersecretlun uf t1uids intu lumen 7 First l 7 3 days ufllfe 7 Vaeeine and speci c eulustrum available Invasive andor destructive 7 Attachingreffaclng a call 7 Sentieemie strains colrsephcemo 7 Qt ers 7 Nu vaeeine available Why young calv Low colostral immunity Buildup ofpathogenic E Cull strains Overcrowdingpoor hygiene Normal oranot fully established so more ecological niches avai able Receptors for K99 rstweek oflife only Stressors such as coldwet conditions Colisepticemia Common due to ANY strain Entry from GIT or elsewhere DinFPT and poor hygiene major factors Dissemination to 7 Intemalurgans 7 Bram and meninges Essentially untreatable by time most calves detected Colisepticemia Salmonellosis Mostcommonin dai thanbeefcalves Salmonella enterica serotypes eg Dublin yp 39murium Newport etc 2 r 12 weeks 01 Also adult cattle 7 dairy opezations T ypes 7 Entenl unly 7 hluudy diarrhea 7 Senueemie7 aeute weakness and death chronic shedding 7 common a er recovery Shedding via MULTIPLE rou es s 39ves months in environmen Antibiotic resistance problems Salmonella Newly emerged strains Resist ampicillin Human infections Deahng w1th salmonellos1s Fluid therapy Antibiotics effective against strain Protect self Isolate affected anim s Consider culling Calf rotavirus and coronavirus Most common viral causes ofdian39hea Loss ofabsorbing ce11s in small intestine Coronavirus gt rotavirus in severity Rotavirus 24 hours Coronavi 5 gt4 days N IOTICS WON T WORK Recovery good ifcalves survive Major problem 7 Reversing uidluss 7 Addressing eleetxulyteluss Vaccinating for rotavirus coronavirus and E coli weeks Kweeks 4 4 4 Year 2 Coccidiosis in calves Generally older calves Older than 3 Weeks Bloodmucus in stool Sanitationrelated Treat with anticoccidial compounds Diarrhea in sheep E L Dll Rotaviral enteritis Salmonellosis Parasitic gastroenteritis Coccidiosis Clostridial enteritis purple gut Johne s disease Treatlng dlarrhea Goal of uid therapy Catch it early 7 Much easier to treat and correct electrolyte 39 Replace lost uid Volume alarms Correct acidosis Gwe slestr ytes39 Replace lost electrolytes esp Na and K e 6 e 8 pints100 lb BW daily m 2 e 4 feedings 7 Reduce to 2 r 4 pints100 lb BW Leave on cow or give milk replacer unless advanced r stomach tube or IV Provide energy source Wh it s in the acket y p HOW to give it Currents acidnsis Esophageal feeder stomach tube lmprnves Na atanan Either standing or In stemal recumbancy 7 mm Emma s Feel for tube as it is being passed 3 glycine Watch for ooding of calt s mouth or In 2 pntassium chlnnde 86Dextxnse cho 39 g 2 Other electxnlytes Up to 2 quarts over severalminutes Replaces K Replace so 45 energy requirements LOW GRADE DEHYDRATION How much uid W cefstmdmg N 5 attains Skin tents lt4 see win nurse electxnlyte snlns 80 lb calf 10 dehydrated 1 What do you g1ve LEAVE on me darn Supplement with several 2 quarts ele ctro lyte fe eds daily MODERATE DEHYDRATI ON SEVERE DEHYDRATION Calflylng but aim Calmat nut 7 uid luss Skm tents 5 see gt 9 uid luss Skm stays tented Eyes sllgh y sunken Eyes sunk L b5 feel culd erbsannrnnutlnenln Oral mvny Warm but streky e 4equarts warrn n n s W energy eleetxolyte Shock too advanced f solal for uld a arrn la e W What NOT to do Stralght water Preventing diarrhea g a e 7 tln mllk co Beware feed store39 eleetrolyte solutrons Just antrbrotres or mrlkreplaeers wlth antrbrotres Avold OTC anabroaes Several weeks before ealvrng move to separate ealvrng ar Move healthy pans to large pasture area Wthln l clay of ealvrn Followlng olarn mlxmg lnstxuctlons g 7 Warm er 7 Alternate mlk with replaca39 unless sellers 7 Dun39tusetuu rnuen pa 37 tan rnueh era guud Lhmg rat AFTER yuu39ve attended halthy Elves Keep pans wrtln dlanhea separate rDONT rntrooluee health pans to group wlth dlanhea Hyg ne Vaeernate olarns forrota eoronavrrus anol K99 E coll 1242009 PATB 4110 7 Diseases ofFood Animals and Horses Respiratory System Overview and Diseases ofHorscs w uNwEnsI39n 0F WYO Dnn Montgomery Veterinary Sciences Rm 114 74245638 ACROSS SPECIES DISEASES OF T RESPIRATOR SYST M ARE ONE OF THE MOST IF NOT THE MOST SIGNIFICANT I In horses respiratory diseases are second only to digestive tract disease colic as the major health pro lern Maj or anatomic components of the Respimtory Sys em Nasal cavi r39 Paranasal sinuses Nasoorop L arynx Trachea Lung Muscles Disorders affecting any or all ofthese components can affect function Functions of the Respimtory System The sole major function oftlle respiratory system is to deliver oxygenrich air to the lung Where gas exchange occurs and to eliminate Waste gases Miscellaneous functions 7 Control ofacidbase balance via exchange of for co2 a Sensory organ smell a Immunologic sentinel Microanatomy Respiratory Epithelium Up to four differenttypes of epithelium Simple or strati ed colnrnnar epithelium e Nasalpassages r Nasnpharynx r Caudal larynx anitraehea r Brnnnhl and brnnnhlnles ciliated Goblet cells 1242009 Brunehr 7 Epithelium ample callxnrur with sun 7 Smamhmmcle 7 mew branch to cansth a rem Alveuli 7meplaeewhere gas exchange eeeurs The Lung 7 Alveoli where gas exchange occurs Twu types ufepithelial eeus 7 Type wmemram 7 Typez7eeemeereere it Simple capillary lined by enduthehal eeus Fibrublasu eeus Mrmma assue betwem the arm alveuh and erythmcytes m capillaries arsease preeess that are capillary and alveular space Defense Mechanisms ofthe Respiratory System Mueeus seereaen and mucuciliary escalatur 7 Meme secrmmshdpmamenthz aeeuee mdemxapbanenaand puhculntemmerthat can thenbe eliminated Residentmcm ura 7 Thenmmal micm ara includes same mama arepvlenhalpathagens but these are keptm eheek by abalmcewithnmpat rmgens Lymphmd assues 7 Lymphmdhssues are scattered throughth resplratmytxacL either as erme a murmur accumuhnms aflymphacytes These are we er mucasal39 immmty mdsecreteIgA 5 Sam emere re ex mchanumx can 5 he mam Neumgemcre exmechamsm 7 cm neumg 7 tlemEmhzrre exesmclu nglaryngulshamare ex Clinical Signs of Respiratory Disease Upper respiratory tract Lower respiratory tract 5 discharge 7 quot Na 31 eep e gh mayurmay nutbepmdu a e 7 Sneezing 7 Taehypnea7rapra 7 Open muuLh breathmg swam speciesvanatmns 7 Dyspneailabmd 7 ryhackmg resprraaen nunpmducnve main 7 Cyanusis 7b1ue culuratmn 7 Unusualrespiratury suunds tn mucuus mambranES such as wheezing whistling etc seasepracessbathwpermdlawer suunds mareaangpeer uxygenatmn ufbluud and assues Respiratory Diseases of the Horse The Upper Respiratory System The Lower Respiratory System Thrsleemre will cuver unly seme ufthe mzjur respiratury diseases in thehurse Spe al emphasis will be given diseases likely re be encuuntered Diseases ofthe nasal passages resistence 1242009 Diseases ofthe nasal passages mus 7 In ammation ofthe nasal cavity nasal passages Can also involve sinuses and other eomponents ofthe upper airways and even lungs 7 Causes yruses mun rnnopnmonusmrpesm e moanr hump mus Allergy mun Ethmoid hematoma Rhinitis Clinical Signs 7 Nasal discharge is rmually elear and eolorlesshutlater ean heeome npaque duetn mueous orpurulentrnclammauon that aeeompames secnndary haetenal infectlnn Treatment 7 Anuhrstamrnes decnnuestants annrln ammatnry e ifallergcrtxy to ldmufy and alleviate eause e Anuhrotres fur secnndary haetenal rnfeeuon usually not indicated unless seyere 0 come 7 lral infectlnns are usually selfrllmltmg with no permanent sequel 7 Scarnngpnlyp formauonufehrome m ammatmnperslsts Ethmoid Hematoma Also called pmgresswe hematoma or hemnrrhagl nasal polyp Usually affects horses gt8 yrs Cause 5 unknown but Treatment Surgcal exclslnn or chemical ahlauon lntraoperauye MW as 13quot rr agemay he aprohlem Can caudally thrnugh the ehoanae Diseases of the Phalynx Chrome pharyngrus e The horse has diffuse lymphmd ussue in manlythe dnrsal pharynx chmmc muge c mul may cause mn39wwmg ufthepharyngeal Vpemng resplratmy umsulty e causesmaymel r t hayepulmonnyyu emans 7 a M 55 m Trenment Usuallypslhauye mu F S h 1 V m ammatmes analgescs muhroucs r Diseases ofthe Pharynx 7 Strangles Distemper Cause Streptococcus cqm subspecies cqm Some analogies can he made with 39stxep throat in humans Highly contagiouspassed from animal to animal from seereu39ons fomites ete Usually alreets horses 1 e 5 years ofa e e Fnals lt 4 months usually prntected by eolostral immunity 7 Horses gt 5years typically have acquiredlmmumty Ineuhau39on period is 34 days 7 Drseasehepns as apharyngltls e Baetena spread to regmnal lymph nudes gtlymphadenltzs andlymph nude ahseessauon Strangles 7 Clinical Signs Sudden onset offever and catarrhal in ammation ofthe upper respiratory tract Enlar ement of m h nodes in neck The l m h nodes are initially rm but then become soft and uctuant 7 r 14 days later heralding abscessation Typical outcome is rupture ofnode abscesses through skin with drainage ofpuss 39 Morbidity 7 30 to 100 Str treatment Isolate cli cally affected and eitposed animals Treatment based on four stages llorses exposed to infeeted animal butno elimeal sigis oticsareosuul ed dcit yn in llorseswith early clinical signs uh cswhelpprevmtspreadarirfectimtolynphmdes llorseswith lymph node abseessation mamenaturationmd damage of abscesses studieshave shown antibiotic treatment at this stage maypmlmgth dsease Complications Dissemmtedfbasmd39 srmgesehppropriata antibiotics Purpurahzmmhagcar antibiotics mdcomcostemids Strangles Management amp Control Separate sick horses Separate recovered horses for 5 weeks Rest contaminated pastures 6 weeks Isolate new retuming horses 1 month Sanitation 7 clean water troughs feed buckets brushes bridles etc Vaccination may only reduce clinical incidence 50 e txep guardm lntervet killed pro duet e Pinnaclem IN Fort Dodge live attenuated Identify carriers by culture or PCR Diseases ofthe Pharynx 7 Guttuml pouches al pouches are saccular ons ofthe audito Major nerves andlarge arteries course thru the wall ofthe pouches Functions unknown 7 Equalizing pressure on ear drums 7 r Resonant chamber for vocalizauum 7 Temp mm mm Complications of gutturil pouch disease may Tympany of the Guttural pouches Definition uni most common or bilateral distension with air Cause undetermined 7 may be a congenital redundancy in a fold ofthe pharyngeal mucosal that acts as a valve al o 39 39 uches clinical signs eNonpainful swelling dysphagia respiratory distress extension ofthe head in horses less than 1 year old Treatment 7 Aspiration of air results in only temporary improvement More effective treatment requires surgery Guttural pouch ernpyerna Empyema distension ofa body cavity with pus Causes 7 Ascendinglnfecuun hom baetenal pharyngitis or rupture of etxupharyngeal lymph node abseess into the guttural poueh mo Inca deem the cause ufstxanrles is eommonl involved clinical si s e Una orbilateral upaquewhlte to tan nenodorous nasal discharge pain dysphaga respiratory distress Diagnosis rCiimcal signs eulture ofaspirates radiography endoscopy Treatment 7 Lavage irrigation ofthe pouch with mhbmtlcrsalme combination parenteral aitibioties surgical drainage Prognosis e Favorable ifdiagnosed andtreated early Guttural pouch ernpyerna I if E with chronicity the disease is more 0 r o ndr i s e accumulations ofhard inspissated exudate Early accurate diagnosis and appropriate treatment are the clues to successful management ofmany diseases 1242009 Guttural pouch 7 Mycotic infection Usually smgle am Chr m 39 39 a Nasal dlscharge um ur bllaterah a Swellmg CommonlyASperglllus Spp Guttumlpouch Mycot nfec on Fungi such as Aspergxlluseommonl eaus invasive type lesi Vessels y e on with extension into blood Severe and sometimes fatal hemorrhage can occur e internal carotid artery that ombination ofmedieal and surgical management Equine Upper Airway Diseas h 5 E h 5 0E a E E E quotE Also ealled roarers Due to damage to the le reeun39ent laryngeal nerve Causerunknown probably multifaetoral Unilateral atrophy ofmost laryngeal museles mainly exieoarytenoid mainly unng inspiration and at exeereise Lower resp atory tract d1 ease Lower respiratory tract disease 7 Anatomic differences Emma UNG n ammat Terminology 7 De nitions 7 pneumugnenarmngtu the lung lastate ufdisease pneumuma Usedtu denote in ammatory disease ufthelun Ermchnprlzumamarlmphesinfechm msngu begnmnglmtla yatthe level ufthe t on nth urways mu rmmal branchales Labarpneunamar mtmlmm rmmypragressngrurm ur lumslmpneunama Pleuapn am maumartnelungmupleuralsurases Embahc pneumamklnfeslaan the lungvutheblaadves els Asmrru mlnal am munamarlnh mmaffarelgamatznal a Pneumupertalmng tn thelung msln ammatlun pneumumus In ammatlunufthe lung Ascamman yusedlssynmymamwlthlmersutlalpmunamar m ammatlanufthzlmgtzssuealvealarseptazperse Lower respiratory tract disease THE LUNG In ammation Various etiologies a Vlr Equine m uenzaf uquot Equine rhinapnzumamhsf rl39nmquot a Fungal a e mmun except me cuveredwl asrue inut eummun see Merek Manual r a Mlscellaneuus cnr thade m s a flnterested mic obstructive nulmanary userse 1242009 Lower respiratory tract disease 7 rl uerlza Orthomyxovirus Clinical signs Two subtypes 7 Highmnrbldltym 7 HENX nmmnnsmce 1963 SEEWMEM SES39 1 tal 7 H7N7raresmcel979 mquot quoty Hih l u 7 inmalhlghlever 8mg quotm 7 Sernus nasal discharge may N 7 neuramlmdase becamepumlentslgnahng Lipid envelope renders the seenniny bacterial infeennn virus suseep39 e o 7 cnugn dry hackinng How mlcroorganlsms disinfectants 7 simple pmduchvemay Signal 2 cause disease chlorine bleaches are bactenalmfecnnn l 7 Pam myalga7depressmn Lower respiratory tract disease Lower respiratory tract disease 7 In uenza 39 Rhlrloprleumorlitis Treatment Herpesvirus7typ s 7 Rest cmughmayperslstup tn Eweeks 7 EHV71 mamly abnrnnnnennatelrnfeennnrnyelneneennelrns Ampmmsv wages 7 EHV74 snmebelleve tlns to be the malnresplratnry natnngen 7 Antibiotics lfneededtn enntrnl secundarybactenal rnfeetrnns EHV EW Y E WmZEd mm m Hrnl contarlous7tmnsmtted by aerosols enge am sernestepurulentnesel senettanerrrseugnbesames Incubation Pmo 3 t0 7 days pmnhchve 7 May ehlghmnrbldltym suscepublemnnalltylnw Prevention High few 7 Depressrnn 7 v t t n th in mam m a 5 VP 7 Semusnasal dischargebemmmgmucnpumlentnrpumlent Mu uplemmufactuers7 lledfmmahnimchmted imualfa awed 7 c h M bybaastennl weeks enmelerserne a masters quotg 0mm Whampmmmwwi mks 7 Clinical signs may belndlstmgulshable 39nm in uenza7rnrnn n m less severe and nrnnaeted Lower respiratory tract disease n Lower respiratory tract disease 7 eumorutls Rhi rloprleumorlitis Treatment 7 Usually suppnmve careandrest 39 Equm Hemesv ms h m agent mpymumfneeded 7EHV1 Pnenmabamkonaeuvated 5 739h9 7 Annbrntres nnly lfnecessan to control z baetena quotmm Wm 7 EHVl Prodigy Inachvated sarne Vaccines B m d d d S M vaccination schedule 7 a t m V aquot m e we 7EHV1 RhmammmeawLV 7 Muluplepmductsandmanufacturers EHV HM P u t d if 7 Several are rnnlnvalen 7enntanbntln EHVMzz 39 39 quot3mgquot m V quotAppmved forusempregnantmaresbutnn label elnrn far 7 Vaccinauzn schedules differ depending nn needs breeding mm mm M label Elms fnrmvemmg rnares at neurnlngreel disease 1242009 Lower respiratory tract disease Lower respiratory tract disease Immunode cienc amp Adenovuus Bacteria Rhodococcus e ui Adenuvirus causes asilent urinapparentinfechun u musthurses The organism Treatrnentcontrol song as indicated by serulugicalte e Facultatzveintracellular 7 Early recugnmun Ade uvuus alune urwith anutherpathugen pusumucysns mm is Amth 4 9 weeks a cumin can cause a fatal pneumumam Arabian fuels with evadehust defenses cumbmum Bf 39 cambmedimmunude eimey syndmme CID e Bacterium um sml erythrumycin andnfampin cu m Arabian fuels Dr crussbreds rare to utherbreeds We m me was havepruven successful 7 Autasamal recesave inheritance nawaym a acorn15 nhalanm ufdust 7 Nu vaccine quotM e Generany e m 7 Prevalence esumated 3 e Fuels 1 tn 6 muums e Nammmnmmumyane ufmrecuwussepucuseaseby5mamhsar e GlTinvulvementin 5W Morbzonusaquihukuhxn age meme nmh mnpniwnx with mommy Grusslesiuns severe Lowerres irato tract seas me with ry Pneumonia amp Pleuri necrusis abduminal lymphadmms Pneumonia caused by bacteria other than Rhuducuccu are generally uncommon in horses and typically occur on a sporadic individual animal basis These may complicate previous viral infection Other bacterial pathogens include 7 Strep equi and zaaepidemicus Bardetella Klebsiella Escherichia Cali others Lower resp atory tract 3911 ease Chronic Obstructive Pulmonary Disease M cellaneous COPD Heaves COPD Heaves The incidence ofdiis disorder increases with age Disease is duc to chronic in ammation ofthe lower Most commou u stabled horses housed indoors in dusty airways small much and bmnchioles or hurmd environments but can occur on pasture m1 chronic in madon mm m hyp plasia CM MY 1quot mmdfa 1 1 3 quot Y P quot 5 7 proliferation and mucoidinetaplasia change from us s an gggjgggfggjggfmmmggs t columto mucous sccecung ccus gnu cprucuum Mild cases may only show respiratory distress and 1 5m w 5 ty coughmg Mm mm o dmng exposure to dug Accumulation ofrriucoid secretions u the lumcus of conditions bronchi and bronchioles More severe cases have respiratory dif culty at rest with Bronchoconstriction narrowing ofairways due to abdominal brea 39ug smooth muscle contraction occurs during attacks 1242009 Chronic Obstructive Pulmonary Disease COPD Heaves 0 Management and Treatment 7 Move horses outdoors if possible 7 Avoid dusty or humid conditions 7 Provide good ventilation 7 Corticosteroids 7 Antihistamines may provide some relief during early stages 7 Bronchodilators Clenbuterol others Atropine ifin a crisis situation Lower respiratory tract disease 7 Exercise Induced Pulmonary I 39 Lower respiratory tract disease 7 Exercise Induced Pulmonary Hemorrhage 0 Common in horses during strenuous exercise 0 Blamed for reduced performance race tracks barrel racers endurance races 0 In mom cases there are no clinical signs 0 In only severe cases may there be a trickle of blood from the external nares 0 Control Diuretics Lasix 7 reduces pulmome blood ow and may not prevent but can lessen the severity of hemorrhage PATB 41 10 Diseases Of Food Animals amp Horses Diseases Causing Sudden Death Don Montgomery DVM PhD Dipl ACVP Sudden Death 7 What Is It I The term sudden death means different things to different people I De nition 7 unexplained death Declining in apparently healthy animals within 12 to 24 hours with NO previous clinical illness or symptomsquot Historical Factors to Consider in Sudden Death I Climactic conditions I Access to dumps etc I Movement ofanimals I Malicious deaths I Water sources I Source of new animals I Legal insurance I Diet dietary changes I Arrival of new I Management changes mals I Location of deads I Age ofthe animals Why are these important Real Life Scenario April 253911 2005 250 cows some with calves moved to a new 900 acre meadow pasture with running cree May 2 6 8 wet snow storm with blowing and dri jng May 4 Five 5 adult cows found dead bloated on and within 250 yards of a knoll where a prairie dog town was located This area had been an area where rnineml blocks were Four 4 additional cows found dead during the next 7 days h manager investigated and sent an autolyzed Ranc carcass to WSVL for exarnination7 had been dead48 hrs How many of these factors are mentioned in the real life scenario I climactic conditions I Access to dumps etc I Movement ofanirnals I Malicious deaths I Water sources I Source of new animals I Legal insurance I Diet dietary changes I Arrival of new I Management changes mals I Location of deads I Age ofthe animals Diagnostics I Necropsy findings 7 Marked autolysis ofall tissues 7 Gaseous distension of the carcass 7 Large bolus of rumen content occluding larynx and extending into tmc ea Possible considerations Choke with 2 bloat Do we stop here with diagnostics or go on Diagnostics mempsyrmngs mgamxmmwg omsm m L bmsurnmmmmmm u pus um Cbhwnhz um 99meme 7x Mwummm why Further Dxagqosucs Hmapa39hnlagy Amwwm aspirsz imman 4am mmmmmmmm mm mm Dowesbpoxg ox theeragqosncs mom Dfmmzncunkm Lesmns 1mm mbxanstnmmm5hmmtnls m kg rum mnmmmmm my mm gym mm M511 Fma agmasiLukupmsmng Physmal Causes of Sudden Death an 39 gammzzzmmumw h ulna 1m uy who 7x mdm 15mmquot ml 9 mme Mwmdnl dagemncnn W 1 Md K n my ham 1 mm rrm a Cardmmsmlar Causes ufSuddEn Bath swt39nlus mm Cardmmsmlar Causes ufSuddEn Bath 7 Banana Rac gmdwxdrumnas rdoczrdms Ba mmmmmammeubmma mum mm cmx ezlhmusmlhs m Mme mm dumme mmuw em 7 Traumaucrenmlupencardms xnreeuuus Sepuc Farasm Causes er dEn DE 4 ml mnvssr km pamus mum an mm aae39eua1 Causes er Sudden Dam Anthrax Bat111A anrhyam a Anya mmbuWA mum MN mu m d Uni lle39 w 53333115 Bae39eual Causes ur SuddEn Bath Enulisn acuan bombmm aquot 135m mp W mum munMam mu m pk Bae39eual Causes ur SuddEn Bath Cxasmuu mwshs fasnms gmgem 1x hmw mum 11 mm museums us my mm M e Mmequot cmusmhsm Eukmmam us mm AlumniKL w mummwm s M 7 7 MW e xmmue e meLhMI mm 1 e u a e mmmmm humu 7 mm um um mm 7 M 7 mm 7 mm m 11m 7 mm Lvu mmsilmm sunmummy dummy r smummum Baamal Causes ur Sldden Bath 39 37333 Named m bad a manual Clmmzl d ease mas Mmmuumwuu mmdwms REE 99km Akawmmdhybmg us m mixde mummuuem gm 9 Mum emuaeme 3923 5 mm 4 Mndmhzmauw sue u m mama 33 Mquot madmwunamn l39mg meme Metabuh at Numuuna1 Causes ur SuddEn Bath mum tweed m mum Metabahc e Nulnuamlcames assume DeathrcapperDe cxency emumwmm mm summmm mm m WWMu m mumu wan mum newsmanmm 39 V23quot may mumquot w quot232 5ng11va Tum Causes ufSuddEn Bath Hewmuls tweed m sum umes when emeMmmmm sum as mmmsmumusmmewu enema 1043meth mm sum as am hmhmwmumnmwgzmynm a Manavenues man me We m mumshsltpm1wsesmmi m 5mm mwg Tum Causes er Sudden Dam Havy me1a1s e Lad pmsumng w mew n4 ha m Tum Causes ufSuddEn Bath mu mm con ned anmdmmx nghms Tum Causes ufSuddEn Bath Pmsmwus warns Mosnt39mla cwendmmmwbgy mm b smwmbe mama use Tum Causes ufhuddeaLhr Kmquot mm n mmm Anaxuk ypuxu W y 8 y mm mm P in 5 5m gamma 7 H mm 7 mmm WM 7m Wm kw 7mm mm W mm 7 m mm mm 7 In 9 qsnh dn V Wv f nmuvw km W lbw m 7 MW Mm MAME 7 cm 7 mm 7 WWW mm m mm mm manna WWW My mum A ugc ReammAmphylaxxs mumsz Mscellaneuus Causes ufSuddEn Bath We39re almnsl dune Chnke blanzrhave ax m be caveredm v1th lecmresrcammn mugs cases can be mmkmrm shake Wm depnwhmrwdlbe amt126m anmhzx mm the mu m afmfa m the class malesde suf ce fax mw Mang m Lessm me In dmce and mum ur Sudden Dam nun hum mm pm A mung Mmmm u mm m mlyunmdlms mm mm Feedlm Sldden Bath Syndrume slant ammmmyhxxs Mum m bemmmmkdmdnmvxphn xemnm vaxmwm m mama mm mm mm umammmmmmxm Umlyunnsnm zmnumm wmm a m Nmbbmdmmhmkmmsmedwm39 vp am nmhlnmxg mmmmmm kwl mbuwmdm mmwmymswmw om absemhms med wxdrlcl39lal39lgls mmum mam yak mMach Aynl my Angus Among thhemcc fad mama mum s ivpmxmtnly Smmu Am 1 madmnmm mam Dramame 2nd um 1mm 3911 rm a m ycmskd ma ematnls PH Dfmmz 9mm zypmmmmlyS whchxs x quotmelanin hnhgulzsm mwu pm rIymsnunnisu nmd Lzmgezl ckmlmx quota Feedlot Sudden Death Syndrome 7 Pathogenesis I Laryngospasm 7 prolonged abnormal re ex closure of the larynx glottis I Along with other physiologic responses may ultimately be signi cant in the cause of death I Lesions can be explained on the basis of go asm 7 sudden increase in negative pressure in tmchea and thorax Sample question for those of you who made it this far You oryourvetennanan are called outto lnvestlgate sudden death ln a goup ofyearllng steas The stees are onnatlve pasture buthav aocess to an old ump and outbulldlngs The door to one ofthe ou ngs ls aarbutlt tbulldl doem t look llke cattle have been ln thae One steer ls nea opsled Dunng the y un when a magaet ls hovered ovathe blts otwne all are attracted and attach to the magnet Whlch ofthe following lsare the conectactlonsgt to takev A BTh c D E Thewlrematenal ls ferrous lron e wlre matenal ls lead and a dlagaosls oflead polsonlng ls made Keep looklng for a cause of sudden death None ofthe above ls conect All ofthe above are conect Sample question for those of you who made it this far I Brie y explain how nitrates in certain plans cause sudden death I How does this differ from cyanide poisoning my W and zlnnwnzx mm mm Feedlot Recommendations w tr swim Reginme Diane con and nvn Prac cehinsecun m m m in dampen In uenzaex Pull k 1 ann39hin nu ramming i2 L an Kg lhnmuguewxdx Pmczsshg 1272mman arrival Vuzim mu misread Cu in 0 Sim arms 1 m Lamam dime Cuuil39n newnm mi Elm 9mm lib mum ya Hing vizan Puunm m imzmzl and xtn39nzl 251 an gaduzny imam mm gain and pmtzin 282008 awhthmmu Manama an and Maxim kvuoxpmnmn39n s mpmm nnmu sum was mm sysmmym ma yams mm s xesxshzwe in 595 as causedbyslrnyplr v 1am Wu gummy ma sand comm ms m a 1mm H39geakxdqanTt damn v yndxswsm gm durum mam mild hug sum mm m c ma 1 mm mm em ccmls m hnkx m5Pamnmem3zrdEmRA P 3quotva mm Manly zmwdlasy hmvlyma mman b 450 Humbug mm W e ma cdama k hug W W rsxshrce 5 lawexed ma we n in desease MWmummumdtmolhlndhm EVD dmlrlml diseases um unmoveth 2nd mm mm human m udpnnii ma mmpmu mmhab maunlu In in me m dimu Wm References lwhwl nwlhylwv mm quotM WWW Wm um rpm um an WWW mu m s 3 a L M 1m Group 5 Members I Giulia Vemati I Gina Marchese I Jessica C00an I Rachelle Jensen I Shannon Brophy Meghan Waldo I Caitlin Blackbum HISTORY n heeausaiorganrsmwas i ehtohaue caused out Europe heio edoeumentation a r ported mongthoroughhre horses red seemto he most affected hydisease 1 i Ame roan hssouation of Equine Practitioners hasshown seueraieasesintheUSsinretheMissouriouthreahihese easeshaue been in Cahiornia Virginia NewJerseyandas st earKentue yiexasandCoiorado 7r History i A have been inked to imported horses from Europe t Organism identified as ioylorello equigenitolis t Organism notshonn to cause disease in humans t Disease has not been compietehreradicated dueto horses beingasumptomatic carriers ETIOLOGY t tequigenitoiis Previously railed Hoemophilus equigenitniis t Gramnegativerocohoridus h two strains with one being resistontto streptomycin 4132009 Organism Identilltlon IMMMm x Strongly oxidase catalase and phosphatase positive x Slide aggulation and latex aggulation used wecembem 2008 According to USDA s Animal and Plant Health Inspection Service I PCR aSSalS lAPHISI a Quarter horse in Kentucky tested positive for contagious o poyymerase chain Reaction equine metritis through routine testing of semen collected for shipment to another facility Currently the resulting investigation involves 608 individual horses located in 45 different states Atotal of 15 stallions have now been confirmed as positive forT equigenitalis by USDA s National Veterinary Services Laboratories vroouces millions of copies ofa sequence of DNA in a snort period of time I ELISA 0 Tests for the presence of antibodies and antigens in serum lNVSLl In addition tothe positive stallions five mares have been found positive forT equigenitalis bythe NVSL IMMMM IMMMm January 7 2009 i April 8 2009 LAKEWOOD Colo One Colorado mare has been identified as a N0 conclusions can be drawn regarding the source of CEM having been in contactwith a stallion infected with contagious The process of tracing locating and treating the exposed and equme metrikis CEMk Old order has been placed on the infected horses is a long and painstaking process accordinga premises umquot m rem have returned spokesperson for Wisconsin s Department of Agriculture 39 Aquarter horse mare in Montana has been quarantined after exposure to CEM The mare was exposed via a semen shipment from a stallion in Kentucky diagnosed with the disease Mar 6 2009 Fourth Wisconsin Stallion Tests Positive for CEM 4132009 CEM Transmission CEM Clinical Signs y venereay disease i Stallions may not have clinical signs but can carry the bacteriaontheir enitals for ears i Direct sexual contact between stallion and mare g y i Indirect by artificial insemination Mares may or may not Show Clinical Signs 0 The uterine body contains mucopurulent exudate i Mares may fail to conceive or spontaneously abort CEM Clinical Signs Diagnosis of Contagious Equine Metritis i 3 general infections in mares i Three different tests available 0 m active inflammation of uterus thick vaginal discharge 0 Bacterial Culture 1014 days afterbreeding 0 M mild inflammation of uterus less vaginal discharge 0 Serum Testing more difficult to treat 0 m mare is not showrng symptoms but is carrying the 0 Test Breeding bacteria and can transmit disease Taylorella equigenitalis 4132009 Diagnosis of CM v Bacterial Culture 0 Swabs taken from stallion s and mare s genitalia 0 Sent to laboratories to test for T equigentolis 0 Must be shipped inspecial transport media under controlled temperature 0 Takes seven days to get results Diagnosis of GEM v SerumTesting 0 The test used is a complement fixation test 0 Must have already developed detectable antiboties to T e of enitolis 0 Can only be used on mares biagnosis of CEM v Test breeding 0 Stallion bred to two pretested negative mares 0 Mares are then tested for the presence of the bacteria 35 days later 0 This method can be more efficient in identifying positive stallions compared to bacterial culturing horses 0 The stallion v Best method for identifying positive 39 Test using both the bacterial culture and the test breeding Diagnosis of CEM The Mare Test using both the bacterial culture and the serology exam 4132009 Prevention Control v QUARANTINEand TEST v Novaccine available 0 All imported fillies mares and stallions olloreian origin v Reportinfected animals to state or federal animal 0 All mares and stallions not previously bred in the US that are heayth authorities older than2years v Noevidence of CEM being zoonotic v Equine carriers may be cleared by washing external genitalia with disinfectants combined with a local antibiotictreatment 0 First3 mares bred toa stallion of foreign origin 0 All suspects until test results are negative v Use strict hygiene practices when handling mares and stallions 0 Use and change gloves between every horse v Mares may take several weeks to become disease free 0 Clean and disinfect intruments Control Treatment v Eradication v Treatment is possiblewiththe use of disinfectantsand o Surveillancetesting topical and systemic antibiotics Quarantine dimmed animals v Once treated maresand stallions cancontinueto be Tlealmenl used forbreeding 0 Suspension of breeding from infected animals 0 Use of PCR polymerase chain reaction to detect disease has been effective in Japan v Fertility is not a problem once the horse has recovered from CEM 4132009 treatment of Stallions Treatmenth Mares r Treatment should be repeated for five Days gt Mares should be able to clear the infection from the uterus r Chlorhexidinesurgicalscrubshoulds be used to clean themse39lestthlscantakeafew WEElStoafew months the entire penis r Mares which become chronically infected require extra care because the contagious equine metritis organism CEMO settles in the clitoral fossa or sinuses gt When this occurs the clitoral area need to be cleaned with Cholrhexidine surgical scrub Then the area should have Nitrofurazone ointmentapplied r Then Nitrofurazone ointement shouldthen beapplied r The stallionshouldthen be tested againten days after treatment is done i In some cases surgery is required In this case the clitoral sinus needs to be removed to rid the mare of the disease Quiz Time Sources gt htt wwwcfs hiastateedu Factsheets dfs Conta ious E vine Metritis df r How is CEMTransmitted r htt wwwa hisusdaov ublications animal healthlcontenthrintable version is ahcem df i What isthebestmethod used to test stallions for CEM i What breed was CEM first reported Beware studs might be affected PATB 4110 Diseases ofthe nervous system Donald Don Montgomery Assoclate Professor amp Pathologist Dept ofVeterinary Sclences ac Wyoming state Veterinary Laboratory gx 39 cagisamarm laiamw There is no other system in the body as complex as the nervous system and no other system comes close to the vanety ofdiseases To some extent neuroscience introduces a new vocabulary providing further challenges to understanding disease ofthe nervous system These lectures Will focus on the type of injury to the nervous system or etiology cause Diseases pertinent to each species Will be covered under the appropriate etiologic classi cation Lecture 1 Will cover General very brief overview of anatomy Terminology amp de nitions Protective mechanisms General functions clinical signs ofnervous system disease Why diseases of the nervous system a important Congenital malformations Hereditary familial genetic diseases Nutritional toxic and metabolic diseases General Overview of Anatomy Central nervous system 7 Brain 7 Spinal cord Peripheral nervous system Microscopic Anatom Terminology amp De nitions Encephalo brain Myelo spinal cord Neuro pertaining to neurons theneryous system or nerves Meningornenin es Polio 7 gay matter ofbrain or spinal cord Leuko white matter ofthe brain or spinal cord otherterrns will be introduced and defined as we come to them These terms can all be used in Combination Terminology amp Definitions 7 Some examples of combined use Degenerative pohornyeiopathy degeneration ofthe gray matter of the spinal cord Encephalomyelitis m ammation ofthe brain and s inai cord Polioencephalomalacia pohoencephaio gray matter of brain rnaiacia softening softening ofthe gray matter ofthe brain Meningoencephahtis in ammation ofthe brain and meninges Protective structures R n mu mu l Meninges Ventricies amp CSF e BrmanSF hamer General Functions The coverage in your c1ass notes will suf ce un1ess you have speci c questions Symptoms of Nervous System Disease rain 7 Different areas ofthe brain have different functions andit is possible to use c1inica1 signs re1ated to these functiona1 areas to localize darnage Very often however damage to the brain does not affect discrete areas so that it is difficuit if not impossible to define the 1ocation ofthe darnage Symptoms of Nervous System Disease I Spinal cord 7 diagnosis of damage to the spinal cord is generally more simplistic I Ifthe damage is focal it may be possible to localize the lesion With some degree 0 certainty I Damage to the spinal cord and peripheral nerves can generally be manifest as changes in sensory perception and motor control Symptoms of Nervous System Disease I In your lecture notes symptoms of various syndromes Will be covered to help localize damage to speci c areas These are guidelines only and dif cult to put in practice Without extensive experience I It is unfortunate but occurs With annoying frequency for us to receive a brain for examination When the clinical signs could easily re ect spinal cord disease and vice versa Why are diseases of the nervous system important I Public health 7 Zoonotic disease diseases spread from animals to humans I RABIES 7 Animals as sentinels of disease West Nile virus Eastern amp Western Equine encephalitis EEE WEE Why are diseases of the nervous system important I Public health I Herd health 7 Although diseases of the nervous system o en occur on an individual animal or spomdic basis some causes ofnervous system disease can affect multiple animals Why are diseases of the nervous system important I Public health I Herd health I Reproductive health 7 Hereditary diseases Why are diseases of the nervous system important Public health Herd health Reproductive health Future health 7 Identify new and emerging diseases B SE that can impact public health herd health or reproductive health 7 The rst con rmed diagnosis of West Nile Virus in the USA Was made by examination ofthe disease in nonhumans birds Congenital Malformations a dD alies Congenital malformations and other deyelopmntal no lies othebraln and spinal cord ar yirtually all species and organogenesis or organ n recognized in are defects that occur during maturation Many brain defects are eampaable Wth life and the ammals are born alive butvvitli severe neuralugeal signs and die shortly after c gmlml is not ous with hereditary disease bmh cmgmmai defects have a hereditary or gm to extreme example is cerebral aplasia that is ufunknuwn eause basis but congenital defects can also be due to toirins lnr WW3 W35 n 3 Wm 535 The was 3 3 b m 3 and have essentaally nu developmentuftlie cerebral cortex They Wm infection and many are of undetemm d can stand and walk and can live far a few days Wth eareful caus ursing Congenital Malformations and Developmental Anomalies Sums uftlie malfurmataun are nigily cumplex and a tliuraugi understanding uf same defects requires a guud vmrkmg knuwledge ufembryulugy and neuru anatomy Formanyaftlie defects diagnosis is obvious astlielesiuns are visible exterally atliers require careful removal and Exzmm uftlie neiy s system assues ataun Congenital Malformations andDevelopmental Anomalies Animals yyitli anomalous development othe spinal cord generally naye sensorya dl comotorproblems fr fbirtli buttliese defects are not Lh The challenge for anima ow ers and yetennarians is accurate characterization othe defect and determination othe cause Information concerning known hereditary defects can be obtained from breed associations your yeterinarian or diagnostic laboratorypersonnel Determination ofa hereditary basis is not easyl Congenital Malformations and Developmental nomali es 7 Toxic causes Cyclops e Oeeursmasteammanlyinlambs Can occur from the ewe ingesting the plant Veratrwn calx lrmmm un urabuuttne 14m day uf gestation 7 Can ueeur un asparadiebasisin atlier speuesbutis ufunknuwn eause Congenital Malformations and Developmental Anomalies rViral infection Hydraneneeplialy is nearly Arilimgrypasis animals barn tvitli cmakzd xated limbs d to vital r calr accusmnybwmmms manna ainmnsmspmlcara annneavmis canoe seenaiarg vita nyannmepiiaiy llypuplasiais failure uf rm upment s it E E 5 a eellsthat wtll farm the ebellum er BVD rhug enuleravirus similarlesiuns alsu produced in pigsby anur parasiaudetaielilarfun Congenital Malformations and Developmental nomalies eHereditary Hereford polled syndrome I e autosomai recessive trait America 7 Calvesbomunabieto rise blind depressed and disoriented Lesions Cerehdlar hypopiasia hypue defective incomplete splasls development formation Congenital Malformations and Anim hydrocephalus commonly menao ed previously th 7 Eyes eataraets abnormal retinal development and retinal polymi o a sho om detachment small optic nerves autosomai recess v an e Fuly many miero small gyna cerebral gynmanysmaii Aquot M 3 mme cerebral gyn hydrocephalus eereb eiiarhypopiasia ete le rent aaon ofvirai versus 7 polymiorogyna also occurs in Murray grey calves is thought mhemed Cerebellar to have agenetiebasis butis unproven hypuplasiacan be dif cult Congenital Malformations and Developmental Hereditary Diseases nom alies rHereditary Hydrocephalus results 39nm uid csF distension ofthe venoneuiar systemin the bran als with eongemtal Congenital hydrocephalus can occur Covered here will be hereditary diseases that do not result in gross malformations in the development ofnervous tissues Cli ical symptoms of some of these diseases are manifested at or very near the time of birth while 39n other diseases clinical signs a ear only after 2 e and x 1 d marinacommimmws a delay during which the animal appears normal have ahereditary basis but is afimdztermmzdcailse thisisunproven GM an liusidusls Hereditary Diseases 7 gaig cmmmmp Hereditary Lysosomal storage diseases GMzganglmsidusis Diseases 7 e Yarkshm pigs Lysosomes are intracellular organelles that contain a Slum celllemdymphy y5 59mal variety ofenzymes that deg de metabolic products and pg D 5quot 51m storage diseases effete structures produced or no iongerneeded by the cells gmmmmm K g e a Inherited disorders termed lysosomal storage diseases o r in a variety o mestic animals These disease are due to deficiencies of specific iysosomai mes that aiiovv nondigested substrate to accumulate i ceiis Mode of inheritance is commonly autosomai recessive It ispossibie to diagnose unaffected carriers es e typically have ya ofthe enzyme activity ofnormai animals us Murraygrcy Ga amy l Mueopoiysaeehandosis e Nubian oats ceroidiipofuseinosis 39 amphetamncc aahbanucisucppmnc p occihasarcaiu Heredltary or Breede Associated Diseases Leukodystrophy e Sp ongy degeneratlon Leulmlwhrte matter clystmphy raultynutrman Swngmsls lmles mmnnlyths whne matter39 ecamnmnlyclus tnvammles mths myzlm sheathss Mans syran utserse ellereranl cattle Status spungmsls arwhue matter m Gelbviehcalves O39Tuule D et al l Velegnlnvesl 176 546553 was Hereditary or Bree Primary Neur dAssociated Diseases tions In euntrasttu hypuplasla onal Degenera eleetaye urmeumplete develupmmt se arseases are ulten referred tu as atxuphy Dr ahmtruphy Ablutmphy eThe lack uf allfersustammg numtaye fatter vlewen as alleetang tlne urgan a ents has develuped lts full cellular cumplement Akuphyr A defect Dr failure ufnumuun mam allay Dr almmutaun m slze uf a cell tassue urg rtlnese diseases that ulstangulshes tlnem hum degeneranun uccurs a er normal maturataun fasted as a wastang an Dr p at The key feature to hypuplasla ls tlnat pnmary neuronal degenerataun pupulaaunsm spen stereutyplcal manne s affect spenlaeneumnal in areas ufbram and mmal curd m a r Hereditary or BreedAssociated Diseases Cerebellar atrophy abiotrophy These anlrnals eanhe affected etlm l Hm mmvmhm tlne unset ufdegenerataun and cmssesGallandpuny ellnleal nse in all weeks tu muntlns a erbmh Heredmy or Ere These ohseases are characte d y degeneration and loss of motor neurons m the spmal Associated Dlseases Motor Neuron D sease cord Species and Breeds r Cattle amwnswtss llereranl shaker calfsyndmme gs yarhshue Hampshue Asimdar disease uccurs m hurses hut ls nutthuught tn be heredltzryrsee elassnutesl Nutritional Toxic amp Metabolic Disease Thiarnine Vit B1 Deficiency arnavnres drugs eats and hulnanshzve an absolute dietary renulrement nrthlzrmne de clmcy syndrumes have been tamed Chastek39s pamlysls earnlyures and Wemlcke39s encephalup athy umans Hahlvnresllnelualngruruinants havenu urllttle dietary Thiarnine Vit B1 De ciency Causes and Clinical Signs Horses n ses thiamine de ciency encephalopathy has been assoclateol with horses eating 1 s contalnlrl thamlnase enzyme such as bmcken fem Ptettdtnm epp hors talls Equlsetum epp or given the coccldlostat amprollum a structural analog of thiamine e name pulluencephalumalacla urlammar eerehmeurueal neerusls Estamaten that tlne daily renulrement uf thamme fur sheep ls 274 mg sllgntlyless tlnan that produced by rumen m erullura Clinical signs e at arrythmlas hlmnness unnaaun eunyulsmns area m these eases e Treatmentrpzrenteml lmeetahle thamme Thiamine Vit B1 Deficien y C Ruminants e functions also applies to other species Function ofthiamine vitamin B is a necessary coe Thiamine Vit B1 De ciency Ruminants r Causal relationships innaayiasiaraes a eaiisaireiaiiaasnpbeiveea absaiiiie aernnnyamnnniae factor for the enzyme transketolase and WW hasheenehsm Tmnsketolase is the rate limiting enzyme in theherose his is the major metabolic pathway for glucose r Thammase cumming r Cuban de nency utilization in the brain plants 7 Sulfur induced etntal lso a cofactor for other enzymes i e pyruvate 2 W 1 m1 le amp Eff decarboxylase in the Kreb s cycle 39 391 quot2 H mm N lo ic disease is thought to re resent an ene quotquot mgm 1 quot quot quot 5 W 9 g P gY prn 39 32mm nfthiaminas xMDlasses mabmd deficit duet the inhibition ofthese metabolic pathways mm ms so involved in neurotransmitter metabolism Ampmimm 7 Hm mm WWW relevance unlmown Thiamine VltBQ Deficiency Ruminants 7 clinical signs are treatment Must commonly seen in the fee Wyoming many cases are assunated with high sulfur in water ccimpciunded by additive levels in the fcirage clinical signs Can d recumbency cipisthcitcinus Treatment 7 SQ lM thhiamineeifgiven iv shciuldbe diluted with 5 dextrose SQ lM dose ID to Zn mgkg 7 Oral administmacin cifthi 7 Others 7 Since stxahl cunvulsiuns the clinical signs cifpciliciencephalcimalaciaoverlap with other ch diseases nervuus cuccidiusis TEME e shutgun appiniach with anabiciacs thiamine etc dlcit situation but cifimpcirtance tci evelcip acutely cir river several days staggering gait bruinsm cidcintcipnsis smus blindness headrpressng Lgiuns nf pnlinsncephalnrualaija in ruminants Nutritional Toxic amp Metabolic Disease Copper de ciencyr small ruminants Occurs worldwide in sheep producing areas 1s associated either with primary copper deficiency absolute copper de ciency in the diet or the de ciency may be secondary to other metals such as molybdenum and zinc that interfere with absorption 39 r Chmcals mare quotsave aeeimoeae iiaeeiaiaiasra at me appear rear V insaaniiaaaan atar may ve area array The pe offood is also important Coppe i CAMDan mm Lesa s poorly absorbed from fresh herbage compared to cmbnlcamx resemth e cansai iesiaas are risen 39 Wm r Degenzntmn af mumnsm CHM gmquot 5quot WWW cerebellumandspinalcard Smybaek Affects lambsrarely s Copper de ciencyr small ruminants nne deficiency can result mivm syrdrannes congenital neuralagis disease at the one arbirihtswayoaslo and auelayedrarrn emaanc ataria Enzuuhc ataxia Affectslambs dalqu clinical signs are evident at Namg atbmh ape imp i P 13quot fb r h tci about a months cifage e Dulnessdsnressianblinuness Emnntic Ataxia 7 goat kid chromatolysis in pinal motor neurons above arrow and pallor w Nutritional Toxic amp Metabolic Disease Many toxins can affect the nervous system in anim s These include many ofthe heavy metals Pb Hg etc bacterial toxins botulism pesticides and plant toxins p fr m sulfurinduced polioencephalomalacia in ruminants which can be considered a toxicity one haveto be differenaated 39um enzootac atama 7 mainl cattle across the US is lead poisoning Nutritional Toxic amp Metabolic Disease Lead Pb poisoning Sources The most common source oflead scans to be old discardedbattenes see sudden death lecture others include old leadrbasedpalnts pipe dope environmental contamination from industrial wastes clinical signs Most cases in cattle are acute Som animals maybe found dead 7 at depression axia ccunvulsluns hyperesthesia l r coma cfasclculanuns rhead pressing 7 death odontopn i Treatment CaNaiEDTA chslates calcium Trombo rmmothsrtissiiss oddly allowing ediulibraoon humins administnition seems to be effechvel Nutritional Toxic amp Metabolic Disease Plant poisons LocoWeed Due to chronic ingestion of plants in the Astrogotue and Oxylmpls genera Many species are recognized but only some are toxic Various toxins are present causing different dromes eLocome and other alkaloids neurologic disease and abortions e Nrnltroso compounds ammonitrile abortions and teratogeinesis e Selenium accumulation selenosis All species can be affected plant poisons horses probably most suscepable sy monly onl after LocoWeed ants 24 weeks 9 E a i Neurologic disease 7 Depression pmpnoceptave de cits hypermeaia tremors ii i i maniacal acavity pathogenesis The toxins inhibit storage disease atmer suppumve therapy and eliminate exposure to plant llorses sall may exhibit penods o f mzma39 l Plant poisons r Moldy corn oisonin in horses Leukoencephalomal acia isolated cases have occurred in horses fed other ranuns clinical signs Rapid onset ofsomnolence depression cramal nerve 1 G it M m mml few days Death can occur within a few hours sudden death lecture Treatment suppomve care prognosis The relatively fewhorses that do not die or not euthamzed will have permanent neurologc deficits Nipnp allidal encephalcimalana CausesCenmmeasp Russian knapwe 7 Death due to starvation Treatment 7 Nu effective treatment nguGub stanaa m a Plant olso l Nutritional Toxic amp Metabolic Disease A variety ofmetabolic disturbances can affect neurological function 7 Electolyte ac mineral disturbances c a Mg 7 Hypoglycemia ketosis pregnancy toxemia 7Acidosis 7Diseases of other organs and tissues liver and kldney Two metabolic diseases will be covered here hepatic encephalopathy and salt poison39 Metabolic Disease Hepatic encephalopathy Neurological disease is a common of severe liver failure in all animal pathogenesis A major function of the liver is to ammonia can have a seiious affect on brain function manifestatj on s eliminate potentially toxic biproducts of normal b t b 39 Metabolic Disease Hepatic encephalopathy In food nimals and horses the underlying liver disease is commonly due to hepatotoxins 7 Acute toiricity with massive liver necrosis cciekleburoranhimrpp 7 igs cattle Gussypul euttunsee 7pigsyuung preruminants ccialtarelaypigennpnisnmng7pigs 7 chronic toiricity Se mo Cmmlamz pyrrcilin dine alkaloidecintaimng ants 7ruminants and hurses itamin E selemum de ciency hepatcisis dieteaea 7 pigs clinical slgls 7 Spungmsls urspungy change all meeies except hurses 7 Allhamertype ll asaueytes Rare cases of dlre Metabolic Disease Salt polsonlng Salt poisoning is generally a misnomer as it applies to imals very few cases are attributable to direct ov erconsumption ofNacl ctNacl poisoning have occurred in saltstarved cattle given free access to loose granular salt and w en milk rep lacers or electrolyte solution young calves have been mixed improperly ses represent either profound dehydration with c in rations will confound the situation and make Water restriction eV serious Metabolic Disease Salt poisoning lugic disease is due tn Sum m the acute dahy xanun N e s with shnnkzge cme mm D memnguencephalms 1302008 Internal parasitesi cattle and sheep and In human Outline Principals of parasitism Important internal parasites 7 Cattle 7 Sheep and goats iHorses Important external parasites Parasitism Association between two species in Which a parasite lives in or on m for signi cant A eriod of its life obtaining nourishment from it Host derives no bene t from relationship Many parasites do little identi able damage to host Age I susceptibility Caveats mmunity and pregnancy status profoundly affect Life 1 Direct cycles Parasites and intermediate hosts depends on intermediate host Control possum by killing intermediate host 1302008 Not all parasites cause clinical disease Some parasites cause disease but it is r 7 r a mistake Culerebm sp Nasal bom ovine sinus Gastric bots equine stomach Rodentbot y Halxeephalobus Meronema 1212er Free living soil nemato e Classifying internal parasites Internal parasites All generalizations are wrong including this one Arthropods gt M m n l h I di Protozoa Flagellates T foetus u ce uar c ronic sease A 1com lexans EPM Helmmths long generation times oor immunity P C111ates Unirnportantquot Protozoa 39 Unicellular7 acute disease7 Ameba Ummpmtant Baoterla short generation times often not always Helmmths Nemamdes Roundworms Vuuses good immunity Cestodestrematodes Tapeworms ukes For species covered in this course andin W Y Sheep tqoeworm PGE Pig tapeworm HOW parasites cause disease migration damage Protein loss Zoonotic diseaxe Competition with host for nutrients Damage tissues l 7 Leakage of blood or protein g 7 Obstruction of hollow organs eg gut S39 7 Ulceration g 7 Migration through tissue Zoonotic disease animalpeople a Lungworm cattle bronchitis Equine axearids obstruction 1302008 Basic nematode life cycle Paras1tic diseases can be dif cult to control Parasitic Preparasitic Antigenically complex due to multiple Comm maturational stages few vaccines with Comm Relatively 1naccess1bie to the immune ammmmms with system 7 esp at mucosal surfaces Ideally kill quotmgquot an Surv1val on pastures andor intermediate V movement AND adults hosts for monthsiyears management Resist some antiparasitic compounds N Larval arrest in tissue hypobiois Peripamment rise in egg output spring rise 39 Mechanism whereby larvae emerge from arrested state when most advantageous Especially sheepgoats Ck zm tquot SP L4 mes39lquot ab m asm mev Sheep Reduced immune suppression due to prolactin an goa s r Cyathosome arrest in large intestine horses Secreuonm late term ewes 39 May be difficult to deliver effective dose of 39 compounded by medication 7 Increased intake of larvae 7 Increased fertility of adult nematodes Now named mmmmgm r Maturation of hypobiotic larvae Nematodes on pasture Important parasites of WY cattle 39 Number of larvae ingested severity ofdisease Ostenagiasis 39 Hatchingdevelopment of larvae determined by TEMPERATURE and HUMIDITY Intestinal cocc1d1051s o a o Optimum18 26 80 100humidity I cryptospondlosls 39 Light aridity and for some parasites freezmg reduces pasture load Trichomonia51s 39 Impact of grazing patterns 39 fecalcontamination 7 Sheep graze pastures short 1302008 Ostertagiasis I Cause Ostertagia ostertagi cattle and O spp sheep I Economically most important nematode of cattle in USA Direct life cycle Larvae live in mucosal lining of abomasum Type 1 ostenagiasis iintake of many larvae gtJuly Type 2 osteragiasis 7 simultaneous emergence of arrested larvae March May Trichostrongyle life cycle ti 1 Ahnmzsumsmzll Intestine 1L3WgtL4WgtAdults 2 Przpzlenipzrind23W221s I TRICHDSTRONGYLES Life Cycles u i Q 5 l l Osmagin fall inhibition 1 onenagia spring inhlbixim Ostertagiosis in Wyoming type climate NORTHERN TEMPERATE CLIMATE Effects of O ostertagi I Usually mature inN3 Weeks I In our climate arrested in fall for 3 7 5 months Damage to parietal cells 4 abomasal pH Pepsinogen not activated Leakage ofprotein Inability to digest protein 4 appetite Treatment Anthelmintics I Dose and move I Alternate sheepcattle 1302008 Pasture control of PGE in cattle in WY If possible DEWORM and MOVE to clean er pasture Low stocking density when possible Use sunlight and drying to kill parasites on pasture 7 Graze pasture once per year 7 Ifheavily used in fall leave idle in spring before reuse in summer or 7 Harrow pasture when hotdry to kill larvae in feces Enteric coccidiosis Multiple species 13 in US 7 important ones E zuemii and E bovis 39 Good immunity in animals exposed to recurrent infections or k recovered youn stoc Large intestine affected red blood passed DIRECT life cycle Especially stressed or recently weaned calves Maturation prepatent period 2 7 3 wks Feces o en contain FEW organisms when disease breaks DISEASE 7 Mild Variable dimhealisdess 7 Severe straining weak i mucoid bloody diarrhea maybe ABSENT Coccidiosis nacyst releasing 1n cattle menteme Bovine Coccidiosis Noah F28260 Treating and preventing coccidiosis Most of damage done when clinical signs occur Move affected calves 7 environment contaminated TREAT 7 Generally3 77 days depending on drug 7 In feed or water drench ifofffeed 7 Corid or sulfo 7 May need to treat dehydration and secondary infections PREVENT 7 Don t feed 39om ground narnades arnon others 7 Avoid fecal eontarninan39on ofwater 7 Same 01 related compounds as fortreatment 7 Rumensin Bovatec Deccox 7 Lower dose Longer treatment Cryptosporidiosis th0 t uin 7 Very small coccidian 7 Calves 1 4Wee s 7 Esp dairy calves 750 infected most subclinical Many infected few deaths Zoonotic Chronic slightmoderate diarrhea for several weeks Often occurs with viral agents rota amp coronavirus Infective when shed Hardy organism 7 resists routine disinfectants 1302008 Cryptosporidiosis tre atrnent control Move calves to clean area No approved treatments for cattle 7 Experimental drugs too exp eusrye to use arm not approved for calves No vaccine Harsh disinfectants formalin ammonia Drying kills cysts Cryptosporidiosis in people ure 5 Waterbome outbreak in Milwaukee Wrseorrsrrr in 1993 300000 people infected Intermittent diarrhea 1 e 2 weeks At risk eluldrerr hikers HIV patients immunotherapy recipients Treatment uids nitazoxanide Avoid boil water lter water pore size lt1 um Trichomoniasis in cattle Cause fragile single celled organism Trich Venereal e transmitted during coitus Esp a common grazing allotments Early fetal death infertility r Cuw 9 clearlnfectlunln 3 munths e Bulls gt munthsryears Esp older bulls THERE ARE NO CLlN39ICAL SIGNS 1N BULLS Poor immunity reinfection may occur Early abortion lt5 months Recognizing trich NO distinctive lesions in bulls or cows 0 e Cummun gazing allutments andurlungpuurly lnes e infected bull lntxuduced Yearl ur wnwmcalvlngsusmpreglmcyratz guesfmm95 saws Yuri preglmcyratzcannnuesmfa 45 7 Impact un pregnancy rate depends un number uflnfected bullslntmduced e Pyumetraln sume euws atpregnzncy eheekmg ume Pyometrar a consequence oftrichomoniais Tnehuruuruasrs m Wyumlng bulls Sept 1 2m rAugust 2007 Purmehullr 50 Intalmmherufhullxtertzd 702007V purme 1302008 Trying the conventional approach I Vaccination 7 WichGuard7 Fort Dodge 7 Speeds up elimination in infected cows 7 Ineffective for bulls I Treatment 7 Theoretically possible based on limited studies 7 Illegalunethical Current control of trichomoniasis Detecteliminate infected BULLS B reporta le 39sease e quarantine hold orders Keep breeding season short lt90 days ifpossible AI will not occur semen checked to Tfaetus Natural servic 39 k nega vebulls e Outufstatebreeding bulls testrneganvewithin in days 7 Cem ed vetmnanan eneek bulls during suundness Examinatmn 7 Keep bulls separate 39um eews Exceptdunngbreed g e Guudfencelines7testingufmarmngbullsatpmducer39srequest e WLSB Vrbrandsinfected bulls e infected suld directly fur slaughter urV lut agreement feedluts e Cull enen aterc vingzn pyumetxacuws e WLSB ve ands and requiresinfectedbulls suldfur slaughter e Cull pyumetracuws Other internal parasites of W St cattle I Liver uke 7 Fasciola hepatica I Lung Worm 7 Dictyocaulur viviparur Fascioliasis I Fasciola hepatica 39 I Indirect life cycle cattlesheep mud snails I Wet areas I L1ve 1n bile ducts 7 Cattle acute chronic Black disease 7 Sheep acute fatal infections I Treatment speci c ukicides eg Curatrern and Ivomec Plus Liver uke 1302008 Flee Meme 9 D as w Spuwcysu a saw Mr Lungworms in cattle 05mm u mum e J a amazithqu 39 0 5 assumes osssszmw Internal parasites of WY cattle Lungworms in cattle SummaIy Parasitic cause of pneumonia FallWeaning Manage pasture 7 NOt maJor m Wyommg too COld coccidia t Diarrhea AnLlCOCCIdlalS Avmd cmwdmg 39l39reated W181 broad spectrum anmelmlntics Trichomonas H t Venereal Cull Sim Vaccination possible 7 one of few examples of such for complex parasites in anima s Liver uke Liver NovDeC Needsmmsture Winter kills Snal disease Cryptosporidia Zoonosis None Fuhllchealthissue Lungworm Pneumonia Ant helmmhcs Wmterkillslarvae mWY Internal paras1tes of W Y sheep Ag nt 1m ct D tment omment Barberpule wum Anem and Amheimue uheummuhm wv sudden death Ostermgm Protein loss Anthelminu C mmnn m wet gumd Nematadmu Diarrhea and Amheimmue medmgrmjur sudden death W Trichwtrulul h mp cheeidm Diarrhea Anncuc d als gigansmm ilaexunuchus 51139 I Tapeworm c cembralx CNS d ease Dewurm dugs Dmtlel ags at sheep msm T gandn Abortion Nuns appmved Keep mts and sheep separate vaer uke e Liver disease offrlabd use Needs mmsture Winter lQllS SrEl 1 302008 Typical roundworm cycle in sheep Ostertqgia circumcincta quotD l r r x a Lt K Eggs lnlechvelmrd 900000 5 ge rewae a Do a a Pasture stages P fln 242 weeks Moisture gt Temperature Frrslslage 7quot ka secund stage I eemec Vesing larvae le Typical buildup on pasture in moist wet summers Perparturiere Roundworms in sheep Parasitic gastroenteritis Affect abomasum small intestine 4 classes ofnematodes 7 EWES majur seuree furlamb erep m 3 e1asses 7 FASTURE then LAMBS seureerrr 1e Most speci c to sheep ass Clinical effects depend on class ofnematode 7 Wegrness g appeme 7 Less ufcundmun peer eece r Diarrhea 7 Sudden death esp Nematodxmxspp 7 Anemiaandbuttlejawesp Haemenshesspp 7 cempheauens7esp pneumum Effective control of roundworms in sheep I Deworm ewes Prelambing or when leaving lambing ground Move to lowrisk pasture I Deworm lambs At Weaning and move to lowrisk pasture High risk at N 6 weeks after beginning to graze Anemic eareass Ostenagiain spiral fulds Ovine parasitic gastroenteritis Ewes produce more eggs 2 weeks before 8 weeks a er lambin 7 Effect ufhurmunal ekaeges assueiatedwith milk pruductmn 7 Tereperaryiessefrrereee 7 Develupment ufanested larvae climate geeeee facturs euntxul Agerelatedresistance 7 disease inlambs Graze close to gro high intake oflarvae 39 n nct hea co taminaho Small fecal pellets break down eas39 y Willing essto cons calcontaminated pastures Eggs in feces may NOTbe goodindex ofparasitiism 7 Esp earlyin uutbreak Wpathugenic species preeeee many eggs 1302008 Nematadirus batlus simultaneous hatch en in inn in M in and um loll sz Jim39s idly 55 Nematodirus battus Hatehing chill followed by mean daynight temperature ofgt10 c Severe damage oflining ofsmall intestine rain and drarmea Lamb gt lamh disease Good immunity in ewes spring MayJune Coneurrent eoeeidiosis eommon Controlling sheep roundworms prossihle avoid using same pastures annually 7 Alternate sheep and eattle pastures Deworm and move to eleaner ground such as e Pastures 39nm whreh a euttrng has heentaken Deworm ewes Zweeks norto larnhing or at lamhingmove ameliorates periparturien rise Regularity oftreatrnent tied to level ofn39sk sheep on wet pastures vs dry open range Alternate wormer annually Dewormers Bumka parasrrrmaloaean m Lengwrtlri wal Lnrlewarrre Awldmbnhhnn ll Tam dlarvas dnsehui dose ynwm lnrdamllnamlss Levasole m slenwrtlrdrawal Lnrlewarrre haest is Many mks eral ml unreal Mansions lverrna m Lm39lgwldrld Lnrlewarrre Awldhchcnn Lroe Many mks lard ml MPKAD Using dewormers and clean vs dilly pastures Ewes e Routine risk deworm prelarnhing or at turnout 7 High risk Heavy stueklng rates Reeurrently used pastures Tumuut and at 3 and 6 Weeks Lambs 7 High risk at 5 weeks 7 Repeat depending on elimate wet warm 7 Repeat at weaning Resistance to dewonners ow incidence ofresistant genes in roundworms Routine useunderdosing select for resistance Esp resistance to henzimidazole elass once on a property permanent feature Avoid by 7 Bene ts efwrthheldrng feed befure desrn 7 7 Maintain lireseeunty lntmduchun efresrstart reundworrns e Quarantinedevverm on entry ufnewly purehased sheep 1302008 Gid 7 Coemm39s cerebralis 5 5 ED 0 e a 525 Imuplmmuw Toxoplasmosis o L 7 f m 7 Qfever K rr m 7 Chlamydmsxs are x w r Tul Toxoplasmosis abom39on sheepgoats Cuntzmmated felme feees 7 WA 1 pm Meagesmen abumun Late nur mal nfected amb Fepperum lesmnquot Dealing with toxoplasmosis abortion Usually undue term shamans 7 Munmxes 7 Placemaa mwm Cuntxul rudents keep ham cats undercuntxul Nu sheepsh Handwashmg Safe dispusal ufdead fetuses and membranes eep txansmxssmn Retain ewes that shun 7 guud 1mmumty Prevent an 7 Deeaeume Deeeaxm 7 Madn edhve Wanne iumpe mdNZunhkelyxnUS Treatment 7 Sulfa ugwdlreduce lasses Neurological dIseases usually affecting Juvenl es and Adults edeiisi Biasmemeendnemmenspneims rzrasmc cimaisi swim Equine pmtazaal myelns even me inwv News eseedisss e mm in esdie hem multicevs eemm insneep Wsi amine new mil encephalamvllms e endemic in mam v wweendene n Wiaiiid Weeenisminmsem hm resin vwv see em in wvem discussed nien dsesses Ri es museum wunval neumlaviulMwmsamqunewnable Sc pie 0 niesmwui at i Mi Yoxic 2rd Nurmmzl Nivmvallidal encephalamlau was in WV esiiseneepneimieeie 4mm in mile in WV demeeneepneismiesemWe wide tseeeedsesvenw laul v Organ zat on of lecture Diseases with brain stem involvement Diseases primarily affecting cerebral hemispheres Diseases primarily affecting spinal cord Clostridial diseases Prion disease Species seen incistccirninciniy in calves butnut neonates Pathugenesis typically an ascending bacterial intecticin supharynx cit tne na Nasaphavvn M edsecnentdae nemesis speues i die eei M mm s inner esi siwseseets me W M W siiepiseseeespeeies assaualed nennees otitis media interna rain Stem meningciencepnaiitis 2 nllgnnsls dniisteisi m hilalemli iscisi nerve Pavalvssi deamessi need tll i pnees Facial nerve Passes tnmuen Right Vaual nerve dsneee in mills nedis i niddieesi inieins Treatment Antlbl tlcs Suppumve sneiten ndtnticin Prevention if huused e clean Envirunment is important Dun tfeed rnastitic mllkt calves Species mminar sgtgtgthmsesandman Znnn IcD emul assuualedwthahamaniCNSmedian Cause tisteiis man cvl genes iniectstne aisinsten in mmlnams aeen sis avveveli n is immanent ta rememhevthal this pain can a muse aculav inlediansi nestitisi shaman due to netmis end septicemia lhe disease mien nouns in wmev in association with ieedin m siis ei hm mses do seem also in sninsis at Pasture Pathogenesis R ummanls L nanacmeenes gainsacuesstathehindebminbvtvavellmg AAst nsaHh is si nee inalnevves tisthaugh acmsstheaml mumsathmughminorahmsianshemreentevmgaxons Lm is n idy sci ii n andVEPlimteseasilvinpamqualnvslagev mevethept l s Disease mien nouns in outbreaks Heises disease isieinnmses Usuallv dimseeneepnsiitis Listeriosis 2 cttnteat Signs 7 Eardruup prehensiun mastteattun enewtng and svtaiiuvving prubiems Ctrettng Necrugg rEiactertai eutture rrum brain stem rcn raetensttetestuns preduminan puns inrtamm u p esen Mi ru eess tiy neutrupntts tn tne meduiia ubiun attun ts ais r t tn the trtgemtnai euntatn gata and gangiiun Bacteria are Gram pusitive and may be intrar eeiiuiar Treatment anttbtuttes Preventiun Nu vaccine avaiiabie tn USA Ensure grind e quaiity siiag N gro pall dal encephalomala 1 spams tntsutseaseatteetsnntsesnntv cause titseauseuta tn esitnnutennetVettnwsiattntsiteCentaurea sotsttttatts m Russian Knapmed Centaurea repens ntsease is vpimiW unu tn summer and tatt tne utteu ptants tn nav ate aim mm Vellnw Slar time and Russtan marwee native in Eumsat tnttnuueeu min USAm tan nemqu Nigropallidal encephalomalacia 2 thnuenms tne ptants mntatn a tune ncipie t Pin tnat meutatestne etteets mine utsease Reptneausesuegenetattnn tatatn tegtnn eatteu tne sutasantta meta anu ginbus natttuus tne sutasiantta meta ts tntne tmnt enu nttnetmtnstem tstetnnatsn Eiinns tn Pavkinsnn s utseas yrmlnms tne tatatn regtnns invnived are tmt arttntneenmmtntmnvemem Pmbiems win pvenensnn ma icalinn swaiinwrig Tongue pmttuues vvetgnt inss dew ia innt aimiessvvan evmg 1mm Once neumns have been ins1 tn tne atteeeuateastnetetsnntegenetattnn Mii iv atteeeu eases mav make a smatt vecnveiv ptettmttnn etaztng anu pas1uve management Avntu making nav ttnm mmaminaie pas1uves substantta mm ttquetaatnn Puttueneepnatumataeta aka erebrai eurtteat e mtn Espunsive eneepnatupatnw erusts tnta 5geetes came sneep anu guais Cause niaminervespunsivePEM nyutugensutnuetunettytunesnuttespunututmamtne eau puisuning DY satt puisuningr may cause testuns simiiaHu FEM Patna enests ceiebvai cunextsmeiabuiicaiiyvevy active and ts A smveiu 212515nienevgymetabuiism ihiamine deiiciencyand H25tntenetethneettutatenetgymetabuttsm s m terns Tnese atetne same vegavdiess utwnetnettmamtne Vespunsive Ciassicaiiy uptstnutunus Ssiavgazin eenttat biindness dueiuinvuivememuivisuaipaviuicuvex vecum ency seizuves Tnete snuutu be nu pytena Polioencephalomalacia 2 lesions A e ts erebrur rtuuresee thn w itgnt E Polioencephalomalacia thiamine responsive A subset er eases respund tn intrarvenuus tntamtne urtiy trtntamtne administered tn eariy stages at ettnteat disease Tnts dues nu necessariiy mean tnat antm is are tntamtne deficient nenee tne term tntamtn rrespunsive True tntamtne deficiency may be impunant tn sume eases nuvvever a e Putenttat urigins urtntamtne deficiency r Thiaminase containing Pianis e g bvacken Hemwm Winmum a rmamtnase pmuetne badevta tn inles1ines e e some Eaciiius speetes m in be mm m speatatnamnas containing Pianis Polioencephalomalacia 4 highsulfur diet associated Hign sultur in Water brtbbd can cause FEM Symptoms usually occur M Weeks after dietary enange FEM is strongly associated Witn ruminal gas cap nydrbgen sultide concentratlun Sultate in dietis epnyerted tn nydrbgen sultide in anaerobic ruminal enyirbnment by sultate reducing bacteria Hydrogen sultide eructatiein and innalatibn is probable meenanism pt absurptlurl into body Leslurls are identical to thlarnlrlerrespurlslve tbrm or disease Diagnosis 7 lesions lack or response to thiamlrlE rule but lead poisoning analyze mod and Waterfur sultur content vvatersulturleyels are nign in many parts ufWY metnibninei as itis more easily reduced to nydrbgen sultide Lead poisoning in ruminants Uncommon cause ofa PEMIike disease in ruminants n e er budlES due El Envlrurlrnerltal Euntamlnatlun 7 Lead induced FEM reguiresyery nign leyel Exposure 7 e g ingestion Likely sources oflead in environmen e Discarded ear batteries 7 Lead paint trbm old buil ings e banned tor residential use since lB7E in USA7 old buildings could still cuntalrl lead paint 7 Oil industry contamination e Fribrtb tne clean air act or map lead Was present in gas luvv leyel pasture cuntarnlrlatlurl along hlghvvays e not suttieient to cause clinical poisoning When should you suspect lead poisoning e Anytime you naye PEMellke symptoms and lesions 7 New untested pasturei possible Exposure to old buildings retuse e g batteries on pasture e AtWSVLe liyer lead leyels are routinely measured in suspect FEM eases LNEHS organ CW EthEE brain levels can also be measured Salt p0lsonlng Species pigsgtmminants Figsareyerysusceptible Cause s most often Waterdepnvatlon e g trozen burst pipes 7 too mucn salt e g chlckerl teed mlstakerlly ted to pigs incorrect mineral additiyes excesslve ingestion aftersalt deprlvatlol l excess concentrate e Sudden cnange to saline Water Pathogenesis Wnen Waterls made ayailable to yerytnirsty pig leads to cerebral edema e Cllrllcally similarto FEM nypomagnesemia ei e symptoms relate to ce 7 SerumbrainCSFtood sodium concentration 7 Microscopy cerebral edema similarto PEM but Witn noreduced tissue deatn eosinopnilic intlammation in porcine salt poisoning Salt Poisoning 2 Treatment remove source of excess salt immediately If dehydrated animals allow small amount ofwater 39n tes or so don t allow gor 39 If severely dehydrated call veterinarian may give intravenous uids slowly Complete recovery is possiblefair1y rapid Prevention Full access to water at all times No sudden change to high salt diet Secure concentrate stores Thrombotic meningoencephalitis TME Species Cattlegt sneep Cause lntection Witn tne bacterium Histopnilus somni Tnis disease ost commonly in teedlot cattle yersus pastured or dairy cattle Fatnogenesis The bacterium gains access to body tnrougn respiratory int ction Once in blood is attacnes to blood yessels in fairly damagingtneiii causingintlammation and tnrombosis Brainlesions S mptoms Pyrexla Acute onsetotneurologic symptomsto sudden deatn Treatment Antibiotics but tne prognosis is yery poor in neurologic animals Freyention yaccine ayailable May not protect against all syndromes c by Histo nilus somni e g cardiac torm or disease yaccine in some instances may also exacerbate tne disease at Hepatic encephalopathy Seyere liyerdamage can result in accumulation or ammoniaWitnin blood resulting in cerebral edema Clinical si ns o gradualonset Excltablllty depression nead pressing abnormal and bizarre benayior Liver toxins Pyn ollzldll le alkalold containing plants e g Ragvvort Senecio yacobeat many otners Cocklebur Xanlniurn slrurnariurn Fungal toxlrls e g aflatoxlrl Many othertoxll l can cause acute or chronlc llver iniury depending on exposure prorile Damageto liyer cells can be ouantitied by measuring enzymatic actiyities Witnin plasma e g GGT Foor prognosis 7 identity underlying cause and preyent cases ll l otheral llmals l mnV causesathDm mnnc WD tamew enewtu va M neeotwteoot Senecmjawbea ts ptesent tn yyy Xammum sttumanum ts ptesent tn yyy thyme Sweets nahnd venaus to USA Eaddebuv 5 quotmo use Coenurtasts Causeo by the tntetmeotate stage otthe tapeyyotm Taenta muItceps usuatty causes ptatn testonsy yanabte tn tocatton occastonatty sptnat coto testons Sheepgtgtgoat t came horas humans Dtsease symptoms oeyetop 278 months attet sheep tngests eggs Symptoms ate yartame oepeno on cyst tocatton most common stte ts tn one ceteptat hemtsphete 7 Cttcttng ts cummun usuaHytu one stoe ttte cycte mTaema mutttceos Howmaythe ttte yoe otthts Pavasnebebmkem Doe ts oetntttye host atso VuxeSt coyotes Evshcmkvmedtaks ve n ootnotsheeome mystte s ve e catteo coenotos Monte Nervous COCCIdIOSIS Neutotogtc synotome tn catyescattte attecteo thh entettc cocctotosts ome The exact cause ott e neutotogtc synotome ts unknuwn 7 Eteatotyte abnotmattttes seconoaty to tntesttnat otsease 7 toun otoouceo by cocctotat soeoes has been oetnonsttateo by one otoub Tteatment 7 cocootostats 7 Tu teouce tnctoenoe otsetzotes7 keep anttnat tn a qutel davk atea 7 suooontye7shetettttutos 7 Cocoootostats7 meotcatton tn ottnttno yyatet 7 tt houseo 7ctean enyttonment ano nesh beootno Locoweed potsontng 1 Sgectes hotses mote suscepttpte than tumtnants Cause tngestton ot seyetat ptants otthe genus OXyImptS ano atso Astraague 72 thropt spectes produce the um pnnctpte catteo swatnsontne7 most ate ptesent tn WY For examgte tnsuttoent otazne Nn an th u t Wmtetncnvyee m semea anmmgtncnvyee m nanat Locoweed poisoning 2 pathogenesis Locoweed poisoning 3 iagnnss Neuinnal aeeuinuiaiien Hisieiv ei exposuie swainsenine ingesien Cum leX SL315 censsieni eiinieai iindlngsr in neisess emessive salivatinri Mn eilngi alteiert gaii weight iess WPeisenstive tn siinuii manlai vies iess inienilnvarirt almmnri siiniiai ndings inea e iameiaiieneiviiieiaieeeeeiis mmaririnsrtase Managem Simple may Pieventamesstnplants cane nuiiiiien Recuveivmavtakesnme time NWW Disease andn vnutniriktnat iii recuveivmavnmbecnmplete in some animals7 valuing an naniiesiaiien West Nile Encephalitis 1 39 History ofWest Nile Encephalitis WNE in USA is a mosquito Dorrie viral infection thatWasfirstideritified in the USA in 1999 The disease occurs in horses birds nuinans and less co morily in inner species Symptoms Clinical sympt ms in noises are varied Most cases have inain s i ai invovement s deniessiunandiiuienisenaiiuiiiuiesiaininiu ement s ataxia lameness tuediaggin piayei pu uie sensitivitytu iuuen spinal euia invulvemen 0 n Pink Positives cieen ubmme s ieiei s lrinialsymptumsmayiesembleiabi as Veiimnei inieiiee Czu WNVis an RNA VlYLlS in tnellaviviius genus OWENlaw r v64 lquot SJVVElllaVVCEi VFW iiiuses also cause encepnaiiiis e g lick borne encepnaiiiis mi sibmit samples in Europe censeeiine Mule eivvv eneeinie VDYWNVi iess siiveiiianee inan a iereais age tn iae West Nile Encephalitis 2 CNS lesions West Nile Encephalitis 3 spinal eiai naiei lesions Spinal penvasmlai niiiaies l unnss s 7 Dmmmalumnanew50mins mesquimmeii wt 3 was aimiin Miami Mm seiiniw csr ivii7mminmmeimiensmis newnineiemmememm mivnmbecause misuse inn iemiemimneisen no rewanse meneiiniesissnpiesmnsses Neeiapsi spinieeie emnmnis ciiiesi ineies quotensupwima veiivseiisi niimmsiien medinv nimiin my maneiepinsi com gt aim stem Miaaisn thalamus andbasalnuclED swimiwaisvnesiiems ineiieeensimminenmnensa naiim Irmlrmm SUPP lvemie inesuivivaliateisalmut Remveivtn ainieiie status in eempeiiiien lvmkirig noises mav not new andn van in Ktnattnis mav iae ine case7 pieiimiinn Aneiiective wmineisavailable Masquiieeeniiei PIEE ullnns merited mien ani e nuinan iiansinissien nas iaeen dummem Wnen handling a suspedWNVnnisetake mmme Pieceulinrisr nu eiieei emesuie tn iaan Midi weai iaiex gloves and Pimedive Clmhl gi wasn hands Equine iaiaies ean pieseni win svmpieins ieseiniaiine WNViriiedinri WNVamigeninspinal Equme herpes Vlral myelItIs Le steamtyne Cause Equthe herpesvtrus an atbna netbesyttus Seen seyetatttmesyeatatvvsyt Pathugehests Attbbme tesbttatetty tnteettetn tnat spreads seebneant tet tnybtyee s tnat E rdgtbram s tnat Curd hurses gm an n eyetbb a tatent tnteettbn The sttatn tnat mustu eh ausesthe neutbtbgtetbtm ett EHW nas been teenttttee e and we ean test tut tt at WSVL Latency ts an tmbetttant feature EHW and uthera pharherpes ytmses such as herpes stmbtex ytms t e tnts causes me sures rrEaEItvatmn uf tatent tnreettbns may exbtatn su e uutbreaks Equthe tabtes may tesembte eany neutbttbbte EHW Equine herpes vIrus LIfecycle and the role of viral latency gt Nasat sheddmg Latent Wedmn senmvv Eanghat LN tnteatnn ntynung butses l hcubman ve rwd2 tam EHV1 strains One studyfuuhd bettnt mutattbn tn 83 ett neutbtbgte dtsease uutbreaks tnat was absent tn 95 ett abbtttbn smrrns F39mm mutattbn tn tne eatatytte subumt ett yttat DNA bbtymetase Hurses thfected wttrt neutbbatnbgettte EHW naye ntgnet dEhVEry ett eukucyte ytms tet CNS enebtnettat eetts Latent tnteettbns ean be detected tn hurses by btbbsy ett tne manetbutat tymbn nude and PCR F39CR ean etsttngutsn neutbttbbte and nunrneurutruptc straws Equme herpes Vlral myelItIs s mbtetms Tybteatty beembenMa seyetat antmats tn wt Pytexta Symmetneat htndrhm Weakness ataxta tnebbtetnattbn tnat may prugrESS tet batabtegta Dtagnbsts Htstbty and ettnteat stgns s tbtbgy 7 may be cumphcated by yaeetnat an r WSVL 7 ms yttus tsettattetn PCR 7 attette dtscrtmtnatmn methud e btbbet csrt Eurd LN gahgha Rue out WNy back INury EPM testt ean use paHEd satnbtes Equme herpes Vlral myeII Is Treatment Subbbmyetanttyttattnaywbtkbutyetyexbenstyet E antt tbttestbebnttbtseebneatytnteettbns Prevemmg secundary ebtnbtteattbns ts ttnbbttant tn batabtegte anttnat Pm nbsts ttanttnatbeebtnes batabtegtettbebtbgnbsts ts puurduem J V Eump teattbns such as secundary tnusete damage obnttbt Neeetbtbtbwyetettnatyaeyteetbteaebspeetnebutbteak eg Ouaramme butseswttbteyetbtwbbtetaettttytebeek tembetatutes dat y etstnteettbn ttbbtses stabtee Pteyenttbn Ouaramme new btsesbn btetntses Ouaramme butses tetutntng ttbtn shuws ete7 Vaccmatmnrnm tum reentry anttnatswttb a tatent tnteettbn by tnanetb btupsyand POW Ahtgh percentage bt teytbustytnteeteeant eeyebb tateney Wbat en yuu en wttb ta ent anttnatswben yuu teenttty tbetnv brat LN tnats Equrne Protozoal Myelltls 1 ne as many teem pmtmt matte arsed by satmeystts m m We 11 Numb hughest 7 ttk cyttz vi ttmtmtu nrlrrurrl W betntttmnagenpassun Abaram tttetneetete hug Nm 7mmquot s w ntesttan at mmatteeaeantmtmawtn bpassunteees t WVrhave been e a setn as1 FeWO ssums n seent rntnngtnn at a a Nebraska humeVl 7 quotWIN an E maa SE ane Meres1 bsA Equ ne protozoalmyel 2 D gnoss Antennae dllgnnsls germane Pnstnnllun lgnnls erhreertherre ear bevaiiable Spinal eere resehs seher exrereeehhee may het ee apparent macroscopically exclude musculaskeletal dsmders herrerrheee ehe necmsis rn earner eere e v hrerres we sent ns w v IParasne eeteetreh eh mm lHC mPCR csr errtr7s heerehe tee csr PcR esr ermremheereterh7heree herher unlkeVINV Rule autWNVand th teeehseeheeseeurtherememeeheeeees rreh rhheheseeeesre memvvm iidisalman etee avert Equine protozoal myelItIs treatment Treatment Cumbinatiun antrbrutre treatment Yrmzmnpnmsumnd nynrrrarturtrhet gtEEI n err herses respund ter therapy ay net recuvertu previuus athletre level 7 Why du yuu t in Cuntrul Seeere herrse reree r e lids Prevent aeeess erreperssernster herrse stables A vaccine rs available 7 her need ter ese rerr WY herrses Clostn al enterotoxem a aka 1 se ynutnmx reehe eeee ustallvpel eete erseese murse eeee h t72 heers Abnormal peserrhe OcmsanallvmavWEsentas suhamte te errehre erseese Dug s r reree eteeherreer ether ererh reerehs rehe eeerre Lenteritis str r PcR 39 m r e en a eetereeheeeers7peerpreehesrs rm e eh Hermon Van2mm en preererr 7 er sheep quot 39V quotquotquot quot m eettre ehe eeetssheere ee vacunated terthrs erseese these vacunes ere multivalent ehe cover ether eestrrerer erseeses rhereerne ereehree bmulism rerre evsehterv tetehes ehe brax Tetanus 1 Species all rarrn mammals herses and humans Cause Clostndium lelani tuxin tetanuspasrnrn Pathegenesrs 7 aaeterrerh earns ehtryte heeythreeeh weehe e e navel tail ducking castratiun eartav HDSEHHV untimun 7 Preirterates rh anaerubic EnvllunmEM she pruducestuxin 7 m s udy ee 7 Tenn enters nervuus systerh at neurumusculauunctlun 7 Transpun up aXDnS rhte one 7 ihhrhrtsrhhrhterytrahsrhrtters eiyerhe she eAEArh one 7 Drsrhhrhrtreh reseits rh excess rheseie tehe uver Extensul gruups 7 Tenn has srrhriarrheehahrsrh etaetreh as butulinum tuxins but sets at erttereht lucatiun tn the nervuus systerh 7see later Tetanus 2 clinical diagnosts hrsterv7 he vacunatia erteh rhteeee eeep heehe Cliniml sre E ehrehreereet Tetanus 3 Treatment Penicillin antitoxin injection poor prognosis Prevention Cleanliness during surgical procedures Vaccination is very effective vaccinate dam to generate maternally derived immunity in calves foals lambs Prompt treatment of infections injuries wounds Botulism l Species a ymammaimbivd Cause Clustndium botumumtaxins lhebadeviumisaneninthe essmimesiinsiiisei athealthy animals m gene is 312 e s 701212 mieeieimsemiseas sievi si eiseni rlhis lly sa disasea x i i navia em in substrate and Wow22s nstaxins tisthen ineesiee For example an atbveakh ieei m spieseinepauiuvimei pssuiemieesiiv DmsinBysanevmge inn Ass mm asphmus eeiiei p encywmch DEM es Pica depraved appeinesne teedirig siisee eanisinine dead animals 2 e rodents ins isthe mas communion atthe iseasein leisheep dhmses e Teviee eeiieu rlhebadeviagrawandpmducestaxinsin iriesinsi tract Shaker mai smemrie 7375 weeks m see 7 Wuund butuiismrbadeviu i gmv ginv uundithist vm maybemme mals i horses Mas likely one animal involved Least a iani m disease Botulism 2 toxins W Heavy chain isieeismiaesiian Wthin ch Liem amiss mote e eBmuiinum toxins are talgeted to theneummuswiallundmn Batuiinum toxin inhibits iisnsiissian m mammal siensis at the neuvamuscuial lundian ecieavsge a sy abrevin i swtaxin SNAPVZS Prevents release m seetvemi a t ine in iespanse action Pa entiai Botulism 3 What symptumswuuld yuu pieeime uncuvwnh butulisrn7 psiesis weakness eiiieuime use lass attangue lane musde tsscicuialians Huw can iii a esisv Demunstvatiun eipieieimee mm is best isl breathing due to mmva ian atabdaminal t 3 ii be e Wound armrcantlycu e 1EIEI anaerobic eeuipmem Treatmentisuppamve maimiesiiwneimmismnaxiniimwsiisin Pieve t e vamine is yew e edive ii used pmpeiiv multivalent m manavslem nest kunds unto Diseassimesiessses Dantteedmmaminatedtuads Large hay bales Provide anaerobic centevs mm to see carcasses my smamsieeisniineriemaes e Damieeesiaeem arses Public heaiihemen is destvayed by heat sames are new resistant to heat Summary Clostridial disease involvin the nervous s stem De nitive diagnosis dif cult for botulism and tetanus as t m es Prognosis is poor for tetanus botulism and enterotoxemia Vaccines are highly effective and cheap there is no excuse for not vaccinati Horses are generally only vaccinated for tetanus ofthe clostridial diseases Can protect young animals by vaccinat39 ing maternally derived Immunity for early protection Pnon Diseases transmissible spongi arm 1 Prions are misfolded proteins that are infectious in the absence of D Prion diseases are neurodegenerative in nature Species in which prion diseases have been described 7 Cattle e buviriE spungifurm Encephaiupathy 7 Sheep and guats e scrapie mink Encephaiupathy e Mule deerEikWhitertaiied deer There is potential for crossspecies transmission eg bovine prion disease is transmissible to man Prion diseases 2 OutbreakinUKinmidJQED sthmughiQ s an At Peak several handled cattle month develaped disease destroyed export View atiive animals and meat e A mse in USA was imi an animal imparted m Canada 7 disease nm Present in usAi as iei as we knew sArveiiianEE piaeisms are in pisee e Yvanmissihie to man rgt1EIEI cases VEPaned in UK nvCJD m early i ssu s iisses excluoed mmmsmmmin Prion diseases 3 Sheep gt goat scrapie present in U gt 2 years chronic progression neurodegeneration rub on objects hence scrapie Prion gene polymorphisms determine susceptibility Can breed scrapie resistant sheep Not knovm to be a 20 Present in USA but rare 7 immunus taining teipiien prutein 7 brain anduriympnuid Liveanimai 7 Tunsii Drthird Eyeiid biupsy and immunustaimng furrnisfuided priuri pruteiri 7 Can use as part at a unk Eradicatiun strategy 3122008 Reproductive and cal iood illness in cowcalf operations Diseases in food animals and horses Typical production cycle Breed1ate spring ear1y summer cow rebred 4590 days after calving Natural service Bulls turned out for 3 months to ensure cows are bred 7 Less lab Dr 7 Own urlase bulls Pregnancy check Vaccinate cows when open preg check 1ate gestation Vaccinate calves branding preweaningweaning Goals Illness and death in calf crop Calf m ortality 50 e 50 within one day ofbinh 70 e 80 in rst 3 weeks ofpostnata11ife oma gt other problems Getting there Proper nutrition ofbrood cowsrep1acement eifer Disease prevention in cows and heifers Minimize calf death 1oss Use healthy ferti1e bulls Cull nonbreeding cows and heifers Breedheifers gt21 days earlierthan cow cohort Disease in periparturient period Hypoglycemiahypothermia Environmental contanination esp in damp crowded conditions FP P Infectious disease greatly in uenced by more ofthese factors Replacement heifers Smaller mean pelvic size at dystocia Differences in measurement Importance of calfbirth weight Feed to allow modest weight gain 0 5kgday Restricting feed does not reduce dystocia rates Third trimester weightioss Tdystocia Heifers bred at 15 months 5055 mature body weight Calve at 24 months Use buiis with low birth weightmoderate weaning or yearling rate EPDs 3122008 Target weight for puberty in heifers 23 mature weight Breed Weight Angus 65 0 lb Hereford 700 lb Charolais 75 0 lb Effect of condition on estrus Body condition score Percent cycling 4 62 5 88 6 98 Bulls Sire selection 7 Calvmg ease EPD expectedprogeny differences gt1518 months old Breeding soundness examination 7 Distinguishes satisfacto from unsatisfactmbulls 7 Observation forphysical proble s r Palpation chests and reproductive glands per rectum r observation ofpenisprepuce feet and leg conformation eyes and penocularpigment 7 Classification of sanen rrnmotiiity7MosT importantpropei ty 7 gt30 motile m rphologyr gt7 quotnnorrnal 7 Saotal circumference Scrotal Circumference All testicles produce same number of spermgm Bigger testicles rnore sperm cells SC predicts earlier puberty in daughters 15 718 month old bulls gt31 cm Adjust for age breed age of dam breed diet Diseases detected by BSE Small asymmetrical in amed or degenerate testes Absent or defective epididymis t er51stent Irenulum tied penisquot gt12 months Short deviated or corkscrew penis Penile hematoma 7 ruptured penis Seminal vesiculitis 7 common In WY and other range states trichomoniasis Common in bulls esp young bulls Ascending infection Various bacteria Pain or asymmetry Recovery unpredictable Control t energy diet Antibiotics for 2 Weeks Seminal vesiculitis 3122008 Bull soundness BSE 9t libido and mating ability It s down to you Feet and legs 7 check while walking Body condition 7too fat or too thin Ocular 7 that s how he nds the ladies Libido mating ability social dominance If he can t nd cows in heat and will not mate or is dominated by other bulls good BSE immaterial Bull cow ratio Allow for terrain Arti cial insemination More labor intensive Better disease control Trichomoniasis Campylobacteriosis vibrio Poor results when Poor nutritional development in replacement heifers Inadequate body condition of cows after calving Failure to identify cows in heat Failure to breed cows at proper time Campylobacteriosis in cattle Now RARE Venereal Bacterial Persists on penis and in female tract EED or abortion Sterili Effective killed Vaccines 7 e g Virbin Campylobacterfetux ssp venerealis Tritrichomonas Natural service bulls Venereal disease due to protozoan Recurring problem in WY esp in grazing assoc1atrons Reportable to WLSB Test bulls during BSE InPouch test 7 3 times is best PCR7 one time is adequate Early returns to service Vaccine 7 ineffective Cull bulls 3122008 Abomon ABORTION PROBLEMS 7 a beef state lt2 ls nurmal 7 Spunkneuus abumuns Tmuma genenc and slamtmn uncummun muses lrlmmmuurls7 rare punda uE pme lucuweed mtmtes m WY Muslunbkelylu gumr ughherd 7 oppunumsuemremlurls permgna wms Excepuuns 7 EVD 7 Tnnhumumasls 7 Campylubadenusls 7 eplusprmsrs 7 Nemurusrs rftr ifr 7 E RUCELLO Sls ABORTION PROBLEMS radalryrbeef state I Ne ospor051s 0 Wm am lo Rare In WY Prmnzul 2 rquot Most Important cause of abortion in dairy industry Protozoan Dogtransrmtte Vertical AND horizontal spread Nu diagnosis 40quot u Emerlsl 17quotquot No as mlnsis r211 leslnns mm 3quotquot Vaccmc 5050 1 Postnatal CNS disease presem 15quot u Brucellosis Leptospil39osis Underdragnosedv GYA Ellmlnated m US Feb 2008 Ba 5 31 abanus r lsease 9 5 7 Laptospmz bovgpatavsam semHaxdja sle hardwme ale term abomon storms 7 plow rmmganrsemarrlr smrmmrm Elk and blson m weslem WY In urlne oonoLlC Some reports ofhlghrates oflnfectlon m herds esp dalry Dlagnosls by serolo Avold by yaccmauon 7cmyenuonal ys Splrovacm Full speclrum dlsease remumto semce early embryonlc death abornonsullbrm weak calves Tesung at slaughter Zoono c USDAregulaLed 3122008 Pasteurellosis39 7 Systemic fever Underdiagnosed Recognized with febn39le viral diseases ers Dif cult to con rm e Nulesluns in fetus 7 Nu lesmns in placmta Ponderosa pine abortion Isocupresslc aeiol Associated With hard Winteis anol shelta seeking in undafed Catt e 3rd tnmes r 2714 olayspost ingestion nflrm Supplem tin 3rd trimester Keep outofslash piles Mummies ath Autolysis in absence of putrefactive baeten a Dned out Maybe dead formonths Minimal diagnosis value in cattle and sheep Vanous eauses Problems due to twins Can be 10 ofpregnancies Many early spontaneous abortions r Recugmzed as lt2 5 Complications 7 Death ufunetwm esp in unilateral pregiancles r Freemamns e Retained plaeentas r Ketusls e Dystueia In event of abortion storm Isolate cowheifer till you know what is going on Protect yourse Su mit etusplacenta if available Serum from cow rpossi le convalescent r llness in cows AIVS natural sa vlce r Otha illness in herd 3122008 Getting ready for calving Catvrng area 7 scraped and alluwed dry ever summ r ll 7 Leave Want 7 Distnfectifpmchcal Move pregnant eattie to eatvrng area 2 7 3 weeks pre7 eatvrn 7 Balance theneed fur guud ubsemuunwlth pnpntaunn dansitypathugen dansity 7 Guud orarnage th g calving dif culty Put parrs out rnto nursrng pasture wrunn 24 hours Calving facilities Best location small Welldrainedpasture Indoor facilities good for people but may be death forc V Dystocia Calving dif culty Most important cause of stillbirth Esp heifer cohort 15 COWS lt3 Strongly associated with subsequent calving morta 7 Deadnlt1znuurspust7parmrn x13 lllwpuw GNVAS Y4 Risk factors 7 Maternatretatrneernpaabrirmesp Thith weightand lpelvic size 7 Overweightde 7 Malpusitmnsmallinbeefcattle 7 Milk fever 7 Fetal malfur manun 11 W wat O Recording dystocia N0 assistance required Easy pull single person pulling Hard pull 2 people pulling Mechanical pull calfj ack Caesariansection Problems due to dystocia calf Traum a call Broken n39bs Internal trauma hemorrhage Swollen head and tongue Hypoxia Esp ifumbilicus compressed or torn Breach presentations Acidbase disturbance 3122008 Problems due to dystocia cow Traumacow Downer cow syndrome 1 ask ofmetritismastitis Tinfenility Metabolic diseases esp dairy 39lk fever Kctosis Abomasal displacement Normal calving 1 25 hours longer in heifers 7 Start oflabora dilated cervix and calf mth canal Waller sac 11 12 hours cows 24 hours heifers III Placenta delivered lt5 hours 2 r 6 hours Calf resuscitation Many stressed calves alert 15 730 mm 7 men crash 39 Position on stemum Removal oralnasalmucus M 7 Sums chemicals 3 g duxapram Dry oireaimoweis hair dryer Disinfectnavel Check for 7 Sleepy aspey urculd 31 2 yes 7 Variable heartrespiratury rates 7 Calves cuveredm mecumum 3122008 Fallure to mgest colostrum Insuf cient ingestion e o i e 7 Low quality 7 Poormo ering r Anatomical mata nal defects 7 eak e a s e Inadequate suckling re ex 7 Management Insuf cient absorption 7 Delayed ingestion r Interference with absorption What s in colostrum Immunoglobulin Lymphocytes VitaminsA D 1312 E x47 8 milk Calcium phosphorus magnesium x2 7 4 milk Copper iron zinc cobalt x5 20 milk Artificially feeding colostrum inimum 5 ofbody weight typically two quarts at each colostral feeding AtZ hours ofbinh Again within 12 hours ofbinh Feed via Nipple feeder Esophageal feeder Hypothermia Brown fat specialized adipose tissue highly vascular with 39 ochondn39al uncoupling protein Keep calf alive and warm for so hours Immersion in warm water 3122008 Navel ill Omphalophlebitis Omphalos Gr 7 center phlebitis 7 in ammation of veins Common bacterial contaminants 39 inurcauon 01 Hygiene iauure Peritonitis Avoid by navel dips keep calf dry colostrum Fetal Circulation Dumas Aneriasus Placenta I oxygeMcn alum Umbilical A EHes Retained fetal membranes Retained gt12 hours postpartum May indicate placentitismetritis In general do not removal manually Damage to uterus Administer antibiotics oxytocin May cut off exposed portion ofplacenta to reduce contamination 3122008 Uterine prolapse Associatedwith Di cultprolonged calving Retained placenta Hypocalcemia Stage 3 ealvmg 73 days postcalving Veterinary emergency May tear middle uterine arteries rbleed out Bacterial contamination Trauma to uterus Keep quite move to clean area r Remuve plaemlalf readllyranuved Epldural to replace Amputatwn may be req d Downer cattle Will be covered under dalry came Obturator paralysis Ketosis Trauma an e Ketosis Acetonernia hypoglycemia Thirl cows LOW carbohydrate low energy diet Stressed from 39 Cold weather Calving Nursing Ket051s recogmtlon and treatm ent Clinical signs 7 Inrcoordlnatlon bellow mg wallowlng and llcklng wlth ton ue e Presslng agalnst walls posts and trees 7 t appetlte and t mllk 7 Immedlate Lreatmmt Treatment 7 50 glucose solutlon W e Propylene glycol drench Control 7 nghpalamble mergyrdmseratlon 3122008 Grass Tetany hypomagnesemia wheat pasture poisoning Thin cows 7Grazing lush pasture high in nitrogen and potassium 7Stress from Cold weather Calving Nursing Tetany 7 recognition and treatment clinical signs 7 Nervous With pncked ears eldhigh staggers M emursespenally rae mrs 7 Aggresslv e staggering tossing head 7 Bellowmg and galloping Treatment magnesiumcalcium solutions Avoid supplement magnesium Acute coliform mastitis Grammegative bacteria 7 E coh Klebnella spp And Aembacter aamganar li Hluhmortalltl lfuntreated Esp dairy cattle7occurs in beefcattle Swollen quarterltsgt With 7 Depressmn 7 shark low temperature 7 Reduced ruminal eunaaeauns Treatwlth systemic and intra7mammary antibiotics Major killer of young postnatal calves Scours enteritis or typhlocoliu39s complicated by septicemia 7 Infected cows 7 contaminated ground 7 Maurampliiieatiun infected calves lsulate these calves 7 Death due to dehydrationsepticemia 7 Scour are caused by bacteria Viruses and protozoa in estlnes c and D mtavuus an uung Elves E coll Salmonella clormdlumpcyfrmgm a d eumnamrus sryptumundia Oldermlves eueudiuss 3122008 Purplegut 7 enterotoxemia Rlngworm derm atophytOSls Clostrldmm perfrmgzrls Lower intestinal tract Esp cowcalf operations in mountain regions cur as outbreaks Seen in calves as yo g as one week of age Acute abdominal pain circumscribed gray lesions 7 Kicking at abdomen Located on the face and neck straining S t No treatment as most found dead or terminal P0quot m0 5mm 39 t Calves separated and treated with antifungal Fungus infection Direct Contact to calves 2 0 Avoid vacclna e ackleg clostndial disease Clasmdlum chanvocr 39 Potent exotoxins Dormant in muscles Sudden death 7 o en better doing calves igns r Lameness and depression 7 suddEn death Gas gangrene 7 Feltunderthe skin as crackling sensatinn Bum dead calves 7way blackleg vaccine Vaccinate herd Tetanus Clustrldmm 2mm Lives in soil Introduced through wounds Muscle spasms induced by sounds or touch Tail stitf ears erect elevated 3m eyelid Ensure pasture free ofobjects cause puncture wounds Treatment penicillin in early stages 3122008 A reasonable vaccination schedule Prebreeding Four way respiratory LV BVD BRSV PI3 andIBR e Boost atpregiancy aiammation With killed product Leptospirosis Carnpy1obacter 7 or 8way clostridiai A reasonable vaccination schedule Precaiving E co1i rotavirus coronavirus 7 or 8way c1ostndia1 Branding repeat at preweaningweaning r wayc1ostndia1 4way res iratory Pasteurenartvianneheiniia Mistakes we see Lack of awareness of established disease BVD and tnchomoniasis My 7 ing on sale bam calves Fai1ure to make effective use ofpregnancy checking Wrecks due to use ofMLV in nonvaccinated pregnant catt1e Bottom line Minimize r Dystocia 7 39FPT Ensure bull soundnessrBSE Pregnancy check Vaccinate appropnate1y and at the right times Separate heiferreplacement from cow cohort for ca1vin Attend to hygiene preca1vingpostca1ving Genetic and congenital diseases D1seases annnd Ammals and Hmrses rPATB 4110 Congenital malformations in PEOPLE births Genetic Environmental Chrnmnsnmal 10715 Mata39nalmfectmns 273 Mendehan 210 Matemald1seases 678 Mulufactnnal 20725 Dmgandchemmal 1 lnad1aunn 1 Unknown 40 7 60 Diseases with genetic component human Insusz D escnbed mu G me lmvwn Described 1942 140 5 0 Gene mlmvwn Genetic diseases characterized at molecular level 7 domestic animals mm 40 16 14 30 Congenital defects in cattle ofunknown origin i t nsfosomus m exus Comnaed zmbm Umbilical hemu rmuluple genes 7mm camman defect in came Schismsamas re zxm e unknnwn headed envese unknnwn mcep yr Wm Absence af cerebelhxn e mlmvwn Chmmasamal ammahesrmanymlmwwn Estimated frequency of congenital disorders in cattle 110071500 ch mm 21 6 lAImn nu39wim meme Emma menwe 11 97 13 7 llEm m 100 noun Congenital defects Genetic 7 Must commonly hnmnlygmls recessive 7 Selecann by inadvertent linkage to a desired trait Milk pmnhchmand wuve39txmtlnErvwnSwlss Leancarcass npamnesaesssyn am Heavym sdmgdeYPPmpmgznyuflmpvesswe r Sums dmninant 7 Chrumusumal abnormaliaes canresultmresmpann early abnmnn nrmalfnrmatmn esp dwar sm Dr infertility ra k cabbage ronmental r Infecnuus BVD BTV Neaxpam 7 Te tngenic plants lupines and skun 7 Nutxmunal iodine and Vitamin A deiinency Suspect genetic defects when More than one born in season or several bom over multiple seasons Stereotyped appearance and outcome Common bloodline eg to halfsisters The problem Many congenital diseases ofanimals can be due to either genetic or environmental 7 war sm 7 Cerebral malformations 7 Many others Terminology Out breeding breeding unrelated or less related animals than average ofthe 0 ulation phenotype 7 physical appearance of individual based on genetic environmental in uences Genntype 7 genetic makeup ofindividual Congenital With bum present at birth Genetic Associated with genes 7 genetic diseases usually evident early in life but some manifest later GENETIC DISEASE CONGENITAL DISEASE Congenital nongenetic disease BVDV encephalopathy Goiter Luw iodine Dr iodine campeatnrs Congenital Viral infecann Inbreeding production of offspring from parents more closely related than the average of population Line breeding inbreeding in which inheritance of a specific ancestor is concentrated by father daughter or granddaughter matings r Herein Rock SpringsPop and sis did a 10 0mm breedin Types of Mendelean inheritance Autosomal recessive Autosomal dominant Xlinked recessive Xlinked dominant Autosome one of the numbered genes carrier non carrier L4 carriers 4 ffected 1 OUT OF A CHANCE 2 OLIT OF A CHANCE 1 OUT OF A CHANCE 25 50 2539 non carrier father 394 non carriers 4 l4 genetic carriers 4 2 OUT OFA CHANCE 2 OUT OF A CHANCE 50 50 Typical homozygous recessive pedigree Ancestral sire As Carrier dam Carrier sire Affected homozygote Some genetic diseases are expressed LATER in life CHAROLAIS ATAXIA HEMOCHROMASIS Salers Seriouslyinbred Charolais Onset at 2 36 mo Homozygous recessive Onset at l 4 2 years CNS disease Excessive upltlake of iron Liver iron epatic Atax1a to recumbency failure with bone Abnormal white matter disease Progression over 1 42 Hemochromatosis Illrmn luss ofineisors deatlr Breedsoeietyunliel ful P umpzratlve disease interest 0 Hemochromatosis in cattle and people Human Bovine 4th 7 5h decade 9 e 22 rnontlis ee R are cyszmyn Farnili Hepahc iron 11680 tig 1500 720000 tieg Tr fe n sat a gtos Cause ofdeatli cirrhosis Hepatic brosis F atio 71 PredominantlyF Jointlesions cliondroealeinosis No Bone lesions No Vetpitlnolzz 372 7321mm Homozygous recessive disease When earner bred to earner 25 elianeetliat uffspnng will av s When canlerbred to anunrczrnEr nu affeeted uffspnng But 50 ufuffspnng will be earners in tlieherd i may seem to skip generations Used to be tested by siredaiglrter Dr sireearner rnatang eif 32 and 16 normal offspring lt1 lEIEI chance lie is earner Dominant traits ON39E affeeted parent required to transmit 11 ratio ofnorrnalaffeeted offspring Canierx earn affeeted 1 nonnal in every generation If11 ratio rnales fernales autosornal dominant lfrnostly fernales sex linked dorninant EXAMPLE HYPP Polygenic traits Multiple genes involved Usually small effect per gene Genes x y z environmental effect disease Example Brisket disease Chrom osom a1 disorders Poorly characterizedin eattle and horses ue to e Transleeatien and deletauns ufparts ufehrurnusurnes ss eornrn u in people 11 of aborted and stillborn calves Types of chromosomal disorders Abnormal chromosome number aneuploidy Extra chromosome 7 trisomy Loss of one chromosome 7m0nosomy Congenital malformations in livestock and horses Breed societies vary in record keeping 7 Some have good genetic disease records available to members Expect AI animals to be tested for diseases of concern If a carrier is found family tree should be tested 7 Others secretive Difficult to investigate with many owners 7 Stigma 7 Economic effect on sale ofseed stock 7 Dif th to trace back sires and dams Horse industry progressive about investigating suspect genetic disease and underwriting genetic test development i N 93 Q99 If you think you have a deleterious genetic trait in herd or flock Blood or hair DNA type to confirm parents esp ifAI 7 eg UC Davis genetics laboratory or private laboratory determined by breed society Contact breed association to see ifrecord of defect in breed Submit typical affected animals for necropsy to characterize de ec Work with geneticist to generate pedigree Avoid andor cull affected blood lines If major problem work with breed association to develop genetic test to pick up carriers Genetic tests Probe for Probe for normal gene abnormal gene m 135Kb NN Nn nn NN NH m PCR ampli cation using allelespeci c oligonucleotides Hyperelastosis cutis in AQH Formal name HEDRA 7 Hereditary equine regional dermal axihenia 7 AQH Paints and Appaloosas I 1978 Homozygous recessive Poco Bueno sireline Damaged dorsal trunk skin 7hematomas seromas scars Horses 6 months 7 2 years old in sites oftrauma and wear 7 White hairs at sites of healed skin 7 Lifespan 2 7 4 years Genetic test available HRD vs HRDHRD Osteopetrosis Hyperkalemic periodic paralysis K Marblehnnedisease Prngenynflmpresswe BlackdeedAngus Uncnntrnll dmuscle twitching as Small premature calves espenallyn kshnuldersnbs s and anks Dead athlnla Failuretn resnrh hnne Nnufy breed assnciatinn Dwarf ism Multiple forms 7 Genetic 7 Growth retardation Proportionate vs short limbs Recessive vs dominan Each breed has its own Syndactyly 7 mule foot Porcine stress syndrome Selection for lean carcassefficient growth Relmively common Single founder 7 Pietran pig Holmm 39 Esp Landrace also Large White Duroc Angus In 1970s prevalence of70 90 in some Many cums European countries Autosomal recessive Minion SEmpork Associated with quotIquot 7 hypenhermia Genetic test Manage to reduce stress Overo lethal white syndrome Breeding paint horses overo x ovei Aganglionisispaia1yze Deana winiin 2 days co1ic Overo x Overo horses 50 overo foal 25 lethal white and 25 nonovero foal Overo x nonOvero 50 chance ofovero foal and no chance onemal white foal Genetic test available foi uaic Genetic test available AQHPaimsAppa1oosas Similarrunrelated ses Polysaccharide stomge myopalliy and tying up syndre 7 r diseas Cryptorchidism Testicles fail to descend to scrotum in last monai gestation Infertileifintemal Inheritedbm mechanismunclear Ifcastxated acts as arig Maybe seatofneoplasia Complex vertebral malformation of Holsteins New disease 7 1999 Genetic defect identi edtest develuped rl l Ongnally Scandinaviarnuw wurldwide USAScandlapan buutZKVobulls s Abumuns saiibinii perinatal deaui M s fusedvene ee ieo Hulstan Assn USAlists ufcamers and Hummers Scolimsmdwll smsxs meiiaedsci so menu Bulldog calves All breeds Common 7 in WY Homozygous recessive O en have cle palate and cardiac anomalies No gmedctest Abnormal giowui ofcartilage Spider lamb Suffulk breed 7 emerged midi ms 7 selectmn fur tall sheep7 e Mastbum alwewithskeletal defamnues 7 some nut Widens an 72 weeksposanoenire e Abmedmsullbmn Limbs dispmpumunately lung and defurmedr knucklmeed a omeiabnmmaliues scoliosis kyphosis Ruman nuse Genetictest avai BLAD Buvmz Leukocyte Adheszun De czemy Holsteins Recognized 1980 now largely elirninated omozygous recessive Inability ofWBCs to stick to blood vessels and kill pathogens due to integrin de ciency Common sires tract back to Osbmmialz Ivanhoe I Cam39er rate was 15 ofAI bulls and 8 ofcows Alfected rate was 6 ofall calves bom 1600020000 calves sickly calvese death due to susceptibility to infection Gme c lest available Parrot mouth Overbite Excessive length maxilla or Inherited but 39 m Care With feed Brain and spinal cord disorders I Multiple I Relatively common I Generally fatal 7 Cerebellar hypoplasia a O en concurrent ocular and spinal defects I Multiple genetic patterns Cardiac disease in calves Multiple cardiac defects Septal defects i Anomalies ofgreat vessels 2 Later onset cardiac disease 7 hypertrophic cardiomyopathy Freemartins NOT genetic Blood test Due to anastomoses of twins placental circulation Male hormones inhibit development of female reproductive tract chimera Detect by physical examination of cervix in female calves twin to male 92 of such females are sterile 7 200000 sets of twin calves born annually in US Also in sheep Polydactyly and syndactyly dactyly related to digits Excessive numbers of digits and ised digits COMM ON Holstein Angus Hereford Simmental among others Homozygous recessive for syns unclear for P01 May be dominant Dr sex Hypotrichosis hairlessness Multiple breeds including Angus and Hereford Cummun Usually recessive linked Can be linked tn anemia and anudunua Other causes BVDV Bn sket Heart failure secondary to pulmonary hypertension Common esp in Angus and gt6000 feet Incidence 05 r 20 Polygenlc inheritance Compoun e y exposure to locoweed Heart failure and diarrhea Test bulls for PAP lt35 mg Hg Affected calves 7 bring to lower altitude Summary genetic disease Considered small problem but in individual nerds affects reputation Have it CHA RIZED esp in intensive line breeding operations simple x identify sire by DNA testing and eliminate Serious for AIhigh dollar sires and breeds with narrow genetic base May be congenital r later onset Importance as animal models ofnuman disease GENETIC DISEASE CONGENITAL DISEASE 4232008 Diseases of Swine Shannon Swis t DViVl MS Gastrointestinal System Gastric ulceiation Causes of diarrhea in swine Gastric Ulceration contributinglactors 7 Feed smallteedparticlesizepeiienngteedsdierswnignieveis o unsaruraredtarsiowtioemgnenergvdiers 7 issuesxhaxieadmlneguiarfeedlng parrems 7 neumnnla pigswsevee smzuizerannnareEdZXmme ilkeivmhlgh iung disease quotgammamarleaatarrresuiarmamspatterns lntzvtwvzm misz in lzspbnszmmizmbnmz bu Wampum vztEDmvs mi pivlzlii tziis Msmmithmnuziszs Hct minim 7 srr ss inanspnnanon twemnwdlng Pigs otten ioqu dead extremeiv ale 7 Gross severegasmzuizerannnwhemnnhageampmeiena 7 Vlgs dietmm exsangulnannn 1255 M av vziziszs Gastric Ulceration Swine Diarrhea Facts Age atwhich pig attected wdiarrhea is an indicator of the cause Diagnosis can be made easier Vaccination hi 7 Have pigs been previously exposed to infectious agents insidious onset slow spread a gradual increase in severity over ime es Explosive onset of diarrhea is rapid spread 7 Usually associated wvirus 4232008 Signs of Diarrhea in Swine Signs associated wdisease of Smaii intestine itirig meiena puuriy digested feces buiky vuiuminuusfeces amp burburygrrius Biuudy fecesgrussmucusunfeces smaii frequent eerecatiun Stteriesrrius tayumiting Ba by Pig Diarrhea Nonrinfeclious contributing factors Effective environmentai temperature Luwer criticai temp tcrHemp beiuwwhich pig must u temp Unweaned 9W weaned 7w iizbiiity urrriiik Ava e Miik pravidesantihadies a energyta maintain hDWtemD Age and Cause Days after birth 172 days Ecoii hypogiycemia Cios tridium 577 days coccidia 1 week TGE rotavirus swine dysentery Saimoneiia Erysipeias 3 weeks May see E coii again associated wagaiactia Agzizctizrizck at ur puur miik arter birth Major Causes of Diarrhea in Swine Suckling iunweanedi Oostridium perrringenstype A Oostridium dif ciie Oostridium erfririgeristype c E coii Transmissibie gastroenteritis hem Roiavirus Coccidia Hypogiycerriia Emaciation amp Dehydration 4232008 Poord oe rs Abdominal Distention amp Pain Clostridium perfringens Type A amp C Low morbidity often biggest healthiest piglets affected High mortality l1ou al ofacule cases chronic infection higher sirvival Other s39gns paddling prostration rv0miling chronic formremacialion rough hair coat Diarrhea is watery yellow to bloody Spread of infection is slow often seen after addition ofnew pigs Clostridium difficile Morbidity 10790 Mortality upto 50 usually 20 Sudden death w no signs dyspnea mild abdominal distention St scrotal edema Diarrhea pasty yellow to walew Associated wantibiotic treatment at birth 4232008 Colibacillosis E coli Morbidity is variable entire litter affected but nearby iitters normai Mortality is variable Occurs anytime of year esp winterwcniiied pigiets is summer wagaiac a Dehydration pasty peritoneum tail may necrose Diarrnea yeiiowis wnite watery wgas a fetid odor Litters ofgi im often worse than those of sows often associated wpoor management dirty environmentamp su ooptimal temp Tra nsmissible Gastroenteritis TGE 39 Cause coronavirus 39 Morbidity ifenzootic 10750 mortality 010 Morbidity amp mortality ifepizootic 100 Vomiting dehydmtion Diarrhea yellowawhite watery distinct odor Epizooticasows sick quick spread to other pigs Associated with addition of new pigs large farms and continual farrowing operations Rotavirus Morbidity variable up to 75 low mortality 510 Gaunt rough hair coat e vomiting Diarrhea wate iy pasty wyeiiow curdalike aterial Coccidiosis Morbidity is variable up to 75 mortality low Infection peaks in August St September Gaunt rough hair coat low weight at weaning 39 Diarrhea Va riable Pasty to profuse watery yellowgray lat fetid or pigs w sneep peiiet feces Associated with solid floors 4232008 Major Causes of Diarrhea in Swine Nursery lweanedl Hemoiytic E coii Saimoneiia septicemia rnucohernorrhagic diarrhea Coccidia TGE Rotavirus Major Causes of Diarrhea in Swine GrowFinisher Lawsonia ereiated enteropathies Saimoneiia Swine dysentery whipworrns rT6E LawsoniaRelated Enteropathies CauseLawsoniaintracellularis rn it re ningmthemumsaaithesmaiiintegine mian Diarrhea may be bioody or not Morbidity 2074095 mortaiity variabie up to 70 esp hemorrhagic form Weig t oss anemia whernorrhagic form Antibiotics Vaccine Swine Dysentery Cause Brachvspira hyodysenteriae spirochete Acute to chronic contagiousinfection ofcolon Morbidity 90 mortality 30 Weight loss dehydration abdominal pain Diarrhea mucohem orrhagic Causes signi cant 55 loses associated wmortality decreased growth rate poor feed conversion amp treatment Antibiotics vaccinesineffeclive 4232008 Stre Eco Salt Central Nervous System ptococcus suis Ii Edema disease toxicosiswater deprivation Skin Foot and mouth disease 39 Par PDN Stap S ine dermatssis nephmpathy syndrome 5 hvlococcus hyicus Greasy pig disease wmepox Pityriasis msea 39 Para 39 Para rRi keratosis si e Mange ngwurm 4232008 Greasy Pig Disease Swine Pox Urinary system 39 Tu rkey egg kid ne quot PDNS bacteriai septicemiaisaimoneiia choieraesuis Erysipeiasi African swine fever and ciassicai swine fever Urate nephrosis Pigweedloxicosis Pamsile Stephanurus dentatus Urate Nephrosis Stephanurus dentatus Liver Parasites 7 Ascend izrvzi migratiun Stephanurus dentatusmigratiun tapewumi cysts Bacteriai septicemia e Szimuneiiz chuieraesuis Virai e Purcine circuvirusrl Pseudurabies Nutritionai e Hepztusisdietmiczmysutuxinsampfattyiiver Neopiastic e Lymphumz 4232008 Hepatosis dietetica Stephanurus dentatus migration Ca rd iova scula r System Mulberw heart disease Musculoskeletal amp Joint Disease Arthritis Monensin loxicosis White muscle disease Porcine stress syndrome Rickels Osteochondrosis Osteopetrosis Porcine Stress Syndrome Osteochondrosis W quot Osteopetrosis 4232008


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Why people love StudySoup

Jim McGreen Ohio University

"Knowing I can count on the Elite Notetaker in my class allows me to focus on what the professor is saying instead of just scribbling notes the whole time and falling behind."

Janice Dongeun University of Washington

"I used the money I made selling my notes & study guides to pay for spring break in Olympia, Washington...which was Sweet!"

Bentley McCaw University of Florida

"I was shooting for a perfect 4.0 GPA this semester. Having StudySoup as a study aid was critical to helping me achieve my goal...and I nailed it!"

Parker Thompson 500 Startups

"It's a great way for students to improve their educational experience and it seemed like a product that everybody wants, so all the people participating are winning."

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