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Final

POPM4230 Final: POPM 4230; Final Exam Review Notes

26 Pages
122 Views
Fall 2015

Department
Population Medicine
Course Code
POPM 4230
Professor
Cathy Bauman
Study Guide
Final

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o$!!%C!D(7"*!*%!"!*&922*(
-6!*%#(
oE&"!&2"7"*!*%+"&""&!.&!")&
*#F*&+"&!7&*"GH(
-6!*
o"""+""*B!**
o*."&"&""&!.&2!)
o*"279""
-6!*$;"&)2"&91+*2"
*"5""2"""% * "2(
."!)6!2rhabovirus%,""**"+!(
-!!"9"#2&!*&
-6"5.!!)+"*")!79&+2!!)
-0";.!
o$!)!!"+"".$!"!&1&
o/""!)""+"&!+
-6!*
oI."!*&922*&+"+"*"
o!!";**".%(
o!";+"&+"&!..)%"(
I.+*"!++%,-(B$
-"B*".!&!!?
o6!""+!&!&
o6">#J12%.6J<(!2A")*I#!
-!!*""*"#K"
-6!*;**".2."&!1!")&9*
-".)
o""*".+!:"1"%=(
o0"!?+"..27+"=
o0)*7".!)"2"
.&*Toxoplasma gondii&+"
-!)."!13!1%+"1("2*!!!
-*;4#1+
-!#"""
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o6!"!%**(++"!
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-6"";!7"!"+"*"&2!"+"*"&#"!"+"*"
%  #3#+*"&*(
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-)2)!;""*
-L"$#"/"+
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o)!"2"*"2+""1
oM"9+"%.")(&9)!"2N"%=E(
o6."!+"!*!,!% * "*!(
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Description
POPM*4230 Animal Health Final Exam Study Notes Pre-Midterm Material Determinants of disease 1. Host factors - Immune status (innate, acquired, etc.) - Herd immunity, nutritional status - Age (physiological effect) - Genetic (phenotypic, genotype, simple) - Physiologic state (i.e. pregnant or lactating) - Production level 2. Agent factors - Virulence determinants - Pathogen challenge 3. Environment factors - Temperature, humidity - Stocking density - Stall design, bedding / flooring - Feeder design Foreign animal disease (FAD): disease that is predominately foreign to Canada (e.g. foot & mouth disease) Reportable animal diseases: economic, trade and/or food security importance for a # of countries, easily spread to other countries & reach epidemic proportions, requires cooperation between countries (e.g. rabies) - Notifiable diseases = communicable diseases identified by federal government for monitoring - All FADs to Canada are reportable animal diseases, but not all reportable animal diseases are FADs Governing agency = Canadian Food Inspection Agency (CFIA) regulates & oversee response to a FAD incursion in Canada, curates list of federally reportable diseases in Canada - Provincial agencies also have their own reportable disease lists as well, usually longer than federal list Reportable animal diseases & FADs are serious because of globalization, consumerism, and economics Foot-and-Mouth Disease (FMD) is the #1 reportable animal disease worldwide, FAD to Canada - Agent is the aphthovirus, highly contagious virus - Multi-species host = wild & domestic cloven-footed mammals (i.e. sheep, cattle, pigs, goats, deer); elephants, rodents, hedgehogs can be carriers o Very rare to infect humans & horses are resistant o Pigs are the most potent excretors of the airborne virus, considered multipliers o Cattle are the most susceptible to the airborne virus o Sheep can be asymptomatic carriers - Transmission  one of the most contagious animal diseases in the world o Direct (contact with infected animals), indirect (fomites, hay, vehicles), airborne (temperature & humidity dependent), humans & fomites - Clinical signs o Vesicular (blisters) eruptions in the mouth, hooves, udder o Acutely high fever, salivating, lameness, loss of appetite, decreased milk production o Many animals recover, but left weakened & debilitated (high morbidity rate) o Rarely fatal but humane euthanasia warranted - Prevention = biosecurity - animals (isolation of new animals, semen, feed, bedding, etc.) and humans (clean clothing & boots, stay off farm if travelled to FMD infected country) o Essential because FMD is very resistant to disinfectants, no treatment Pseudorabies – Aujeszky’s Disease is a FAD – reportable disease, viral disease of swine, agent is herpesvirus - Swine is the natural host, but there are dead-end hosts (die before they shed the virus) - Transmission o Horizontal transmission – pig-to-pig via oral & nasal secretions o Vertical transmission (trans-placental, milk, vaginal mucosa, semen) o Possibly airborne – farm-to-farm o Indirect – fomites - Clinical signs in the dead-end host (all livestock mammals, cats, dogs, raccoons, skunks) o Infected animals die within 1-2 days o Intense pruritus (“mad itch”) & neurological signs (circling, wobbly gait) - Clinical signs in neonatal pigs (age is a host factor) o Listless, anorexic, febrile & neurological signs (depression, tremors, convulsions, incoordination, dog-sitting, posture, coma & death, high mortality at ~100%) - Clinical signs in older pigs o Primarily respiratory signs – coughing o High fever, anorexia, tremors, convulsions, loss of body condition o High morbidity & low to moderate mortality - Clinical signs in sows = abortions, stillbirths, weak pigs if born Zoonotic disease: naturally transmissible from animals to humans or from humans to animals (e.g. rabies) Rabies is a fatal viral infection of CNS that is caused by rhabovirus (different strains geographically) - Occurs in all warm-blooded animals, including humans, is a reportable disease - Control: vaccination program in domestic animals & wild animals, public education - Transmission = via saliva of an infected animal o Infection occurs primarily via bite wounds or open cuts in mouth, skin, eyes o Virus remains at infection site for a short period, travels up nerves to brain & salivary glands - Clinical signs o Behaviour changes, wobbly gait, paralysis that progresses to death o Furious form = aggressive (usually seen in mammals) o Dumb form = depression, paralysis, excessive salivation (seen in ruminants) Bovine Spongiform Encephalopathy (BSE) – Mad Cow Disease is a reportable disease - Prion disease – damages nerve cells, mainly infects cattle o Can infect other ruminant species, cats, humans o Creutzfeldt-Jakob disease (vCJD) can be seen in humans after eating BSE-infected meat - Onset of clinical signs normally ranges from 4-5 years - Clinical signs = aggressive behaviour, lack of coordination, weight loss - Prevention o Human health is ensured through removal of specified risk material (SRM) o Transmission to cattle is prevented via the mammalian feed ban & disposal of all ruminant SRM o Testing & surveillance is almost entirely about trade Toxoplasmosis, agent is Toxoplasma gondii, a parasite - Human infection via undercooked/uncooked (pork) meat or by handling infected cat feces - Signs = flu-like symptoms - Fecal-oral route of transmission o Cats excrete oocysts (eggs) of toxoplasma parasite in feces o Pigs become infected by consuming oocysts, oocysts mature in muscle - Control measures = cat & rodent control programs, biosecurity programs, on-farm control programs (i.e. all-in/all-out pig farms, hygiene) Antimicrobial & antibiotic: kills / inhibits microbial growth yet results in minimal or no damage to host - Antimicrobial = natural, semi-synthetic or synthetic origin - Antibiotic = natural origin - Used in animals for growth promotion, disease prevention & disease treatment Antimicrobial resistance ≠ antimicrobial residue - Antimicrobial residue is a chemical hazard o Antimicrobial drug or metabolite is present in the meat or milk of an animal o Withdrawal period ( over time), done when antimicrobial < maximum residue limit (MRL) o Can have direct pharmacological effect on human (e.g. allergic) o Consumer perception & export / trade can be affected - Antimicrobial resistance (AMR) is a microbial hazard o Resistant bacteria / genes are isolated from meat or milk of an animal o Dissemination of resistant bacteria / genes continues beyond the residue withdrawal period o AMR = normally susceptible bacterium, grow in presence of antimicrobial(s) at levels which normally suppress growth / kill the bacterium o Bacteria can develop genes for resistance through mutation, or from other bacteria o Organisms resistant to one antimicrobial are typically resistant to multiple drugs  AMR in one area will eventually appear in other areas  Once AMR appears, it is unlikely to decline spontaneously o AMR reduces ability to effectively treat bacterial infections & transmission through food supply is a food safety concern  Economic implications, occupational health implications, human clinical issues (i.e. greater morbidity & mortality), Public Health Issue, public concern, etc. o Use antimicrobials only when needed, use right antimicrobial, use correct dosage Lecture 14, 15, 16, 17 & 18: Swine Health of Canadian pig herd is important due to the high amount of exporting ∴ have to maintain reputation All in / all out Continuous flow Room / barn filled all at once New pigs constantly Room / barn completely emptied Room / barn never & cleaned before new pigs enter completely empty Decreased disease spread More risk of disease - Quality assurance programs (Canadian Quality Assurance, Animal Care Assurance, Biosecurity Standards, Code of Practice) Marketing System = marketed at 110-125kg - Gestation length is ~115 days - Sows farrow in crates (no crushed piglets) - Piglets are weaned at 14 to 28 days old - Move into nursery at ~3 weeks old & 5kg, move out at ~10 weeks old & 25kg - In finishing production, housed in groups & remain here until they reach their market weight (~110kg) - Spend 100-120 days in finishing barn, pigs are ~6 months old when they reach market weight Biosecurity of pigs - New pigs arriving in a herd are most common source of disease ∴ buy pigs from 1 source with known health status & w/ good biosecurity & quarantine new boars/gilts for ~60 days (test for disease, etc.) - Disease can also enter a herd by semen from boar stud, trucks & equipment, contaminated feed, rats etc., people or via aerosol Suckling piglet production targets Parameter Target Birth weight 1.5kg Pre-weaning < 10% (farm level target) mortality Weaning age ~21 days of age (17-28 days of age) Weaning weight > 5kg Stillbirths - ~5% of all births - Last pigs in the litter to be born - Broken umbilical cord - Host issues for stillbirths: Fatter sows Age Larger litters Previous stillbirths Overheating PIGLET health – pre-weaning mortality - Target < 10%, major causes are management (crushing, chilling, starvation) or disease (diarrhea) - Prevention of crushing o Use farrowing crates, non-slip flooring under sow o Heat lamps to attract piglets away from sow (for warmth, light) o See more crushing in the summer because it is too hot for the sow - Prevention of chilling o Provide supplemental heat, creep area, mats in crates o Warm up cold piglets (dry them, warming box) because piglets are ~1.5kg at birth, no fat stores - Prevention of starvation o Make sure small / weak-born pigs are nursing o Split-suckle – remove large piglets for short period so small piglets can nurse o Cross-fostering to ensure enough teats for # of piglets (i.e. sick sow or sow not milking well)  Disadvantage of cross fostering is the sow could carry disease - Piglet processing o Iron administration prevents anemia o Clip needle teeth to prevent injury & disease (i.e. greasy pig disease) o Castrate males to prevent boar taint, dock tails to reduce tail-biting - Diarrhea: colibacillosis, transmissible gastroenteritis (TGE), porcine epidemic diarrhea (PED), coccidiosis Colibacillosis agent is E. coli, normal inhabitants of GIT ∴ pathogenic E. coli must be present (ETEC) - Pathogenesis = fecal-oral route o Attachment to & colonization of villi of SI, bacteria produces enterotoxins o Excess fluid secretion into lumen - Clinical signs o Watery to creamy diarrhea that can begin within hours of birth (< 12 hours of age) o Piglets become dehydrated & weak o More common in gilt litters o Morbidity & mortality rates can be high - Maximize lactogenic immunity by vaccinating sows prior to farrowing o Vaccinate gilts twice, sows once with a commercial (killed) vaccine o Reduce culling rate of sows - Minimize challenge by using all in / all out farrowing rooms, cleaning & disinfecting, perforated floors - Keep piglets warm (chilling reduces gut mobility, decreases suckling) - Minimize transmission Colibacillosis Environmental Agent Factors Host Factors Factors Dirty farrowing crates E. coli pili for attachment Piglet age Cold / drafts Produces endotoxin Genetics Careless workers Immune status Sow age / health Nursing ability Transmissible Gastroenteritis (TGE) virus - Agent is transmissible gastroenteritis virus (TGEv), a coronavirus - Heat labile (room temp.), stable when frozen, seasonal disease (highest incidence in winter months) - Pathogenesis = fecal-oral (or nasal) route o Severe villous atrophy in neonates, enterocyte growth from base of crypt to tips of villi o Speed of regeneration varies with age (neonates are slow ~3wks, adults are ~3 days) - Clinical signs o Vomiting & watery diarrhea o All ages of pigs affected (more severe in younger piglets) o High mortality in young piglets, see diarrhea start at 2 days of age o All piglets born over the next 6wks will die, rapid spread through herd - Expose all animals (feedback program, especially pregnant sows), institute strict biosecurity, close herd, clean & disinfect barn TGE Environmental Agent Factors Host Factors Factors Season – winter TGE virus Age – more severe in neonates Poor biosecurity Survives in cold environment Affects all ages Highly contagious Lactogenic immunity protects neonates Porcine Epidemic Diarrhea (PED) agent is porcine epidemic diarrhea virus, a coronavirus - Heat labile (room temp.), stable when frozen, seasonal disease (highest incidence in winter months) - Same clinical signs as TGE ∴ vomiting & watery diarrhea - All ages affected, see diarrhea starting at 2 days of age PED Environmental Agent Factors Host Factors Factors Season – winter PED virus Age – more severe in neonates Poor biosecurity Survives in cold environment Affects all ages Highly contagious Lactogenic immunity protects neonates Cystisospora suis (Coccidiosis) starts at 5 days but could be 1-3 weeks - Agent is a protozoal parasite – Cystisospora suis - Pathogenesis o Coccidia grow in enterocytes of SI, cause mild to moderate villous atrophy o Oocysts are resistant to disinfection o Predisposing factors are cement floors & late summer - Clinical signs o Mild creamy diarrhea, slow growth o Affects older piglets – at least 5 days old, but usually 1-3 weeks of age o High morbidity, but low mortality - Antibiotic treatment is ineffective, no vaccine, anti-parasite medication available - Long-term solution is to change flooring to perforated, raised floors Coccidial Diarrhea Environmental Agent Factors Host Factors Factors Dirty farrowing crates Parasite – Isospora suis Age of piglet (5 days, 1-3 weeks) Cement floors “Sticky” oocysts, resist disinfection Immunity NURSERY PIGS (weaners / weanling pigs) - Typically in nursery barn / room from 3 weeks until 10 weeks of age (∴ 7wks in nursery) - Target is minimum 5kg into nursery and 25kg out of nursery (ADG is ~0.4kg/day) - Feed to gain ratio is about 1.5:1 (very efficient) Weaning is a gradual process in nature, but is a sudden event in modern pig farming Liquid feed – milk containing Abs  Solid feed – grain-based, possible GI inflammation Stable social order  New penmates & possibly new pathogens Same environment from birth  New environment, need to find water & feed Nursery pig health - Stress of weaning - Declining immunity (Abs from colostrum begin to decrease, developing active immunity) - Change in GI flora (amylase activity increases, lactase activity decreases) & dietary change - Anorexia – some pigs may refuse to eat but are otherwise healthy - Other conditions seen in nursery pigs = ear hematomas, hernias, tail biting, ear necrosis & ear biting - Tail biting / chewing is a significant economic & welfare issue o Systemic abscessation & condemnation at slaughter o Noted in late nursery & older, highly variable incidence o Multifactorial triggers that are poorly understand (e.g. discomfort, boredom, gender, etc.) o Prevention: dock tails, provide and rotate toys & pen enrichments, eliminate stresses through good production practices (e.g. feeding & nutrition, satiety, pen density & overcrowding, temperature, tail length) - Umbilical hernias affect either gender, difficult to detect in early nursery o Risk factors are tension on umbilicus at birth (long wet cord) & umbilical abscessation o Baseball size in early grower, may be basketball size in finisher o Treatment options: market hogs early at ~75kgs or euthanize if large (cannot be transported) - Scrotal hernias are a common congenital defect, detect at castration, primarily males & unilateral o Enlarge & potentially strangulate SI o Treatment: surgery (remove testicle, replace SI, close ring), ship at light weight to BBQ pig market or euthanize - Common infectious diseases of nursery pigs = greasy pig disease, streptococcal meningitis, porcine circovirus associated diseases, post weaning E. coli diarrhea Greasy Pig Disease etiologic agent is Staphylococcus hyicus (common bacteria on skin) - General pathogenesis o Abrasion occurs (usually due to fighting, mixing of pigs or fighting during nursing) o Opportunist S. hyicus enters the body & produces a toxin, infection develops o Dark crusty lesions beginning on face, can spread over entire body o Lesions ooze a greasy substance - Prevention / control = clip needle teeth, reduce fighting (do not mix pigs), reduce humidity in barn - Treat with injectable & topical antibiotics Greasy Pig Disease Environmental Agent Factors Host Factors Factors Pigs with needle teeth S. hyicus secretes toxin Cuts & abrasions on skin High humidity Secondary infection Low immunity Mixing of pigs Virtually all pigs are carriers Streptococcal Meningitis etiologic agent is Streptococcus suis, a normal inhabitant of respiratory & genital tract, lives for a long time in the environment - Neurological disease, potential zoonotic disease (rare but often fatal in humans, entry via skin wounds) - Transmission o Sow-piglet via genital tract (parturition) or via respiratory & alimentary routes (lactation) o Pig-pig in nurseries & beyond o Onset of disease typically 5-10 weeks of age - Early clinical signs = head tilt, circling, trembling - Clinical signs = pig lying on side, paddling, ataxia, convulsions, found dead - Prevention = avoid overcrowding & frequent mixing of pigs, reduce stress - Treatment = isolate sick pigs, injectable antibiotics (early treatment) Streptococcal Meningitis Environmental Factors Agent Factors Host Factors Overcrowding & mixing Strep. suis bacteria Immunity – other diseases present Poor ventilation ZOONOSIS Porcine Circovirus Associated Disease (PCVAD) etiologic agent is porcine circovirus type 2 (PCV-2) - Clinical signs = weight loss / emaciation, enlarged lymph nodes, respiratory signs (coughing, rapid breathing), diarrhea, skin lesions (scabs) - Prevention / control – highly efficacious vaccine ∴ vaccinate (administer at weaning) PCVAD Environmental Agent Factors Host Factors Factors Mixing pigs Porcine circovirus type 2 (PCV- Other disease? Genetics? 2) Overcrowding, etc. Vaccination Post-weaning E. coli diarrhea (PWECD) - Clinical signs = watery diarrhea, red perineum - Some pigs may die suddenly before signs of diarrhea occur – purple discolouration of abdomen - Prevention o Warm & dry pens, all in / all out flow o Antibiotics? Acidifiers in feed / water? o Other feed additives such as very high levels of zinc oxide Post-weaning E. coli Diarrhea (PWECD) Environmental Agent Factors Host Factors Factors Poor sanitation E. coli Immunity Cold rooms Pili for attachment Age Feed Toxin production Genetics FINISHING PHASE - Housed in groups, remain here until reach market weight (~110kg) - Spend 100-120 days in finishing barn, pigs are ~6 months old when they reach market weight - Production goals o ADG = 800 gm per day (or better) o Feed to gain ratio = 3:1 or better o Mortality = < 2% Maturation of tissues occurs in the following order: nervous tissue, bone, muscle, fat - Genotype affects growth - Barrows grow faster than gilts, but are fatter while boars grow fastest & are the leanest - Low protein = slow growth, nutritional influences - Overcrowding & temperature can affect ADG - Among most economically significant diseases in pigs are subclinical infections causing  growth rates - Growth promotants (i.e. antimicrobial agents) can positively affect young pigs’ growth Feed efficiency is important because cost of feed is 60% or more of total cost of producing a market hog - Feed to gain ratio = total feed used / (live weight of pigs marketed – weight of feeder pigs entering) - Feed quality (composition, preparation, antimicrobial agents) affects feed efficiency - Restricted feeding improves efficiency - Feed conversion remains very efficient until hogs approach 100kg - Hot weather, disease, overcrowding, etc. result in slower growth & more feed for maintenance - Mortality (<2%) has a minor impact on herd feed efficiency if mortality is early in grow-finish stage o Respiratory disease is the most common & costly disease of finisher pigs o Gastrointestinal disease is also important Enzootic Pneumonia etiologic agent is Mycoplasma hyopneumoniae (MH) - Clinical signs include dry, hacking cough, reduced growth rate - Spreads slowly, rarely fatal  high morbidity, low mortality - Pigs are now more susceptible to other disease when they have enzootic pneumonia - Horizontal transmission by sow-to-piglet in crates or pig-to-pig in grower/finisher - Regional spread via aerosol (in moist, cool, wet weather) - Typical expression in grower pigs (> 12 weeks old) - MH colonizes trachea & bronchial epithelial cells, clumps cilia (impairs ciliary clearance) o Secretory & cellular debris gravitate from bronchi to alveoli (deeper into the lung) o Secondary invasion occurs in virtually all cases (mixed bacterial & viral infections) - Vaccination reduces prevalence & severity of disease, but does not prevent colonization or infection o Vaccinate pigs at weaning - Strategic medication with antibiotics prior to or during peak exposure, reduces infection pressure but do not eliminate MH infection (essential to control secondary bacterial infections) - Prevent by buying MH-free pigs, having good air quality, all in / all out flow, vaccinating in nursery & using antibiotics if necessary Enzootic Pneumonia Environmental Factors Agent Factors Host Factors Carrier pigs present Mycoplasma hyopneumoniae Vaccine status Mixing & overcrowding of Presence of infected pigs is source Other underlying diseases pigs Poor air quality Near other pig barns? Pleuropneumonia etiologic agent is Actinobacillus pleuropneumoniae (APP) - Acute disease outbreak: sudden death of pigs close to market weight, abdominal breathing, cyanosis - Chronic problem: poor growth rate, dyspnea, coughing, pleural adhesions at market - Treat by injecting antibiotics (be wary of withdrawal times) - Ensure good air quality, minimize mixing, do not crowd & avoid adding new pigs to barn - Prevent by avoiding introducing APP to naïve herd, use all in / all out & use antibiotics if necessary Pleuropneumonia Environmental Factors Agent Factors Host Factors Carrier pigs Actinobacillus Naïve herd pleuropneumoniae Mixing & overcrowding Good air quality Swine Influenza etiologic agent is influenza virus A - Textbook clinical signs = sudden outbreak, barking cough, higher fever, spreads rapidly & lasts ~1wk - In reality, clinical signs = influenza is present on many farms, cycles of reoccurring respiratory disease, often in combination with other pathogens - Control by vaccinating, control secondary diseases, all in / all out, not allowing humans with flu-like symptoms into barn Swine Influenza Environmental Factors Agent Factors Host Factors Present on many farms Influenza virus A Vaccinated? All in / all out Secondary diseases present? Porcine Reproductive & Respiratory Syndrome (PRRS) etiologic agent is the PRRS virus - In the sow herd, clinical signs include abortions & dramatic increase in pre-weaning mortality - In grower pigs, clinical signs are coughing, difficulty breathing, increased mortality & slower growth - Controlling PRRS in grower-finisher barns: o Management factors (especially all in / all out), environmental factors (e.g. control of temperature fluctuations, stresses), disease control (especially of MH), immunity PRRS Environmental Factors Agent Factors Host Factors Temperature PRRS virus Sow herd or grower pigs fluctuations Stresses (mixing, etc.) Control of other Immunity? diseases Ileitis is a gastrointestinal disease, etiologic agent is Lawsonia intracellularis - See poor growth, variation in pig size, sporadic diarrhea - May have sudden death with severe bloody diarrhea - Bacteria invade cells of intestine (intracellular) cause thickening of SI wall - Difficult to eliminate (some piglets likely infected by sow as young as 6 days old, mice carry it) - Prevent / control by sanitation (slatted floors, all in / all out flow), vaccinate via water (may be inconsistent in protection though) or feed medication (i.e. low levels of antibiotics improves growth) Ileitis Environmental Factors Agent Factors Host Factors Presence of carrier pigs Lawsonia intracellularis Vaccination status Continuous flow Mice as host Stresses Temperature Growth & inflammation in infected Feed antibiotics fluctuations cells Gastric ulcers are another gastrointestinal disease, exact cause(s) not completely understood - Anything that causes  fluidity of stomach contents allowing acid & bile from distal region to contact unprotected area around esophageal opening (pars esophagea), causes bleeding into stomach  death can occur from acute blood loss of due to perforation of the stomach - Clinical signs: o Might contribute to slow growth o Pale (reflects degree of blood loss), anemic, anorexic pig o Black tarry feces, abdominal pain, bruxism (teeth grinding) o May vomit & then eat again (healed, stenosis) o Found dead o Pneumonia, associated with removing feed before shipping Gastric Ulcers Environmental Factors Agent Factors Host Factors Particle size of feed Non-infectious Underlying diseases (especially respiratory disease) Pelleted feed Exact cause(s) not Anything that makes a pig go off-feed completely understood Disruption in feed delivery Periparturient sows, finisher pigs BREEDING HERD - Goal is to fill each farrowing spot with a sow that will produce a large litter with robust healthy piglets o Not to breed too many sows or too few o Not to have poor quality sows taking up farrowing spaces (i.e. small litters, poor mothers) - Need available gilts to replace older sows to maintain optimum parity distribution, gilt development program to achieve optimum fertility & longevity, short predictable weaning to breeding interval, good estrus detection & good breeding management, high farrowing rate & minimal embryo losses - Gilt development o Choose prolific breeds, use crossbred o Boar exposure to induce puberty (then avoid continual boar exposure) o Breed on second or third heat o Gilts stay in heat for shorter time than sows o Avoid  in feed intake, want a rising plane of nutrition - Parity distribution o Ideally would have all sows between 2-5 parities (i.e. litters), at least cull after 6 litters o Cull rate is 40-50% per year - Weaning to breeding interval – 4 or 5 days for most sows o Biggest problem is first parity o Sign of problem is second parity litter size drop o Major reasons for problems in WBI are disease & improper heat detection - Controlling boar exposure can be challenging (use robotic movers, leashes, panels) - Small litter size may be the result of genetics or quality of breeding o Gilts – bred on first heat, nutrition (flushing), quality & timing of breeding o Sows – 2 parity drop, short lactation length, old sows with drop in live borns - Farrowing rate - non-reproductive reasons for culling, regular / irregular returns, abortions - Breeding herd health o Reproductive problems  Management problem – chronic losses (> 3 months)  Disease problem – rapid change from good to poor production, reductions in multiple areas (increased stillbirths, decreased litter size, low pregnancy rate, etc.) o Reproductive targets  Farrowing rate  85% (# of sows that farrow / # sows bred)  Total born per litter ~12  Born alive per litter ~11  Stillborn pigs per litter  0.5  Mummified pigs < 1.5% Parvovirus causes embryonic & fetal death endemically worldwide, stable virus (~ impossible to eliminate) - Agent is porcine parvovirus (PPV), a ubiquitous virus, endemic infection in most herds - Clinical signs o Increase in # of sows returning to estrus post-breeding o Decrease in # of piglets born alive (some affected litters only have 2-3 live per litter) o Increase in # of mummified piglets (mummified fetuses are of different sizes) o Mainly gilt litters affected (less developed immunity) - Virus crosses placenta & travels along uterine horn, replicates in cells undergoing mitosis - Many killed vaccines available  administer prior to conception (before breeding) o Gilts – twice (5 & 2 weeks pre-breeding) o Sows – revaccinated 2 weeks pre-breeding o Boars – twice annually Parvovirus Environmental Factors Agent Factors Host Factors Contaminated Porcine parvovirus Immunity facilities Carrier pigs present Survive in environment for Gilts months, resistant to disinfectants Erysipelas agent is Erysipelothrix rhusiopathiae bacterium (resistant to drying but susceptible to disinfectants) - All age groups susceptible - Infected swine shed the bacteria & contribute to contaminating the environment - Systemic vasculitis – toxins circulate in bloodstream then become localized in skin, joints, heart - Clinical signs: o High fever, can cause abortion o Resist getting up – squeal because joints are painful o Purplish skin on snout, abdomen, ears o Diamond skin lesions – raised, red o Develop arthritis & vegetative endocarditis later - Potential zoonosis (causes erysipeloid skin lesions in rendering plant workers, vets, etc.) - Prevention / control o Vaccination – every weaning vaccinate o Quarantine incoming stock, cull animals with joint lesions, treat affected animals with antibiotics / water medication o Good sanitation & hygiene – reduce infection pressure Erysipelas Environmental Factors Agent Factors Host Factors Contaminated Erysipelothrix rhusiopathiae Immunity facilities Poor sanitation Survives well in environment Poor biosecurity Killed by disinfectants Carrier pigs present Produces toxin that damages blood vessels Porcine Reproductive & Respiratory Syndrome virus (PRRSv) is one of the most significant diseases in the swine industry today - Etiologic agent is the PRRS virus, from the genus Arteriveridae o Genus can cause asymptomatic persistent infections, can cause severe fatal disease, replicates in macrophages & exhibits considerable genetic mutation & recombination o Considerable strain variation & variation in virulence among strains nd o Antigenic drift within a herd, positive herds can become infected with a 2 strain o Approximately 80% of herds in Ontario are positive (not all positive herds have clinical signs) - Highly infectious – low minimum infectious dose - Persistent – prolonged carrier state (> 100 days), pigs viremic within 24h, shed virus for 60-90 days in feces, urine, semen & nasal secretions - Heterologous strains are not fully cross-protective (one strain does not protect against another) - Passed in urine, feces, blood, saliva & semen (needles can also transfer virus from one litter to another) - Pig-to-pig contact (especially if pigs fight) & farm-farm via pigs, semen, trucks, flies & mosquitoes - In the sow herd, clinical signs include abortions & dramatic increase in pre-weaning mortality o Anorexia, fever, sow mortality if virulent strain o 1 & 2 trimester – minimal impact o 3 trimester – transplacental infection (>72d gestation), reproductive failure & infertility  Abortions, premature farrowing (<110d)  Stillbirths, mummified; weak, liveborn piglets; neonatal diarrhea  Elevated pre-weaning mortality (25-50%) o Respiratory disease in congenitally infected suckling pigs (vertical transmission), nursery & grower pigs (horizontal transmission)  Dyspnea, cyanosis of extremities  Minimal coughing in pure PRRS pneumonia (more common following secondary bacterial invasion)  Immunosuppressive (virus results in mixed infections, important when trying to control enzootic pneumonia) - In late gestation, crosses placenta (>72d), causing fetal death due to vasculitis of umbilical vessels o Vasculitis in neonates  periorbital edema, persistently infected - Treatment of affected animals o Supportive – anti-inflammatories (aspirin) o Prevent secondary infections, strategic medication as required - Controlling PRRS in breeding herd: o Mass exposure via vaccination, serum inoculation (vaccine can revert to virulence though) o Depopulation – clean, disinfect & dry all barns (twice), repopulate with negative stock o Herd closure to incoming breeding stock for 6-12 months PRRS Environmental Factors Agent Factors Host Factors Poor biosecurity PRRS virus Sow herd or grower pigs Season Mutates rapidly – many Immunity? strains Proximity to other herds Lecture 19 & 20: Poultry Broiler chickens & turkeys are raised for meat, are heavy-boned, large body, genetically selected for fast growth & high breast meat yield Layer chickens produce table eggs, are lightweight & genetically selected for high egg production Breeders produce hatching (i.e. fertilized) eggs for the next generation of broilers, layers or turkeys BROILER BREEDERS - Begin laying at ~26wks of age, average hatchability is 82.8% - Hens & roosters are housed at a ratio of ~10 hens to 1 rooster & mating is natural - Total incubation time is 21 days - Setter – 1 stage of incubation (day 1 – 18), must pay attention to temperature, humidity, turning o On day 18 of incubation, eggs are transferred from the setter to the hatcher o In ovo vaccination for Marek’s disease occurs at this time nd - Hatcher – 2 stage of incubation (day 18 – 21), humidity is increased - At one day of age, chicks are processed o Health che
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