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Prevention & Production Medicine > Swine P+P > Flashcards

Swine P+P Flashcards

1
Q

Define the following terms:

  • Gilt
  • Barrow
  • Sow
  • Boar
  • Weaner
  • Piglet
  • Shoat
  • Fat hog/finisher
  • Feeder pig
A
  • Gilt: female that has not farrowed
  • Barrow: castrated male
  • Sow: female that has farrowed (typically older)
  • Boar: intact male
  • Weaner: piglet that has been weaned
  • Piglet: suckling pigs, < 15lbs and <28d
  • Shoat: older than a weaner, but has been weaned
  • Fat hog/finisher: finishing wt and age
  • Feeder pig: around shoat age, around 50-80lbs
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2
Q

Define the following terms:

  • All In/All Out
  • Depop/Repop
  • PRDC
  • Farrow
  • Parity
  • Feedback
  • Biosecurity
A
  • All in/all out: everyone comes in and leaves at once, all pigs of same age, same level of dz susceptibility, deep cleaning of barn after
  • Depop/Repop: take the herd and depopulate/repopulate; sow farms - continuous cycle
  • PRDC: shipping fever - combo of resp dz
  • Farrow: parturition
  • Parity: # of times she’s already farrowed; avg P3-P6
  • Feedback: system utilized to perform oral inoculations on a farm
  • Biosecurity: cleanliness and sanitation, critical to minimize dz transmission
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3
Q

Define the following terms:

  • Non-productive Sow Day (NPSD)
  • PEDV
  • McREBEL
  • Batch farrowing
A
  • NPDS: day sow is neither gestating or lactating; should not be > 5-7d in b/t breeding days
  • PEDV: Porcine Epidemic Diarrheal Virus;
  • McREBEL: management changes that go along with biosecurity principles to prevent animals acquiring multiple diseases
  • Batch farrowing: spread out breeding, and thus farrowing; 3 wks most common - allows for piglets with same level of dz susceptibility
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4
Q

Define the following terms:

  • SEW
  • MEW
  • MMEW
  • 2 Site Production
  • 3 Site Production
  • Isowean
A
  • SEW: segregated early weaning, move piglets to a nursery to minimize vertical spread of dz
  • MEW: medical early weaning
  • MMEW: modified medical early weaning
  • 2 site prod: sows at one site, weaning pigs and older at another
  • 3 site prod: sows at one site, weaners at another, finishing pigs at another; minimizes dz spread b/t life stages
  • Isowean: brand of SEW
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5
Q

Define the following terms:

  • SPF “Specific Pathogen Free”
    • Primary SPF
    • Secondary SPF
A

Primary: C-section derived; mom has a dz so piglet removed surgically and raised somewhere else to prevent dz

Secondary: piglets from the primary SPF pigs

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6
Q

What is a farrow to finish operation?

A
  • sows farrow –> piglets move to nurseries –> conditioning areas –> move off the farm at finishing wt
  • great way of containing cycle of dz - have all ages on the farm and have continuous inventory
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7
Q

What are the various types of pig industry operations?

A
  1. Farrow to Finish
  2. Feeder Pig Producer (traditional/weaner)
  3. Feeder Pig Finisher/Contract Finishing
  4. Pure Bred Producer
  5. Breeding/geneti companies
  6. Specialty/Niche Market
    • Show pigs
    • Roasters
    • Producer/Retailers
    • Process Verified
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8
Q

What are the three maternal line pig breeds?

A
  • Yorkshire, Landrace, Chester White
    • all white
  • Features: long under lines and grow a little bit slower
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9
Q

What are the 5 colored/dark/terminal line breeds of pigs?

A
  • Duroc, Berkshire, Hampshire, Spot, Poland China
  • Features: produce semen meant for the maternal line to breed fast-growing market pigs
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10
Q

What are the various pig breeding systems?

A
  • Synthetic breeds - genetic companies
  • Terminal cross - use semen from one of our colored breeds to make that market breed
  • Maternal cross - producing sows for the maternal line, can make lesser quality males
  • Rotational cross (3 way/4 way) - maximize heterosis
  • Heterosis - the tendency of a crossbred individual to show qualities superior to those of both parents.
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11
Q

What are the three reasons you can use antibiotics in your feed in the swine herd?

A
  1. Prevention
  2. Treatment
  3. Control

NOT for gain/feed efficiency

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12
Q

What does the Veterinary Feed Directive state?

A

No extra label drug usage permitted

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13
Q

How do you use antibiotics in the swine herd?

A
  • Water tx (Prescription)
    1. to tx dz
    2. to prevent major outbreak
    • water soluble
    • palatable
    • residues/compatibility
    • cost effective
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14
Q

What are your criteria for individual antibiotic treatment in pigs?

A
  1. Cost of drug vs. animal
  2. Withdrawal times
  3. Ease of administration
  4. Is animal marketable afterwards?
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15
Q

List some general biosecurity and prevention practices

A
  • all in/all out
  • truck washes/bakes
  • shower in/shower out
  • Danish entry
  • filtration of barns
  • raising pigs indoors

Essentially boils to:

  1. exclusion
  2. segregation
  3. dedication
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16
Q

What are the acceptable methods of euthanasia for swine?

A

No conditions:

  • carbon dioxide
  • captive bolt (penetrating or non-penetrating)
  • anesthetic overdose

When conditions are met:

  • gunshot
  • electrocution
  • blunt force trauma
  • +/- followed by exsanguination
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17
Q

What are the various routes of administration for vaccines in pigs?

A
  • IM and SQ: most common, depends on needle length
  • IV - ear vein
  • IP - often in neonates, hang by back legs and inject between last two pairs of nipples
  • IN - anesthesia overdose
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18
Q

What are the benefits of all in/ all out productions?

A
  • increases feed efficiency and average daily give by 8-25%
  • decr death loss
  • incr use of facility
  • ease of management
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19
Q

What are the weights of pigs at various important landmark stages?

A
  • Birth: 3-3.5 lbs
  • Weaning: 21d - 12 lbs; 28d - 17 lbs
  • @ 8wks: 40 lbs
  • Market: 250-280 lbs
  • Age @ market wt: 6 mo - US avg 205d
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20
Q

Describe rescue maneuvers for swine herd health

A
  • Antibiotics
    • water
    • feed
    • parenteral
  • Antiserums
  • Euthanasia
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21
Q

What are common prevention practices in swine herd health?

A
  • Sanitation
  • Vaccination
  • Antibiotics
  • Management
  • Genetics
  • Biosecurity!!
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22
Q

What are the goals of an animal health program?

A
  1. Prevention of morbidity and mortality
  2. Optimize utilization of facilities
  3. Optimize utilization of genetic potential
  4. Optimize utilization of nutrition
  5. Optimize ROI/ROE
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23
Q

What are your goals for swine herd health for days 1-3 of life?

A
  • Iron (200mg) - pigs born on cusp of Fe deficiency
  • Warmth
  • Dry
  • Navel
  • +/- tail
  • +/- ear notch
  • +/- antibiotics/coccidiostats
  • +/- antiserums
  • castration (surgical)
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24
Q

What are your goals for swine herd health for day 7 of life?

A
  • Castrate (surgical) - if not done days 1-3
  • Gilt/boar selection
  • Underline screening
  • Vaccination?
    • Bordetella
    • Pastuerella
    • Erysipelas
    • Circovirus
  • Creep feed
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25
Q

What are your goals for swine herd health for days 14-28 of life?

A
  • Iron (repeat if necessary)
  • Vaccination
    • Mycoplasma
    • PRRS
    • Circovirus
    • Erysipelas
  • Parasite control
  • wean/split weaning
  • management/facilities considerations
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26
Q

What are your goals for swine herd health for the first 6-8 weeks of life?

A
  • vaccination
  • site specific factors
  • management factors
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27
Q

What are your goals for swine herd health for prebreeding gilts?

A
  • selection @ 180lbs (before? after?)
  • flush feeding
  • boar exposure
  • parasites
  • vaccinations
    • Parvo
    • Lepto
    • Erysipelas
  • Herd immunity/biosecurity issues/acclimatization
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28
Q

What are your goals for swine herd health for prebreeding sows?

A
  • vaccinations
    • Parvo
    • Lepto
    • Erysipelas
    • SIV
    • PRRSV
  • Herd immunity
  • Biosecurity
  • Parasites
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29
Q

What are your goals for swine herd health for prefarrowing gilts/sows?

A
  • colostrum management
  • vaccination
    • E. coli
    • TGE
    • Rotavirus
    • Mycoplasma
    • Clostridium perfringens
  • Two doses for gilts starting 4-6 wks prefarrowing
  • Booster sow/gilt 2 wks prefarrowing
  • Parasites
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30
Q

What is the equation for disease?

A

Disease = (Dose x virulence)/Resistance

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31
Q

How do you diagnose enteric disease in swine?

A
  1. Case hx:
    • morbidity
    • age @ onset
    • duration of signs
    • body condition after cessation of diarrhea
  2. Clinical exam
    • consistency, color, odor, volume
    • pH - # of samples
    • body temp - usually not helpful
    • dehydration
  3. Necropsy and specimen selection
    • untreated
    • C/S <1d
    • Several animals
    • specimen collection
    • diagnostic test choice: gross pathology, bacterial culture, virology, EM, serology, histopath, PCR
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32
Q

Describe Colibacillosis

A
  • aka: white scours, wet tail scours, ETEC
    • diarrhea and septicemia (usu < 4d)
  • incidence: everywhere
  • etiology: pili attach to enterocytes
    • enterotoxins - LT (labile toxins), STA (stable toxins), STB
  • pathogenesis:
    • E. coli attach –> toxin secretion of fluid into SI –> acidosis –> dehydration –> death
  • epidemiology:
    • up to 100% of litters - 100% morbidity/60-75% mortality
    • oral/fecal infection route
    • dirty environment; decr temp, decr colostrum
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33
Q

What are the clinical signs for colibacillosis, and how is it diagnosed and treated?

A
  • C/S: profuse watery diarrhea 12-24hr after birth or infection –> dehydration –> death
  • Dx:
    • hx
    • culture pillus antigen
    • PCR
    • histopath
    • response to tx
    • impression smear
    • mixed infections
    • pH - basic
  • Tx:
    • Antibiotics
    • Fluids
    • Probiotics
    • Antibody Preps - Monoclonal
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34
Q

What are your differentials for Colibacillosis?

A
  • TGE
  • Clostridial enteritis
  • Coccidiosis
  • Strongyloides
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35
Q

How do you control Colibacillosis?

A
  • vaccination
    • milk
    • killed bacterins - commecial/autogenous
    • subunit - pillus antigens
    • J-5 (core antigens)
  • genetics
  • management
    • temperature, drafts
    • clean environment
  • sow
  • AI/AO
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36
Q

Describe Transmissible Gastroenteritis

A
  • highly infectious viral dz
  • worldwide incidence, but incr problem in US
  • etiology: coronavirus (RNA) - 1 serotype
  • epidemiology:
    • epizootic: classical outbreaks in late fall, winter and spring
    • enzootic: year round
      • virus presents in feces in large quantities and may be excreted for up to 10 wks
      • spread by fecal/oral and fomites
      • airborne transmission - up to 1 mile
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37
Q

What are the clinical signs of TGE, and how is it diagnosed and treated?

A
  • C/S:
    • Epizootic: morbidity = 100%, mortality = 0-100%, profuse watery diarrhea, milk curds, vomiting, incubation 1-2d
    • Enzootic: signs variable but usally in weaned pigs; Morb 0-100%, Mort 0-10%
  • Dx:
    • necropsy- thin-walled SI
    • C/S
    • no response to tx
    • histopath
    • VI, EM, FAT
    • serology
    • pH acidic
  • Tx:
    • pray! (age dependent), fluids, abx, wean, incr temp - sow
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38
Q

Describe the pathogenesis of TGE

A
  • virus replication (lung, duodenum, jejunum, ileum)
  • villi damaged, malabsorption, diarrhea, dehydration, death/recovery
  • 7-10d recovery for enterocytes
  • viral excretion maximum 1-2d
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39
Q

How do you control TGE?

A
  • immunity
    • IgG in response to infection
    • Serum Ab fo 7 wks PI
    • Maternal Ab in piglets 6-12wks
  • epizootics - every 2 yrs
  • vaccination
    • oral, IM, IP, MLV/killed
  • feed back
  • quarantine, test
  • bird, animal control
  • biosecurity
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40
Q

Describe Porcine Epidemic Diarrhea Virus (PEDv)

A
  • incidence: found in China, Europe, and now US
  • Etiology: coronavirus
  • Morbidity: up to 100% (all age groups affected)
  • Mortality: 0-100%
  • Fecal-oral transmission
  • Pathogenesis: replicates in enterocytes in SI, destroys villi –> erosion/ulceration of enterocytes, fluid loss into the lumen, diarrhea
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41
Q

Describe the clinical signs of PEDv, and how you would diagnose and treat it?

A
  • C/S: profuse water diarrhea, less vomiting reported compared to TGE, all ages affected, suckling pigs - death 3-4d, growing/breeding, sows severe MMA
  • Dx:
    • necropsy - thin walled SI
    • PCR
    • direct electron microscopy
    • serology - ELISA
  • Tx:
    • prayer! (age dependent)
    • fluids
    • biosecurity
    • vaccination
    • feed back
    • quarantine, test
    • bird, animal control
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42
Q

Describe coccidiosis

A
  • incidence - worldwide
  • etiology - Isospora suis
  • epidemiology - sow not source, oocysts in piglet environment
  • pathogenesis: oocysts, sporozoites (24hrs), merozoites, secondary meronts (72-96hrs), large merozoites (type I), tertiary merozoites, merozoites (type II), oocysts remain infective for up to 10 mo
43
Q

What are the clinical signs of coccidiosis, and how to you diagnose and treat this?

A
  • C/S: must be 4.5-5d old!, usually very time specific, diarrhea –> watery to pasty, gaunt and rough hair coat, recovery slow –> stunted/runts, mortality/morbiditiy variable
  • Pathology: gross lesions - jejunum and ileum are thickened and turgid, diarrhea, histopath: villous atrophy, merozoites, micro/macro gametes SI
  • Dx:
    • age, C/S, no response to standard tx, fecal, impression smears, histopath
  • Tx:
    • amprolium, decoquinate, sulfas,antibiotics, ponazuril, toltrazuril, ALL ELDU
44
Q

How do you control coccidiosis?

A
  • hygiene
  • heat tx
  • quaternary ammonia compounds
  • chlorox (dosium hypochlorite bleach)
  • live stream
  • lime treatment pens
  • preventive drugs to baby pigs
45
Q

Describe Clostridial enteritis

A
  • necrotic, hemorrhagic enteritis in pigs <7d of age; chronic form may hit older piglets
  • incidence: common, but distribution variable
  • etiology: C. perfringens Type C
  • epidemiology:
    • geographical area, soil, wind, contaminated sows, building, crates, ingested, toxin, death, morbidity variable, mortality up to 100%
  • pathogenesis: adheres to intestinal epithelium in jejunum –> beta toxin –> villi damaged –> blood/death
46
Q

What are the clinical signs of Clostridial enteritis, and how do you diagnose and treat it?

A
  • C/S: peracute, acute, subacute, and chronic, death, bloody diarrhea, poor doers
  • Pathology:
    • Gross: SI hemorrhagic, swollen, gas bubbles in serosa, bloody lumen
    • Histo: large #s of bacteria, villous damage, diptheric membrane in subacute/chronic
  • Dx: hx, C/S, post mortem, impression smear, culture
  • Tx: antibiotics, antitoxin
47
Q

How do you control clostridial enteritis?

A
  • vaccination
  • antitoxin
  • hygiene
  • feed antibiotics to lactating sows
    • e.g. bacitracin
48
Q

Describe Rotavirus

A
  • porcine strain of rotavirus; diarrhea may be profuse and lead to significant mortality
  • incidence: probably endemic in all if not most swine herds
  • etiology: can get cross infection w/ other species, diff antigenic types, virus can be killed by ethanol, iodine, or bleach
  • epidemiology: very common, sow–> piglet at farrowing
  • pathogenesis: viral replication SI (jejunum to ileum), villous damage, malabsorption, diarrhea, lactogenic immunity
49
Q

What are the clinical signs of Rotavirus, and how is this diagnosed and treated?

A
  • C/S: 7-14d old piglets most common, incubation 18-24h, anorexia, lethargy, depression, vomiting, diarrhea, dehydration, death, regeneration of villus epithelium 7-10d (young), 3-4d older
  • Pathology: dehydration, emaciation, histopath: loss of villus tips and clumping of villi, peroxidase staining (neg. after 8d)
  • Dx: EM, serology, R/O
  • Tx: fluids, antibiotics, TLC
50
Q

How do you prevent Rotavirus?

A
  • vax - MLV/killed (serotypes)
    • piglets
    • sows
  • feed back
  • sow management
51
Q

What are management principles for disease prevention for weaned pigs (up to 40lbs/20kg)

A
  • Preferably no age separation
  • creep feeding of fresh, palatable feed freq from 10-14d of age
  • no feed change
  • provide feeder space sufficient for all pigs to eat together
  • feed ad libitum, intake severely restricted for 18-24h
  • water: provide nipple drinkers - 2/pen, good quality water + electrolytes
  • runts: delayed weaning, match for size
  • navel suckling: abnormal behavior assoc w/ early weaning
  • hygiene: clean up b/t groups, all in/all out
52
Q

Describe colibacillosis in weaned pigs

A
  • E. coli that causes post-weaning diarrhea (PWD) or edema dz (ED)
  • Incidence: PWD common; ED rare
  • Etiology: specific strains of E. coli cause either ED or PWD
  • Epidemiology: PWD d/t loss of lactogenic immunity @ weaning, pathogenicity and management determines severity of dz; 20-50% morbidity: < 10% mortality
53
Q

What are the clinical signs of colibacillosis in weaned pigs? How is it diagnosed and treated?

A
  • C/S:
    • PWD: diarrhea, wt loss, stunting, death - may have fever
  • Pathology: dehydration, congested liver, SI contains thin watery material, no villous damage
  • Dx: C/S or hx, culture of pathogenic E. coli
    • DDx: endemic TGE, rotavirus, swine dysentery, Salmonella
  • Tx: Feed or H2O meds, parenteral tx
54
Q

What is the pathogenesis of colibacillosis in weaned pigs?

A

loss of lactogenic immunity, high stomach pH (decr acidity), environ E. coli overgrowth, enterotoxins, secretory diarrhea

55
Q

How do you control colibacillosis in weaned pigs?

A
  • creed feeding?
  • vaccination? rota/E.coli/oral?
  • split feedings
  • acidified H2O
  • decr #s/pen
  • environ/feed pads
  • diet - complex
56
Q

Describe edema disease in weaned pigs

A
  • sudden death of “good doing” pigs, edema of gut, eyelids, nervous signs
  • incidence: low to variable - usually <10% affected - most die
  • etiology: specific strains of E. coli - usually pillous? verotoxigenic or shiga-like toxin
  • epidemiology: genetic; runs course in 7-10d (3d for a litter)
  • pathogenesis: oral exposure, stomach SI toxin (EDP) –> blood vessels damaged –> edema
57
Q

What are the clinical signs of edema disease in swine, and how do you diagnose and treat it?

A
  • C/S: within 10d of weaning; best pigs affected; dull, blind, head pressing, incoordination, recumbancy, convulsions/padding, death
    • Transient diarrhea, constipation, edema of forehead, eyelids, larynx, colon, no fever
  • Pathology: edema, esp stomach wall; thoracic cavity fluid, stomach full - SI/colon empty, histo: brain malacia/angiopathy
  • Dx: C/S, P.M., culture (O serotype - hemolytic), histopath, bioassay for EDP
  • Tx: antibiotics, decr cerebral edema
58
Q

How do you control edema disease in weaned pigs?

A
  • vaccination
  • management
  • genetics
  • acidification of H2O/feed
  • decr feed intake
59
Q

What are some other post-weaning diseases?

A
  • rotavirus
  • endemic TGE
60
Q

Describe salmonellosis

A
  • infection w/ any of the strains of Salmonella that result in septicemia, and acute or chronic enteritis
  • incidence: not Salmonella that people get, but incr feeder pig operations may have incr incidence
  • etiology: S. cholerasuis
    • S. typhimurium: may survive in meat/bone meal?, survive - drying/freezing, killed - heat, sunlight, phenols. I2, chlorine
  • epidemiology: primary dz of grow/finish pigs
    • Salmonella cholerasuis - pigs
    • S. typhimurium - other sources and pigs, shedding 4 mo, may be induced by stress
61
Q

What are the clinical signs of salmonellosis, and how is it diagnosed and treated?

A
  • C/S:
    • septicemic form: fever, restless, anorexia, cyanosis –> diarrhea (watery, feces “yellow”), M lo : M hi; incubation 24-48h
    • enteric form: fever, dehydration, decr body condition –> fast spreading diarrhea; M hi: M lo; recurring diarrhea w/ carriers
    • S. cholerasuis - pneumonia, septicemia
    • S. typhimurium - rectal strictures
  • Pathology: septicemic - skin discoloration, incr l.n., incr spleen
    • histo: focal necrosis, hyaline capillary thrombosis, “parathypoid nodule” in liver, pathognomic
    • enteric: focal of diffuse necrotic colitis/typhilitis, “button ulcers”, mesenteric l.n. incr, colon/cecum fluid filled
  • Dx: culture, C/S, hx, histo
  • Tx: early aggressive Abx
62
Q

What is the pathogenesis of Salmonella?

A
  • bacteria invade intestinal mucosa –> phagocytized by macrophages –> septicemic/enteric dz
63
Q

How do you control Salmonellosis?

A
  • isolate sick animals
  • single source pigs
  • decr stress
  • hygiene
  • avoid meat/bone meal?
  • prophylactic abx
  • vaccines - core antigen, ML, killed
  • medication (feed/water)
64
Q

Describe swine dysentery

A
  • Brachyspira (serpulina) Hyodysenteriae; previously Treponema hyodysenteria
  • mucohemorrhagic colitis characterized by decr performance, death loss, and bloody/mucous diarrhea
  • incidence: widespread; economic losses
  • etiology: brachyspira hyodysenteriae; anaerobic spirochete found in the colon
  • epidemiology: common in feeder pigs, affected may be of any size, oral/fecal route of transmission, carriers or infected pigs main source of transmission; M 100%/M 30%, cyclical on some farms, can shed for 70d PI
65
Q

What are the clinical signs of swine dysentery, and how is it diagnosed and treated?

A
  • C/S: incubation 2d up to 3 mo - usually 10-14d, diarrhea of varying intensity, occasional peracute death, pasty diarrhea w/ decr appetite –> mucoid diarrhea w/ blood, watery diarrhea w/ blood
  • Pathology: poor body condition; colitis (spiral colon) - flaccid, red, congestion, fluid contents, flood, necrotic matter and food particles; histo - lesions limited to mucosa - wet mount BEWARE!
  • Dx: C/S, hx, p.m., culture, FA, serology
  • Tx: antibiotic tx
66
Q

What is the pathogenesis of swine dysentery?

A
  • gains entrance to colon wall via goblet cells –> epithelial cells of the colon –> destruction of cells –> inflammation, histamine release, failure of fluid transport
67
Q

How does one control swine dysentery?

A
  • depopulation/repopulation
  • strategic abx tx
  • control animal movement
  • fomites
  • vaccines
68
Q

Describe Porcine Intestinal Adenomatosis Complex

A
  • aka: necroproliferative enteritis (NPE), regional ileitis (RI), ileitis, proliferative hemorrhagic enteropathy (PHE), garden hose gut, “necr” (Necrotic enteritis - NE)
  • complex syndrome displaying a variety of pathological changes; limited to small and large intestine
    • PIA - thickening of intestinal mucosa
    • NE - deep coagulative necrosis of adenomatous surface
    • RI - granulation tissue proliferation in lamina propria and submucosa of PIA w/ hypertrophy of mm
    • PHE - massive hemorrhage into lumen w/o visible bleeding points in the thickened proliferated mucosa
69
Q

What is the incidence, etiology, epidemiology and pathogenesis of PIA Complex?

A
  • Incidence: incr prevalence, high health herds
  • Etiology: Lawsonia intracellularis
  • Epidemiology: carriers; fecal/oral, 6-20 wks most common, but can affect all ages
  • Pathogenesis:
    • oral ingestion –> infection –> proliferation of immature glandular epithelial cells –> elongation of the glands
      • PHE: rupture of capillaries @ tips of villi
      • NE: necrosis of regressing mucosa
      • RI: cycles of proliferation and necrosis
70
Q

What is the pathology of PIA Complex, and how is it diagnosed, treated and controlled?

A
  • Pathology: us. ileum, occ. upper colon and cecum
    • NE: yellow masses of friable necrotic matter
    • RI: wall is smooth and rigid, lining ulcerated or granulation
    • PHE: SI distended w/ blood, no bleeding points noticeable, melena, anemia
    • Histo: silver staining, see organisms, proliferative enteritis
  • Dx: hx/clinical signs, PM/histopath, clean herd
  • Tx: antibiotics - parenteral, food, water
  • Control: feed meds, pulse tx, cost: benefit
71
Q

Describe gastric ulcers in swine

A
  • ulceration of the pars esophagus
  • incidence: 2-100% of animals @ slaughter
  • etiology: copper, stress, gastric acidity, whey feeding, corn starch, feed processing, fatty acids, Vit E, Se, finely ground feed, off feed, etc
72
Q

What are the clinical signs of gastric ulcers, and how are they diagnosed, treated, and controlled?

A
  • C/S:
    • Peracute: dead (hemorrhage/peritonitis) - sows, boars*, fast growing pigs
    • Chronic: melena, wt. loss, anemia, abd pain
  • Pathology:
    • Acute: blood in stomach, GI tract, or peritonitis
    • Chronic: craters
  • Dx: hx, C/S, melena, anemia, PM, endoscope
  • Tx: cost: benefit, cimetidine/ranitidine/omeprazole for indiv. high value pig
  • Control: check factors, min stressors, out of feed events, feed! - grind, pellets
73
Q

Describe Porcine Respiratory Disease Complex

A
  • resp dz of grow/finisher pigs
  • pneumonia in nursery thru finisher
  • multifactorial
    • infectious organisms
    • environmental factors
    • management factors
    • pig flow and comingling
  • 2-10% mortality; 20-80% mortality, poor growth, the “+18 week wall”
74
Q

What are the four main agents involved in PRDC?

A
  1. M. hyo
  2. PRRSV
  3. SIV
  4. Bacteria: P. multocida, Strep suis, H. parasuis
75
Q

How do you diagnose respiratory disease in swine?

A
  1. Hx: m/m, age/time of onset (movement), duration
  2. Clinical exam: temp, coughing, thumping, nasal/ocular d/c, facilities/stocking rates, ventilation
  3. Necropsy and specimen collection: all dead?, euthanize and post several untreated, gross, histo and IHC, C&S, virology, FAT, serology, PCR
76
Q

Describe Mycoplasma pneumonia

A
  • “enzootic pneumonia” - resp infection characterized by coughing, poor FCR, ADR and very low mortality
  • Incidence: common - up to 90% of herds
  • etiology: M. hyopneumoniae primary, occ M. hyorhinus
    • complex media for growth, survives in rain water for 17d, dies quickly (48h) on clothing/hair
  • epidemiology: carrier pig –> herd; airborne transmission possible, aerosol or direct contact usual transmission; sow –> pig or pig –> pig
77
Q

What are the clinical signs of Mycoplasma Pneumonia?

A
  • Chronic dz w/ high (90%) morbidity and low (<5%) mortality
  • 3-10 wk old pigs most common (10-16d incubation)
  • chronic, non-productive cough
  • rough hair coat, change in body condition
  • infection of SPF herds can lead to severe clinical signs w/ incr mortality
  • decr growth may/may not be related to % of lung dz
  • coughing - may be worst in a.m. or w/ exercise
78
Q

Describe the pathogenesis of Mycoplasma pneumonia

A
  • infection of cilia of URT (cilia clumped –> shed), probably due to a cytotoxin
  • mucociliary apparatus affected –> LRT (cranial ventral pattern)
  • lesions start red—> grayish/pink
  • secondary invader
79
Q

What are the pathological issues caused by mycoplasma pneumonia?

A
  • gross - consolidation of anterior/ventral lobes, in severe cases into diaphragmatic lobes
  • lower surface than surrounding “normal” lung, meaty consistency
  • catarrhal exudate
  • lymphadenomegaly
  • histopath - peribronchiolar lymphocytic hyperplasia
80
Q

How do you diagnose, treat and control mycoplasma pneumonia?

A
  • Dx: C/S, culture, serology, histopath, IF, laryngeal swab
  • Tx: antibiotic therapy
  • Control: AI/AO, SEW/MEW/MMEW, SPF, depop/repop, vaccination, old sows
81
Q

Describe the influenza A virus

A
  • resp tract infection w/ influenza A virus
    • H1N1, H3N2, H2N1
  • common in hog raising areas (slaughter/breeding pigs)
  • epidemiology: pig –> pig by aerosol, carrier pigs introduce into naive herds, fomites - man, migratory birds, airborne transmission, most outbreaks occur fall–> spring
  • pathogenesis: virus –> resp tract –> replication –> viremia –> fetus(?)
82
Q

What are the clinical signs of influenza A virus, and how is it diagnosed, treated and controlled?

A
  • C/S: explosive outbreaks of coughing (100% morbidity), fever, prostration, anorexia, dyspnea, conjunctivitis, coughing, sneezing, wt loss, resolve in 5-7d unless secondary dz
  • Pathology: purple-red pneumonic lesions, mucus and exudate in airways and congestion of the mucosa; histo - thickened alveolar sepate and bronchial epithelial changes
  • Dx: C/S, hx, serology, FAT/VI
  • Tx: antibiotics for secondary
  • Control: vaccines, ventilation, pig movement, bird control
83
Q

Describe actinobacillus pleuropneumoniae (APP)

A
  • aka Hemophilus
  • contagious resp dz of grow-finish pigs assoc w/ pleurisy, infarcts and variable mortality rates
  • incidence: widespread, serotyepes vary worldwide
  • etiology: dz caused by one of 12/13 serotypes of APP, requires NAD/nurse colony staph
  • epidemiology: fragile organism - nose to nose contact or direct aerosolization probably necessary for infection; carrier pigs (tonsils/lungs) responsible for transmission
84
Q

What are the clinical signs of actinobacillus pleuropneumoniae?

A
  • acute: incr temp, anorexia, dyspnea –> death (6h), bloody nose, cyanosis
  • subacute: same as above but milder and decr death; decr performance
  • chronic: same as above, decr performance, may affect all ages (nursing and sow), abortions, maternal Ab lasts 6-8wks
  • pathology: diaphragmatic lobes; infarcts, pleuritis, blood in airways/nose, interlobular edema; histo - infarct, alveolar hemorrhage
85
Q

How is actinobacillus pleuropneumoniae diagnosed, treated and controlled

A
  • Dx: c/s, culture, p.m. - pathognomic lesions?, serology, poor performance/incr # of problems, hx of new additions
  • Tx: parenteral abx, chronics - Pb tx, feed/H2O meds, tx early and often
  • Control: lower stress, ventilation, mixing, vaccinate, serotype, commercial/autogenous, adjuvant, cross protection, concurrent dz - PRV esp
86
Q

Describe Porcine Reproductive Respiratory Syndrome (PRRS)

A
  • dz syndrome characterized by reproductive disorders (late term abortions, premature farrowings, stillborns, mummies, and weak liveborn pigs), high piglet mortality, and resp dz in neonates to market pigs
  • etiology: Lelystad virus (togavirus) (arterivirus)
  • epidemiology: aerosol, pig to pig, semen
  • pathogenesis: infection –> viremia –> C/S; immunosuppression
87
Q

What are the clinical signs of PRRS, and how is it diagnosed, treated and controlled?

A
  • C/S:
    • acute: late term abortions, premature farrowings, stillborns, mummies, and weak liveborn pigs (epizootic)
    • chronic: resp. dz in nursery (endemic)
  • Pathology: piglets - NGL, pneumonic - interstitial pneumonia
  • Dx: C/S, hx, VI, serology
  • Tx: none
  • Control: match health profiles, acclimatize new animals well, control animals movement, semen, vax (killed/MLV)
88
Q

Describe Pasteurella multocida

A
  • etiology: pneumonia - 90% P. multocida Type A; 10% P. multocide Type D, serotype (A3)
  • epidemiology: tonsils/resp tract of healthy pigs –> aerosol/oral –> secondary to some primary dz (PRV, M. hyo, SIV) or some non-infectious agents
  • pathogenesis: immune suppression/decr mucociliary tract function; primarily secondary management, death d/t endotoxic shock
89
Q

What are the clinical signs of Pasteurella multocida, and how is it diagnosed, treated and controlled?

A
  • C/S: dyspnea, mouth breathing, abd breathing (thumping), exercise incr signs, fever early
  • Pathology: mycoplasma lesions, bronchopneumonia, consolidation, atelectasis, pleuritis, pericarditis; histo - bronchopneumonia/bacteria
  • Dx: C/S, culture
  • Tx: antibiotics
  • Control: vaccination, control other resp dz, environment, strategic meds, high health status herd
90
Q

Describe atrophic rhinitis

A
  • progressive atrophic rhinitis
  • incidence: typically seen where air quality is poor, overcrowding of pigs, can be seen w/ any group of pigs
  • etiology: coinfection of Bordetella bronchiseptica and toxigenic pasteurella multocide (type D)
  • epidemiology: spread by nose to nose contact w/ infected pigs
  • pathogenesis: toxigenic strains of pasteurella colonize following rhinitis induced by bordetella, chemical irritant or other; produces potent toxin that causes osteopathy and destruction of turbinates
91
Q

What are the clinical signs of atrophic rhinitis, and how is it diagnosed, treated, and controlled?

A
  • C/S:
    • mild/early - sneezing, mucopurulent nasal d/c
    • chronic - ocular d/c, shortened/deviated snout, epistaxis
  • Pathology: deformed, missing nasal turbinates
  • Dx: post mortem analysis of snout at level of first cheek tooth
  • Tx: individual tx unrewarding
  • Control: air quality, appropriate stocking densities, vaccines
92
Q

Describe Haemophilus parasuis (Glasser’s disease)

A
  • multisystem involvement w/ meningitis, polyarthritis, and polyserositis
  • etiology: H. parasuis
  • epidemiology: endemic on farm, stress –> outbreak
  • pathogenesis: aerosol transmission
93
Q

What are the clinical signs of H. parasuis, and how is it diagnosed, treated and controlled?

A
  • C/S: fever, anorexia, dyspnea, hunched appearance, lethargy, swollen joints, meningitis, death in 2-5d “acute death”
  • Pathology: polyserositis, pericarditis, pleuritis, peritonitis, orchitis
  • Dx: C/S, post mortem culture difficult
  • Tx: abx, indiv tx
  • Control: decr stress, vaccination
94
Q

Describe Strep suis

A
  • incidence: ubiquitous when raising pigs, subclinical carriers are open
  • epidemiology: transmitted via aerosol route, unlikely to be eliminated, high health pigs seem more susceptible
  • pathogenesis: colonizes the tonsil and is phagocytized by monocytes, travels in circulation and causes inflamm response where trapped
95
Q

What are the clinical signs of Strep suis, and how is it diagnosed, treated and controlled?

A
  • C/S: dyspnea, fever, anorexia, lethargy, hunched posture, CNS signs, death
  • Pathology: suppurative meningitis, meningeal edema, polyserositis, pneumonia
  • Dx: gross lesions on post mortem, culture of CSF/meningeal swab
  • Tx: aggressive abx tx, anti-inflammatory drugs
  • Control: vaccines, autogenous/commercial, minimize stress, prophylactic abx
96
Q

Describe actinobacillus suis

A
  • septicemia
  • epidemiology: healthy pigs carry the bacteria in tonsil and upper resp tract
  • pathogenesis: invasion of tonsil-spreading to bloodstream likely; believed to produce a toxin similar to APP
97
Q

What are the clinical signs of actinobacillus suis, and how is it diagnosed, treated and controlled?

A
  • C/S: sudden death, cyanotic extremities, dyspnea, cough, lameness, fever, weakness, wasting, CNS signs possible
  • Pathology: widespread petechial and ecchymotic hemorrhage, hemorrhagic/necrotizing pneumonia, serous/serofibrinous exudate in thoracic or abd cavity
  • Dx: hx, culture
  • Tx: antibiotics - but often too late
  • Control: vaccines, prophylactic antibiotics in feed/water
98
Q

Describe Erysipelas

A
  • infectious dz characterized by sudden death, skin lesions, arthritis, vegetative endocarditis, abortion
  • Erysipelothrix rhusiopathiae, gram + bacteria
  • Epidemiology: tonsils = 30-50% healthy pigs - shed in feces, urine, saliva, nasal secretions; carriers shed via feces
  • Pathogenesis: can enter via skin lesions or oral –> bacteremia
99
Q

What are the clinical signs of Erysipelas?

A
  • C/S:
    • hyperacute (peracute): depression, fever (high), cyanosis –> death
    • acute: high temp, dyspnea, cyanosis –> death (24-48h) (young pigs); anorexia, thirst, incr temp, skin lesions 24-48h, abortion (older pigs)
    • chronic: necrotic skin lesions, arthritis, endocarditis
  • Pathology:
    • Hyperacute: congestion/skin discoloration
    • Acute: skin discoloration, diamond skin lesions, splenomegaly
    • Chronic: necrotic skin, non-suppurative arthritis, endocarditis
100
Q

How do you diagnose, treat, and control Erysipelas?

A
  • Dx: culture, C/S, response to tx, *skin lesions
  • Tx: antibiotics, antiserum
  • Control: vaccines - maternal Ab 6-8wks, antibiotics, killed bacterins, 2x/yr
101
Q

Describe Postweaning Multisystemic Wasting Syndrome

A
  • congenital tremors
  • etiology: Porcine Circovirus Type II; DNA virus
  • epidemiology: oral, fecal, nasal
102
Q

What are the clinical signs of PMWS?

A
  • C/S: 5 wks +, wasting, dyspnea, enlarged l.m. primary symptoms
    • may also see diarrhea, palor, jaundice, epizootic: mortality to 40%, endemic: decr M/M
  • Pathology: poor BCS, enlarged l.n., pallor, icterus, mottled red/grey lungs, enlarged and waxy kidneys, white foci under renal capsule, fluid filled SI; histo: basophilic, cytoplasmic inclusion bodies in l.n., macrophages
103
Q

How do you diagnose, treat and control PMWS?

A
  • Dx: post mortems, C/S, virus isolation, histo/IHC, PCR, serology
  • Tx: none; supportive care, TLC
  • Control: vaccination for PCV II, biosecurity, isolation, acclimatization, stocking density, ventilation, mixing, mud and feces (all in/all out)

Prevention & Production Medicine (17 decks)

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