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
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
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
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
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
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
7
Q
What are the various types of pig industry operations?
A
- Farrow to Finish
- Feeder Pig Producer (traditional/weaner)
- Feeder Pig Finisher/Contract Finishing
- Pure Bred Producer
- Breeding/geneti companies
- Specialty/Niche Market
- Show pigs
- Roasters
- Producer/Retailers
- Process Verified
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
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
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.
11
Q
What are the three reasons you can use antibiotics in your feed in the swine herd?
A
- Prevention
- Treatment
- Control
NOT for gain/feed efficiency
12
Q
What does the Veterinary Feed Directive state?
A
No extra label drug usage permitted
13
Q
How do you use antibiotics in the swine herd?
A
- Water tx (Prescription)
- to tx dz
- to prevent major outbreak
- water soluble
- palatable
- residues/compatibility
- cost effective
14
Q
What are your criteria for individual antibiotic treatment in pigs?
A
- Cost of drug vs. animal
- Withdrawal times
- Ease of administration
- Is animal marketable afterwards?
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:
- exclusion
- segregation
- dedication
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
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
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
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
20
Q
Describe rescue maneuvers for swine herd health
A
- Antibiotics
- water
- feed
- parenteral
- Antiserums
- Euthanasia
21
Q
What are common prevention practices in swine herd health?
A
- Sanitation
- Vaccination
- Antibiotics
- Management
- Genetics
- Biosecurity!!
22
Q
What are the goals of an animal health program?
A
- Prevention of morbidity and mortality
- Optimize utilization of facilities
- Optimize utilization of genetic potential
- Optimize utilization of nutrition
- Optimize ROI/ROE
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)
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
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
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
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
28
Q
What are your goals for swine herd health for prebreeding sows?
A
- vaccinations
- Parvo
- Lepto
- Erysipelas
- SIV
- PRRSV
- Herd immunity
- Biosecurity
- Parasites
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
30
Q
What is the equation for disease?
A
Disease = (Dose x virulence)/Resistance
31
Q
How do you diagnose enteric disease in swine?
A
- Case hx:
- morbidity
- age @ onset
- duration of signs
- body condition after cessation of diarrhea
- Clinical exam
- consistency, color, odor, volume
- pH - # of samples
- body temp - usually not helpful
- dehydration
- Necropsy and specimen selection
- untreated
- C/S <1d
- Several animals
- specimen collection
- diagnostic test choice: gross pathology, bacterial culture, virology, EM, serology, histopath, PCR
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
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
34
Q
What are your differentials for Colibacillosis?
A
- TGE
- Clostridial enteritis
- Coccidiosis
- Strongyloides
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
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
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
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
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
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
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
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
- oral ingestion –> infection –> proliferation of immature glandular epithelial cells –> elongation of the glands
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
- M. hyo
- PRRSV
- SIV
- Bacteria: P. multocida, Strep suis, H. parasuis
75
Q
How do you diagnose respiratory disease in swine?
A
- Hx: m/m, age/time of onset (movement), duration
- Clinical exam: temp, coughing, thumping, nasal/ocular d/c, facilities/stocking rates, ventilation
- 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)
