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3. Food Animal > Swine 2 > Flashcards

Swine 2 Flashcards

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1
Q

piglet birth weight

A

1.5kg

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2
Q

piglet wean weight and age

A
  • Wean: @ 16-28 days (~21 days)
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3
Q

piglet pre-weaning mortality

A
  • Pre-weaning mortality: <8-10%
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4
Q

Diarrhea due to various agents begins at a different time in the pig’s life

The age/timing of the earliest start of clinical signs helps to determine the causal agent

What are the common 5 causes of diarrhea in piglets, and when do they occur?

A
  • Escherichia coli (colibacillosis) (<12 hrs)
  • Clostridium perfringens (<12 hrs)
  • Swine enteric coronavirus diseases (SECD): PED and TGE virus (2 d)
  • Isospora suis (coccidiosis) (5 d)
  • Rotavirus (5 d)
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5
Q

is E. coli normally found in the pig GI tract? what two broad categories are there that must be distinguished?

A

E. coli are normal inhabitants of GIT, therefore pathogenic and non-pathogenic E. coli’s must be distinguished……

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6
Q

Pathogenic E. coli’s of swine:

A
  • ETEC: Enterotoxigenic E. coli
  • VTEC: Verotoxigenic E. coli (Edema disease)
  • SEPEC: Septicemic E. coli
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7
Q

ETEC – Clinical signs; Severity dependent on:

A
  • Virulence factors of E. coli strain
  • Age and genetics of piglet
  • Vaccination status of dam
  • Environmental factors (temperature, cleanliness, etc)
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8
Q

ETEC – Clinical signs? what portion of litter affected? is the appearance of the diarrhea notable? peractue form signs?

A
  • Single, multiple, or all pigs within the litter affected
  • Colour & appearance of feces is not pathognomonic
  • Diarrhea, dehydration, weakness, lethargy, death
  • Peracute form: death before onset of diarrhea
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9
Q

ETEC – Common clinical signs in newborns

A

Newborns with severe dehydration, watery diarrhea and high mortality

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10
Q

ETEC – Common clinical signs in older nursing pigs

A

Older nursing pigs (i.e., still on sow) with creamy, mild diarrhea
* Severity can vary within and between litters

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11
Q

what type of antibodies are very important for E. coli defence? therefore, what condition can cause problems?

A

Lactogenic antibodies very important- agalactia leads to E coli diarrhea

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12
Q

how many pigs of the litter are typically affected with E. coli diarrhea?

A

Typically, multiple pigs to entire litter is affected.

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13
Q

difference in diarrhea appearance for day-old pigs vs later with E. coli

A

In day-old pigs – feces may be clear. Later feces is colour of ingested feed.

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14
Q

ETEC - Pathogenesis

A
  • Adherence to small intestinal mucosa by means of fimbrial adhesins:
  • F4 (K88), F5 (K99), F6 (987P), F41
  • Colonization of jejunal/ileal mucosa
  • Production of 1 or more enterotoxins
    > Sta (ST1), STb (ST11) (heat-stable toxin)
    > LT (heat-labile toxin)
  • Secretory diarrhea (alkaline pH)
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15
Q

fimbrial adhesins of ETEC

A
  • F4 (K88), F5 (K99), F6 (987P), F41
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16
Q

enterotoxins of ETEC

A
  • Sta (ST1), STb (ST11) (heat-stable
    toxin)
  • LT (heat-labile toxin)
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17
Q

ETEC – Pathology (PM findings)

A
  • Usually unrewarding
  • Dehydration
  • Dilated, fluid filled small intestine
  • Congestion of SI vasculature
  • Dilated stomach, may contain undigested curd
  • Venous infarcts on greater curvature
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18
Q

ETEC – Diagnosis & Distinguishing features; on farm

A

1) History & epidemiology
* Age of earliest onset, gilt litters, severity, status of dams
2) Fecal pH (on farm)
* Secretory diarrhea – alkaline

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19
Q

ETEC – Diagnosis & Distinguishing features; at laboratory

A

3) Culture & sensitivity
* Gut loop (tied) or rectal swabs from affected pigs
4) Histopathology (fresh gut essential due to epithelial sloughing)
* Live piglets or place gut in formalin within 15 min
* Minimal villus atrophy
5) PCR: expression of fimbria & enterotoxin genes

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20
Q

Necropsy submissions for neonatal diarrhea

A
  • Piglets in acute stage - ill <24 hrs. (best if <12 hrs)
  • Not treated with oral or parenteral antimicrobials
  • Typical clinical signs
  • Live preferred (gut rapidly decomposes)
  • Minimum of 2-3 piglets (not littermates)
  • Provide detailed history (age, clinical signs, morbidity/mortality, etc)
21
Q

ETEC – Control & Prevention general considerations

A

1) Environment
* Prevent chilling

2) Sanitation & hygiene

3) Pig management
* Stop cross-fostering

4) Commercial killed bacterins

5) Autogenous bacterins (no toxoid)

6) Treatment of affected litters or piglets:
* Dehydration
* Antimicrobials
* NOT penicillin (not effective)***

22
Q

how should the environment be regulated for control and prevention of ETEC? why?

A
  • Prevent chilling (drafts, room & creep temperature)
  • Intestinal peristalsis greatly reduced if ambient temperature falls below 25oC, or piglets are chilled
23
Q

how should sanitation and hygeine be regulated for control and prevention of ETEC? why?

A
  • Farrowing crate (quality of wash, disinfection, dry time)
  • Instruments & equipment (fomites)
  • Personnel – handling affected piglets
24
Q

how should pig management be regulated for control and prevention of ETEC? why?

A
  • Stop cross-fostering between affected/unaffected litters
  • Reduce/avoid excessive number of gilts farrowing (immunity)
25
Q

what commercial killed bacterins should be used for control and prevention of ETEC? schedule?

A

Must offer protection against:
* Adhesins: F4, F5, F6, F41
* Toxoids: Sta, STb, LT

Schedule:
* Sows: 2 wks pre-farrowing
* Gilts: 5 & 2 wks pre-farrowing

26
Q

how should autogenous bacterins be used for control and prevention of ETEC? what are the diagnostic steps in autogenous vaccine prep?

A

Autogenous bacterins (no toxoid)
* Farm specific pathotypes – for farms that are usually negative for F4, F5, F6, F41

Diagnostic steps in autogenous vaccine preparation:
* Submit rectal swabs from 3-4 affected piglets (untreated)
* Submit E. coli isolated at diagnostic lab
* Test for virulence (PCR, serotype)
* Prepare autogenous bacterin

27
Q

what treatments should we give to litters or piglets affected with ETEC?

A

Dehydration - Electrolyte/dextrose solutions
* Syringe (individual), dish (litter)
* Warm
* Sparingly and frequently

Antimicrobials - Choice depends on
sensitivity, target piglets not sows:
* Parenteral (preferred):
> Ceftiofur, trimethoprim sulfa
* Oral (pump): Neomycin
* NOT penicillin (not effective)***

28
Q

what can help us determine the causal agent for diarrhea in the young pig?

A

The age/timing of the earliest start of clinical signs helps to determine the causal agent

29
Q

what diseases cause diarrhea in pigs at 2d old

A
  • Swine enteric coronavirus diseases (SECD): PED and TGE virus (2 d)
  • Porcine epidemic diarrhea & transmissible gastroenteritis
30
Q

Coronavirus: TGE & PED Virus; etiology

A
  • Coronaviridae
  • Enveloped, club-shaped surface projections,
    single stranded RNA
  • Heat labile (room temperature)
  • Very stable when frozen
  • Seasonal disease - highest in winter
31
Q

Acute SECD (TGE & PED) – Clinical signs in suckling piglets

A
  • Transient vomiting
  • Diarrhea: profuse watery, odoriferous, may contain milk curd
  • Rapid weight loss, severe dehydration
  • High mortality
  • Rapid spread
32
Q

Acute SECD (TGE & PED) – Clinical signs in all other ages except suckling piglets

A
  • Inappetance, agalactia (sows)
  • Mild diarrhea, sporadic vomiting
  • Mortality rare
  • Recovery in 1-2 days
33
Q

how much of a litter is generally affected by SECD? what will they look like, collectively and individually?

A
  • Whole litter affected
  • Piling (cold)
  • Thin (dehydrated)
  • Dirty (diarrhea on pigs)
  • Vomitus
  • Curds of milk
  • Pigs keep nursing until acutely ill
34
Q

if coronavirus is introduced to a new pig farm, what will we see (epidemiology)? incubation, transmission, who is affected, mortality, season.

A

Introduction into naïve farm (100% animals susceptible):
* Short incubation & rapid transmission throughout herd (2-
3 days)
* All ages clinically affected
* Mortality
> Near 100% in piglets less than 2-3 wks old (until maternal IgA response infers protection)
> Very low in older pigs
* Season: Generally, in winter/spring
> TGEv/PEDv preserved by freezing
> Inter-herd transmission by fomites, birds

35
Q

Endemic TGE (rare now) – Epidemiology; where it occurs, transmission, mortality

A
  • Occurs in positive farms that fail to eradicate or eliminate
  • Viral persistence in herd associated with ongoing infection
    of piglets weaned each week
  • Transmission from old to youngest nursery pigs coinciding with loss of maternal IgA (milk) at weaning
  • In older piglets low mortality, variable morbidity (varies with coinfections)
36
Q

swine Coronavirus: Pathogenesis - transmission, incubation, mechanism

A
  • Oral or nasal route
  • Virus is shed in feces in large amounts!!
  • Incubation period 2-3 days
  • Lysis and sloughing of cells and blunting of villi
  • Severe intestinal villous atrophy; malabsorption of nutrients
  • Nursing pigs die of acute dehydration
  • Older pigs tend to recover in one week but have low ADG
37
Q

main pathogenesis of swin ecoronavirus, and easy PM test

A
  • Severe villous atrophy
  • Thin walled SI
    > “HB test”
  • Malabsorptive diarrhea
38
Q

typical intestinal lesion of TGE/PED? how does this differ from ETEC?

A

Paper thin intestinal wall, typical of TGE/PED

(ETEC – comparatively thicker intestinal wall seen grossly)

39
Q

Coronavirus: Pathogenesis - why is it more severe in neonates

A
  • Enterocyte growth from base of crypt to tips of villi
  • Speed of regeneration varies with age:
    > Neonate ~ 3 weeks…..SLOW regrowth in piglets
    > Adult ~ 3 days
  • Villus atrophy more severe in neonates
40
Q

Diagnosis & distinguishing features for swine coronavirus; mortality, nature of the scours, fecal pH, methods and definitive methods

A
  • Near 100% mortality in young piglets
  • Persistent non-responsive post-weaning scours (possible
    endemic state)
  • Fecal pH: acidic
  • Histology: severe villous atrophy of distal SI
  • Fecal PCR
  • Definitive: IHC, PCR
  • Tissues: must have acute cases, with minimal epithelial sloughing
41
Q

Treatment & Control of swine coronaviruses; in endemic cases and outbreaks

A

TGE endemic (thankfully rare) infections:
§ Control secondary infections contributing to post-
wean diarrhea
§ Supportive care (no effective vaccine available – off
market many years ago)

Coronavirus Outbreaks:
* Eradicate the virus completely from the herd by “feeding the contents of intestines” of scouring piglets back to all pigs within the farm (feedback or intentional exposure)
* Creates protective herd immunity by eliminating susceptible animals from the population

42
Q

Steps in a PCED eradication program

A
  1. Purchase all breeding replacements
  2. Close herd (for 6 months)
  3. Harvest & feedback the intestinal contents from clinical piglets to all other healthy pigs (gestating sows) on the farm. Observe.
  4. Wash & disinfect entire barn
  5. After 6 months, then introduce sentinels (naïve animals – replacement gilts will be needed)
  6. Expose to feces from all ages
  7. Observe clinically for diarrhea
  8. After ~2-3 wks, measure serologic response in sentinel animals (seronegative if successful)
43
Q

sequelae of coronavirus on a breeding herd

A
  • Sows are ill and then all of their pigs die
    > Sows do not come back into estrus properly
  • Reduced reproductive productivity in sows
    > Reduced born alive, lose litter and longer wean to breed interval, reduced farrowing rate
  • Boars: experience high body temperature and illness
    > Low fertility
    > Producer should use AI or a combination of AI and natural breedings for six weeks following the outbreak
44
Q

where is PED found geographically

A
  • Porcine epidemic diarrhea virus (Coronavirus)
  • Present in EU, UK, Asia for decades
  • Recent introduction to USA in May 2013
  • First introduction to NA, now widespread in USA

> Emerged in Canada Jan 2014

45
Q

PED piglet mortality

A
  • 90-100% mortality in piglets < 2 weeks
46
Q

does TGE protect from PED? reportable?

A

n TGE does NOT protect against PEDV (and vv)
n Emerged in Canada Jan 2014
n Looks just like TGE – confirm diagnosis!
n Reportable disease under the Animal Health Act 2009

47
Q

what is PRCV and what are its origins? what is it similar to?

A
  • Evolved from TGE in mid-80’s (EU) thru genetic mutation
  • Changes tissue tropism from gut to lung
  • Antigenically similar to TGE
48
Q

does PRCV protect from TGE and PED? significance?

A

n Partially protects against TGE (masks clinical disease)
n DOES NOT protect against PED
n Reduced incidence of TGE worldwide

49
Q

when did delta coronavirus come to ontario? How does it compare to PED?

A
  • Also entered Ontario in winter of 2014
  • Causes similar clinical signs but a milder disease
  • Herds can be infected with PED and SDCV at the same time * Canadian herds are trying to eliminate both viruses

3. Food Animal (22 decks)

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