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3. Food Animal > Swine 5 > Flashcards

Swine 5 Flashcards

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1
Q

Porcine Circovirus Associated Diseases
Includes:

A
  • Post-weaning Multi-systemic Wasting Syndrome (PMWS)
  • Porcine Dermatopathy and Nephropathy Syndrome

Porcine circovirus type 2 (PCV2)

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2
Q

PCVAD etiology; what circovirus types cause disease

A
  • Porcine circovirus type II (PCV2)
    – Isolates from 2a and 2b
    – PCV1 is non-pathogenic
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3
Q

PCVAD pathogenesis

A
  • Largely unknown – may occur after immune stimulation
  • Viremia (variable duration) replicates in lymphoid tissues
    – Immuno-suppression – reduction in lymphocytes, macrophages
    – Sets the pigs up for 2o diseases
  • Variation in lesions and clinical appearance
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4
Q

PCV2 - Epidemiology; what type of virus, environment, disease and clinical presentation considerations

A
  • Non-enveloped ssDNA virus - Ubiquitous
  • Potential rodent reservoirs
  • Hardy in environment and organic substrates
    – Stable, resistant to heat, cold & many disinfectants
  • PCV2 infection alone results in subclinical disease
  • Overt disease expression requires PCV2 infection plus co-factors that enhance PCV2 replication
  • PCV2 = necessary but insufficient agent in PCVAD
  • PVC3 emerging
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5
Q

Factors influencing expression of PCV2:

A
  • Known co-infections: – PRRS, MH, SIV, PPV
  • Unknown co-infections: – Agent “X”
  • Non-infective co-factors & inappropriate management
    – Lack of Good Production Practices (GPP) – Immune stimulation (i.e. vaccinations??)
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6
Q

(PCV2- Clinical Signs) - PMWS; when do we see signs / what age? what do mortality and morbidity look like?

A

Post-weaning multisystemic wasting syndrome (PMWS)

Clinical signs vary: not all signs are noted in the same pig, but most are evident on an affected farm over time:
- Can begin at 6-8 weeks of age (nursery phase)
* Can affect pigs as old as into grower phase (~20 weeks of age)
* Rare in nursing pigs

-Elevated mortality
– Often morbidity rate is low BUT high case fatality rate
– Severely affected herds: 70% morbidity, 50% mortality
* Poor growth, weight loss, wasting, emaciation – gradual wasting
* Anemia, pallor

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7
Q

PMWS (PCV2)- Clinical Signs for individual pig

A
  • Weight loss/emacitation*
  • Dyspnea, tachypnea
    – coughing
  • Enlarged lymph nodes*
  • Jaundice*
  • May include diarrhea (grow/finish)
  • +/- Enlarged spleen
  • May include neurological signs
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8
Q

PCVAD wasting - what is it and when does it usually develop?

A

PCVAD Wasting:
Wasting is usually noted in the late nursery or early grower barns (top). Severe weight loss (emaciation) develops in chronic PCVAD cases if animals are not euthanized

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9
Q

PCVAD lymphadenopathy; what LN are affected?

A

PCVAD Lymphadenopathy:
Enlarged LN are a prominent feature of PCVAD. Generally, all LN are affected. Superficial inguinal (top) and mesenteric
LN (bottom) are easy to find.

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10
Q

PCVAD Skin abnormalities:

A
  • Pallor is the most prominent skin lesion and is seen in many wasting pigs.
  • Jaundice is less frequently noted but is remarkable and terminal.
  • Cyanotic scabs initially seen over the rump and perineal area can be seen in PCVD affected herds (referred to as PDNS (usually from 8-18 weeks), but PDNS has not been experimentally reproduced by PCV2.
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11
Q

PMWS effect on internal organs

A
  • severe liver atrophy (end-stage liver) possible
  • enlarged kidney; chrnoic interstitial nephritis
  • splenic infarcts, splenomegalu
  • excessive fluid in gut resulting in profuse diarrhea
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12
Q

PDNS (PCV2) - Clinical Signs; when do they show up, what do we commonly expect

A

Porcine Dermatopathy & Nephropathy Syndrome
- Clinical Signs:
* 8- to 18-week old pigs
* Red to purple skin lesions on hind quarters, flank and perineum

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13
Q

PDNS (PCV2) - Clinical Signs; pathology

A
  • Kidneys are large, with white spots and/or hemorrhage in the parenchyma
  • Immune mediated vasculitis?
  • Pigs usually die of 2o infections
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14
Q

PCV2 - PDNS; treatment

A
  • Supportive * Euthanasia
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15
Q

PCV2 - PDNS; prevention

A
  • None, unclear
  • Review vaccine protocols
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16
Q

PCVAD - Diagnosis (IMPORTANT)

A

Clinical signs and gross pathology
* Emaciated, pale pigs
* +/- skin lesions
* large lymph nodes
* +/- enlarged and meaty spleen
* +/- icteric liver, +/-, mottled liver
* +/- spotted kidney, enlarged
* Cecum, colon: mottled, hyperemic, petechiated

PCR, RFLP, - typically positive – this virus is ubiquitous

**Must confirm through immuno-histochemistry (IHC)
- and histology showing large numbers of virus (PCV2) particles in the affected tissues
**Virus isolated in the affected organ

17
Q

PMWS/PCVAD Control

A

Control
- Commercial Vaccines
* 1 and 2 dose piglet vaccines
* Sow vaccines

Management
* Control other diseases
– Control PRRS
* Reduce secondary pathogen challenge
* Prophylactic antibiotics and vaccination for secondary infections

Implement Good Production Practices
* Less mixing of pigs
* Strict all-in-all-out movement
* Proper stocking density
* Adequate air & environment quality
* Sanitation

18
Q

Impact of PCV2 Vaccination? for piglets and sows:

A

Vaccination is extremely efficacious
- Many PCV2 vaccines available in Canada - all unique

  • Piglet vaccination (1 or 2 dose products):
    – Decreased mortality
    – Decreased viral load in serum (do not prevent viremia)
    – Increased ADG
    – Decreased growth variation
  • Sow vaccination
    – Same benefits as piglet vaccination, prolonged maternal antibodies
19
Q

Post-weaning E. Coli Diarrhea; what causes it? what virulence factors does the organism have?

A
  • Caused by Enterotoxigenic E. coli
    – Possess adhesion factors
    – Fimbrial type F4 (K88) is associated with most outbreaks
    – Four main enterotoxins
  • STa, STb, LT, and VT
20
Q

four main challenges for nursery pigs?

A
  • Stress of weaning
  • Declining immunity
  • Change in GI flora
  • Dietary change
21
Q

how does digestive enzyme activity change as a function of age for piglets?

A

-start with mostly lactase, very little amyalse
- lactase amount declines, while amylase increases
-amylase surpases lactase around 4 wks old, and trends continue

22
Q

clinical presentation of post-weaning E. coli

A
  • May occur sporadically
  • Sudden death (no previous signs)
  • Distended abdomens, sunken eyes & discoloured skin
  • Fluid-filled intestinal tract

Clinically affected pigs
* Pasty to watery diarrhea
* Depression
* Irritated perineum

23
Q

Post-weaning E. coli; diagnosis

A
  • History
    – Recently weaned
  • Clinical signs
  • Necropsy-fluid filled intestines & dehydration
  • Culture and serotyping
  • Histology-bacteriain intestines, vascular congestion & hemorrhage
24
Q

Post-weaning E. coli; feed treatments

A
  • Reduce quantity of substrates for E. coli proliferation
    – Poorly digested or absorbed carbohydrates may provide substrate for E coli proliferation. Excess protein – can act as a substrate for E coli growth
    > Hence, high quality ingredients used = $$$
  • Acidify gastrointestinal pH
    – Reduce excessive levels of calcium
    – Add acidifiers to feed or water (COMMON)
  • Add fibre to the diet
    – However, this reduces the growth rate
  • Medication
    – Zinc oxide can control diarrhea (1500-3000 ppm)
25
Q

Post-weaning E. coli; water treatment

A
  • Acidify water (citric acid) – Use water of pH 5-6
  • Large amounts of readily available water
  • Medication
    – Use results of culture & sensitivity
    – Problems with resistance
    – Apramycin in the water
    – Neomycin in the water /feed
26
Q

vaccination for post-weaning E. coli

A

Vaccines variable efficacy – typically do not work well

27
Q

Post-weaning E. coli; environmental management

A
  • Chilling reduces peristalsis & encourages E.coli proliferation
    – Maintain optimum room temperatures
  • Dirtier floor surfaces have higher prevalence
    – Hygiene important
    – Disinfectants are ineffective in presence of organic matter – clean with a detergent, disinfect and let dry
  • Clean water lines and water nipples with chlorine
28
Q

Edema Disease; what is the pathogen, what does it cause and to what host?

A
  • Verotoxigenic E.coli (VTEC)
  • Acute, fatal enterotoxemia of recently
    weaned pigs
29
Q

Edema Disease; VTEC strains and virulence factors

A
  • E.coli producing Shiga-like toxin (SLT-IIe)
  • Four pathogenic E.coli:
    – 0138:K81:NM
    – 0139:K12
    – 0141:K85a,c:H4
    – 0141:K85a,b:H4

NB: not the same strains that cause either neonatal colibacillosis or post weaning E coli diarrhea

30
Q

Edema Disease; is organism and disease widespread?

A

Organisms widespread but disease is rare

31
Q

at what age does edema disease usually strike? what pigs are typically affected?

A
  • 1-3 weeks after weaning
  • “Found dead” & “Best pigs” usually affected
32
Q

edema disease: what is the impact of nutrition and environmental temp?

A

Nutrition appear to be important
– Pigs with high feed intake - feed as substrate for E coli
– Or cold environmental temperature (slows GIT)

33
Q

edema disease: morbidity and mortality

A
  • Morbidity low, case mortality high
34
Q

how do other diseases impact edema disease?

A

Concurrent diseases add stress, make things worse

35
Q

Edema Disease; pathogenesis

A
  • E. coli colonize and proliferate in small intestine and release enterotoxins into circulation
  • Enterotoxins damage arteries causing edema
    – Shiga toxins (Stx2e)
  • May damage arteries in brain and meninges
    – Leads to increased vascular permeability and
    accumulation of edema at various sites
  • Notably the colon, stomach, small intestines, brain, eyelids
36
Q

Edema Disease; clinical signs

A
  • Unthriftiness in a high proportion of the pigs
  • Anorexia
  • Nervous signs – ataxia, recumbency, paddling
  • Edema - of eyelids, gastric submucosa & mesentery
  • “squeaky” squeal – laryngeal edema
  • Death within 24h
  • Course of ED in a herd is usually ~ 2 weeks
    – May re-appear in next batch
37
Q

Edema Disease; diagnosis

A
  • Clinical signs and evidence of edema at necropsy
  • Culture of small intestine (non-treated pig)
  • Genotyping to identify pilus type responsible for production of shiga-like toxin (Stx2e)
38
Q

Edema Disease; Differential diagnoses:

A
  • Strep suis, Hemophilus suis, others….
    – Water deprivation, organic arsenical poisoning, septicemia
39
Q

Edema Disease; control

A
  • Attention to details of husbandry and GPPs
    – Feed change, restricted feeding, minimize stresses (temp variations, drafts)
  • Antibiotics in feed or water – limited efficacy***
  • Autogenous and commercial (US) vaccines
  • May resolve spontaneously
  • Biosecurity
    – Most recent case (2015) in Ontario associated with purchase of Boar

3. Food Animal (22 decks)

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