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3. Food Animal > Swine 10 > Flashcards

Swine 10 Flashcards

1
Q

Porcine Proliferative enteropathy (PPE) is caused by what pathogen

A
  • lawsonia intracellularis
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2
Q

Swine dysentery is caused by what pathogen

A

brachyspira hyodysenteriae

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3
Q

Pathogens associated with diarrhea in grower-finisher pigs

A

n Coronaviruses (TGE, PED, delta)
n Porcine circovirus
n Trichuris suis
n Lawsonia intracellularis (PPE)
n Brachyspira spp
n Salmonella spp

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4
Q

Porcine Proliferative Enteropathy (PPE):
Before a causative agent was identified, there was a confusing group of diseases classified by pathological lesions
> what are the diseases associated with the chronic manifestation ( in grower & finisher hogs):

A
  • PIA – Porcine Intestinal Adenomatosis (proliferative enteropathy)
  • NE - Necrotic Enteritis (coagulative necrosis of mucosa)
  • RI - Regional Ileitis (granulomatous inflammation, hypertrophy of muscle layers
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5
Q

Porcine Proliferative Enteropathy (PPE):
Before a causative agent was identified, there was a confusing group of diseases classified by pathological lesions
> what are the diseases associated with the Acute manifestation (in finisher hogs & adults):

A

PHE – Proliferative Hemorrhagic Enteropathy (severe GIT haemorrhage)

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6
Q

what does porcine intestinal adenomatosis look like on PM?

A

Porcine intestinal adenomatosis with no necrosis, only mucosal proliferative changes is seen involving mainly the ileum, with a thick-walled intestine (top) and a corrugated, hyperplastic appearance on the serosal surface visible (bottom right).

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7
Q

what happens if a pig lives long enough with necrotic enteritis? (visible on PM)

A

In necrotic enteritis, if the pig lives long enough, the necrotic membrane will slough off.

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8
Q

when does regional ileitis occur? what does its pathology look like?

A

Regional ileitis (hose pipe gut) occurs when the necrotic mucous membrane has sloughed away resulting in smooth muscle hypertrophy of the tunica muscularis, a natural response in a pig that survives the necrotic enteritis stage. It can be difficult to find the organisms in remnants of hyperplastic crypts in such cases. Most pigs have died by this stage.

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9
Q

characteristics of lawsonia intracellularis? what does it cause pathologically?

A

-Obligate intracellular bacterium
-Gram negative, non-spore forming, curved shaped rod
-Causes intestinal crypt epithelial cell proliferation

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10
Q

in what part of the intestine does lawsonia intracellularis generally live?

A

end of small intestine (ileum), beginning of spiral colon

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11
Q

pathogenesis of proliferative enteritis

A
  • Exposure to Lawsonia intracellularis begins in nursery (fecal- oral)
  • Incubation period: ~ 2-3 wks
  • Penetrates the dividing crypt cells
  • Infected cells:
    > Fail to mature and continue to divide
    > Result is hyperplastic crypts ->
    “adenomatosis”
    > Intestinal mucosa becomes: Thickened, inflamed, necrotic > Proliferative & necrotic lesions
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12
Q

is proliferative enteritis common? where geographically?

A

Infection is very prevalent and of worldwide significance

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13
Q

where does lawsonia live outside of pigs?

A

lives on rodents, carried on flies, boots

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14
Q

when L intracellularis infects grow-finish pigs, what do we see?

A

chronic disease:
PIA, NE, RI

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15
Q

when L intracellularis infects finish and gestation pigs, what do we see?

A

acute disease, PHE

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16
Q

clinical signs of chronic Lawsonia intracellularis infection? when is onset? how and when is it shed, and when is it common seasonally?

A

Onset:
- 6–20 weeks of age

  • Slow growth, lethargy, weight loss
    > Thin, razor backs, poor-doers
  • Diarrhea
    > Normal to greyish colour, homogenous in appearance

Subclinical disease common:
§ Poor feed intake to anorexia
§ Weight variation in the pen
§ Some loose stool
§ Economic loss is important

Fecal shedding:
§ in subclinical animals may begin as
early as 3 weeks of age
§ May shed for ~10 weeks post
recovery

§ Common when temperature fluctuates – spring and fall.

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17
Q

Rule-out for chronic form of Lawsonia intracellularis infection?

A

Porcine circovirus type 2

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18
Q

Lawsonia intracellularis Clinical Signs: Acute (PHE)? who does it affect?

A
  • Older finisher hogs (80+kg)
  • Gilts and boars – breeding herd (4-12 months old)
  • Acute to peracute death
  • Acute blood loss anemia (pale)
  • Anorexia
  • Dark tarry (melena) to bloody diarrhea

ACUTE
n Young adults
n Recently moved
n Black diarrhea
n Pale
n Sudden death

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19
Q

Rule-out for acute form of Lawsonia intracellularis infection?

A

n Bleeding out from gastric ulcer
n Hemorrhagic bowel syndrome
n Twisted gut (intestinal accident)

20
Q

Epidemiology: Acute (PHE); when does it occur? what can reduce incidence?

A

Sporadic, but sometimes predictable occurrence:
- E.g., introduction of naïve replacement gilts from high health source
- E.g., Removal of antibiotics from feed midway through G-F barn

-Vaccination has reduced incidence

21
Q

black tarry to hemorrhagic diarrhea from PHE is considered a:

A

– a medical emergency

22
Q

pathogenesis of acute PHE

A
  • Degeneration of epithelial cells, leakage of capillary bed
  • Acute haemorrhage with underlying chronic proliferative lesions
23
Q

Lawsonia intracellularis: Diagnosis of Ileitis (PIA & PHE)

A

Necropsy: examination of ileum
> Chronic: corrugated mucosa and/or “hose-pipe”
> Acute: presence of blood/melena

  • Histo: intracellular bacteria
    > Special stains: (silver, Ziehl-Nielsen stains)
  • PCR – feces (from clinically affected animals – but cannot rule out carrier status)
  • Culture – difficult (intracellular bacteria)
  • Serology: IFA
    > 90% sensitive (poor), 100% specific
24
Q

Lawsonia intracelluaris Treatment

A

Treatment with antimicrobials
- Parenteral for animals demonstrating clinical signs
- Water and feed grade products for herd treatment
> Many options- tetracyclines, macrolides, tiamulin
> Need to treat early
> Metaphylactic
> Medical emergency

25
Q

Lawsonia intracellularis prevention

A

Vaccination

26
Q

what vaccine options are available for Lawsonia intracellularis? when are they administered and what is the duration of activity?

A

-Enterisol Ileitis (oral)** (modified live)
> **No antimicrobials can be administered 3 days pre- and 3 days post-vaccination

-Porcilis Ileitis (IM injection)

-Both vaccines administered in nursery
-Long duration of activity (> 22 wks)

27
Q

Swine Dysentery (SD) and Spirochetal colitis; caused by what pathogen? what might farmers call it?

A

Brachyspira hyodysenteriae
- Formerly: Serpulina or Treponema hyodysenteriae

  • Farmers may refer to swine dysentery as bloody scours.
  • It was once called vibrionic dysentery

Other Bracyspira species can cause colitis For example: B. hampsonii, B. pilosicoli

28
Q

Brachyspira hyodysenteriae
characteristics? how to differentiate from other brachyspira?

A
  • Gram negative, oxygen-tolerant, anaerobic spirochete
  • Strongly beta-haemolytic on blood agar – one test used to differentiate from other Brachyspira sp.
29
Q

B. hyodysenteriae virulence

A
  • Hemolysins involved in virulence
  • Flagella and motility is also required for virulence
  • penetrates mucous to reach epithelial cells
30
Q

B. hyodysenteriae epidemiology; how severe is disease? what variants exist?

A

Traditionally a severe disease
n Recent emergence of mild and non-pathogenic variants

31
Q

B. hyodysenteriae affects what age group? how is it transmitted? incubation? environmental survival?

A
  • Pigs >8 weeks of age
  • Fecal-oral transmission
  • Extremely contagious:
    > low infective dose
  • Between farms via fomites
  • ‘Short’ incubation (strain dependent):
    > 5 - 21 days (usually 2-3 days)
  • Rapid spread
    -Long term survival in the environment
  • Can survive under wide range of environmental conditions & many reservoirs i.e. mice, rats, dogs, flies, birds, pigs
32
Q

B. hyodysenteriae morbidity and mortality

A

Morbidity high ~90%, mortality up to 30%

33
Q

B. hyodysenteriae environmental suvival and susceptibility

A

Long term survival in the environment
- Can survive under wide range of environmental conditions & many reservoirs i.e. mice, rats, dogs, flies, birds, pigs:
> Manure storage lagoons & pits – 60 d
> Mice–1yr
> Carriers – recovered pigs shed up to 90 days

  • Susceptible to heat, UV, desiccation, disinfectants
34
Q

B. hyodysenteriae Clinical Signs of acute onset

A
  • Mucohemorrhagic diarrhea
  • Copious mucus and flecks of blood
    > Usually within 2-3 days
    > As long at 21 days
  • May be profuse & watery
  • May contain frank blood
  • Mucofibrinous exudate

Other Clinical Signs:
n Partial anorexia and pyrexia (40-40.5C)
n Abdominal pain
n Weak, gaunt, incoordination, emaciation
n Death due to dehydration, acidosis, hyperkalemia
n Peracute to acute deaths without evidence of diarrhea reported but is uncommon
n If left untreated herds can have
> Morbidity >50%
> Mortality >50%
- Can result in stunted growth

35
Q

chronic vs acute swine dtsentery presentation

A

acute: bloody diarrhea
chronic: Thin, unthrifty finisher hog
> endemic herds may have mostly subclinical disease

36
Q

what part of the intestine does Brachyspira hyodysenteriae generally affect?

A

colon

37
Q

B. hyodysenteriae pathology:

A

n Caecum & colon only
n Fibrinous necrotizing haemorrhagic colitis & typhlitis
n Mucosa covered by mucus, fibrin, flecks of blood
n Mesentery and LI walls: edematous and hyperemic
n Thick fibrinonecrotic pseudomembrane if chronic

38
Q

acute swine dysentery PM lesions

A

Swine dysentery (SD) lesions are confined to the colon and cecum and in acute stages are hemorrhagic, fibrinous and necrotizing

39
Q

B. hyodysenteriae diagnosis

A

Distinguishing features:
- History – traditionally explosive outbreak bloody diarrhea in naïve herd
> May be variable due to feed antimicrobials, strain variation
- Diarrhea – mucofibrinohaemorrhagic
- Gross lesions – confined to caecum & colon
- Presence of hemolysis on blood culture
- Spirochetes on mucosa smears
- PCR is definitive and specific (tissue, feces)
- Culture – can have false negatives, need to use colonic scrapings from acute, untreated pigs.

40
Q

swine dysentery differential diagnosis; SD vs PPE ileitis for ilial lesions, colonic lesions, leocecal lymph nodes, extraintestinal lesions

A

Swine dysentery:
> Ileal lesion - Absent
> Colonic lesion - Superficial, diffuse necrosis, blood and/or mucus
> Ileocecal lymph nodes - Normal to slightly enlarged
> Extra- intestinal lesions - None except gastric fundic infarction in natural death

PPE ileitis:
> Ileal lesion - Hemorrhagic to necrotic to proliferative
> Colonic lesion - Milder than ileum, only spiral colon if severe
> Ileocecal lymph nodes - Variable with stage of disease
> Extra- intestinal lesions - None

41
Q

Spirochaetal colitis vs B. hyo disease

A

Spirochaetal colitis – Brachyspira pilosicoli or other Bracyspira
Virtually “the same” as B Hyo with the exception that the disease is much milder

42
Q

Other differentials for severe diarrhea GF pigs, aside from SD, PPE ileitis

A

whipworm, salmonellosis

43
Q

B. hyodysenteriae Treatment & Control; short term

A

Biosecurity and prevention is high priority
Short-term control in severe animals or farms:
n Parenteral antimicrobials for affected individual
n Mass medication of water (acute) or feed (strategic)
n Effective vaccines - unavailable

44
Q

B. hyodysenteriae; Treatment & Control;
Long term control & elimination:

A

n Eradicate
- Medicate [tiamulin] to eliminate clinical disease
- Empty, clean & disinfect pens
> Room by room in AIAO GF barn may be successful
> Rodent control must be excellent
> Prevent from contamination by effluent/pit manure

  • Off-site wean
    > Transmission prior to weaning does not seem to occur
  • +/- Depopulate – during warm weather
45
Q

“Spirochetal diarrhea” caused by? similar to? how do we differentiate and control?

A

n Brachyspira pilosicoli
n Considered similar to B. Hyo only milder
disease
> More likely to see in practice
n PCR to differentiate
n Control is same principles of sanitation,
husbandry
> Responds to same antimicrobials as B. hyo

3. Food Animal (22 decks)

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