Swine 11 Flashcards

1
Q

most common cause of diarrhea in swine???

A

Salmonellosis

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2
Q

types of salmonellosis in swine and what causes them? hosts?

A

-Enteric form caused by S.Typhimurium
> Can infect other livestock, poultry, mice, and people
> Pigs are considered most likely source of S. Typhimurium DT104 in people

-Systemic form caused by S. Cholerasuis
> Host-adapted** i.e., considered restricted to swine
> Rare reports in humans out of Asia (**zoonotic potential)
> Can live in mice

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3
Q

salmonella seotype diversity? general characteristics? toxins? how to inactivate?

A

n >2000 Salmonella serotypes
n Salmonella are notoriously diverse
n Hardy, small, ubiquitous, gram-negative bacilli
n Contain ENDOTOXIN
n Inactivated by iodine and phenol-based disinfectants

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4
Q

where in the host in salmonella generally found? how does it spread? are there always clinical signs? when do we usually see a clinical outbreak?

A
  • Salmonella in gastrointestinal tracts (of many hosts)
  • Spreads via fecal-oral route
  • New infections in pig herds
    > Usually, fecal contaminated feed or water
    > Pigs may act as asymptomatic carriers = source of infection especially if comingling pigs or new introductions into herd
  • Farm may be positive with no clinical signs of disease
  • Clinical outbreak typically follows a stressful event
    > Shipping, mixing, overcrowding, concurrent disease
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5
Q

S. Typhimurium causes:

A

enterocolitis

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6
Q

Enterocolitis form of salmonella:
how it spreads? who it affects? prevalence?

A
  • Fecal-oral route
  • Typically pigs in nursery to mid-grower
    > ~50% herd prevalence in Ontario
    > ~2% recognize as a problem
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7
Q

S. Typhimurium: pathogenesis

A
  • Endotoxin results in mucosal GIT damage and endothelial necrosis
    > Vasculitis, microvascular thrombosis
  • Diarrhea attributed to tissue fluids leaking from damaged mucosa. Malabsorption diarrhea
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8
Q

S. Typhimurium – Clinical signs? sequelae?

A

Enterocolitis form of salmonella:
- Moderate pyrexia, anorexia and dehydration
- Typically, a yellow-coloured diarrhea due to fluids leaking through the damaged mucosa
> As progresses more mucus, fibrin, and blood in feces. But blood is not a primary feature
- Morbidity high (over time) and mortality low
- May cause emaciation and slow growth
- Sequelae: rectal stricture …….rectal prolapse

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9
Q

S. Typhimurium – public health concerns

A

Public heath issue:
- Concern due to pigs shedding in abattoir DT104
- Multi-drug resistant strains

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10
Q

S. Typhimurium - lesions

A
  • Lower small intestine and large intestine are heavy, edematous and thickened
  • Enlarged, congested mesenteric lymph nodes
  • Focal necrosis on intestinal mucosa
  • Chronic cases may have raised circular lesions in the colon (button ulcers)
  • Excess peritoneal fluid and strands of fibrin – peritonitis
    > pigs have small amount of abdominal fibrin which is normal. Look for “excess fibrin”
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11
Q

S. Typhimurium – laboratory Diagnosis

A

Culture & Sensitivity
- Untreated animal and demonstrating typical signs
- Culture multiple organs
- PCR
- Serotype
> Special test for DT 104 by Public health Agency of Canada - zoonotic

Histopathology
- Rule-out other enteric and septicemic diseases

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12
Q

S. Cholerasuis causes what form of salmonellosis?

A

Septicemic form

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13
Q

Pathogenesis and transmission
Septicemic form of salmonellosis

A
  • Fecal-oral route or inhalation of organism
  • Invades tonsil (Mr. Tonsil!) and mucosa of small intestine
  • Spreads to regional lymph nodes and can survive in macrophages
  • Results in a septicemia and localizes in tissues where cause lesions:
    > Releases endotoxin, vasculitis (present in all forms of salmonellosis)
    > Liver, lung, brain, meninges, joints, lymph nodes
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14
Q

S. Cholerasuis - what age affected, what immunity usually protects?

A

All ages of pigs but usually nursery to mid-grower
- Lactogenic immunity is usually protective

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15
Q

S. Cholerasuis - Clinical Signs? common in ontario?

A
  • Clinical signs mediated by endotoxin - variable
  • Inappetance, depression, high fever, acute death
  • Discolored skin (red to purple), cyanosis
  • Diarrhea may develop later (if pig lives) but not a typical clinical sign
  • Respiratory signs - dyspnea and cough
  • High mortality, low morbidity
  • VERY VERY rare in Ontario (last reported in 2015)
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16
Q

S. Cholerasuis - lesions

A
  • Cyanotic extremities
  • Enlarged spleen, lymph nodes and liver
  • Liver may have white/ grey necrotic foci
  • Petechial hemorrhage of the kidneys
  • Interstitial pneumonia – congestion, interlobular edema, fibrinous pleuritis
  • Congestion, fibrinous inflammation, of the intestinal mucosa
  • Necrotic entero-colitis if the pig lives long enough
17
Q

S. Cholerasuis - lab and histo Diagnosis

A

Laboratory
- Culture from multiple organs of septicemic pigs
- Differentiate from other septicemic diseases and causes of interstitial pneumonia

Histopathology:
- Unique paratyphoid nodules in liver

18
Q

Salmonellosis - Control

A

Prevention preferred! Good production practices
- Introductions from single source, quarantine
- AI/AO management
- Minimize stress
- Control rodents, birds, wildlife

But when outbreaks occur
- Provide clean, warm environment
- +/- antibiotics

Vaccine – oral/intranasal
- Avirulent live culture
- Increase ADG in enteric disease
- Limited value economically
> Remember ~2% Ontario herds perceive a
problem with S. typhimurium

FYI: 2015 Salmonella cholerasuis in Ontario linked to vaccine use

19
Q

rectal prolapse in common in what age group

A

Common in grower finisher age group
- seldom seen in nursery pigs

20
Q

rectal prolapse risk factors

A
  • Diarrhea – irritation, tenesmus, prolapse
  • Increased abdominal pressure
    > Straining, piling (cold environment)
  • Zearalenone (mycotoxin, estrogen-like compound)
  • Antibiotics- lincomycin, tylosin may result in rectal prolapse
21
Q

what is Porcine hemorrhagic bowel syndrome

A

Excessive gas production in intestines leading to extreme distension (bloat) causing venous blockage, rapid necrosis, shock and sudden death
- Etiology unknown
- Usually in grower-finisher (4-6 months of age)
- Found dead, pale, distended carcass
- Lesion similar to mesenteric torsion but there is no torsion

22
Q

GI torsions that can occur in swine

A
  • Gastric torsion or volvulus
    -Torsion of the bowel
23
Q

rectal prolapse diagnosis

A

n Clinical signs
n Other pigs with blood on their nose/face

24
Q

Rectal Prolapse treatment

A
  • Move pig to hospital pen
  • +/- Surgical correction - reinsert and purse string or surgical removal
  • Address underlying infectious disease, management
  • May develop rectal stricture as sequelae
25
Q

general look of pig with rectal stricture

A

emaciated but with distended abdomen

26
Q

gastric ulcerns in swine - what is the common location

A

Ulceration of the Pars Esophagea (UPE)

27
Q

Ulceration of the Pars Esophagea (UPE) - how common? is it important and why? what ages and types of pigs are affected?

A
  • Widespread and common
    > Slaughter surveys have shown 90% with range from 2-90%
    > Important cause of mortality in adult pigs/finishers
  • Herd to herd variation in severity and prevalence
  • Affects any aged pig but more commonly >3 months of age
  • Peripartuient sows are at higher risk
28
Q

gastric ulcers of the pars esophagea can lead to what

A

Chronic scarring > stenosis

29
Q

Ulceration of the Pars Esophagea (UPE)
- cause, risk factors, typical presentation

A
  • Exact cause or causes not completely understood
  • Risk factors well known
  • Typical presentation
    > Healthy pig found dead, pale
30
Q

UPE - Pathogenesis
> what is the structure of the pars esophagea?

A
  • Pars esophagea – stratified squamous epithelium
    > Does not secrete protective mucus
  • Chronic insult results in hyperplasia of epithelial cells
    > Tight junctions between cells break down
    > Allows digestive juices access to deeper layers
    > Erosions develop
  • Lesions can be acute
    > Conditions that cause increase fluidity of stomach contents
    > Change from normal to ulcerated can take < 24 hours
31
Q

UPE – Clinical signs

A

n Might contribute to slow growth
n Pale (reflects degree of blood loss)
n Anorexic pig
n Black tarry feces, abdominal pain, bruxism n +/- vomit and then eat again (healed, stenosis)
n Found dead

32
Q

UPE - general Risk Factors

A

Anything that leads to a breakdown in the
division between the very acidic distal portion of the stomach and the neutral “rumen-like” proximal stomach

33
Q

UPE - Risk Factors, more specific

A

Feed Factors
- Rapid passage
> Fine particle size
> Pelleting or heating
- No feed intake
> Empty feeder
> Crowded pen, poor access
> Hot weather
> Disease causing anorexia
> Vomitoxin

Other possible factors
-Infectious component?
> E.g., Helicobactor spp

34
Q

what feed particle size is more likley to contribute to gastric ulcers?

A

fine feed

35
Q

UPE- Diagnosis and differentials

A
  • Gross post-mortem exam
  • Clinical history
  • Differentials for anemia/found dead/pale pig
    > Acute form of Lawsonia infection (PHE)
    > Intestinal torsion or hemorrhagic bowel syndrome.
36
Q

UPE - Control Measures

A

n Avoid feed disruption
n Encourage increased feed particle size
> But this increases feed:gain (fine balance)
n Encourage feed intake
n Infectious disease control
n Monitor with postmortem exams and slaughter checks
n Good production practices