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3. Food Animal > Swine 13 > Flashcards

Swine 13 Flashcards

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1
Q

Pyelonephritis affects sows how?

A

n A very common cause of sow death

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2
Q

Pyelonephritis; pathogens, where they come from

A

Wide variety of bacteria, most associated with manure
> Leptospirosis, or fecal source of bacteria such as E coli, Actinobaculum suis (sheath of boars)

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3
Q

Pyelonephritis Transmisson and herd spread

A

moves between sows via urine, dirty environment, venereal spread

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4
Q

Pyelonephritis clinical signs

A

n thin sows
n +/- anorexic
n strain to urinate
n blood (+ mucus) on floor (usually indicates cystitis)

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5
Q

Pyelonephritis -
prevention and control:

A
  • Water access important
    > flow: 1 litre/minute, check regularly, drinkers break frequently
  • Parenteral antibiotics to affected sows
    > tetracycline are usual choices
  • Clean environment – behind sows
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6
Q

Vaginal discharge syndrome Clinical signs? when they occur?

A
  • May present as an “outbreak” of a large number of open sows (Not-in-pig; NIP)
  • Repeat breedings
  • +/- sow mortality
  • Purulent vaginal discharge
    > 15 - 25 days post breeding
    > Offensive odour
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7
Q

Vaginal discharge syndrome
Control

A
  • Cull affected sows
    > i.e., that ‘repeat’ or have discharge
  • Purchase clean gilts & boars
  • AI with purchased semen
    > Review AI procedure
    > Avoid breeding late estrous
  • Cull contaminated boars
  • Medicated feed if herd problem (tetracycline)
  • Clean and disinfect barn
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8
Q

Zearalenone toxicity Fungal source

A

Fusarium graminearum

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9
Q

Zearalenone toxicity clinical effects

A
  • Estrogenic
  • Vulvovaginitis
  • Vaginal and rectal prolapse
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10
Q

zearalenone toxicity common complaint

A

Common scenario is complaint that gilts look to be in heat but won’t stand to be bred.

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11
Q

oxytocin effect on breeding? what can go wrong?

A

reduce Farrowing duration

  • Increased stillbirth if dosage too high
  • Aggitated sow if dosage is too high
  • Increased stillbirths if given before cervix is fully dilated
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12
Q

Prosteglandin effect on breeding? drawbacks?

A

induce partuition

  • Piglets born < 113 d gestation may be small and weak
  • Prostaglandins will induce abortion
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13
Q

PG600 (eCG & hCG) effect on breeding? uses and things to watch for?

A

induce puberty
- Useful for inducing a group of gilts to begin cycling together
- If a gilt has already reached puberty and has started to cycle, then PG600 will not have an effect
> Does not make up for lack of observation

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14
Q

Regu-Mate (altrenogest) effect on breeding? drawbacks? route of admin?

A

stop the estrous cycle to synchronize breeding
- Under-dosing will cause cystic ovaries
- Oral product
> Need to ensure each gilt receives full dose

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15
Q

Swine Erysipelas (SE) is caused by what bacteria? is it G+/-? is it common?

A

Erysipelothrix rhusiopathiae
- Gram-positive bacteria
- Assume it is in all pig barns!

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16
Q

Erysipelas: how many serovars? which are problematic? how is it carried?

A
  • About 26 different serovars
  • 80% of swine serovars are 1 & 2
  • Other serovars of questionable significance in swine
  • 30-50% of healthy swine are carriers (tonsils, lymph)
  • Also isolated from sheep, turkeys, fish
17
Q

Erysipelas: issues for people

A

Potential zoonosis – causes “erysipeloid” skin lesion
* meat, leather, rendering plant workers, vets

18
Q

Erysipelas survival in environment and susceptibility? how is it shed?

A

Survival in environment:
* Resistant to drying
* Susceptible to common disinfectants
* Remains viable for months in animal tissues
* Acutely infected swine shed profusely

19
Q

Erysipelas - which age groups are susceptible? what type of immunity is protective? other issues?

A
  • Passive antibody is protective and may interfere with vaccine-induced active immunity
    > i.e. maternal antibody interference
  • All age groups are susceptible
20
Q

Erysipelas - Pathogenesis, incubation

A
  • Usually ingestion of contaminated feed/water, short incubation (~36hrs)
    > environment, feed/water, skin wounds, or Mr. Tonsil (again!)
  • Swelling of endothelium, adherence of monocytes
  • Systemic vasculitis (enzyme neuramidase may cause vascular damage)
  • Fibrinous thrombosis & necrosis

From here, can:
> Localization in: Skin, Joints, Heart
> Septicemia: peracute death

21
Q

Erysipelas – Pathology

A
  • Vasculitis, thrombosis & necrotizing dermatitis
  • Chronic valvular endocarditis
  • Chronic fibrosing, non-suppurative arthritis of major joints with villonodular hypertrophy
  • Destruction of articular cartilage in chronic arthritis
  • Lesions of a septicemia in parenchymal organs

§ Petechial & ecchymotic haemorrhages on epicardium
§ Spleen – enlarged & congested
§ Kidney – petechial hemorrhages

22
Q

Erysipelas – Clinical Signs, acute (septicemia)

A

Acute (Septicemia):
* Often starts with peracute deaths – deaths rare in NA
* Pyrexia: Temp 41°- 42.5°C, anorexia
* Depressed, reluctant to move, shifting weight leg-leg
* Diamond Skin Disease:
– Localized hyperemia > edema > piloerection > cyanosis > ischemic necrosis
* Severe: widespread ischemic necrosis (eg. of tail, scrotum, etc)
* Commonly seen in pregnant sows before farrowing – stress suspected

23
Q

skin lesions caused by acute erysipelas

A

Diffuse skin lesions, some of which should be diamond shape.

24
Q

Erysipelas – chronic disease processes

A

Chronic (Endocarditis):
* Begins with vasculitis & myocardial infarcts
* Bacterial emboli, fibrin deposition leads to destruction of valvular endocardium
* Vegetative valvular endocarditis

Chronic (Arthritis):
* Begins as acute synovitis within 4-10 days
* Fibrinous exudation, synovial proliferation, fibrosis & destruction of articular cartilage within 3-8 mo
* Weight bearing to non-weight bearing lameness depending on severity

25
Q

Erysipelas – Clinical Signs of chronic endocarditis

A

§ Cardiac insufficiency
§ Peripheral cyanosis
§ Dyspnea
§ Sudden death

26
Q

Erysipelas – Diagnosis, for different forms

A

Culture:
a) Acute cases
* Systemic sites (LN, liver, spleen)
* Acute skin lesions (pink or white; not purple) from junctional areas (biopsy can be used)
* Blood culture (EDTA, serum) – from several septicemic animals

b) Arthritis (difficult)
* Synovial fluid or 2.5 cm^2 villonodular synovial tissue

c) Endocarditis
* Culture lesion

27
Q

Erysipelas - description of chronic arthritis found in large feeder-finisher pigs. How do we culture? are vaccinated pigs safe from this lesion?

A

A very chronic rheumatoid like arthritis with villonodular hypertrophy occurs in large feeder-finisher pigs. E. rhusiopathiae is hard to grow from joint tissues. Submit 5 gm villonodular tissue, centrifuge and culture the pellet. This lesion can even occur in vaccinated pigs.

28
Q

Erysipelas – Treatment & Control

A

1) Good hygiene and sanitation (reduce infection pressure)
– Infected pigs shed profusely
– Erysipelas readily killed by disinfectants

2) Parenteral treatment: required for sick animals:
– Penicillin, or tetracyclines are drugs of choice
– Early treatment, rapid response of acute cases expected

3) Water medication: could be used for mass medication with variable success in acute outbreaks
– Variable intake because animals reluctant to move

4) vaccine

29
Q

Erysipelas – Vaccination; when should we do it? when is it not effective? what vaccine options do we have?

A

Finishing pig problem:
– Vaccination of pigs in nursery or early grow-finish
– Vaccination in the face of an outbreak is recommended
– Little efficacy for chronic lameness, valvular endocarditis
– Killed bacterins and live avirulent oral vaccines

30
Q

Erysipelas – Vaccination; how should we vaccinate the breeding herd? what types do we have? skin disease commonly seen in what pigs?

A

Breeding herd vaccination:
* Killed bacterin – single antigen or multivalent
* Pre-breeding or pre-farrowing
* Skin disease most commonly seen in sows pre-farrowing

31
Q

Osteochondrosis dessicans (OCD); what is it and what does it cause?

A
  • One of the major causes of lameness in adult pigs
  • Non-infectious degenerative condition of epiphyseal cartilage
32
Q

Osteochondrosis dessicans (OCD); what are some possible associations / causes?

A

Multifactorial - possibly associated with:
* High growth rate of modern genotypes that deposit more body weight prior to skeletal maturity at 18 months
* Breed & confirmation abnormalities - particularly broad hams, short hind legs, sloping pasterns
* Compression, joint overloading & mechanical stresses attributed to overcrowding, breeding, fighting

33
Q

Osteochondrosis dessicans (OCD) Clinical signs, when they occur?

A
  • 4-18 months of age
  • Weight bearing (WB) or non-WB lameness:
    > Reluctance to rise, lie down quickly after standing
  • Chronic, progressive, shifting lameness, affecting one or more limbs
  • Painful, due to inflammation, increased joint fluid and swelling
34
Q

Osteochondrosis dessicans (OCD) common locations of lesions:

A
  • Medial articular surfaces most likely affected
  • Articular cartilage
    > stifle, elbow, hock, shoulder
  • Growth plates
    > distal ulna & femur, femoral & humeral heads, ischiatic tuberosity
  • Epiphysiolysis
    > glenoid cavity (scapula), capital femoral epiphysis
35
Q

Osteochondrosis dessicans (OCD) pathogenesis

A
  • Articular cartilage thickens, depriving deeper chondrocytes of nutritional support
  • Chondrocyte necrosis
  • Mechanical stress & trauma results in cracks & fissures on articular surface
  • Synovial fluid leakage induces inflammatory response
    > synovitis
  • When cartilage flap or fragment develops on articular surface > termed OCD
36
Q

Osteochondrosis dessicans (OCD) treatment and contol? when to euthanize?

A

1) Pain control / anti-inflammatories (Predef, dex, ketoprofen) can be used short term to improve level of comfort

2) Prevent mechanical stresses:
o Non-slip floors
o Reduce pen density, fighting & competition o Provide partially slatted floors

3) Euthanize if:
o Experiencing unrelenting pain
o Unable to walk onto transport vehicle (unfit)
o Animal is non-ambulatory

3. Food Animal (22 decks)

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