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3. Food Animal > Swine 12 > Flashcards

Swine 12 Flashcards

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1
Q

Systemic Infectious Reproductive Diseases of swine

A
  • Porcine reproductive and respiratory syndrome (PRRS)
  • Pseudorabies (foreign animal disease)
  • Porcine parvovirus infection (SMEDI)
  • Leptospirosis
  • Brucellosis (foreign animal disease)
  • Erysipelas (does not infect fetus)
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2
Q

Overview of Swine Reproduction

A

gilt pool enters, also use older sows
-mating
>regular repeats (18-24d)
>irregular repeats (>25d)
-gestation (115d)
>cull, death, abortino, NIP / open sows
-farrowing
-lactation (14-28d)
-weaning
>cull
-wean to breed interval (5-7d)

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3
Q

normal abortion target and level of concern

A

target: <2%
concern: 5-10%

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4
Q

normal stillbirth target and level of concern

A

target: <7%
concern: 10-15%

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5
Q

normal mummies target and level of concern

A

target: 0.5%
concern: >3 pigs in 10% of litters

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6
Q

normal farrowing rate and level of concern

A

target: >85%
concern: <80%

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7
Q

Leptospira interrogans:
characteristics? what serovars are swine susceptible to? which are most common?

A
  • Thin, motile Gram neg organisms which spin or undulate on long axis.
  • Swine susceptible to all serovars
    Most common:
    L. pomona, L. Bratislava
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8
Q

is leptospirosis common in modern swine production

A

Now fairly uncommon in modern swine production

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9
Q

maintenance hosts of L pomona

A

swine, skunk, raccoon, opossum

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10
Q

maintenance hosts of L bratislava

A

swine, horse

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11
Q

importance of leptospirosis for humans?

A

Important zoonotic disease – “Swine herders disease”
– Women of child bearing years
– Bacteremia, abortions, flu-like with cyclical fever

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12
Q

general presentation of lepto in swine? importance varies with what? where does it generally live in the host?

A

In pigs:
* Infection largely subclinical
* Importance varies with geographic regions due to serovar and local maintenance hosts which act as reservoirs
* Affinity for and persistence in kidneys of all animals

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13
Q

where does lepto live in the host? how is it passed on? how does an infection usually enter a herd?

A
  • Predilection for kidneys and persist there
    > also in genitalia
  • Pass large numbers of pathogen in urine
    > often lasts for weeks to months after clinical signs have concluded
  • Infection into a herd is usually introduced via infected swine
    > Purchased animals.
    > Fetus’ infected in utero may survive as infected piglets and become adult carriers
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14
Q

where does lepto generally live in the environment?

A
  • Incidental host – rats, mice raccoon, etc
  • Can survive in damp soil and water
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15
Q

lepto transmission

A

Horizontal:
* Direct or indirect contact (urine, placental fluids, milk)
* Wildlife & contaminated environment (soil, water etc)

Vertical:
* Venereal & transplacental

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16
Q

Leptospira survival in environment enhanced by? susceptible to?

A
  • Moisture & warmth
    > optimal 28OC; brief survival if less than 10oC or greater than 34oC
  • Access to wildlife, stagnant water (dugouts, wallows, effluent) associated with incidental infections
  • Susceptible to desiccation
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17
Q

Pathogenesis of lepto

A
  • Penetrate mucous membranes (ocular, nasal, vaginal) brief bacteremia
    – Exact mechanism unknown but capillary damage is major feature – Produce hemolysins, hemoglobinuria, hemolytic anemia
  • Persistence in kidneys resulting in leptospiruria for weeks (common) to months (less common)
    – Interstitial nephritis
  • Persistence in genital tract
    – Uterus non-pregnant females and genitals of males
  • Transplacental infections if pregnant
  • Abortions – toxic material from autolyzing fetuses trigger abortion
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18
Q

lepto Clinical signs of acute infections

A

Acute infections:
* Coincides with bacteremia (can see petechial haemorrhages eg. on skin of piglet)
> Depends on virulence of serovar
involved
* Transient anorexia, pyrexia, listlessness in young piglets
> Rare jaundice, hemoglobinuria
> Failure to grow (low ADG)
* Sometimes unnoticed in mature animals
> Spontaneous recovery

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19
Q

is acute lepto common? in what type of pigs generally?

A

Acute lepto in pigs is less common but when does occur it is more likely in young piglets

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20
Q

lepto clinical signs of chronic infections for different serovars

A

Chronic infections: (most common) Reproductive failure and infertility most
common in North America

L. Pomona:
* Pregnant females - transplacental infection resulting in abortion storms, stillborns, & live weak piglets resulting in high PWM
***Late stage abortions

L. Bratislava:
***Increased returns to estrus – bacteria “lives” in fallopian tubes

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21
Q

lepto - pathology of acute infections

A
  • Limited due to mild clinical disease
  • Petechial haemorrhages, mild renal tubular damage, focal liver necrosis
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22
Q

lepto - pathology of chronic infections

A
  • Grow-finish: kidneys may have scattered small grey foci due to diffuse focal interstitial nephritis (may involve renal tubules)
23
Q

lepto - pathology of fetal infection

A
  • Edema and fibrin - in body cavities
  • Petechial haemorrhages various organs & skin
  • Focal liver necrosis – less common but very suggestive
24
Q

are lesions of lepto nephritis consistent between animals? how do we differentiate from other diseases?

A
  • With Lepto nephritis, the severity of lesions varies tremendously from one pig to another and histologic
  • IHC differentiation from lymphosarcoma, PCV2 or PDNS lesions is needed.
25
Q

what type of ‘streaks’ do we often see in lepto nephritis?

A

Typical lymphoplasmacytic infiltrations often present as pale streaks in the cortical regions

26
Q

lepto diagnosis

A
  1. History of abortions in late gestation along with lesions in fetuses.
  2. Serology: MAT (microscopic agglutination test)
  3. Demonstration of Leptospires or antigen
27
Q

why is herd screening for lepto serology difficult?

A
  • High titers usually present at time of abortion – paired samples may be needed
  • Cross reactions among serotypes common > serotype specific
  • Considerable problem when interpreting vaccinated pigs
    > Breeding animals vaccinated
    > Titers from infection higher then from vaccination
28
Q

Demonstration of Leptospires or antigen; troubles with this approach for diagnosis? methods?

A
  • Generally low sensitivity/specificity especially in chronic infection
  • Generally unable to differentiate serovar
  • Special stains: histopathology tissues (IHC, silver stains)
  • PCR: urine, tissues
  • Dark field microscopy: urine
  • Immunofluorescence: tissues, blood, urine sediment
  • Bacterial culture: tissues, blood, urine
    > 10 days post infection, prior to antimicrobial treatment
29
Q

stains to use for lepto histo

A

histopathology tissues (IHC, silver stains)

30
Q

lepto vaccination: what is its use? how does it work and when must / should we give it?

A

Vaccination
* Provides partial protection; serotype specific
– Prevent abortions
– Reduce renal shedding
* Numerous polyvalent bacterins (parvo, lepto, erysipelas)
* Must vaccinate prior to infection as kidney is immune privileged site (cannot clear infection once established)

Recommended vaccination program on sow farms:
* Pre-breeding in sows (administered during lactation) and gilts (administered 5 & 2 wks pre-breeding)

31
Q

medication for lepto

A
  • Oxytetracycline, tylosin, erythromycin (high doses, 3-5 days may eliminate L. pomona from kidney
  • Levels of feed medication (if used in feed) must be very high (800 ppm tetracyclines)
32
Q

biosecurity important for lepto contol

A
  • Eliminate contact with wildlife & contaminated environment
  • Rodent control, stagnant water
33
Q

is porcine parvovirus common? are outbreaks common?

A
  • Ubiquitous virus, endemic infection in most herds
  • World wide distribution
  • outbreaks rare
34
Q

is PPV stable in the environment?

A

Very stable DNA virus – virtually impossible to eliminate

35
Q

PPV economic significance?

A

Economically significant cause of embryonic and fetal death, prior to fetal immunocompetence
– Especially gilts

36
Q

PPV disease in post-natal animals?

A
  • Absence of clinical disease in post-natal animals
37
Q

parvovirus structure, stability, environmental survival ability?

A
  • Small single stranded DNA
  • Stable, resistant to heat, many disinfectants
  • Virus in environment remains infectious for 4 months
38
Q

parvovirus property with red blood cells? what does this let use do?

A
  • Agglutinates erythrocytes
    – basis of hemagglutination (HA) serologic test
39
Q

parvo transmission / how are swine generally exposed to parvo?

A

Oronasal, transplacental (viremia), seminal exposure

40
Q

how is PPV spread by boars?

A

PPV shed by acutely infected boars in semen and other excretions

41
Q

parvovirus immunity; how it works, consequences for vaccination? gilts vs sows?

A
  • High levels of passive immunity found in most growing pigs which degrade over 3-6 months
  • Passive antibody interferes with the development of active immunity
    > High passive antibody levels prevent infection and horizontal transmission, creating naïve populations of gilts
  • Gilts should be vaccinated or exposed naturally prior to conception
  • Sows generally immune, active immunity through natural infection persists for life
42
Q

parvovirus clinical signs? in naive pregnant females? in first half of gestation?

A
  • Disease is subclinical in all pre-pubertal pigs, in spite of extensive viral replication in many tissues
    > Mild leukopenia with 10 days of infection
  • PPV infection of naïve pregnant females results in SMEDI
    (stillbirths, mummies, early embryonic death and infertility)
    – Irregular return to estrus (< 35 days of gestation)
    – Anestrus
    – Small litter sizes
    – Mummies!
    – Fail to farrow

Clinical manifestations of embryonic death & fetal mummification during first half of gestation:
* Small litters and/or mummies of various sizes up to about 17 cm (day 70)
* RARELY abortion

43
Q

if only a portion of a litter in utero is infected with PPV, what will happen? what do we see? what about with piglets after day 70?

A
  • If only a portion of the litter is initially infected, PPV gradually spreads in utero and kills more conceptuses sequentially resulting in mummies of various sizes
  • Because PPV usually infects a portion of the litter and spreads laterally to other piglets in the litter, various sizes of mummies are seen.
  • However, piglets after day 70 are immunocompetent. Thus, PPV may not be the cause of all dead/decomposing piglets.
44
Q

pathogenesis of parvovirus?

A
  • Infected dams develop viremia and virus crosses placenta(s)
    > All or some of fetuses are affected
  • Virus can replicate only in cells undergoing mitosis
    & has predilection for fetus.
  • Virus may slowly spread from fetus to fetus
  • Appears to have predilection for endothelium causing vascular necrosis
  • Transplacental infections after gestation day 70 rarely results in death due to fetal immunocompetence
45
Q

PPV; time of fetal exposure vs outcome

A

< 14 days: Death of fetus, regular return to estrus

10-35 days: Death of fetus, resorption, irregular return to estrus

35-70 days: Death of fetus, mummification

70 – 115d (term): Immune response, usually survival

46
Q

diagnosis of PPV?

A
  1. Demonstration of antigen or DNA
    * Several mummified fetuses (<17 cm), lungs of such fetuses for immunofluorescent antibody test IFA or PCR
  2. Serology
    * Seroconversion in many gilts with paired serology but acute samples often not available.
    * Can generally distinguish vaccine and natural induced titres based on level
    > Vaccination: titres less than 1:1,000
    > Natural infection: titres generally greater than 1:1,000
47
Q

porcine parvo control / vaccine - what types available, when to administer, duration of immunity, effects?

A
  • Many killed vaccines available, most multivalent combined with lepto & erysipelas
  • Must be administered prior to conception, after maternal antibody decay
  • Duration of immunity unknown, thought to be about 4 months
  • Vaccination prevents fetal disease, but not infection of pregnant dams natural exposed to PPV

Recommended vaccination program:
> Gilts – Twice - 5 & 2 wks pre-breeding
> Sows – revaccinated 2 wks pre-breeding
> Boars – twice annually

48
Q

what proportion of herds are affected by seasonal infertility? which pigs are at more risk? what are some factors that lead to this?

A
  • ~10% of Ontario herds affected
  • Late summer (Jul, Aug, Sept)
  • Pigs raised outdoors more at risk
  • Photoperiod thought to be of importance
  • Restricted feeding and heat stress appear to be factors
49
Q

seasonal infertility clinical signs

A

Increase in number of sows returning to heat at irregular times (>25 days)
* Especially in gilts
* Reduce farrowing rate
* Increased irregular returns to estrus
* Increased wean-to-breed interval
* Delayed puberty in gilts
Or increase in ‘NIP’ sows at farrowing

50
Q

seasonal infertility pathogenesis?

A
  • Wild pigs are seasonal breeders – trait still carried by domestic pigs
  • Decreasing day length triggers reduced fertility
51
Q

seasonal infertility treatment

A
  • Confinement housing with 18 hrs artificial light/day
  • Housing: individual/gestating sows in stalls**
  • Group/pen sows together by parity
  • Increase feed intake in 1st 3-wks of gestation
52
Q

in what season are abortions common in sows and why?

A

Autumn abortions
* October and November
* Common in sows exposed to cool/cold temperatures at night

53
Q

treatment for autumn abortions

A
  • increase feed intake and
  • increase ambient temperature (close air inlets at night)

3. Food Animal (22 decks)

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