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3. Food Animal > Swine 12 > Flashcards

Swine 12 Flashcards

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
what type of 'streaks' do we often see in lepto nephritis?
Typical lymphoplasmacytic infiltrations often present as pale streaks in the cortical regions
26
lepto diagnosis
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
why is herd screening for lepto serology difficult?
- 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
Demonstration of Leptospires or antigen; troubles with this approach for diagnosis? methods?
* 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
stains to use for lepto histo
histopathology tissues (IHC, silver stains)
30
lepto vaccination: what is its use? how does it work and when must / should we give it?
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
medication for lepto
* **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
biosecurity important for lepto contol
* Eliminate contact with wildlife & contaminated environment * Rodent control, stagnant water
33
is porcine parvovirus common? are outbreaks common?
* Ubiquitous virus, endemic infection in most herds * World wide distribution - outbreaks rare
34
is PPV stable in the environment?
Very stable DNA virus – virtually impossible to eliminate
35
PPV economic significance?
Economically significant cause of embryonic and fetal death, prior to fetal immunocompetence – Especially gilts
36
PPV disease in post-natal animals?
* Absence of clinical disease in post-natal animals
37
parvovirus structure, stability, environmental survival ability?
* Small single stranded DNA * Stable, resistant to heat, many disinfectants * Virus in environment remains infectious for 4 months
38
parvovirus property with red blood cells? what does this let use do?
* Agglutinates erythrocytes – basis of hemagglutination (HA) serologic test
39
parvo transmission / how are swine generally exposed to parvo?
Oronasal, transplacental (viremia), seminal exposure
40
how is PPV spread by boars?
PPV shed by acutely infected boars in semen and other excretions
41
parvovirus immunity; how it works, consequences for vaccination? gilts vs sows?
* 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
parvovirus clinical signs? in naive pregnant females? in first half of gestation?
* 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
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?
- 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
pathogenesis of parvovirus?
* 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
PPV; time of fetal exposure vs outcome
< 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
diagnosis of PPV?
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
porcine parvo control / vaccine - what types available, when to administer, duration of immunity, effects?
* 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
what proportion of herds are affected by seasonal infertility? which pigs are at more risk? what are some factors that lead to this?
* ~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
seasonal infertility clinical signs
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
seasonal infertility pathogenesis?
* Wild pigs are seasonal breeders – trait still carried by domestic pigs * Decreasing day length triggers reduced fertility
51
seasonal infertility treatment
* 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
in what season are abortions common in sows and why?
Autumn abortions * October and November * Common in sows exposed to cool/cold temperatures at night
53
treatment for autumn abortions
* increase feed intake and * increase ambient temperature (close air inlets at night)

3. Food Animal (22 decks)

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