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Respiratory > Respiratory Diseases Of Swines > Flashcards

Respiratory Diseases Of Swines Flashcards

1
Q

Define all in/all out. How does that help contain infectious pathogens?

A

A management style of raising pigs (though sometimes cattle) where animals are born or bought into a facility at the same time, age, weight, etc. then all leave at the same time.
This principally aids in reducing transmission of pathogens from older animals to younger susceptible animals. When the animals depart a facility thorough cleaning helps prevent residual environmental contamination.

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2
Q

Define vertical integration.

A

Full-service swine operation that houses breeders, new- borns, weanlings, and feeder stock

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3
Q

What are the most important stressors and risk factors of neonatal piglets?

A
  1. Nutritional stress: milk diet to plant protein diet –> they may experience negative energy balance
  2. Cold stress: piglets are extremely susceptible to cold and drafts
  3. Respiratory stress: ammonia and hydrogen sulfide lev- els in poorly ventilated barns can damage resp. mucosa
  4. Social stress: leaving mom, establishing a hierarchy, overstocking
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4
Q

What is the greatest reservoir of pathogens for piglets?

A

mom

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5
Q

What gases are produced in underground manure pits that might damage the respiratory tract of pigs?

A

ammonia and hydrogen sulfide

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6
Q

List the stressors in neonatal and growing pigs.

A
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7
Q

What is atrophic rhinitis and what 2 agents cause this?

A

synergistic infection -> two bacteria work together to cause this disease:
1. Bordetella bronchiseptica
2. Pasteurella multocida (Type D toxin)(AR+ strains)

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8
Q

Describe the pathophysiology of atrophic rhinitis. What makes the strain of P. multocida
associated with atrophic rhinitis distinct?

A
  1. Pigs acquire B. bronchiseptica from the sow
  2. Damage to mucos (virus, ammonia, etc.)
  3. Co-colonization of P. multocida
  4. Toxins induce osteoclastic activity
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9
Q

Who is more at risk for developing more severe turbinate atrophy with atrophic rhinitis?

A

The younger the pigs at infection, the more severe the turbinate atrophy

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10
Q

Can B. bronchiseptica induce pathology by itself?

A

yes

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11
Q

clinical signs of atrophic rhinitis

A

Early signs farrowing or nursing: sneezing, snuffling, mucopurulent nasal discharge

Later signs finishing: twisted/shortened snouts, excess lacrimation, epistaxis, decreased growth rate

50% of market hogs have at least mild lesions

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12
Q

What are the keys to preventing atrophic rhinitis in piglets?

A
  1. Vaccine: given to sows reduces her mucosal load and reduces colonization of pigs
  2. Improved management
  3. Ventilation
  4. Continuous slaughter checks
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13
Q

Treatment of atrophic rhinitis?

A

Mass medication-ABX added to feed

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14
Q

Describe necrotic rhinitis.

A

caused by Fusobacterium necrophorum
- colonizes damaged mucosa, sometimes follows trauma

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15
Q

Clinical signs of Necrotic Rhinitis

A

NEONATES/WEANERS
- severe swelling of the nose (cellulitis)
- abscessation
- foul breath bc its an anaerobe
- chronic infections : facial deformities, bull nose

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16
Q

Whats the treatment for necrotic rhinitis?

A

antibiotic therapy is unrewarding, most pigs are eutha- nized
- would debridement

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17
Q

How is necrotic rhinitis prevented?

A

keep the area clean
- poor sanitation is listed as a risk factor, F. necrophorum is found in feces (different from AR)

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18
Q

what is inclusion body rhinitis?

A

caused by a GAMMA herpesvirus -> porcine cytomegalovirus

Gamma herpes, latency in leukocytes

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19
Q

What is the pathophysiology of inclusion body rhinitis?

A

Sow is reservoir (latently infected) –>stressful event, sheds virus and exposes
piglets–>virus replicates in the nasal and ocular tissue (can move
horizontally between pigs)

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20
Q

Clinical signs of inclusion body rhinitis?

A

NEONATES Sneezing, snorting, ocular-nasal discharge SOWS-mummification, still born pigs

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21
Q

TX for inclusion body rhinitis?

A

Most cases are self-limiting Treatment is unnecessary

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22
Q

What is the reservoir of porcine cytomegalovirus for piglets in inclusion body rhinitis?

A

The sow

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23
Q

What is the viral classification of influenza?

A

orthomyxovirus, RNA virus, segemented genome

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24
Q

Influenza strains are named for
the proteins on the envelope surface: _______ and _______

A

hemagglutinin and neuraminidase
H: used to enter cells N: used to leave cells
Pig strains:
- H1N1 (2 of these)
- H3N2
- H1N2

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25
Q

The predominant influenza strain that circulates in pigs is?

A

H1N1

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26
Q

How are influenza strains described?

A
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27
Q

Define antigenic drift and antigenic shift for influenza virus.

A

Antigenic drift: mutations in the genetic structure of the virus, some are dead ends and others arent
Antigenic shift: reassortment (mixing and matching) of genetic segments which leads to the opportunity of pandemics

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28
Q

Why are pigs predisposed to uniquely capable of increasing the risks of pandemic re-assortment
events?

A

Pigs can be infected with both the avian and the human influenza strains increasing their opportunity of pandemic re-assortment events due to the fact that they have BOTH alpha 2,6 sugars and alpha 2,3 sugar.

Alpha 2,6 sugar is on a lot of human strains
Alpha 2,3 sugar is on a lot of avian strains

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29
Q

How is influenza transmitted and describe its replication?

A
  • Transmission occurs through respiratory secretion
  • Viral replication occurs in the nasal, tracheal, and bronchial epithelium
30
Q

What are the clinical manifestations of influenza in pigs?

A

Mild to moderate necrosis of respiratory epithelium –> lung cell death and consolidation

same as humans
- intestinal diarrhea - coughing
- sore throat
- lethargy
- lack of appetite
- sneezing
- mucous: nose/eye
- fever
- weight loss
- poor growth

HIGH morbidity rate, thumping (exaggerated abdominal breathing), paroxysmal cough, huddling together

Most pigs recover in 6-7 days

31
Q

How does influenza maintain itself in a population of pigs?

A

viral shedding can occur within 48 hours of infection, CSs appear in 4 days
**Post-Infection virus CAN SHED UP TO 30 DAYS, some virus cultrured from clinically normal animals

SIV likely circulates at low levels waiting for a herd wide increase in susceptibility

32
Q

How do you diagnose swine influenza?

A

PCR, Virus isolation, serology, indirect fluorescent antibody

33
Q

Are the vaccines for swine influeza reliable?

A

No because they arent reformulated fast enough to provide good immunity
Better prevention is all in/all out and reduction of stress and abrupt changes in stress
Depopulation is necessary in severe epidemics

34
Q

What is Pseudorabies?

A

Caused by Porcine herpesvirus 1: alpha herpesvirus

35
Q

What are the clinical manifestations of pseudorabies virus? Are these manifestations different
than those described for BHV-1?

A

Respiratory
- URI
- nasal discharge
- sneezing
- coughing
- dyspnea

Neurologic:
Most common and more severe in piglets: ataxia, paddling, convulsions
Incidental hosts: ruminants “mad itch”

Reproductive
- sows: infertility, abortion, mummified feti

36
Q

Why is pseudorabies and classical swine fever still relevant to large/mixed animal veterinarians?

A
  1. it causes “mad itch” in cattle
  2. in feral hog population
37
Q

Is pseudorabies a concern in commercial hog populations?

A

Currently it is eradicated in the commercial hog population of the US
Most herds require serosurviellence

38
Q

What is Porcine Reproductive Respiratory Syndrome? What does it infect? How is it transmmitted?

A

Arterivirus

PRRS infects pulmonary macrophages
- replicates initially in PAMs then viremia disseminates the virus to multiple tissues

transmission via direct contact, aerosol, semen

39
Q

In PRRS, describe the reproductive manifestations and the respiratory manifestations in Sows.

A

Abortions
- Fetal mummification
- Stillborn pigs
- weak pigs with high mortality
- anorexia - lethargy - fever

40
Q

In PRRS, described the reproductive manifestations and the respiratory manifestations in Piglets.

A

Anorexia
- Fever
- Dyspnea
- Cyanosis of the ears and extremities

41
Q

How long do PRRS clinical signs last?

A

4-5 months
Environmental persistence is high –> once its on the farm its extremely hard to get rid of and there can be alot of subclinical longterm carriers
males are lifelong carriers

42
Q

How does PRRS virus maintain itself in a population of hogs?

A

Subclinical carriers are long-term infected carriers and are key to maintaining the virus in the herd

43
Q

What is a rolling epidemic?

A

In a naive population all animals have no background immunity.
Then initial outbreak will move rapidly and persist for several months creating a pandemic like outbreak with severe clinical illness as animals have no standing immunity.
Eventually its followed by a return to normal or almost normal production. But when a naive group of animals enters into the group it reemerges.
It is the idea that after that initial outbreak there is a slow smoldering attenuation of the effect where it is on again and off again but it is never as severe as it initially was.

Subclinical carriers animals (long-term infected animals) are key to maintaining the virus in the herd

44
Q

Why
are subsequent outbreaks never as severe as the initial outbreak?

A

Because there are animals in the population already that have had the infection prior.
It is the idea that after that initial outbreak there is a slow smoldering attenuation of the effect where it is on again and off again but it is never as severe as it initially was.

45
Q

What are the options for controlling PRRS? What is a controlled infection?

A
  1. Eradication
    - removing all hogs from the premise - repopulating with virus-free
    - stock
    - $$$$$
  2. Control of the infection (better option)
    - nursery depopulation –> pigs are exposed here and piglets show worse signs
    - managing gilts
    - decrease the subpopulations of naive gilts (decrease sick pigs in the nursery)
    - select replacement gilts from the herd instead of bringing in new gilts
    - vaccinate upon entry
    - Controlled infection
46
Q

Vaccines for PRRS?

A

Doesnt prevent infection
Best used to produce consistent immunity
Vaccinate gilts prior to entry in the herd
Boars-reduces shedding the semen
MLV have been associated with reversion to virulence

47
Q

What are the predisposing risks for the development for bronchopneumonia in pigs?

A

Stress+virus = Bacterial pneumonia

Agalactia, poor colostrial immunity
Cold stress due to poor nursery temps
Dust, overcrowding, poor ventilation
Viral primary infection

48
Q

What is Porcine Respiratory Disease Complex

A

Its alot like BRD Complex
P. Multocida is the most common isolated pathogen in PRD

49
Q

Clinical signs of PRD

A
  • Fever
  • Anorexia
  • Depression
  • Cough
  • Vomiting
50
Q

Diagnosis of PRD

A
  • Culture at necropsy
  • Nasal/ Pharyngeal swabs
  • Tonsilar scraping
51
Q

What is Actinobacillus pleuropneumoniae (APP)

A
  • gram (-) primary pathogen
  • very aggressive
  • very contagious
52
Q

What is APP virulence mechanism?

A

virulence mechanisms:
- anti-phagocytic capsule

cytotoxins:
- macrophages
- Neutrophils
- endothelium
- pneumocytes

endotoxin

Once the lower lung is colonized a necrotizing fibrino-hemorrhagic pneumonia ensues

53
Q

Which cattle pathogen is Actinobacillus pleuropneumoniae (APP) most like? Why?

A

Manhheimia
- both viruses create a leukotoxin

54
Q

What is the main source of infection for APP?

A

Subclinical carrier sows
Subclinical carriers were most likely mildly infected individuals, now chronic lifelong carriers.
- Tonsils and nasal passahes harbor the organism

Outbreak occurs following cold snaps and ventilatory stress

55
Q

APP clinical signs

A

death, dyspnea, depression, pyrexia, anorexia
Blood stained froth is consistent finding in highly virulent infections

Case attack rate: 30-50% in nursery and finishing pigs
Case fatality rate: up to 50%

56
Q

What are the defining pathologic characteristics of APP bronchopneumonia?

A

Hemorrhagic necrosis at necropsy

57
Q

TX and control of APP

A

Difficult
Mass medication is frequently employed due to the high morbidity
Commercial vaccine can attenuate clinical signs
Autogenous vaccines may stimulate the best protection
Eradication and depopulation

58
Q

Describe how Mycoplasma hyopneumonia leads to bronchopneumonia.

A

causes bronchopneumonia and acts as a primary infection leading to PRD

sows/gilts= carriers, M. hyo acts as a commensal organism

  • piglets are colonized in farrowing house
  • disease manifests in the nursery
  • Infection is characterized by a slow smoldering inflammation
  • Bronchitis, bronchioloitis, and mild pneumonia
  • Predisposes to more severe pathogens of PRD
59
Q

How to control M. hyo?

A

vaccines can be effective at attenuating the clinical signs, but doesnt prevent infection
Best control is all in/all out
Beginning with pathogen free females

Improved management is important

60
Q

Define polyserositis.

A

infection of all serosal membranes
-> pericardium, pleura, synovium, and meninges

61
Q

What is Glasser’s Disease?

A

Glasserella (Haemophilus) parasuis
- characterized by polyserositis (pericardium, pleura, syn- ovium, and meninges)

62
Q

Clincial signs of Glasser’s Disease

A

CNS
- TremorsAtaxia
- Recumbency
- Depression
- Opisthodomos

Septic arthritis: swollen lame joints, pigs standing on their toes

Respiratory:
- dyspnea
- cyanosis

63
Q

Pathophysiology of Glasser’s Disease

A

Commensal Organism in some animals –> spreads to naive pigs –> septicemia –> colonization of multiple membrane bound structures and organs

64
Q

Control of Glasser’s Disease

A

Vaccines attenuate clinical signs –> not good
ALl in/all out
and good management

65
Q

What clinical presentation differentiates Glasser’s disease and Mycoplasma hyorhinis?

A

like Glasser’s disease but WITHOUT the CNS signs
- characterized by polyserositis (pericardium, pleura, syn- ovium)

Septic arthritis: swollen lame joints, pigs standing on their toes

Respiratory:
- dyspnea
- cyanosis

66
Q

How can M.Hyor and Glasser’s
disease be differentiated?

A

Only culture can differentiate Glasser’s from M. hyorhinis

67
Q

Control of M. Hyorhinis?

A

No effective vaccine
Pathogen free breeding stock
All in/all out

68
Q

What is Salmonella Cholerasuis?

A

GI disease gone bad
This is a host adapted strain in pigs, it starts as GI then gains access to vasculature and causes septicemia, bacteremia and that spreads to respiratory tract

69
Q

Clinical signs of Salmonella Cholerasuis?

A

High fever
depression
anorexia
diarrhea occurs 3-4 days after the other signs develop.
Septicemia
Cyanosis of extremities and belly
Dyspnea
Death

CNS:
Meningitis, arthritis, liver, kidneys

70
Q

Control of Salmonella Cholerasuis?

A

Attenuated vaccine shows promise at containing teh disease

Best way to manage is starting with pathogen free pigs, eliminating stress, eliminating the reservoir of infection (mostly sows and gilts)

Respiratory (9 decks)

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