Swine Respiratory Diseases

Question 1

contrast interstitial disease pattern to bronchopneumonia pattern

Answer 1

interstitial:
-inflammation, maybe hemorrhagic
-diffuse edema between the lung tissue causes the pattern, animal has very hard time breathing (will not be able to stand)
-lung feels squishy/spongy
-seen more commonly with viruses

bronchopneumonia:
-can be localized to one or a few lobes; animal can still breathe! may present with coughing, dyspnea or thumping (abdominal effort to expel air)
-still standing up and walking around
-consolidated = fluid takes the place of air
-lung feels firm
-seen more commonly with bacteria

Question 2

compare normal lung histology to interstital and bronchopneumonia patterns

Answer 2

normal: plenty of room for air

interstitial: edema compresses normal tissue

bronchopneumonia: no ability to exchange air through affected tissue
-will see lots of WBCs

Question 3

describe atrophic rhinitis

Answer 3

1. characterized by snuffling, sneezing, and sometimes nosebleeds
   -due to atrophy and distortion of nasal turbinates
2. symptoms can appear as young as 1 week of age
3. etiology:
   -toxigenic strains of bordetella bronchiseptica and pasteurella multicoda type D
   -both can be normal nasal flora!
   -endotoxin from gram negative bacteria causes pathology

Question 4

describe management standpoint of atrophic rhinitis

Answer 4

1. management and husbandry linked
   -dust
   -endotoxin from gram negative bacteria overgrowth
   -ventilation is important!
2. infection can result in carrier pigs
   -may lead to introduction into naive herds
3. control:
   -improve husbandry
   -vaccination
   -medication
   -depopulation/repopulation (slaughter surveillance)

Question 5

describe symptoms and diagnostics of atrophic rhinitis

Answer 5

symptoms:
1. sneezing
2. snorting
3. serous or mucopurulent nasal discharge
4. facial staining due to obstruction of tear ducts

diagnostics:
1. history, lesions, clinical signs!!
2. can bacterial culture from affected animals

Question 6

describe mycoplasma hyopneumoniae, include clinical signs

Answer 6

1. enzootic disease of swine (endemic)
   -NUMBER ONE BACTERIAL RESPIRATORY DISEASE OF SWINE
2. component of porcine respiratory disease complex (PRDC)
3. carrier swine are most common source of infection
4. clinical signs:
   -chronic persistent, non-productive cough
   -suppressed growth rates despite normal appetites
   -morbidity is high, mortality is usually low

Question 7

describe epidemiology of mycoplasma hyopneumoniae

Answer 7

1. does not survive well in the environment but will survive in the pig for months (at least 5 months)
2. not believed to be spread by other animals
3. spread is usually by nose-to-nose contact or aerosol transmission

Question 8

describe pathogenesis of mycoplasma hyopneumonia

Answer 8

1. cranioventral lung consolidation
2. poor air quality may predispose to infection
3. initial lesions are bronchitis and bronchiolitis, which leads to hyperplasia of mucus secreting cells
   -this results in an inflammatory reaction spreading into alveoli leading to alveolitis, pneumonia, and airway obstruction

-increased accumulation of lymphoid tissue around airways and blood vessels (perivascular cuffing)

-these pigs cough a LOT

Question 9

describe necropsy lesions, diagnosis, treatment, and control of mycoplasma hyopneumoniae

Answer 9

necropsy lesions:
-well demarcated cranio-ventral lung consolidation!!

2. diagnosis:
   -IHC
   -PCR
   -serologic tests for previous exposure needed in addition to tracheal swab
   -tracheal swab is ideal sample to collect and look for the organism itself!
3. treatment: parenteral antibiotics or water or feed grade
   -NOT beta lactams (mycoplasma have no cell wall; need macrolides, tetracyclines, aminoglycosides)
4. control:
   -vaccine is somewhat efficacious, need continuous boosters
   -herd elimination programs

Question 10

describe actinobacillus pleuropneumoniae (APP)

Answer 10

1. hemolytic gram negative capsulated coccobacillary rod
   -HOST SPECIFIC for swine
2. two biotypes present: distinguish by dependency for nicotinamide adenine dinucleotide in culture
3. 15 serotypes: 1 and 5 considered most virulence
4. does not persist in the environment (enveloped)
5. 4 exotoxins, also called RTX toxins
   -cytotoxic or hemolytic
   -antibodies to exotoxins are important in protective immunity

Question 11

describe epidemiology of APP

Answer 11

1. survivors remain carriers
2. subclinical carriers also possible
3. transmission by direct contact through nasal secretions and aerosol
4. fomites can spread but don’t remain infectious for long

Question 12

describe pathogenesis of APP

Answer 12

1. hemolysin and toxins are active against endothelial cells and pulmonary alveolar macrophages
2. vasculitis in lungs:
   -proceeds thrombosis and followed by infarction and sequestration of infarct in the lungs
3. sudden death by endotoxic shock
4. colostral immunity may allow gradual development of immunity
5. naive pigs develop fulminating disease
6. easy to diagnose in the field
   -lots of fibrosis
   -cut into tissue and it just bleeds everywhere

Question 13

describe clinical signs of APP

Answer 13

1. acute outbreaks; sudden death is common
2. prostration, high temp, apathy, anorexia, stiffness, vomiting, diarrhea
3. shallow, non-productive cough
4. as disease progresses, dyspnea with mouth breathing and possibly foamy bloody discharge from mouth and nose
5. peripheral cyanosis of extremities
   -generalized cyanosis follows
6. morbidity and mortality varies but can be very high
7. chronic cough may be present following acute outbreak
   -also see slow growth

Question 14

describe lesions of APP

Answer 14

usually restricted to respiratory tract

1. necro-hemorrhageic consolidation accompanied by fibrinous pleuritis
2. thoracic cavity contains blood-tinged fluid
3. hemorrhage and necrosis in dorsal portion of diaphragmatic lobes
4. lesions in lungs are dark red to black, firm, and develop infarction
5. bloody froth may fill larger airways leading to interlobular edema
6. serofibrinous pericardiits
7. pharyngitis
8. occasional polyarthritis
9. chronic cases may have large sequestered or encapsulated nodules of necrosis in the lungs that incompletely resolve
   -fibrous adhesions to rib cage = slaughter condemnation

Question 15

describe diagnosis of APP

Answer 15

1. onset of acute rapidly spreading disease with high morbidity and mortality
2. dark red infarcts in lungs
3. isolation and ID of organism through culture
4. PCR is available and can ID toxin genes
5. complement fixation and ELISA may also be used for diagnosis

Question 16

describe control of APP

Answer 16

1. limit new swine introduction in APP-free herds
2. quarantine at least 30 days
3. vaccination with subunit vaccines or older type vaccines (not as cross protective)
4. depopulation of positive sow farms is economically efficient
   -thorough cleaning and disinfection of facilities
   -restock with APP-free breeding stock
5. early weaning or medicated early weaning (<17d of age) is effective at reducing spread of disease to youngstock

Question 17

describe antibiotics for APP

Answer 17

1. chronic cases generally unresponsive

see ppt for types

Question 18

describe PRRS

Answer 18

1. porcine repro and resp syndrome
   -can see repro failure in breeding animals: abortions, increased mummies and stillbirths, conception failure, boar sterility)
   -resp syndrome is more common in growing animals
2. European and North America Strains
3. widely considered the most economically important disease affecting swine producers
   -uncomplicated outbreaks could easily cost >1million
4. HIGH prevalence in commercial pigs and also frequently ID in exhibition swine

Question 19

describe the PRRS virus

Answer 19

1. enveloped RNA virus: high rate of mutation!! can fine 2-3 strains on just one farm
   -significant heterogenicity
2. moderately resistant to environmental degradation
3. inactivated by phenol, formaldehyde, and most common disinfectants
4. predilection for immune cells:
   -pulmonary intravascular macrophages
   -pulmonary alveolar macrophages (use to isolate virus in vitro)
   -can replicate significantly inside these cells
5. strains vary widely in virulense
6. can see significant interaction with other diseases
   -esp M. hyopneumoniae

Question 20

describe epidemiology of PRRS

Answer 20

1. persists longterm in carrier pigs (>200 days) however most stop shedding by 60d post infection
2. decrease in antibody titers 4-8 months after infection
3. highly infectious (10 virions can cause disease)
   -not highly contagious
4. found in nasal secretions, urine, semen, mammary secretions, feces
   -rapid spread through infected semen: boar stud = major control point, can shed PRRS for up to 92 days post infection in semen, impact dams during breeding
5. aerosol spread is possible
6. sows infected while pregnant become viremic, persistently infected pigs
   -results in shedding and ifnection to other pigs during lactation and nursery/growing phases of production
   -older infected pigs held back in nurseries, hold-back litters, or cross-fostered can infect younger pigs

Question 21

describe pathogenesis of PRRS

Answer 21

1. transmission of virus to tonsils or upper resp system leads to primary replication in lymphoid tissues and persistent viremia
2. infects and compromises the function of PMS and PAMS leads to interstitial pneumonia
   -increases susceptibility of lungs to other pathogens
3. can cross placenta in late gestation and may reach higher titers in fetus
4. may kill all, part, or non of fetus
   -hypoxia as a result of arteritis in umbilical vessels
   -abortions are common as well as mummies

Question 22

describe general clinical signs of PRRS

Answer 22

many herds have subclinical disease and do not recognize symptoms

-symptoms influenced by: virulence, ongoing or new infection, age group, other disease agents present, and herd size

include:
-anorexia
-fever
-lethargy
-depression
-resp distress
-mild cyanosis of ears, abdomen, and vulva

Question 23

describe reproductive syndrome of PRRS

Answer 23

1. decreased live borns and increased still borns
2. late term abortions
3. premature farrowings
4. pre-weaning mortality can be high
5. still born or weak piglets and increased mummified fetuses
6. nursing pigs may have dyspnea/thumping
7. repro symptoms may last 2-3 months followed by slow improvement in repro performance without intervention
8. may see cyclical disease if naive animals are introduced for certain populations are not infected during initial outbreak
9. can see outbreaks with multiple heterologous strains at the same time
10. boars: decrease in semen quality

Question 24

describe clinical signs of PRRS in growing pigs (6)

Answer 24

1. fever, depression, lethargy, stunting due to systemic illness and pneumonia
2. followed by expiratory dyspnea and stunting
3. peak disease occurs 4-10 weeks of age
4. post-weaning mortality is significantly, particularly with virulent strains and co-infections
5. older pigs may have significant signs, particularly if naive
6. heterologous strains may make it worse

Question 25

describe PRRS lesions

Answer 25

1. mild to severe lesion in lungs and lymph nodes
2. interstitial pneumonia varies from multifocal to lobular to diffuse in distribution
3. lungs may be mottled and tan in appearance
4. lymph nodes are generally swollen, tan, and edematous or cystic
5. microscopic lesions may include nonsuppurative interstitial pneumonia, mild nonsuppurative encephalitis, myocarditis, rhinitis, and depletion of germinal centers of lymph nodes

Question 26

describe diagnosis of PRRS

Answer 26

1. clinical signs and history
2. tests:
   -virus isolation
   -IFA
   -PCR: sequencing
   -serology: indicates past exposure; useful for indicating age of infection
3. best to look at affected pigs during early stages of disease
   -abortions, weakborn neonates, clinically affected pigs/sows
   -serum, BAL, lung, lymph nodes, tonsil, and spleen
   -sows not sick at time of abortion are usually not viremic but have high levels of circulating antibodies
   -fresh tissue can be tested with IHC or PCR

Question 27

describe control of PRRS

Answer 27

1. quarantine affected animals (may shed for 60-200d)
2. avoid moving pigs between litters
3. control secondary pathogens
4. acclimation strategies if in endemic regions
   -vaccination
   -live-virus inoculation
   -animal exposure
5. depopulation/repopulation
6. herd closure for at least 200 days

potentially use of CRISPR in future

Question 28

describe influenza A virus of swine

Answer 28

1. type A orthomyxoviridae virus
2. glycoprotein spikes on surface as major antigens
   -hemagglutinin
   -neuraminidase
3. classic subtype in swine is H1N1, with emergence of H3N2 and H1N2
4. survival outside host is short (<2 weeks) and virus is easily inactivated
5. zoonotic potential!!
6. characteristic by sudden onset of fever, oculonasal discharge, prostration, weakness, anorexia, and coughi ng
7. uncomplicated SIV rarely causes mortality, but may cause significant weight loss, BCS changes, and medication costs associated with disease
8. morbidity is super high while mortality super low
   -concurrent infections can increasing culling risk and death loss
9. illness during pregnancy may lead to abortion due to acute illness in the sows

Question 29

describe influenza A pathogenesis

Answer 29

1. nasopharyngeal access and enters through respiratory epithelium, where it can cause severe inflammation with degeneration and necrosis of cells lining bronchi and bronchioles
2. virus can be found in interlobular septa, sometimes in turbinate epithelium and mediastinal lymph nodes
3. in the lung, alveolar Type 2 pneumocytes are most commonly affected and they produce less surfactant, impairing phagocytosis of secondary organisms by alveolar macrophages
   -inflam exudate may block smaller airways leading to atelectasis, emphysema, and bronchointerstitial pneumonia

-epi damage can be repaired in 5-7 days in most cases

4. IAV can combine with other viral subtypes to produce novel strains in pigs and can be transferred to other species

Question 30

describe influenza A clinical signs

Answer 30

1. respiratory illness appears suddenly in a group of pigs
   -prostration, weakness, high fevers (104-106), coughing, anorexia, and conjunctivitis
   -herd usually is recovered within 2 weeks
2. uncomplicated SIV rarely causes mortality
   -may be significant wt loss, BCS changes, and medication costs associated though
3. morbidity very high, mortality remains low
   -concurrent infections can increase culling risk and death loss
4. illness during pregnancy may lead to abortion due to acute illness
   -transplacental infection is rare

Question 31

describe influenza A lesions

Answer 31

1. lobular distribution of congestion, firmness, atelectasis, emphysema, perhaps pneumonia
2. gross lesions usually restricted to apical and cardiac lobes but may be more widespread
3. airways have blood tinged exudate
4. regional lymph nodes may be moderately enlarged
5. degeneration and necrosis of the airway epithelium and obstruction of airways with exudate
6. +/- bronchointerstitial pneumonia
7. edema and congestion of entire lung lobes may be present
8. characteristic lesion of necrotizing bronchiolitis

Question 32

describe influenza A diagnosis

Answer 32

1. sudden onset of disease with rapid recovery in widespread nature across herd
2. IFA test on fresh lung secretions or IHC on formalin fixed lung secretions
3. virus may be isolated from nasal swabs or lung tissue in chick embryos
4. PCR on nasal swabs or lungs
5. paired serologic tests demonstrating a rising tier to SIV
6. common to have co-infections including mycoplasma hyopneumoniae but also other diseases

Question 33

describe influenza A control

Answer 33

1. vaccination of the breeding herd with killed vaccine prior to farrowing will help stabilize herds
   -differences in subtypes may decrease efficacy
   -maternal immunity may block vaccination
2. modified live virus vaccination: intranasal vaccine
   -may reduce shedding in pigs and reduce infection opportunities throughout production

Question 34

describe porcine respiratory coronavirus

Answer 34

NOT ZOONOTIC

does not cause clinical infection in pigs!!!
-can ID asymptomatic herd through serology