Swine Respiratory Diseases Flashcards
1
Q
contrast interstitial disease pattern to bronchopneumonia pattern
A
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
2
Q
compare normal lung histology to interstital and bronchopneumonia patterns
A
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
3
Q
describe atrophic rhinitis
A
- characterized by snuffling, sneezing, and sometimes nosebleeds
-due to atrophy and distortion of nasal turbinates - symptoms can appear as young as 1 week of age
- etiology:
-toxigenic strains of bordetella bronchiseptica and pasteurella multicoda type D
-both can be normal nasal flora!
-endotoxin from gram negative bacteria causes pathology
4
Q
describe management standpoint of atrophic rhinitis
A
- management and husbandry linked
-dust
-endotoxin from gram negative bacteria overgrowth
-ventilation is important! - infection can result in carrier pigs
-may lead to introduction into naive herds - control:
-improve husbandry
-vaccination
-medication
-depopulation/repopulation (slaughter surveillance)
5
Q
describe symptoms and diagnostics of atrophic rhinitis
A
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
6
Q
describe mycoplasma hyopneumoniae, include clinical signs
A
- enzootic disease of swine (endemic)
-NUMBER ONE BACTERIAL RESPIRATORY DISEASE OF SWINE - component of porcine respiratory disease complex (PRDC)
- carrier swine are most common source of infection
- clinical signs:
-chronic persistent, non-productive cough
-suppressed growth rates despite normal appetites
-morbidity is high, mortality is usually low
7
Q
describe epidemiology of mycoplasma hyopneumoniae
A
- does not survive well in the environment but will survive in the pig for months (at least 5 months)
- not believed to be spread by other animals
- spread is usually by nose-to-nose contact or aerosol transmission
8
Q
describe pathogenesis of mycoplasma hyopneumonia
A
- cranioventral lung consolidation
- poor air quality may predispose to infection
- 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
9
Q
describe necropsy lesions, diagnosis, treatment, and control of mycoplasma hyopneumoniae
A
necropsy lesions:
-well demarcated cranio-ventral lung consolidation!!
- 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! - treatment: parenteral antibiotics or water or feed grade
-NOT beta lactams (mycoplasma have no cell wall; need macrolides, tetracyclines, aminoglycosides) - control:
-vaccine is somewhat efficacious, need continuous boosters
-herd elimination programs
10
Q
describe actinobacillus pleuropneumoniae (APP)
A
- hemolytic gram negative capsulated coccobacillary rod
-HOST SPECIFIC for swine - two biotypes present: distinguish by dependency for nicotinamide adenine dinucleotide in culture
- 15 serotypes: 1 and 5 considered most virulence
- does not persist in the environment (enveloped)
- 4 exotoxins, also called RTX toxins
-cytotoxic or hemolytic
-antibodies to exotoxins are important in protective immunity
11
Q
describe epidemiology of APP
A
- survivors remain carriers
- subclinical carriers also possible
- transmission by direct contact through nasal secretions and aerosol
- fomites can spread but don’t remain infectious for long
12
Q
describe pathogenesis of APP
A
- hemolysin and toxins are active against endothelial cells and pulmonary alveolar macrophages
- vasculitis in lungs:
-proceeds thrombosis and followed by infarction and sequestration of infarct in the lungs - sudden death by endotoxic shock
- colostral immunity may allow gradual development of immunity
- naive pigs develop fulminating disease
- easy to diagnose in the field
-lots of fibrosis
-cut into tissue and it just bleeds everywhere
13
Q
describe clinical signs of APP
A
- acute outbreaks; sudden death is common
- prostration, high temp, apathy, anorexia, stiffness, vomiting, diarrhea
- shallow, non-productive cough
- as disease progresses, dyspnea with mouth breathing and possibly foamy bloody discharge from mouth and nose
- peripheral cyanosis of extremities
-generalized cyanosis follows - morbidity and mortality varies but can be very high
- chronic cough may be present following acute outbreak
-also see slow growth
14
Q
describe lesions of APP
A
usually restricted to respiratory tract
- necro-hemorrhageic consolidation accompanied by fibrinous pleuritis
- thoracic cavity contains blood-tinged fluid
- hemorrhage and necrosis in dorsal portion of diaphragmatic lobes
- lesions in lungs are dark red to black, firm, and develop infarction
- bloody froth may fill larger airways leading to interlobular edema
- serofibrinous pericardiits
- pharyngitis
- occasional polyarthritis
- chronic cases may have large sequestered or encapsulated nodules of necrosis in the lungs that incompletely resolve
-fibrous adhesions to rib cage = slaughter condemnation
15
Q
describe diagnosis of APP
A
- onset of acute rapidly spreading disease with high morbidity and mortality
- dark red infarcts in lungs
- isolation and ID of organism through culture
- PCR is available and can ID toxin genes
- complement fixation and ELISA may also be used for diagnosis
16
Q
describe control of APP
A
- limit new swine introduction in APP-free herds
- quarantine at least 30 days
- vaccination with subunit vaccines or older type vaccines (not as cross protective)
- depopulation of positive sow farms is economically efficient
-thorough cleaning and disinfection of facilities
-restock with APP-free breeding stock - early weaning or medicated early weaning (<17d of age) is effective at reducing spread of disease to youngstock
17
Q
describe antibiotics for APP
A
- chronic cases generally unresponsive
see ppt for types
18
Q
describe PRRS
A
- 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 - European and North America Strains
- widely considered the most economically important disease affecting swine producers
-uncomplicated outbreaks could easily cost >1million - HIGH prevalence in commercial pigs and also frequently ID in exhibition swine
19
Q
describe the PRRS virus
A
- enveloped RNA virus: high rate of mutation!! can fine 2-3 strains on just one farm
-significant heterogenicity - moderately resistant to environmental degradation
- inactivated by phenol, formaldehyde, and most common disinfectants
- predilection for immune cells:
-pulmonary intravascular macrophages
-pulmonary alveolar macrophages (use to isolate virus in vitro)
-can replicate significantly inside these cells - strains vary widely in virulense
- can see significant interaction with other diseases
-esp M. hyopneumoniae
20
Q
describe epidemiology of PRRS
A
- persists longterm in carrier pigs (>200 days) however most stop shedding by 60d post infection
- decrease in antibody titers 4-8 months after infection
- highly infectious (10 virions can cause disease)
-not highly contagious - 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 - aerosol spread is possible
- 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
21
Q
describe pathogenesis of PRRS
A
- transmission of virus to tonsils or upper resp system leads to primary replication in lymphoid tissues and persistent viremia
- infects and compromises the function of PMS and PAMS leads to interstitial pneumonia
-increases susceptibility of lungs to other pathogens - can cross placenta in late gestation and may reach higher titers in fetus
- may kill all, part, or non of fetus
-hypoxia as a result of arteritis in umbilical vessels
-abortions are common as well as mummies
22
Q
describe general clinical signs of PRRS
A
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
23
Q
describe reproductive syndrome of PRRS
A
- decreased live borns and increased still borns
- late term abortions
- premature farrowings
- pre-weaning mortality can be high
- still born or weak piglets and increased mummified fetuses
- nursing pigs may have dyspnea/thumping
- repro symptoms may last 2-3 months followed by slow improvement in repro performance without intervention
- may see cyclical disease if naive animals are introduced for certain populations are not infected during initial outbreak
- can see outbreaks with multiple heterologous strains at the same time
- boars: decrease in semen quality
24
Q
describe clinical signs of PRRS in growing pigs (6)
A
- fever, depression, lethargy, stunting due to systemic illness and pneumonia
- followed by expiratory dyspnea and stunting
- peak disease occurs 4-10 weeks of age
- post-weaning mortality is significantly, particularly with virulent strains and co-infections
- older pigs may have significant signs, particularly if naive
- heterologous strains may make it worse
25
Q
describe PRRS lesions
A
- mild to severe lesion in lungs and lymph nodes
- interstitial pneumonia varies from multifocal to lobular to diffuse in distribution
- lungs may be mottled and tan in appearance
- lymph nodes are generally swollen, tan, and edematous or cystic
- microscopic lesions may include nonsuppurative interstitial pneumonia, mild nonsuppurative encephalitis, myocarditis, rhinitis, and depletion of germinal centers of lymph nodes
26
Q
describe diagnosis of PRRS
A
- clinical signs and history
- tests:
-virus isolation
-IFA
-PCR: sequencing
-serology: indicates past exposure; useful for indicating age of infection - 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
27
Q
describe control of PRRS
A
- quarantine affected animals (may shed for 60-200d)
- avoid moving pigs between litters
- control secondary pathogens
- acclimation strategies if in endemic regions
-vaccination
-live-virus inoculation
-animal exposure - depopulation/repopulation
- herd closure for at least 200 days
potentially use of CRISPR in future
28
Q
describe influenza A virus of swine
A
- type A orthomyxoviridae virus
- glycoprotein spikes on surface as major antigens
-hemagglutinin
-neuraminidase - classic subtype in swine is H1N1, with emergence of H3N2 and H1N2
- survival outside host is short (<2 weeks) and virus is easily inactivated
- zoonotic potential!!
- characteristic by sudden onset of fever, oculonasal discharge, prostration, weakness, anorexia, and coughi ng
- uncomplicated SIV rarely causes mortality, but may cause significant weight loss, BCS changes, and medication costs associated with disease
- morbidity is super high while mortality super low
-concurrent infections can increasing culling risk and death loss - illness during pregnancy may lead to abortion due to acute illness in the sows
29
Q
describe influenza A pathogenesis
A
- nasopharyngeal access and enters through respiratory epithelium, where it can cause severe inflammation with degeneration and necrosis of cells lining bronchi and bronchioles
- virus can be found in interlobular septa, sometimes in turbinate epithelium and mediastinal lymph nodes
- 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
- IAV can combine with other viral subtypes to produce novel strains in pigs and can be transferred to other species
30
Q
describe influenza A clinical signs
A
- 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 - uncomplicated SIV rarely causes mortality
-may be significant wt loss, BCS changes, and medication costs associated though - morbidity very high, mortality remains low
-concurrent infections can increase culling risk and death loss - illness during pregnancy may lead to abortion due to acute illness
-transplacental infection is rare
31
Q
describe influenza A lesions
A
- lobular distribution of congestion, firmness, atelectasis, emphysema, perhaps pneumonia
- gross lesions usually restricted to apical and cardiac lobes but may be more widespread
- airways have blood tinged exudate
- regional lymph nodes may be moderately enlarged
- degeneration and necrosis of the airway epithelium and obstruction of airways with exudate
- +/- bronchointerstitial pneumonia
- edema and congestion of entire lung lobes may be present
- characteristic lesion of necrotizing bronchiolitis
32
Q
describe influenza A diagnosis
A
- sudden onset of disease with rapid recovery in widespread nature across herd
- IFA test on fresh lung secretions or IHC on formalin fixed lung secretions
- virus may be isolated from nasal swabs or lung tissue in chick embryos
- PCR on nasal swabs or lungs
- paired serologic tests demonstrating a rising tier to SIV
- common to have co-infections including mycoplasma hyopneumoniae but also other diseases
33
Q
describe influenza A control
A
- 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 - modified live virus vaccination: intranasal vaccine
-may reduce shedding in pigs and reduce infection opportunities throughout production
34
Q
describe porcine respiratory coronavirus
A
NOT ZOONOTIC
does not cause clinical infection in pigs!!!
-can ID asymptomatic herd through serology
