Swine Respiratory Diseases PDF

Swine Respiratory Diseases University of Georgia College of Veterinary Medicine Brad Heins DVM, MFAM, DACVPM [email protected] Swine Respiratory System Pneumonia Interstitial pattern – think more Bronchopneumonia pattern – think about viruses than other causes m...

Swine Respiratory Diseases University of Georgia College of Veterinary Medicine Brad Heins DVM, MFAM, DACVPM [email protected] Swine Respiratory System Pneumonia Interstitial pattern – think more Bronchopneumonia pattern – think about viruses than other causes more about bacteria Normal Lung Histology Pneumonia Interstitial pattern – think more Bronchopneumonia pattern – think about viruses than other causes more about bacteria Respiratory: Atrophic Rhinitis Characterized by snuffling, sneezing and sometimes nosebleeds Atrophy and distortion of nasal turbinates Symptoms can appear as young as 1 week of age Etiology Toxigenic strains of Bordetella bronchiseptica and Pasteurella multocida Type D Both can be normal nasal flora Endotoxin from Gram - Bacteria Chih-MingLiaoacChienjinHuangbShih-LingHsuanaZeng-WengChenbWei- ChengLeeaCheng-ILiuaJames R.WintondMaw-ShengChiena. Immunogenicity and efficacy of three recombinant subunit Pasteurella multocida toxin vaccines against progressive atrophic rhinitis in pigs. Vaccine vol 24, issue 1, p 27-35. 2006. Respiratory: Atrophic Rhinitis Management and Husbandry linked Dust Endotoxin from Gram – bacteria Ventilation is important Infection can result in inapparent carrier pigs May lead to introduction into naïve herds Control: Improve husbandry Vaccination Medication https://www.minipiginfo.com/mini- pig-artophic-rhinitis.html Depopulation/Repopulation Respiratory: Atrophic Rhinitis Symptoms: Sneezing Snorting Serous or mucopurulent nasal discharge Facial staining due to obstruction of tear ducts Diagnostics: History, lesions, clinical signs Bacterial culture from affected animals Respiratory: Mycoplasma hyopneumoniae Enzootic disease of swine Component of the Porcine Respiratory Disease Complex (PRDC) Carrier swine are most common source of the infection Clinical Signs: Chronic, persistent and non-productive cough Suppressed growth rates despite normal appetites Morbidity is high, but mortality is usually low Respiratory: Mycoplasma hyopneumoniae Epidemiology Does not survive well in the environment but will survive in the pig for months Not believed to be spread by other animals Spread is usually by nose-to-nose contact or aerosol transmission Pathogenesis Cranioventral lung consolidation Poor air quality may predispose to infection Initial lesions are bronchitis and bronchiolitis → hyperplasia of mucus secreting cells → inflammatory reaction spreading into alveoli leading to alveiolitis, pneumonia, and airway obstruction Increased accumulation of lymphoid tissue around airways and blood vessels (perivascular cuffing) Respiratory: Mycoplasma hyopneumoniae Necropsy Lesions Well demarcated cranio-ventral lung consolidation Diagnosis Immunohistochemistry PCR Serologic tests for previous exposure Treatment Parenteral antibiotics or water or feed grade Control Vaccine is somewhat efficacious Herd elimination programs https://www.merckvetmanual.com/respira tory-system/respiratory-diseases-of- pigs/mycoplasmal-pneumonia-in-pigs Actinobacillus pleuropneumoniae (APP) Actinobacillus pleuropneumoniae is a hemolytic Gram- capsulated coccobacillary rod and is host specific for swine. Two biotypes are present (Distinguished by dependency for nicotinamide adenine dinucleotide in culture) 15 serotypes (1,3,5,7 are the most common in the US) (1 and 5 considered more virulent) Does not persist in the environment 4 exotoxins (ApxI, ApxII, ApxIII, ApxIV) also called RTX toxins Cytotoxic or hemolytic Antibodies to exotoxins are important in protective immunity Actinobacillus pleuropneumoniae (APP) Epidemiology Survivors remain carriers Subclinical carriers Transmission by direct contact through nasal secretions, aerosol Fomites can spread but don’t remain infectious long Pathogenesis Hemolysin and toxins are active against endothelial cells and pulmonary alveolar macrophages Vasculitis in lungs Proceeds thrombosis and followed by infarction and sequestration of infarcts in the lungs Sudden death by endotoxic shock Colostral immunity may allow gradual development of immunity Naïve pigs develop fulminating disease Actinobacillus pleuropneumoniae (APP) https://www.ksvdl.org/reports/april_2017/porcine.html Actinobacillus pleuropneumoniae (APP) Clinical Signs Acute outbreaks → sudden death is common Prostration, high temperatures, apathy, anorexia, stiffness, vomiting and diarrhea Shallow, non-productive cough may be present 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 Actinobacillus pleuropneumoniae (APP) Lesions Usually restricted to respiratory tract Necro-hemorrhagic consolidation accompanied with 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 → interlobular edema Serofibrinous pericarditis 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 Actinobacillus pleuropneumoniae (APP) Diagnosis Onset of acute, rapidly spreading disease with high morbidity and mortality Dark red infarcts in lungs Isolation and identification of the organism through culture PCR is available and can identify toxin genes Complement fixation and ELISA may also be used for diagnosis Control 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 effective Thorough cleaning and disinfection of facilities Restock with APP-free breeding stock Early weaning or medicated early weaning ( $1M due to lost production, animal loss, medication expenses, poor feed conversion etc High prevalence in commercial pigs and also frequently identified in exhibition swine Respiratory: PRRS Enveloped RNA arterivirus Significant heterogeneity in PRRS genome due to common transcription errors in RNA. Genetic and antigenic variability between isolates is a significant challenge to control disease Moderately resistant to environmental degradation Inactivated by phenol, formaldehyde and most common disinfectants Predilection for immune cells including pulmonary intravascular macrophages (PIMs) and pulmonary alveolar macrophages (PAMs) where it can replicate significantly PAMs can be used to isolate and replicate the virus in vitro Strains vary widely in virulence Can see significant interaction with other diseases, particularly M. hyopneumoniae. Respiratory: PRRS Epidemiology Persists long term in carrier pigs (>200 days) however most stop shedding by 60 days post infection Decrease in antibody titers 4-8 months after infection Virus is highly infectious (10 virions can cause disease) but it is not highly contagious Found in nasal secretions, urine, semen, mammary secretions and feces Rapidly spreads through infected semen (Boar stud is major critical control point) Boars can shed PRRS for up to 92 days post infection in semen and this can impact dams during breeding Aerosol spread is possible Sows infected while pregnant → viremic, persistently infected pigs → shedding and infection 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 Respiratory: PRRS Pathogenesis Transmission of virus to tonsils or upper respiratory system → primary replication in lymphoid tissues → persistent viremia Infects and compromises the function of PIMS and PAMS → interstitial pneumonia Increases susceptibility of lungs to other pathogens Can cross placenta in late gestation and may reach higher titers in the fetus May kill all, part or none of fetuses Hypoxia as a result of arteritis in umbilical vessels Abortions are common as well as mummies Respiratory: PRRS Clinical Signs (May see Reproductive and Respiratory Syndromes simultaneously) Many herds have subclinical disease and do not recognize symptoms Influenced by: Virulence of the virus Whether it is an ongoing or new infection The age group affected Other disease agents present Herd size Anorexia, fever, lethargy, depression and respiratory distress. Mild cyanosis of ears, abdomen and vulva may be seen Respiratory - PRRS Clinical Signs – Breeding Age (reproductive syndrome) Decrease live borns and increased still borns Late term abortions Premature farrowings Stillborn or weak piglets and increased mummified fetuses Pre-weaning mortality can be high Decrease in the number of dams that conceive and farrow Nursing pigs may have dyspnea (thumping) Reproductive symptoms may last for 2-3 months followed by a slow improvement in reproductive performance (if intervention does not occur) May see cyclical disease if naïve animals are introduced for certain populations are not infected during the initial outbreak. Can see outbreaks with multiple heterologous strains simultaneously Boars → decrease in semen quality Respiratory - PRRS Clinical Signs – Growing Pigs Fever, depression, lethargy, stunting due to systemic illness and pneumonia Sneezing, fever and lethargy are followed by expiratory dyspnea and stunting Peak disease occurs 4-10 weeks of age Post weaning mortality is significantly increased, particularly with virulent strains and co-infections Older pigs may have significant signs, particularly if naïve Heterologous strains may make it worse Respiratory: PRRS Lesions Mild to severe lesions 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 Respiratory: PRRS Diagnosis Clinical signs and history suggest PRRS Tests Virus isolation Fluorescent antibody tests Immunohistochemistry PCR – allows sequencing Serology – indicates past exposure 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 the time of abortion are usually not viremic but have high levels of antibodies circulating Fresh tissue can be tested with IHC or PCR Serology is useful for determining age of infection, exposure status but may not differentiate between strains or vaccination status IFA ELISA Sequencing using restriction enzymes and RNA fragments (RFLP) Respiratory: PRRS Control Quarantine affected animals (may shed for 60-200 days) Avoid moving pigs between litters (MCREBEL) Control secondary pathogens Acclimation strategies if in an endemic regions Vaccination Live-virus inoculation Animal Exposure Depopulation/Repopulation Herd closure for at least 200 days Future control strategy? CRISPR technology to eliminate receptors for virus within pigs Respiratory: Influenza A Virus of Swine Type A Orthomyxoviridae virus Glycoprotein spikes on the surface serve as major antigens Hemagglutinin (H) – 16 varieties Neuraminidase (N) – 9 varieties Classic subtype in swine is H1N1, with emergence of H3N2 and H1N2 Survival outside the host is short (