About: Coinfection modulates inflammatory responses, clinical outcome and pathogen load of H1N1 swine influenza virus and Haemophilus parasuis infections in pigs

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About: Coinfection modulates inflammatory responses, clinical outcome and pathogen load of H1N1 swine influenza virus and Haemophilus parasuis infections in pigs Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Coinfection modulates inflammatory responses, clinical outcome and pathogen load of H1N1 swine influenza virus and Haemophilus parasuis infections in pigs
Creator	Pejsak, Zygmunt Kwit, Krzysztof Pomorska-Mól, Małgorzata Czyżewska-Dors, Ewelina Dors, Arkadiusz
Source	Medline; PMC
abstract	BACKGROUND: Respiratory co-infections are important factor affecting the profitability of pigs production. Swine influenza virus (SIV) may predispose to secondary infection. Haemophilus parasuis (Hps) can be a primary pathogen or be associated with other pathogens such as SIV. To date, little is known about the effect of coinfection with SIV and Hps on the disease severity and inflammatory response and the role of Hps in the induction of pneumonia in the absence of other respiratory pathogens. In the study we investigated the influence of SIV and Hps coinfection on clinical course, inflammatory response, pathogens shedding and load at various time points following intranasal inoculation. The correlation between local concentration of cytokines and severity of disease as well as serum acute phase proteins (APP) concentration has been also studied. RESULTS: All co-infected pigs had fever, while in single inoculated pigs fever was observed only in part of animals. Necropsy revealed lesions in the lungs all SIV-inoculated and co-inoculated pigs, while in Hps-single inoculated animals only 1 out of 11 pigs revealed gross lung lesions. The SIV shedding was the highest in co-inoculated pigs. There were no differences between Hps-single inoculated and co-inoculated groups with regard to Hps shedding. The significant increase in Hps titre in the lung has been found only in co-inoculated group. All APP increased after co-infection. In single-inoculated animals various kinetics of APP response has been observed. The lung concentrations of cytokines were induced mostly in SIV + Hps pigs in the apical and middle lobe. These results correlated well with localization of gross lung lesions. CONCLUSIONS: The results revealed that SIV increased the severity of lung lesions and facilitated Hps (PIWetHps192/2015) replication in the porcine lung. Furthermore, Hps influenced the SIV nasal shedding. Enhanced Hps and SIV replication, together with stronger systemic and local inflammatory response contributed to a more severe clinical signs and stronger, earlier immune response in co-inoculated animals. We confirmed the previous evidence that single-Hps infection does not produce significant pneumonic lesions but it should be in mind that other strains of Hps may produce lesions different from that reported in the present study.
has issue date	2017-12-04(xsd:dateTime)
bibo:doi	10.1186/s12917-017-1298-7
bibo:pmid	29202835
has license	cc-by
sha1sum (hex)	cf08012c131b34b073bc10b82fcb6574b17d13b8
schema:url	https://doi.org/10.1186/s12917-017-1298-7
resource representing a document's title	Coinfection modulates inflammatory responses, clinical outcome and pathogen load of H1N1 swine influenza virus and Haemophilus parasuis infections in pigs
has PubMed Central identifier	PMC5716233
has PubMed identifier	29202835
schema:publication	BMC Vet Res
resource representing a document's body	covid:cf08012c131b34b073bc10b82fcb6574b17d13b8#body_text
is schema:about of	named entity 'CLINICAL' named entity 'PATHOGEN LOAD' named entity 'RESPONSE' named entity 'MIDDLE LOBE' named entity 'CORRELATION' named entity 'RESULTS' named entity 'HPS' named entity 'NECROPSY' named entity '2015' named entity 'FOUND' named entity 'VARIOUS' named entity 'RESPIRATORY' named entity 'INFLUENCE' named entity 'SINGLE' named entity 'CONCENTRATION OF' named entity 'EVIDENCE' named entity 'FEVER' named entity 'LITTLE' named entity 'SERUM' named entity 'SWINE INFLUENZA VIRUS' named entity 'ENHANCED' named entity 'LOCALIZATION' named entity 'DATE' named entity 'OBSERVED' named entity 'ROLE' named entity 'PNEUMONIC' named entity 'SYSTEMIC' named entity 'SEVERITY' named entity 'MIND' named entity 'IMPORTANT' named entity 'CORRELATED' named entity 'PART OF' named entity 'CO-INFECTIONS' named entity 'LOCAL' named entity 'TITRE' named entity 'SHEDDING' named entity 'PRODUCTION' named entity 'PORCINE' named entity 'INTRANASAL INOCULATION' named entity 'EARLIER' named entity 'SIGNIFICANT' named entity 'BACKGROUND' named entity 'LESIONS' named entity 'HIGHEST' named entity 'INCREASE' named entity 'IMMUNE RESPONSE' named entity 'ACUTE PHASE PROTEINS' named entity 'ABSENCE OF' named entity 'PRIMARY PATHOGEN' named entity 'EFFECT' named entity 'ANIMALS' named entity 'ASSOCIATED WITH' named entity 'NASAL' named entity 'ABOUT' named entity 'LOAD' named entity 'PRODUCE' named entity 'INDUCED' named entity 'CLINICAL COURSE' named entity 'PIGS' named entity 'THESE' named entity 'COINFECTION' named entity 'INFLAMMATORY RESPONSE' named entity 'CYTOKINES' named entity 'KNOWN' named entity 'PREVIOUS' named entity 'BUT' named entity 'REPLICATION' named entity 'SIV' named entity 'INCREASED' named entity 'APICAL' named entity 'APP' named entity 'KINETICS' named entity 'CONCLUSIONS' named entity 'THE LUNGS' named entity 'DISEASE SEVERITY' named entity 'PATHOGENS' named entity 'INFECTIONS'

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