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Canine influenza virus coinfection with Staphylococcus pseudintermedius enhances bacterial colonization, virus load and clinical presentation in mice.

ABSTRACT: Canine influenza virus (CIV) and Staphylococcus pseudintermedius (Sp) are pathogens that cause respiratory disease in dogs. Considering bacterial infections following influenza are a leading cause of illness and death, it is of particular meaning to investigate the interaction between these two pathogens. In this study, BALB/c mice were used as a mouse model to assess whether inoculation with CIV H3N2 followed by S. pseudintermedius 72 h later resulted in exacerbation of disease. Disease was characterized by assessment of body weight loss, titration of virus and bacteria, histopathology, and cytokine production.There was a significantly greater decrease in body weight in the co-infected group compared with the CIV-only and SP-only groups. CIV inoculation increased bacterial colonization, whereas secondary infection with S. pseudintermedius elevated the viral RNA load of CIV in tissues. The histological lesions in the brain, spleen and lung were more severe in the CIV/Sp group than in the singly treated groups. Infection with CIV alone, Sp alone or coinfection stimulated a significantly higher release of cytokines, such as interferon-gamma (IFN)-?, interleukin 6 (IL)-6, tumor necrosis factor (TNF-?) and lymphotactin (Lptn), than was observed in the mock-infected group (PBS). Moreover, the levels of IFN-? in the spleen and lung were higher in the CIV/Sp group compared with the CIV-only and Sp-only groups.Our findings provide the first demonstration that the secondary infection of mice with Sp leads to increased clinical signs and lesions during canine influenza.

SUBMITTER: Kalhoro DH

PROVIDER: S-EPMC4893303 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature

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Canine influenza virus coinfection with Staphylococcus pseudintermedius enhances bacterial colonization, virus load and clinical presentation in mice.

Kalhoro Dildar Hussain DH Gao Shanshan S Xie Xing X Liang Shan S Luo Su S Zhao Yanbing Y Liu Yongjie Y

BMC veterinary research 20160604

<h4>Background</h4>Canine influenza virus (CIV) and Staphylococcus pseudintermedius (Sp) are pathogens that cause respiratory disease in dogs. Considering bacterial infections following influenza are a leading cause of illness and death, it is of particular meaning to investigate the interaction between these two pathogens. In this study, BALB/c mice were used as a mouse model to assess whether inoculation with CIV H3N2 followed by S. pseudintermedius 72 h later resulted in exacerbation of disea ...[more]

PMID: 27259293

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Project description:Community interactions at mucosal surfaces between viruses, like influenza virus, and respiratory bacterial pathogens are important contributors toward pathogenesis of bacterial disease. What has not been considered is the natural extension of these interactions to live attenuated immunizations, and in particular, live attenuated influenza vaccines (LAIVs). Using a mouse-adapted LAIV against influenza A (H3N2) virus carrying the same mutations as the human FluMist vaccine, we find that LAIV vaccination reverses normal bacterial clearance from the nasopharynx and significantly increases bacterial carriage densities of the clinically important bacterial pathogens Streptococcus pneumoniae (serotypes 19F and 7F) and Staphylococcus aureus (strains Newman and Wright) within the upper respiratory tract of mice. Vaccination with LAIV also resulted in 2- to 5-fold increases in mean durations of bacterial carriage. Furthermore, we show that the increases in carriage density and duration were nearly identical in all aspects to changes in bacterial colonizing dynamics following infection with wild-type (WT) influenza virus. Importantly, LAIV, unlike WT influenza viruses, had no effect on severe bacterial disease or mortality within the lower respiratory tract. Our findings are, to the best of our knowledge, the first to demonstrate that vaccination with a live attenuated viral vaccine can directly modulate colonizing dynamics of important and unrelated human bacterial pathogens, and does so in a manner highly analogous to that seen following wild-type virus infection.Following infection with an influenza virus, infected or recently recovered individuals become transiently susceptible to excess bacterial infections, particularly Streptococcus pneumoniae and Staphylococcus aureus. Indeed, in the absence of preexisting comorbidities, bacterial infections are a leading cause of severe disease during influenza epidemics. While this synergy has been known and is well studied, what has not been explored is the natural extension of these interactions to live attenuated influenza vaccines (LAIVs). Here we show, in mice, that vaccination with LAIV primes the upper respiratory tract for increased bacterial growth and persistence of bacterial carriage, in a manner nearly identical to that seen following wild-type influenza virus infections. Importantly, LAIV, unlike wild-type virus, did not increase severe bacterial disease of the lower respiratory tract. These findings may have consequences for individual bacterial disease processes within the upper respiratory tract, as well as bacterial transmission dynamics within LAIV-vaccinated populations.

Project description:S. pseudintermedius is a known resident of the skin and mucous membranes and a constituent of the normal microbiota of dogs. It has also been recognized as an opportunistic and zoonotic pathogen that is able to colonize humans and cause severe diseases, especially in immunocompromised hosts. Most importantly, methicillin-resistant S. pseudintermedius (MRSP), which is intrinsically multidrug-resistant, has emerged with serious public health consequences. The epidemiological situation is further exacerbated with reports of its zoonotic transmission and human infections which have been mostly attributed to the increasing frequency of dog ownership and close contact between dogs and humans. Evidence on the zoonotic transmission of MRSP from pet dogs to humans (such as dog owners, small-animal veterinarians, and other people in close proximity to dogs) is limited, especially due to the misidentification of S. pseudintermedius as S. aureus. Despite this fact, reports on the increasing emergence and spread of MRSP in humans have been increasing steadily over the years since its first documented report in 2006 in Belgium. The emergence of MRSP strains has further compromised treatment outcomes in both veterinary and human medicine as these strains are resistant to beta-lactam antimicrobials usually prescribed as first line treatment. Frustratingly, the limited awareness and surveillance of the zoonotic transmission of S. pseudintermedius have underestimated their extent of transmission, prevalence, epidemiology, and public health significance. In order to fill this gap of information, this review focused on detailed reports on zoonotic transmission, human colonization, and infections by S. pseudintermedius, their pathogenic features, antimicrobial resistance profiles, epidemiology, risk factors, and treatment. In writing this review, we searched Web of Science, PubMed, and SCOPUS databases using the keyword "Staphylococcus pseudintermedius AND humans". A phylogenetic tree to determine the genetic relatedness/diversity of publicly available genomes of S. pseudintermedius was also constructed.

Dataset Information

Canine influenza virus coinfection with Staphylococcus pseudintermedius enhances bacterial colonization, virus load and clinical presentation in mice.

Publications

Canine influenza virus coinfection with Staphylococcus pseudintermedius enhances bacterial colonization, virus load and clinical presentation in mice.

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