#Canine #infectious #respiratory disease: New insights into the #etiology and #epidemiology of associated pathogens (PLoS One, abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

PLoS One. 2019 Apr 25;14(4):e0215817. doi: 10.1371/journal.pone.0215817. eCollection 2019.

Canine infectious respiratory disease: New insights into the etiology and epidemiology of associated pathogens.

Maboni G1, Seguel M2, Lorton A1, Berghaus R3, Sanchez S1,4.

Author information: 1 Athens Veterinary Diagnostic Laboratory, University of Georgia, Athens, Georgia, United States of America. 2 Odum School of Ecology, University of Georgia, Athens, Georgia, United States of America. 3 Department of Population Health, College of Veterinary Medicine, University of Georgia, Athens, Georgia, United States of America. 4 Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, Georgia, United States of America.

 

Abstract

Canine infectious respiratory disease (CIRD) is a syndrome where multiple viral and bacterial pathogens are involved sequentially or synergistically to cause illness. There is limited information regarding the prevalence of pathogens related to CIRD in the United States as well as the role of co-infections in the pathogenesis of the syndrome. We aimed to conduct a comprehensive etiologic and epidemiologic study of multiple CIRD agents in a diverse dog population using molecular methods and statistical modeling analyses. In addition, a novel probe-based multiplex real-time PCR was developed to simultaneously detect and differentiate two species of Mycoplasma (M. canis and M. cynos). Canine adenovirus, canine distemper virus, canine parainfluenza virus, coronavirus, influenza A virus (H3N2 and H3N8), Bordetella bronchiseptica, M. canis, M. cynos and Streptococcus equi subsp. zooepidemicus were investigated in specimens from clinically ill and asymptomatic dogs received at the Athens Veterinary Diagnostic Laboratory. Results showed low occurrence of classical CIRD agents such as B. bronchiseptica, canine adenovirus and distemper virus, while highlighting the potential role of emerging bacteria such as M. canis and M. cynos. Statistical modeling analyses of CIRD pathogens emphasized the impact of co-infections on the severity of clinical presentation, and showed that host factors, such as animal age, are the most important predictors of disease severity. This study provides new insights into the current understanding of the prevalence and role of co-infections with selected viruses and bacteria in the etiology of CIRD, while underscoring the importance of molecular diagnosis and vaccination against this disease.

PMID: 31022218 DOI: 10.1371/journal.pone.0215817

Keywords: Dogs; Canine Avian Influenza; H3N2; H3N8; Mycoplasma canis; Bordetella bronchiseptica; Canine adenovirus.

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#Equine #influenza virus in #Asia: phylogeographic pattern and molecular features revealed the circulation of an autochthonous lineage (J Virol., abstract)

[Source: Journal of Virology, full page: (LINK). Abstract, edited.]

Equine influenza virus in Asia: phylogeographic pattern and molecular features revealed the circulation of an autochthonous lineage

Samuel Miño, Laura Mojsiejczuk, Wei Guo, Haili Zhang, Ting Qi, Cheng Du, Xiang Zhang, Jingfei Wang, Rodolfo Campos, Xiaojun Wang

DOI: 10.1128/JVI.00116-19

 

ABSTRACT

Equine influenza virus (EIV) causes severe acute respiratory disease in horses. Currently, the strains belonging to the H3N8 genotype are divided into two clades, Florida clade 1 (FC1) and Florida clade 2 (FC2) which emerged in 2002. Both FC1and FC2 clades were reported in Asian and Middle East countries in the last decade. In this study, we described the evolution, epidemiology and molecular characteristic of the EIV lineages, with focus on those detected in Asia from 2007 to 2017. The full genome phylogeny showed that FC1 and FC2 constituted separated and divergent lineages, without evidence of reassortment between the clades. While FC1 evolved as a single lineage, the FC2 showed a divergent event around 2004 giving rise to two well supported and coexisting sub-lineages, European and Asian. Furthermore, two different spread patterns of EIV in Asian countries were identified. The FC1 outbreaks were caused by independent introductions of EIV from the Americas, being the Asian isolates genetically similar to the contemporary American lineages. On the other hand, the FC2 strains detected in Asian mainland countries conformed an autochthonous monophyletic group with a common ancestor dated in 2006 and showed evidence of an endemic circulation in local host. Characteristic aminoacidic signature patterns were detected in all viral proteins in both Asian-FC1 and FC2 populations. Several changes were located at the top of the HA1 protein, inside or near to antigenic sites. Further studies are needed to assess the potential impact of these antigenic changes in vaccination programs.

 

IMPORTANCE

The complex and continuous antigenic evolution of EIVs remains a major hurdle for vaccine development and the design of effective immunization programs. The present study provides a comprehensive analysis showing the EIV evolutionary dynamics, including the spread and circulation within the Asian continent and its relationship to global EIV populations over a 10-year period. Moreover, we provide a better understanding of EIV molecular evolution in Asian countries and its consequences on the antigenicity. The study underscores the association between the global horse movement and the circulation of EIV in this region. Understanding EIV evolution is imperative in order to mitigate the risk of outbreaks affecting horse industry and to help with the selection of the viral strains to be included in the formulation of future vaccines.

Copyright © 2019 American Society for Microbiology. All Rights Reserved.

Keywords: Equine Influenza; Horses; Asia Region.

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#Attenuation of highly pathogenic #avian #influenza A(#H5N1) viruses in #Indonesia following the #reassortment and acquisition of genes from low pathogenicity avian influenza A virus progenitors (Emerg Microbes Infect., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Emerg Microbes Infect. 2018 Aug 22;7(1):147. doi: 10.1038/s41426-018-0147-5.

Attenuation of highly pathogenic avian influenza A(H5N1) viruses in Indonesia following the reassortment and acquisition of genes from low pathogenicity avian influenza A virus progenitors.

Dharmayanti NLPI1, Thor SW2, Zanders N2, Hartawan R1, Ratnawati A1, Jang Y2, Rodriguez M3, Suarez DL3, Samaan G4, Pudjiatmoko5, Davis CT6.

Author information: 1 Indonesian Research Center for Veterinary Science, Bogor, Indonesia. 2 Influenza Division, Centers for Disease Control and Prevention, Atlanta, GA, USA. 3 Southeast Poultry Research Laboratory, USDA, Athens, GA, USA. 4 Australian National University, Canberra, Australia. 5 Ministry of Agriculture, Jakarta, Indonesia. 6 Influenza Division, Centers for Disease Control and Prevention, Atlanta, GA, USA. ctdavis@cdc.gov.

 

Abstract

-The highly pathogenic avian influenza (HPAI) A(H5N1) virus is endemic in Indonesian poultry and has caused sporadic human infection in Indonesia since 2005. Surveillance of H5N1 viruses in live bird markets (LBMs) during 2012 and 2013 was carried out to provide epidemiologic and virologic information regarding viral circulation and the risk of human exposure. Real-time RT-PCR of avian cloacal swabs and environmental samples revealed influenza A-positive specimens, which were then subjected to virus isolation and genomic sequencing. Genetic analysis of specimens collected at multiple LBMs in Indonesia identified both low pathogenicity avian influenza (LPAI) A(H3N8) and HPAI A(H5N1) viruses belonging to clade 2.1.3.2a. Comparison of internal gene segments among the LPAI and HPAI viruses revealed that the latter had acquired the PB2, PB1, and NS genes from LPAI progenitors and other viruses containing a wild type (wt) genomic constellation. Comparison of murine infectivity of the LPAI A(H3N8), wt HPAI A(H5N1) and reassortant HPAI A(H5N1) viruses showed that the acquisition of LPAI internal genes attenuated the reassortant HPAI virus, producing a mouse infectivity/virulence phenotype comparable to that of the LPAI virus. Comparison of molecular markers in each viral gene segment suggested that mutations in PB2 and NS1 may facilitate attenuation. The discovery of an attenuated HPAI A(H5N1) virus in mice that resulted from reassortment may have implications for the capability of these viruses to transmit and cause disease. In addition, surveillance suggests that LBMs in Indonesia may play a role in the generation of reassortant A(H5) viruses and should be monitored.

PMID: 30131494 PMCID: PMC6104089 DOI: 10.1038/s41426-018-0147-5 [Indexed for MEDLINE] Free PMC Article

Keywords: Avian Influenza; H5N1; H3N8; Reassortant Strain; Poultry; Human; Indonesia.

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#Influenza in #NZ Before 1918: A Preliminary #Report (Am J Epidemiol., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Am J Epidemiol. 2018 Aug 22. doi: 10.1093/aje/kwy180. [Epub ahead of print]

Influenza in New Zealand Before 1918: A Preliminary Report.

Rice GW1.

Author information: 1 Department of History, University of Canterbury, New Zealand.

 

Abstract

This paper aims to test the hypothesis of possible fatal immunological reactions to the A/H1N1 virus of the 1918 “Spanish” influenza pandemic caused by previous exposure to the A/H3N8 virus of the 1890-2 “Russian” influenza pandemic. Reconstruction of mortality peaks from influenza and excess pneumonia deaths in New Zealand before 1918 from newspapers and official death records enables comparison with peaks of influenza mortality by age in 1918 from individual death records. Influenza outbreaks in 1885, 1890-2, 1894 and 1898 appear to match mortality peaks for males in the 1918 pandemic. Peaks of female deaths in 1918 correspond to the previous influenza outbreaks of 1887 and 1890-2. The peak mortality for both sexes was in the age-groups 28-32 years. While lending strong support to the hypothesis of fatal immunological reaction derived from early exposure to a different influenza virus, this study also raises more puzzles: given that the A/H1N1 virus of 1918 was exceptionally virulent, why did so few children aged 5-15 die from it? Influenza normally kills only the very young and the very old. And why did twice as many European males than females die in the young-adult age-groups, while Māori males and females died at almost identical rates?

PMID: 30137202 DOI: 10.1093/aje/kwy180

Keywords: Influenza A; Pandemic Influenza; Spanish Flu; H1N1; H3N8; New Zealand.

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#Mutation W222L at the receptor binding site of #hemagglutinin could facilitate viral adaption from #equine #influenza A(#H3N8) virus to #dogs (J Virol., abstract)

[Source: Journal of Virology, full page: (LINK). Abstract, edited.]

Mutation W222L at the receptor binding site of hemagglutinin could facilitate viral adaption from equine influenza A(H3N8) virus to dogs

Feng Wen a, Sherry Blackmon a, Alicia K. Olivier b, Lei Li c, Minhui Guan a, Hailiang Sun a, Peng George Wang c and Xiu-Feng Wan a*

Author Affiliations: a Department of Basic Sciences, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS 39762 USA; b Department of Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS 39762 USA; c Department of Chemistry, Georgia State University, Atlanta, GA 30303 USA

 

ABSTRACT

An outbreak of respiratory disease caused by the equine-origin influenza A(H3N8) virus was first detected in dogs in 2004 and since then, has been enzootic among dogs. Currently, the molecular mechanisms underlying host adaption of this virus from horses to dogs is unknown. Here, we have applied quantitative binding, growth kinetics, and immunofluorescence analyses to elucidate these mechanisms. Our findings suggest that a substituation of W222L in the hemagglutinin of the equine-origin A(H3N8) virus facilitated its host adaption to dogs. This mutation increased binding avidity of the virus specifically to receptor glycans with N-glycolylneuraminic acid (Neu5Gc) and sialyl Lewis X (SLeX) motifs. We’ve demonstrated these motifs are abundantly located in the submucosal glands of dog trachea. Our findings also suggest that in addition to the type of glycosidic linkage (e.g., α 2,3-linkage or α2,6-linkage), the type of sialic acid (Neu5Gc or 5-N-acetyl neuraminic acid) and the glycan substructure (e.g., SLeX) also play an important role in host tropism of influenza A viruses.

 

Significance statement

Influenza A viruses (IAVs) cause a significant burden on human and animal health, and mechanisms for interspecies transmission of IAVs are far from being understood. Findings from this study suggest that an equine-origin A(H3N8) IAV with mutation W222L at its hemagglutinin increased binding to canine-specific receptors with sialyl Lewis X and Neu5Gc motifs and, thereby, may have facilitated viral adaption from horses to dogs. These findings suggest that in addition to the glycosidic linkage (e.g., α2,3-linked and α2,6-linked), the substructure in the receptor saccharides (e.g., sialyl Lewis X and Neu5Gc) could present an interspecies transmission barrier for IAVs and drive viral mutations to overcome such barriers.

 

FOOTNOTES

*Correspondence: Dr. Xiu-Feng Wan by wan@cvm.msstate.edu.

Copyright © 2018 American Society for Microbiology. All Rights Reserved.

Keywords: Equine Influenza; Canine Influenza; H3N8; Dogs.

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Isolation and characterization of an #avian-origin #H3N8 #canine #influenza virus from a #dog in eastern #China (Arch Virol., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Arch Virol. 2018 Jul;163(7):1955-1960. doi: 10.1007/s00705-018-3818-6. Epub 2018 Mar 20.

Isolation and characterization of an avian-origin H3N8 canine influenza virus from a dog in eastern China.

Cao X1, Liu X2, Zheng S3, Xu L4, Wu H5, Liu J6.

Author information: 1 Dezhou College, Dezhou, 253023, Shandong, China. xueliangcao@163.com. 2 Shandong Vocational Animal Science and Veterinary College, Weifang, 261061, Shandong, China. 3 Dezhou College, Dezhou, 253023, Shandong, China. 4 Animal Husbandry and Veterinary Institute, Zhejiang Academy of Agricultural Science, Hangzhou, 310021, Zhejiang, China. 5 State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, Zhejiang, China. 6 Animal Hospital of Zhejiang University, Hangzhou, 310058, Zhejiang, China.

 

Abstract

Previous studies have shown that dogs are susceptible to influenza A viruses, and the close contact between dogs and humans poses a threat to public health. In 2015, a novel H3N8 influenza virus was isolated from a dog in eastern China. This strain was characterized by whole-genome sequencing with subsequent phylogenetic analysis and genetic comparison and found to be most closely related to avian influenza viruses co-circulating in China. It was able to replicate in mice without prior adaptation. The continued circulation of this novel H3N8 influenza virus in dogs could endanger other mammalian species.

PMID: 29556821 DOI: 10.1007/s00705-018-3818-6 [Indexed for MEDLINE]

Keywords: Avian Influenza; Canine Avian Influenza; H3N8; China; Dogs.

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#Age-specific excess #mortality #patterns and #transmissibility during the 1889-1890 #influenza #pandemic in Madrid, #Spain (Ann Epidemiol., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Ann Epidemiol. 2017 Dec 27. pii: S1047-2797(17)30684-1. doi: 10.1016/j.annepidem.2017.12.009. [Epub ahead of print]

Age-specific excess mortality patterns and transmissibility during the 1889-1890 influenza pandemic in Madrid, Spain.

Ramiro D1, Garcia S1, Casado Y1, Cilek L1, Chowell G2.

Author information: 1 Institute of Economics, Geography and Demography, Center for Humanities and Social Sciences, CCHS-CSIC, Spanish National Research Council, Madrid, Spain. 2 Division of Epidemiology and Biostatistics, School of Public Health, Georgia State University, Atlanta, GA; Division of International Epidemiology and Population Studies, Fogarty International Center, National Institutes of Health, Bethesda, MD. Electronic address: gchowell@gsu.edu.

 

Abstract

PURPOSE:

Although the 1889-1890 influenza pandemic was one of the most important epidemic events of the 19th century, little is known about the mortality impact of this pandemic based on detailed respiratory mortality data sets.

METHODS:

We estimated excess mortality rates for the 1889-1890 pandemic in Madrid from high-resolution respiratory and all-cause individual-level mortality data retrieved from the Gazeta de Madrid, the Official Bulletin of the Spanish government. We also generated estimates of the reproduction number from the early growth phase of the pandemic.

RESULTS:

The main pandemic wave in Madrid was evident from respiratory and all-cause mortality rates during the winter of 1889-1890. Our estimates of excess mortality for this pandemic were 58.3 per 10,000 for all-cause mortality and 44.5 per 10,000 for respiratory mortality. Age-specific excess mortality rates displayed a J-shape pattern, with school children aged 5-14 years experiencing the lowest respiratory excess death rates (8.8 excess respiratory deaths per 10,000), whereas older populations aged greater than or equal to 70 years had the highest rates (367.9 per 10,000). Although seniors experienced the highest absolute excess death rates, the standardized mortality ratio was highest among young adults aged 15-24 years. The early growth phase of the pandemic displayed dynamics consistent with an exponentially growing transmission process. Using the generalized-growth method, we estimated the reproduction number in the range of 1.2-1.3 assuming a 3-day mean generation interval and of 1.3-1.5 assuming a 4-day mean generation interval.

CONCLUSIONS:

Our study adds to our understanding of the mortality impact and transmissibility of the 1889-1890 influenza pandemic using detailed individual-level mortality data sets. More quantitative studies are needed to quantify the variability of the mortality impact of this understudied pandemic at regional and global scales.

Copyright © 2017 Elsevier Inc. All rights reserved.

KEYWORDS: 1889–1890 influenza pandemic; Age-specific mortality; Madrid; Reproduction number; Spain

PMID: 29336941 DOI: 10.1016/j.annepidem.2017.12.009

Keywords: Pandemic Influenza; H3N8; Spain.

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