Phylodynamic signatures in the emergence of community-associated MRSA
- Steinig, Eike, Aglua, Izzard, Duchene, Sebastian, Meehan, Michael, Yoannes, Mition, Firth, Cadhla, Jaworski, Jan, Drekore, Jimmy, Urakoko, Bohu, Poka, Harry, Wurr, Clive, Ebos, Eri, Nangen, David, Müller, Elke, Mulvey, Peter, Jackson, Charlene, Blomfeldt, Anita, Aamot, Hege, Laman, Moses, Manning, Laurens, Earls, Megan, Coleman, David, Greenhill, Andrew, Ford, Rebecca, Stegger, Marc, Syed, Muhammad, Jamil, Bushra, Monecke, Stefan, Ehricht, Ralf, Smith, Simon, Pomat, William, Horwood, Paul, Tong, Steven, McBryde, Emma
- Authors: Steinig, Eike , Aglua, Izzard , Duchene, Sebastian , Meehan, Michael , Yoannes, Mition , Firth, Cadhla , Jaworski, Jan , Drekore, Jimmy , Urakoko, Bohu , Poka, Harry , Wurr, Clive , Ebos, Eri , Nangen, David , Müller, Elke , Mulvey, Peter , Jackson, Charlene , Blomfeldt, Anita , Aamot, Hege , Laman, Moses , Manning, Laurens , Earls, Megan , Coleman, David , Greenhill, Andrew , Ford, Rebecca , Stegger, Marc , Syed, Muhammad , Jamil, Bushra , Monecke, Stefan , Ehricht, Ralf , Smith, Simon , Pomat, William , Horwood, Paul , Tong, Steven , McBryde, Emma
- Date: 2022
- Type: Text , Journal article
- Relation: Proceedings of the National Academy of Sciences of the United States of America Vol. 119, no. 45 (2022), p.
- Full Text:
- Reviewed:
- Description: Community-associated, methicillin-resistant Staphylococcus aureus (MRSA) lineages have emerged in many geographically distinct regions around the world during the past 30 y. Here, we apply consistent phylodynamic methods across multiple community-associated MRSA lineages to describe and contrast their patterns of emergence and dissemination. We generated whole-genome sequencing data for the Australian sequence type (ST) ST93-MRSA-IV from remote communities in Far North Queensland and Papua New Guinea, and the Bengal Bay ST772-MRSA-V clone from metropolitan communities in Pakistan. Increases in the effective reproduction number (Re) and sustained transmission (Re > 1) coincided with spread of progenitor methicillin-susceptible S. aureus (MSSA) in remote northern Australian populations, dissemination of the ST93-MRSA-IV genotype into population centers on the Australian East Coast, and subsequent importation into the highlands of Papua New Guinea and Far North Queensland. Applying the same phylodynamic methods to existing lineage datasets, we identified common signatures of epidemic growth in the emergence and epidemiological trajectory of community-associated S. aureus lineages from America, Asia, Australasia, and Europe. Surges in Re were observed at the divergence of antibiotic-resistant strains, coinciding with their establishment in regional population centers. Epidemic growth was also observed among drug-resistant MSSA clades in Africa and northern Australia. Our data suggest that the emergence of community-associated MRSA in the late 20th century was driven by a combination of antibiotic-resistant genotypes and host epidemiology, leading to abrupt changes in lineage-wide transmission dynamics and sustained transmission in regional population centers. Copyright © 2022 the Author(s).
- Authors: Steinig, Eike , Aglua, Izzard , Duchene, Sebastian , Meehan, Michael , Yoannes, Mition , Firth, Cadhla , Jaworski, Jan , Drekore, Jimmy , Urakoko, Bohu , Poka, Harry , Wurr, Clive , Ebos, Eri , Nangen, David , Müller, Elke , Mulvey, Peter , Jackson, Charlene , Blomfeldt, Anita , Aamot, Hege , Laman, Moses , Manning, Laurens , Earls, Megan , Coleman, David , Greenhill, Andrew , Ford, Rebecca , Stegger, Marc , Syed, Muhammad , Jamil, Bushra , Monecke, Stefan , Ehricht, Ralf , Smith, Simon , Pomat, William , Horwood, Paul , Tong, Steven , McBryde, Emma
- Date: 2022
- Type: Text , Journal article
- Relation: Proceedings of the National Academy of Sciences of the United States of America Vol. 119, no. 45 (2022), p.
- Full Text:
- Reviewed:
- Description: Community-associated, methicillin-resistant Staphylococcus aureus (MRSA) lineages have emerged in many geographically distinct regions around the world during the past 30 y. Here, we apply consistent phylodynamic methods across multiple community-associated MRSA lineages to describe and contrast their patterns of emergence and dissemination. We generated whole-genome sequencing data for the Australian sequence type (ST) ST93-MRSA-IV from remote communities in Far North Queensland and Papua New Guinea, and the Bengal Bay ST772-MRSA-V clone from metropolitan communities in Pakistan. Increases in the effective reproduction number (Re) and sustained transmission (Re > 1) coincided with spread of progenitor methicillin-susceptible S. aureus (MSSA) in remote northern Australian populations, dissemination of the ST93-MRSA-IV genotype into population centers on the Australian East Coast, and subsequent importation into the highlands of Papua New Guinea and Far North Queensland. Applying the same phylodynamic methods to existing lineage datasets, we identified common signatures of epidemic growth in the emergence and epidemiological trajectory of community-associated S. aureus lineages from America, Asia, Australasia, and Europe. Surges in Re were observed at the divergence of antibiotic-resistant strains, coinciding with their establishment in regional population centers. Epidemic growth was also observed among drug-resistant MSSA clades in Africa and northern Australia. Our data suggest that the emergence of community-associated MRSA in the late 20th century was driven by a combination of antibiotic-resistant genotypes and host epidemiology, leading to abrupt changes in lineage-wide transmission dynamics and sustained transmission in regional population centers. Copyright © 2022 the Author(s).
Influenza A virus causes maternal and fetal pathology via innate and adaptive vascular inflammation in mice
- Liong, Stella, Oseghale, Osezua, To, Eunice, Brassington, Kurt, Erlich, Jonathan, Luong, Raymond, Liong, Felicia, Brooks, Robert, Martin, Cara, O'Toole, Sharon, Vinh, Antony, O'Neill, Luke, Bozinovski, Steven, Vlahos, Ross, Papagianis, Paris, O'Leary, John, Brooks, Doug, Selemidis, Stavros
- Authors: Liong, Stella , Oseghale, Osezua , To, Eunice , Brassington, Kurt , Erlich, Jonathan , Luong, Raymond , Liong, Felicia , Brooks, Robert , Martin, Cara , O'Toole, Sharon , Vinh, Antony , O'Neill, Luke , Bozinovski, Steven , Vlahos, Ross , Papagianis, Paris , O'Leary, John , Brooks, Doug , Selemidis, Stavros
- Date: 2020
- Type: Text , Journal article
- Relation: Proceedings of the National Academy of Sciences of the United States of America Vol. 117, no. 40 (2020), p. 24964-24973
- Full Text:
- Reviewed:
- Description: Influenza A virus (IAV) infection during pregnancy causes severe maternal and perinatal complications, despite a lack of vertical transmission of IAV across the placenta. Here, we demonstrate a significant alteration in the maternal vascular landscape that underpins the maternal and downstream fetal pathology to IAV infection in mice. In IAV infection of nonpregnant mice, the local lung inflammatory response was contained to the lungs and was self-resolving, whereas in pregnant mice, virus dissemination to major maternal blood vessels, including the aorta, resulted in a peripheral "vascular storm," with elevated proinflammatory and antiviral mediators and the influx of Ly6Clow and Ly6Chigh monocytes, plus neutrophils and T cells. This vascular storm was associated with elevated levels of the adhesion molecules ICAM and VCAM and the pattern-recognition receptors TLR7 and TLR9 in the vascular wall, resulting in profound vascular dysfunction. The sequalae of this IAV-driven vascular storm included placental growth retardation and intrauterine growth restriction, evidence of placental and fetal brain hypoxia, and increased circulating cell free fetal DNA and soluble Flt1. In contrast, IAV infection in nonpregnant mice caused no obvious alterations in endothelial function or vascular inflammation. Therefore, IAV infection during pregnancy drives a significant systemic vascular alteration in pregnant dams, which likely suppresses critical blood flow to the placenta and fetus. This study in mice provides a fundamental mechanistic insight and a paradigm into how an immune response to a respiratory virus, such as IAV, is likely to specifically drive maternal and fetal pathologies during pregnancy. © 2020 National Academy of Sciences. All rights reserved.
- Authors: Liong, Stella , Oseghale, Osezua , To, Eunice , Brassington, Kurt , Erlich, Jonathan , Luong, Raymond , Liong, Felicia , Brooks, Robert , Martin, Cara , O'Toole, Sharon , Vinh, Antony , O'Neill, Luke , Bozinovski, Steven , Vlahos, Ross , Papagianis, Paris , O'Leary, John , Brooks, Doug , Selemidis, Stavros
- Date: 2020
- Type: Text , Journal article
- Relation: Proceedings of the National Academy of Sciences of the United States of America Vol. 117, no. 40 (2020), p. 24964-24973
- Full Text:
- Reviewed:
- Description: Influenza A virus (IAV) infection during pregnancy causes severe maternal and perinatal complications, despite a lack of vertical transmission of IAV across the placenta. Here, we demonstrate a significant alteration in the maternal vascular landscape that underpins the maternal and downstream fetal pathology to IAV infection in mice. In IAV infection of nonpregnant mice, the local lung inflammatory response was contained to the lungs and was self-resolving, whereas in pregnant mice, virus dissemination to major maternal blood vessels, including the aorta, resulted in a peripheral "vascular storm," with elevated proinflammatory and antiviral mediators and the influx of Ly6Clow and Ly6Chigh monocytes, plus neutrophils and T cells. This vascular storm was associated with elevated levels of the adhesion molecules ICAM and VCAM and the pattern-recognition receptors TLR7 and TLR9 in the vascular wall, resulting in profound vascular dysfunction. The sequalae of this IAV-driven vascular storm included placental growth retardation and intrauterine growth restriction, evidence of placental and fetal brain hypoxia, and increased circulating cell free fetal DNA and soluble Flt1. In contrast, IAV infection in nonpregnant mice caused no obvious alterations in endothelial function or vascular inflammation. Therefore, IAV infection during pregnancy drives a significant systemic vascular alteration in pregnant dams, which likely suppresses critical blood flow to the placenta and fetus. This study in mice provides a fundamental mechanistic insight and a paradigm into how an immune response to a respiratory virus, such as IAV, is likely to specifically drive maternal and fetal pathologies during pregnancy. © 2020 National Academy of Sciences. All rights reserved.
- «
- ‹
- 1
- ›
- »