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5. SARS-CoV-2 evolution during treatment of chronic infection

Author

Kemp, S. A., Collier, D. A., Datir, R. P., Ferreira, I. A. T. M., Gayed, S., Jahun, A., Hosmillo, M., Rees-Spear, C., Mlcochova, P., Lumb, I. U., Roberts, D. J., Chandra, A., Temperton, N., Baker, S., Dougan, G., Hess, C., Kingston, N., Lehner, P. J., Lyons, P. A., Matheson, N. J., Owehand, W. H., Saunders, C., Summers, C., Thaventhiran, J. E. D., Toshner, M., Weekes, M. P., Bucke, A., Calder, J., Canna, L., Domingo, J., Elmer, A., Fuller, S., Harris, J., Hewitt, S., Kennet, J., Jose, S., Kourampa, J., Meadows, A., O'Brien, C., Price, J., Publico, C., Rastall, R., Ribeiro, C., Rowlands, J., Ruffolo, V., Tordesillas, H., Bullman, B., Dunmore, B. J., Fawke, S., Graf, S., Hodgson, J., Huang, C., Hunter, K., Jones, E., Legchenko, E., Matara, C., Martin, J., Mescia, F., O'Donnell, C., Pointon, L., Pond, N., Shih, J., Sutcliffe, R., Tilly, T., Treacy, C., Tong, Z., Wood, J., Wylot, M., Bergamaschi, L., Betancourt, A., Bower, G., Cossetti, C., De Sa, A., Epping, M., Gleadall, N., Grenfell, R., Hinch, A., Huhn, O., Jackson, S., Jarvis, I., Lewis, D., Marsden, J., Nice, F., Okecha, G., Omarjee, O., Perera, M., Richoz, N., Romashova, V., Yarkoni, N. S., Sharma, R., Stefanucci, L., Stephens, J., Strezlecki, M., Turner, L., De Bie, E. M. D. D., Bunclark, K., Josipovic, M., Mackay, M., Rossi, S., Selvan, M., Spencer, S., Yong, C., Ansaripour, A., Michael, A., Mwaura, L., Patterson, C., Polwarth, G., Polgarova, P., di Stefano, G., Fahey, C., Michel, R., Bong, S. -H., Coudert, J. D., Holmes, E., Allison, J., Butcher, H., Caputo, D., Clapham-Riley, D., Dewhurst, E., Furlong, A., Graves, B., Gray, J., Ivers, T., Kasanicki, M., Le Gresley, E., Linger, R., Meloy, S., Muldoon, F., Ovington, N., Papadia, S., Phelan, I., Stark, H., Stirrups, K. E., Townsend, P., Walker, N., Webster, J., Robson, S. C., Loman, N. J., Connor, T. R., Golubchik, T., Martinez Nunez, R. T., Ludden, C., Corden, S., Johnston, I., Bonsall, D., Smith, C. P., Awan, A. R., Bucca, G., Estee Torok, M., Saeed, K., Prieto, J. A., Jackson, D. K., Hamilton, W. L., Snell, L. B., Moore, C., Harrison, E. M., Goncalves, S., Fairley, D. J., Loose, M. W., Watkins, J., Livett, R., Moses, S., Amato, R., Nicholls, S., Bull, M., Smith, D. L., Barrett, J., Aanensen, D. M., Curran, M. D., Parmar, S., Aggarwal, D., Shepherd, J. G., Parker, M. D., Glaysher, S., Bashton, M., Underwood, A. P., Pacchiarini, N., Loveson, K. F., Carabelli, A. M., Templeton, K. E., Langford, C. F., Sillitoe, J., de Silva, T. I., Wang, D., Kwiatkowski, D., Rambaut, A., O'Grady, J., Cottrell, S., Holden, M. T. G., Thomson, E. C., Osman, H., Andersson, M., Chauhan, A. J., Hassan-Ibrahim, M. O., Lawniczak, M., Alderton, A., Chand, M., Constantinidou, C., Unnikrishnan, M., Darby, A. C., Hiscox, J. A., Paterson, S., Martincorena, I., Robertson, D. L., Volz, E. M., Page, A. J., Pybus, O. G., Bassett, A. R., Ariani, C. V., Spencer Chapman, M. H., K. K., Li, Shah, R. N., Jesudason, N. G., Taha, Y., Mchugh, M. P., Dewar, R., Jahun, A. S., Mcmurray, C., Pandey, S., Mckenna, J. P., Nelson, A., Young, G. R., Mccann, C. M., Elliott, S., Lowe, H., Temperton, B., Roy, S., Price, A., Rey, S., Wyles, M., Rooke, S., Shaaban, S., de Cesare, M., Letchford, L., Silveira, S., Pelosi, E., Wilson-Davies, E., O'Toole, A., Hesketh, A. R., Stark, R., du Plessis, L., Ruis, C., Adams, H., Bourgeois, Y., Michell, S. L., Gramatopoulos, D., Edgeworth, J., Breuer, J., Todd, J. A., Fraser, C., Buck, D., John, M., Kay, G. L., Palmer, S., Peacock, S. J., Heyburn, D., Weldon, D., Robinson, E., Mcnally, A., Muir, P., Vipond, I. B., Boyes, J., Sivaprakasam, V., Salluja, T., Dervisevic, S., Meader, E. J., Park, N. R., Oliver, K., Jeffries, A. R., Ott, S., da Silva Filipe, A., Simpson, D. A., Williams, C., Masoli, J. A. H., Knight, B. A., Jones, C. R., Koshy, C., Ash, A., Casey, A., Bosworth, A., Ratcliffe, L., Xu-McCrae, L., Pymont, H. M., Hutchings, S., Berry, L., Jones, K., Halstead, F., Davis, T., Holmes, C., Iturriza-Gomara, M., Lucaci, A. O., Randell, P. A., Cox, A., Madona, P., Harris, K. A., Brown, J. R., Mahungu, T. W., Irish-Tavares, D., Haque, T., Hart, J., Witele, E., Fenton, M. L., Liggett, S., Graham, C., Swindells, E., Collins, J., Eltringham, G., Campbell, S., Mcclure, P. C., Clark, G., Sloan, T. J., Jones, C., Lynch, J., Warne, B., Leonard, S., Durham, J., Williams, T., Haldenby, S. T., Storey, N., Alikhan, N. -F., Holmes, N., Carlile, M., Perry, M., Craine, N., Lyons, R. A., Beckett, A. H., Goudarzi, S., Fearn, C., Cook, K., Dent, H., Paul, H., Davies, R., Blane, B., Girgis, S. T., Beale, M. A., Bellis, K. L., Dorman, M. J., Drury, E., Kane, L., Kay, S., Mcguigan, S., Nelson, R., Prestwood, L., Rajatileka, S., Batra, R., Williams, R. J., Kristiansen, M., Green, A., Justice, A., Mahanama, A. I. K., Samaraweera, B., Hadjirin, N. F., Quick, J., Poplawski, R., Kermack, L. M., Reynolds, N., Hall, G., Chaudhry, Y., Pinckert, M. L., Georgana, I., Moll, R. J., Thornton, A., Myers, R., Stockton, J., Williams, C. A., Yew, W. C., Trotter, A. J., Trebes, A., MacIntyre-Cockett, G., Birchley, A., Adams, A., Plimmer, A., Gatica-Wilcox, B., Mckerr, C., Hilvers, E., Jones, H., Asad, H., Coombes, J., Evans, J. M., Fina, L., Gilbert, L., Graham, L., Cronin, M., Kumziene-Summerhayes, S., Taylor, S., Jones, S., Groves, D. C., Zhang, P., Gallis, M., Louka, S. F., Starinskij, I., Jackson, C., Gourtovaia, M., Tonkin-Hill, G., Lewis, K., Tovar-Corona, J. M., James, K., Baxter, L., Alam, M. T., Orton, R. J., Hughes, J., Vattipally, S., Ragonnet-Cronin, M., Nascimento, F. F., Jorgensen, D., Boyd, O., Geidelberg, L., Zarebski, A. E., Raghwani, J., Kraemer, M. U. G., Southgate, J., Lindsey, B. B., Freeman, T. M., Keatley, J. -P., Singer, J. B., de Oliveira Martins, L., Yeats, C. A., Abudahab, K., Taylor, B. E. W., Menegazzo, M., Danesh, J., Hogsden, W., Eldirdiri, S., Kenyon, A., Mason, J., Robinson, T. I., Holmes, A., Hartley, J. A., Curran, T., Mather, A. E., Shankar, G., Jones, R., Howe, R., Morgan, S., Wastenge, E., Chapman, M. R., Mookerjee, S., Stanley, R., Smith, W., Peto, T., Eyre, D., Crook, D., Vernet, G., Kitchen, C., Gulliver, H., Merrick, I., Guest, M., Munn, R., Bradley, D. T., Wyatt, T., Beaver, C., Foulser, L., Churcher, C. M., Brooks, E., Smith, K. S., Galai, K., Mcmanus, G. M., Bolt, F., Coll, F., Meadows, L., Attwood, S. W., Davies, A., De Lacy, E., Downing, F., Edwards, S., Scarlett, G. P., Jeremiah, S., Smith, N., Leek, D., Sridhar, S., Forrest, S., Cormie, C., Gill, H. K., Dias, J., Higginson, E. E., Maes, M., Young, J., Wantoch, M., Jamrozy, D., Lo, S., Patel, M., Hill, V., Bewshea, C. M., Ellard, S., Auckland, C., Harrison, I., Bishop, C., Chalker, V., Richter, A., Beggs, A., Best, A., Percival, B., Mirza, J., Megram, O., Mayhew, M., Crawford, L., Ashcroft, F., Moles-Garcia, E., Cumley, N., Hopes, R., Asamaphan, P., Niebel, M. O., Gunson, R. N., Bradley, A., Maclean, A., Mollett, G., Blacow, R., Bird, P., Helmer, T., Fallon, K., Tang, J., Hale, A. D., Macfarlane-Smith, L. R., Harper, K. L., Carden, H., Machin, N. W., Jackson, K. A., Ahmad, S. S. Y., George, R. P., Turtle, L., O'Toole, E., Watts, J., Breen, C., Cowell, A., Alcolea-Medina, A., Charalampous, T., Patel, A., Levett, L. J., Heaney, J., Rowan, A., Taylor, G. P., Shah, D., Atkinson, L., Lee, J. C. D., Westhorpe, A. P., Jannoo, R., Lowe, H. L., Karamani, A., Ensell, L., Chatterton, W., Pusok, M., Dadrah, A., Symmonds, A., Sluga, G., Molnar, Z., Baker, P., Bonner, S., Essex, S., Barton, E., Padgett, D., Scott, G., Greenaway, J., Payne, B. A. I., Burton-Fanning, S., Waugh, S., Raviprakash, V., Sheriff, N., Blakey, V., Williams, L. -A., Moore, J., Stonehouse, S., Smith, L., Davidson, R. K., Bedford, L., Coupland, L., Wright, V., Chappell, J. G., Tsoleridis, T., Ball, J., Khakh, M., Fleming, V. M., Lister, M. M., Howson-Wells, H. C., Boswell, T., Joseph, A., Willingham, I., Duckworth, N., Walsh, S., Wise, E., Moore, N., Mori, M., Cortes, N., Kidd, S., Williams, R., Gifford, L., Bicknell, K., Wyllie, S., Lloyd, A., Impey, R., Malone, C. S., Cogger, B. J., Levene, N., Monaghan, L., Keeley, A. J., Partridge, D. G., Raza, M., Evans, C., Johnson, K., Abnizova, I., Aigrain, L., Ali, M., Allen, L., Anderson, R., Ariani, C., Austin-Guest, S., Bala, S., Bassett, A., Battleday, K., Beal, J., Beale, M., Bellany, S., Bellerby, T., Bellis, K., Berger, D., Berriman, M., Betteridge, E., Bevan, P., Binley, S., Bishop, J., Blackburn, K., Bonfield, J., Boughton, N., Bowker, S., Brendler-Spaeth, T., Bronner, I., Brooklyn, T., Buddenborg, S. K., Bush, R., Caetano, C., Cagan, A., Carter, N., Cartwright, J., Monteiro, T. C., Chapman, L., Chillingworth, T. -J., Clapham, P., Clark, R., Clarke, A., Clarke, C., Cole, D., Cook, E., Coppola, M., Cornell, L., Cornwell, C., Corton, C., Crackett, A., Cranage, A., Craven, H., Craw, S., Crawford, M., Cutts, T., Dabrowska, M., Davies, M., Dawson, J., Day, C., Densem, A., Dibling, T., Dockree, C., Dodd, D., Dogga, S., Dougherty, M., Dove, A., Drummond, L., Dudek, M., Durrant, L., Easthope, E., Eckert, S., Ellis, P., Farr, B., Fenton, M., Ferrero, M., Flack, N., Fordham, H., Forsythe, G., Francis, M., Fraser, A., Freeman, A., Galvin, A., Garcia-Casado, M., Gedny, A., Girgis, S., Glover, J., Goodwin, S., Gould, O., Gray, A., Gray, E., Griffiths, C., Gu, Y., Guerin, F., Hamilton, W., Hanks, H., Harrison, E., Harrott, A., Harry, E., Harvison, J., Heath, P., Hernandez-Koutoucheva, A., Hobbs, R., Holland, D., Holmes, S., Hornett, G., Hough, N., Huckle, L., Hughes-Hallet, L., Hunter, A., Inglis, S., Iqbal, S., Jackson, A., Jackson, D., Verdejo, C. J., Jones, M., Kallepally, K., Kay, K., Keatley, J., Keith, A., King, A., Kitchin, L., Kleanthous, M., Klimekova, M., Korlevic, P., Krasheninnkova, K., Lane, G., Langford, C., Laverack, A., Law, K., Lensing, S., Lewis-Wade, A., Liddle, J., Lin, Q., Lindsay, S., Linsdell, S., Long, R., Lovell, J., Mack, J., Maddison, M., Makunin, A., Mamun, I., Mansfield, J., Marriott, N., Martin, M., Mayho, M., Mccarthy, S., Mcclintock, J., Mchugh, S., Mcminn, L., Meadows, C., Mobley, E., Moll, R., Morra, M., Morrow, L., Murie, K., Nash, S., Nathwani, C., Naydenova, P., Neaverson, A., Nerou, E., Nicholson, J., Nimz, T., Noell, G. G., O'Meara, S., Ohan, V., Olney, C., Ormond, D., Oszlanczi, A., Pang, Y. F., Pardubska, B., Park, N., Parmar, A., Patel, G., Payne, M., Peacock, S., Petersen, A., Plowman, D., Preston, T., Puethe, C., Quail, M., Rajan, D., Rance, R., Rawlings, S., Redshaw, N., Reynolds, J., Reynolds, M., Rice, S., Richardson, M., Roberts, C., Robinson, K., Robinson, M., Robinson, D., Rogers, H., Rojo, E. M., Roopra, D., Rose, M., Rudd, L., Sadri, R., Salmon, N., Saul, D., Schwach, F., Scott, C., Seekings, P., Shirley, L., Simms, A., Sinnott, M., Sivadasan, S., Siwek, B., Sizer, D., Skeldon, K., Skelton, J., Slater-Tunstill, J., Sloper, L., Smerdon, N., Smith, C., Smith, J., Smith, K., Smith, M., Smith, S., Smith, T., Sneade, L., Soria, C. D., Sousa, C., Souster, E., Sparkes, A., Spencer-Chapman, M., Squares, J., Steed, C., Stickland, T., Still, I., Stratton, M., Strickland, M., Swann, A., Swiatkowska, A., Sycamore, N., Swift, E., Symons, E., Szluha, S., Taluy, E., Tao, N., Taylor, K., Thompson, S., Thompson, M., Thomson, M., Thomson, N., Thurston, S., Toombs, D., Topping, B., Tovar-Corona, J., Ungureanu, D., Uphill, J., Urbanova, J., Jansen Van, P., Vancollie, V., Voak, P., Walker, D., Walker, M., Waller, M., Ward, G., Weatherhogg, C., Webb, N., Wells, A., Wells, E., Westwood, L., Whipp, T., Whiteley, T., Whitton, G., Whitwham, A., Widaa, S., Williams, M., Wilson, M., Wright, S., Farr, B. W., Quail, M. A., Thurston, S. A. J., Bronner, I. F., Redshaw, N. M., Lensing, S. V., Balcazar, C. E., Gallagher, M. D., Williamson, K. A., Stanton, T. D., Michelsen, M. L., Warwick-Dugdale, J., Manley, R., Farbos, A., Harrison, J. W., Sambles, C. M., Studholme, D. J., Lackenby, A., Mbisa, T., Platt, S., Miah, S., Bibby, D., Manso, C., Hubb, J., Dabrera, G., Ramsay, M., Bradshaw, D., Schaefer, U., Groves, N., Gallagher, E., Lee, D., Williams, D., Ellaby, N., Hartman, H., Manesis, N., Patel, V., Ledesma, J., Twohig, K. A., Allara, E., Pearson, C., Cheng, J. K. J., Bridgewater, H. E., Frost, L. R., Taylor-Joyce, G., Brown, P. E., Tong, L., Broos, A., Mair, D., Nichols, J., Carmichael, S. N., Smollett, K. L., Nomikou, K., Aranday-Cortes, E., Johnson, N., Nickbakhsh, S., Vamos, E. E., Hughes, M., Rainbow, L., Eccles, R., Nelson, C., Whitehead, M., Gregory, R., Gemmell, M., Wierzbicki, C., Webster, H. J., Fisher, C. L., Signell, A. W., Betancor, G., Wilson, H. D., Nebbia, G., Flaviani, F., Cerda, A. C., Merrill, T. V., Wilson, R. E., Cotic, M., Bayzid, N., Thompson, T., Acheson, E., Rushton, S., O'Brien, S., Baker, D. J., Rudder, S., Aydin, A., Sang, F., Debebe, J., Francois, S., Vasylyeva, T. I., Zamudio, M. E., Gutierrez, B., Marchbank, A., Maksimovic, J., Spellman, K., Mccluggage, K., Morgan, M., Beer, R., Afifi, S., Workman, T., Fuller, W., Bresner, C., Angyal, A., Green, L. R., Parsons, P. J., Tucker, R. M., Brown, R., Whiteley, M., Rowe, W., Siveroni, I., Le-Viet, T., Gaskin, A., Johnson, R., Sharrocks, K., Blane, E., Modis, Y., Leigh, K. E., Briggs, J. A. G., van Gils, M. J., Smith, K. G. C., Bradley, J. R., Doffinger, R., Ceron-Gutierrez, L., Barcenas-Morales, G., Pollock, D. D., Goldstein, R. A., Smielewska, A., Skittrall, J. P., Gouliouris, T., Goodfellow, I. G., Gkrania-Klotsas, E., Illingworth, C. J. R., Mccoy, L. E., Gupta, R. K., Medical Microbiology and Infection Prevention, AII - Infectious diseases, Collier, Dami A [0000-0001-5446-4423], Jahun, Aminu [0000-0002-4585-1701], Temperton, Nigel [0000-0002-7978-3815], Modis, Yorgo [0000-0002-6084-0429], Briggs, John AG [0000-0003-3990-6910], Goldstein, Richard A [0000-0001-5148-4672], Skittrall, Jordan P [0000-0002-8228-3758], Gkrania-Klotsas, Effrossyni [0000-0002-0930-8330], McCoy, Laura E [0000-0001-9503-7946], Gupta, Ravindra K [0000-0001-9751-1808], and Apollo - University of Cambridge Repository

Subjects
0301 basic medicine, Male, Time Factors, viruses, Passive, Antibodies, Viral, CITIID-NIHR BioResource COVID-19 Collaboration, 2.1 Biological and endogenous factors, Viral, Aetiology, Neutralizing, Lung, Phylogeny, neutralising antibodies, Infectivity, education.field_of_study, Genome, Multidisciplinary, Alanine, biology, High-Throughput Nucleotide Sequencing, Viral Load, Spike Glycoprotein, Virus Shedding, Adenosine Monophosphate, Aged, Antibodies, Neutralizing, COVID-19, Chronic Disease, Genome, Viral, Humans, Immune Evasion, Immune Tolerance, Immunization, Passive, Immunosuppression Therapy, Mutagenesis, Mutant Proteins, Mutation, SARS-CoV-2, Spike Glycoprotein, Coronavirus, Evolution, Molecular, Infectious Diseases, Pneumonia & Influenza, Antibody, Infection, Viral load, Biotechnology, Evolution, General Science & Technology, antibody escape, Convalescent plasma, 030106 microbiology, Population, evasion, Antibodies, Virus, Article, Vaccine Related, resistance, 03 medical and health sciences, Immune system, COVID-19 Genomics UK (COG-UK) Consortium, Biodefense, Genetics, Viral shedding, education, COVID-19 Serotherapy, QR355, Prevention, Wild type, Molecular, Pneumonia, Virology, COVID-19 Drug Treatment, Coronavirus, Emerging Infectious Diseases, Good Health and Well Being, 030104 developmental biology, biology.protein, Immunization, immune suppression, mutation
Abstract

The spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is critical for virus infection through the engagement of the human ACE2 protein1 and is a major antibody target. Here we show that chronic infection with SARS-CoV-2 leads to viral evolution and reduced sensitivity to neutralizing antibodies in an immunosuppressed individual treated with convalescent plasma, by generating whole-genome ultra-deep sequences for 23 time points that span 101 days and using in vitro techniques to characterize the mutations revealed by sequencing. There was little change in the overall structure of the viral population after two courses of remdesivir during the first 57 days. However, after convalescent plasma therapy, we observed large, dynamic shifts in the viral population, with the emergence of a dominant viral strain that contained a substitution (D796H) in the S2 subunit and a deletion (ΔH69/ΔV70) in the S1 N-terminal domain of the spike protein. As passively transferred serum antibodies diminished, viruses with the escape genotype were reduced in frequency, before returning during a final, unsuccessful course of convalescent plasma treatment. In vitro, the spike double mutant bearing both ΔH69/ΔV70 and D796H conferred modestly decreased sensitivity to convalescent plasma, while maintaining infectivity levels that were similar to the wild-type virus.The spike substitution mutant D796H appeared to be the main contributor to the decreased susceptibility to neutralizing antibodies, but this mutation resulted in an infectivity defect. The spike deletion mutant ΔH69/ΔV70 had a twofold higher level of infectivity than wild-type SARS-CoV-2, possibly compensating for the reduced infectivity of the D796H mutation. These data reveal strong selection on SARS-CoV-2 during convalescent plasma therapy, which is associated with the emergence of viral variants that show evidence of reduced susceptibility to neutralizing antibodies in immunosuppressed individuals.

Published
2021

7. Mycoplasma taxonomy: what’s in a name and where to submit?

Author

Chalker V., M. Balish, A. Bertaccini, A. Blanchard, D. Brown, J. Frey, G. Gasparich, L. Hölzle, C. Knox, C. -H. Kuo, L. Manso-Silvan, M. May12, A. S. Ramírez Corbera, J. Spergser, B. Spiller, D. Volokhov, W. Wei, and Chalker V., M. Balish, A. Bertaccini, A. Blanchard, D. Brown, J. Frey, G. Gasparich, L. Hölzle, C. Knox, C.-H. Kuo, L. Manso-Silvan, M. May12, A.S. Ramírez Corbera, J.Spergser, B. Spiller, D. Volokhov, W. Wei

Subjects
Mollicutes, Taxonomy, repository, rules
Abstract

The International Committee on Systematics of Prokaryotes (ICSP) oversees the nomenclature of prokaryotes, naming rules and issues Judicial Commission Opinions concerning taxonomy, Bacteriological Code revisions, etc. Mycoplasmology is represented by a subcommittee of experts on behalf of the International Organization for Mycoplasmology (IOM). Taxonomy of Mollicutes standards (Brown et al., 2007) include deposition: (i) type strains into two culture collections; (ii) 16S rRNA gene sequences with phylogenetic analysis; (iii) demonstration type strains differ from known valid species; (iv) assignment to an order, family and genus in the class. (v) description of novel Mollicutes species should also follow the proposed minimal standards for the use of genome data for the taxonomy of prokaryotes in which genome sequence (complete or draft) the proposed type strain is required (this is not required for Candidatus assignment) (Chun et al., 2018). Antiserum is no longer required (Firrao and Brown 2012); Submission of Mollicutes to culture collections is imperative to assist the community longer term by accessing strains, retaining them for future work and is required when describing a new species. In 2021 the ICSP reviewed international culture collections accepting depositions of Mollicutes. The following collections indicated they accept strains (*with no charge for deposition, shipping fees apply): USA: ATCC* (https://www.lgcstandards-atcc.org/?geo_country=es) France: CIP* (https://catalogue-crbip.pasteur.fr/resultatRecherche.xhtml) Germany: DSMZ* (https://www.dsmz.de/search?tx_kesearch_pi1[sword]=mycoplasma&cHash=e52a26740bdd69d3bf55a6bca2fe6d74) Japan: NBRC (https://www.nite.go.jp/nbrc/catalogue/NBRCDispSearchServlet?lang=en) UK: NCTC* (https://www.phe-culturecollections.org.uk/) Taiwan: BCRC (https://catalog.bcrc.firdi.org.tw/Welcome) (case by case review) Taxonomic naming of new species: Recent publications suggest renaming of species to unusual/unconventional names (Gupta and Oren, 2020). The ICSP Mollicutes Subcommittee is committed to retaining nomenclature aligned to the agreed code and existing scientific/clinical practice, retaining standards for authors naming Mollicutes. Balish et al., 2020 recommended rejection of published names within the class Mollicutes. When considering naming new species, we recommend contacting the committee for advice prior to publication, engage with the Mollicute community prior to publication of controversial changes, especially impacting pathogenic relevant bacteria.

Published
2021

9. Genomic reconstruction of the SARS-CoV-2 epidemic in England

Author

Vöhringer, HS, Sanderson, T, Sinnott, M, De Maio, N, Nguyen, T, Goater, R, Schwach, F, Harrison, I, Hellewell, J, Ariani, CV, Gonçalves, S, Jackson, DK, Johnston, I, Jung, AW, Saint, C, Sillitoe, J, Suciu, M, Goldman, N, Panovska-Griffiths, J, Abnizova, I, Aigrain, L, Alderton, A, Ali, M, Allen, L, Amato, R, Anderson, R, Ariani, C, Austin-Guest, S, Bala, S, Barrett, J, Bassett, A, Battleday, K, Beal, J, Beale, M, Beaver, C, Bellany, S, Bellerby, T, Bellis, K, Berger, D, Berriman, M, Betteridge, E, Bevan, P, Binley, S, Bishop, J, Blackburn, K, Bonfield, J, Boughton, N, Bowker, S, Brendler-Spaeth, T, Bronner, I, Brooklyn, T, Buddenborg, SK, Bush, R, Caetano, C, Cagan, A, Carter, N, Cartwright, J, Monteiro, TC, Chapman, L, Chillingworth, T-J, Clapham, P, Clark, R, Clarke, A, Clarke, C, Cole, D, Cook, E, Coppola, M, Cornell, L, Cornwell, C, Corton, C, Crackett, A, Cranage, A, Craven, H, Craw, S, Crawford, M, Cutts, T, Dabrowska, M, Davies, M, Davies, R, Dawson, J, Day, C, Densem, A, Dibling, T, Dockree, C, Dodd, D, Dogga, S, Dorman, M, Dougan, G, Dougherty, M, Dove, A, Drummond, L, Drury, E, Dudek, M, Durham, J, Durrant, L, Easthope, E, Eckert, S, Ellis, P, Farr, B, Fenton, M, Ferrero, M, Flack, N, Fordham, H, Forsythe, G, Foulser, L, Francis, M, Fraser, A, Freeman, A, Galvin, A, Garcia-Casado, M, Gedny, A, Girgis, S, Glover, J, Goncalves, S, Goodwin, S, Gould, O, Gourtovaia, M, Gray, A, Gray, E, Griffiths, C, Gu, Y, Guerin, F, Hamilton, W, Hanks, H, Harrison, E, Harrott, A, Harry, E, Harvison, J, Heath, P, Hernandez-Koutoucheva, A, Hobbs, R, Holland, D, Holmes, S, Hornett, G, Hough, N, Huckle, L, Hughes-Hallet, L, Hunter, A, Inglis, S, Iqbal, S, Jackson, A, Jackson, D, James, K, Jamrozy, D, Verdejo, CJ, Jones, M, Kallepally, K, Kane, L, Kay, K, Kay, S, Keatley, J, Keith, A, King, A, Kitchin, L, Kleanthous, M, Klimekova, M, Korlevic, P, Krasheninnkova, K, Lane, G, Langford, C, Laverack, A, Law, K, Lawniczak, M, Lensing, S, Leonard, S, Letchford, L, Lewis, K, Lewis-Wade, A, Liddle, J, Lin, Q, Lindsay, S, Linsdell, S, Livett, R, Lo, S, Long, R, Lovell, J, Ludden, C, Mack, J, Maddison, M, Makunin, A, Mamun, I, Mansfield, J, Marriott, N, Martin, M, Mayho, M, McCarthy, S, McClintock, J, McGuigan, S, McHugh, S, McMinn, L, Meadows, C, Mobley, E, Moll, R, Morra, M, Morrow, L, Murie, K, Nash, S, Nathwani, C, Naydenova, P, Neaverson, A, Nelson, R, Nerou, E, Nicholson, J, Nimz, T, Noell, GG, O’Meara, S, Ohan, V, Oliver, K, Olney, C, Ormond, D, Oszlanczi, A, Palmer, S, Pang, YF, Pardubska, B, Park, N, Parmar, A, Patel, G, Patel, M, Payne, M, Peacock, S, Petersen, A, Plowman, D, Preston, T, Prestwood, L, Puethe, C, Quail, M, Rajan, D, Rajatileka, S, Rance, R, Rawlings, S, Redshaw, N, Reynolds, J, Reynolds, M, Rice, S, Richardson, M, Roberts, C, Robinson, K, Robinson, M, Robinson, D, Rogers, H, Rojo, EM, Roopra, D, Rose, M, Rudd, L, Sadri, R, Salmon, N, Saul, D, Scott, C, Seekings, P, Shirley, L, Simms, A, Sivadasan, S, Siwek, B, Sizer, D, Skeldon, K, Skelton, J, Slater-Tunstill, J, Sloper, L, Smerdon, N, Smith, C, Smith, J, Smith, K, Smith, M, Smith, S, Smith, T, Sneade, L, Soria, CD, Sousa, C, Souster, E, Sparkes, A, Spencer-Chapman, M, Squares, J, Stanley, R, Steed, C, Stickland, T, Still, I, Stratton, MR, Strickland, M, Swann, A, Swiatkowska, A, Sycamore, N, Swift, E, Symons, E, Szluha, S, Taluy, E, Tao, N, Taylor, K, Taylor, S, Thompson, S, Thompson, M, Thomson, M, Thomson, N, Thurston, S, Tonkin-Hill, G, Toombs, D, Topping, B, Tovar-Corona, J, Ungureanu, D, Uphill, J, Urbanova, J, Van Vuuren, PJ, Vancollie, V, Voak, P, Walker, D, Walker, M, Waller, M, Ward, G, Weatherhogg, C, Webb, N, Weldon, D, Wells, A, Wells, E, Westwood, L, Whipp, T, Whiteley, T, Whitton, G, Whitwham, A, Widaa, S, Williams, M, Wilson, M, Wright, S, Robson, SC, Connor, TR, Loman, NJ, Golubchik, T, Martinez Nunez, RT, Bonsall, D, Rambaut, A, Snell, LB, Corden, S, Nastouli, E, Nebbia, G, Lythgoe, K, Torok, ME, Goodfellow, IG, Prieto, JA, Saeed, K, Houlihan, C, Frampton, D, Hamilton, WL, Witney, AA, Bucca, G, Pope, CF, Moore, C, Thomson, EC, Harrison, EM, Smith, CP, Rogan, F, Beckwith, SM, Murray, A, Singleton, D, Eastick, K, Sheridan, LA, Randell, P, Jackson, LM, Fairley, DJ, Loose, MW, Watkins, J, Moses, S, Nicholls, S, Bull, M, Smith, DL, Aanensen, DM, Aggarwal, D, Shepherd, JG, Curran, MD, Parmar, S, Parker, MD, Williams, C, Glaysher, S, Underwood, AP, Bashton, M, Pacchiarini, N, Loveson, KF, Byott, M, Carabelli, AM, Templeton, KE, de Silva, TI, Wang, D, Langford, CF, Gunson, RN, Cottrell, S, O’Grady, J, Kwiatkowski, D, Lillie, PJ, Cortes, N, Moore, N, Thomas, C, Burns, PJ, Mahungu, TW, Liggett, S, Beckett, AH, Holden, MTG, Levett, LJ, Osman, H, Hassan-Ibrahim, MO, Simpson, DA, Chand, M, Gupta, RK, Darby, AC, Paterson, S, Pybus, OG, Volz, EM, de Angelis, D, Robertson, DL, Page, AJ, Bassett, AR, Wong, N, Taha, Y, Erkiert, MJ, Spencer Chapman, MH, Dewar, R, McHugh, MP, Mookerjee, S, Aplin, S, Harvey, M, Sass, T, Umpleby, H, Wheeler, H, McKenna, JP, Warne, B, Taylor, JF, Chaudhry, Y, Izuagbe, R, Jahun, AS, Young, GR, McMurray, C, McCann, CM, Nelson, A, Elliott, S, Lowe, H, Price, A, Crown, MR, Rey, S, Roy, S, Temperton, B, Shaaban, S, Hesketh, AR, Laing, KG, Monahan, IM, Heaney, J, Pelosi, E, Silviera, S, Wilson-Davies, E, Fryer, H, Adams, H, du Plessis, L, Johnson, R, Harvey, WT, Hughes, J, Orton, RJ, Spurgin, LG, Bourgeois, Y, Ruis, C, O’Toole, Á, Fraser, C, Edgeworth, J, Breuer, J, Michell, SL, Todd, JA, John, M, Buck, D, Gajee, K, Kay, GL, Peacock, SJ, Heyburn, D, Kitchman, K, McNally, A, Pritchard, DT, Dervisevic, S, Muir, P, Robinson, E, Vipond, BB, Ramadan, NA, Jeanes, C, Catalan, J, Jones, N, da Silva Filipe, A, Fuchs, M, Miskelly, J, Jeffries, AR, Park, NR, Ash, A, Koshy, C, Barrow, M, Buchan, SL, Mantzouratou, A, Clark, G, Holmes, CW, Campbell, S, Davis, T, Tan, NK, Brown, JR, Harris, KA, Kidd, SP, Grant, PR, Xu-McCrae, L, Cox, A, Madona, P, Pond, M, Randell, PA, Withell, KT, Graham, C, Denton-Smith, R, Swindells, E, Turnbull, R, Sloan, TJ, Bosworth, A, Hutchings, S, Pymont, HM, Casey, A, Ratcliffe, L, Jones, CR, Knight, BA, Haque, T, Hart, J, Irish-Tavares, D, Witele, E, Mower, C, Watson, LK, Collins, J, Eltringham, G, Crudgington, D, Macklin, B, Iturriza-Gomara, M, Lucaci, AO, McClure, PC, Carlile, M, Holmes, N, Storey, N, Rooke, S, Yebra, G, Craine, N, Perry, M, Alikhan, N-F, Bridgett, S, Cook, KF, Fearn, C, Goudarzi, S, Lyons, RA, Williams, T, Haldenby, ST, Davies, RM, Batra, R, Blane, B, Spyer, MJ, Smith, P, Yavus, M, Williams, RJ, Mahanama, AIK, Samaraweera, B, Girgis, ST, Hansford, SE, Green, A, Bellis, KL, Dorman, MJ, Quick, J, Poplawski, R, Reynolds, N, Mack, A, Morriss, A, Whalley, T, Patel, B, Georgana, I, Hosmillo, M, Pinckert, ML, Stockton, J, Henderson, JH, Hollis, A, Stanley, W, Yew, WC, Myers, R, Thornton, A, Adams, A, Annett, T, Asad, H, Birchley, A, Coombes, J, Evans, JM, Fina, L, Gatica-Wilcox, B, Gilbert, L, Graham, L, Hey, J, Hilvers, E, Jones, S, Jones, H, Kumziene-Summerhayes, S, McKerr, C, Powell, J, Pugh, G, Trotter, AJ, Williams, CA, Kermack, LM, Foulkes, BH, Gallis, M, Hornsby, HR, Louka, SF, Pohare, M, Wolverson, P, Zhang, P, MacIntyre-Cockett, G, Trebes, A, Moll, RJ, Ferguson, L, Goldstein, EJ, Maclean, A, Tomb, R, Starinskij, I, Thomson, L, Southgate, J, Kraemer, MUG, Raghwani, J, Zarebski, AE, Boyd, O, Geidelberg, L, Illingworth, CJ, Jackson, C, Pascall, D, Vattipally, S, Freeman, TM, Hsu, SN, Lindsey, BB, Tovar-Corona, JM, Cox, M, Abudahab, K, Menegazzo, M, Taylor, BEW, Yeats, CA, Mukaddas, A, Wright, DW, de Oliveira Martins, L, Colquhoun, R, Hill, V, Jackson, B, McCrone, JT, Medd, N, Scher, E, Keatley, J-P, Curran, T, Morgan, S, Maxwell, P, Eldirdiri, S, Kenyon, A, Holmes, AH, Price, JR, Wyatt, T, Mather, AE, Skvortsov, T, Hartley, JA, Guest, M, Kitchen, C, Merrick, I, Munn, R, Bertolusso, B, Lynch, J, Vernet, G, Kirk, S, Wastnedge, E, Idle, G, Bradley, DT, Poyner, J, Mori, M, Jones, O, Wright, V, Brooks, E, Churcher, CM, Fragakis, M, Galai, K, Jermy, A, Judges, S, McManus, GM, Smith, KS, Westwick, E, Attwood, SW, Bolt, F, Davies, A, De Lacy, E, Downing, F, Edwards, S, Meadows, L, Jeremiah, S, Smith, N, Charalampous, T, Patel, A, Berry, L, Boswell, T, Fleming, VM, Howson-Wells, HC, Joseph, A, Khakh, M, Lister, MM, Bird, PW, Fallon, K, Helmer, T, McMurray, CL, Odedra, M, Shaw, J, Tang, JW, Willford, NJ, Blakey, V, Raviprakash, V, Sheriff, N, Williams, L-A, Feltwell, T, Bedford, L, Cargill, JS, Hughes, W, Moore, J, Stonehouse, S, Atkinson, L, Lee, JCD, Shah, D, Alcolea, A, Ohemeng-Kumi, N, Ramble, J, Sehmi, J, Williams, R, Chatterton, W, Pusok, M, Everson, W, Castigador, A, Macnaughton, E, El Bouzidi, K, Lampejo, T, Sudhanva, M, Breen, C, Sluga, G, Ahmad, SSY, George, RP, Machin, NW, Binns, D, James, V, Blacow, R, Coupland, L, Smith, L, Barton, E, Padgett, D, Scott, G, Cross, A, Mirfenderesky, M, Greenaway, J, Cole, K, Clarke, P, Duckworth, N, Walsh, S, Bicknell, K, Impey, R, Wyllie, S, Hopes, R, Bishop, C, Chalker, V, Gifford, L, Molnar, Z, Auckland, C, Evans, C, Johnson, K, Partridge, DG, Raza, M, Baker, P, Bonner, S, Essex, S, Murray, LJ, Lawton, AI, Burton-Fanning, S, Payne, BAI, Waugh, S, Gomes, AN, Kimuli, M, Murray, DR, Ashfield, P, Dobie, D, Ashford, F, Best, A, Crawford, L, Cumley, N, Mayhew, M, Megram, O, Mirza, J, Moles-Garcia, E, Percival, B, Ensell, L, Lowe, HL, Maftei, L, Mondani, M, Chaloner, NJ, Cogger, BJ, Easton, LJ, Huckson, H, Lewis, J, Lowdon, S, Malone, CS, Munemo, F, Mutingwende, M, Nicodemi, R, Podplomyk, O, Somassa, T, Beggs, A, Richter, A, Cormie, C, Dias, J, Forrest, S, Higginson, EE, Maes, M, Young, J, Davidson, RK, Jackson, KA, Turtle, L, Keeley, AJ, Ball, J, Byaruhanga, T, Chappell, JG, Dey, J, Hill, JD, Park, EJ, Fanaie, A, Hilson, RA, Yaze, G, Afifi, S, Beer, R, Maksimovic, J, Masters, KM, Spellman, K, Bresner, C, Fuller, W, Marchbank, A, Workman, T, Shelest, E, Debebe, J, Sang, F, Zamudio, ME, Francois, S, Gutierrez, B, Vasylyeva, TI, Flaviani, F, Ragonnet-Cronin, M, Smollett, KL, Broos, A, Mair, D, Nichols, J, Nomikou, K, Tong, L, Tsatsani, I, O’Brien, S, Rushton, S, Sanderson, R, Perkins, J, Cotton, S, Gallagher, A, Allara, E, Pearson, C, Bibby, D, Dabrera, G, Ellaby, N, Gallagher, E, Hubb, J, Lackenby, A, Lee, D, Manesis, N, Mbisa, T, Platt, S, Twohig, KA, Morgan, M, Aydin, A, Baker, DJ, Foster-Nyarko, E, Prosolek, SJ, Rudder, S, Baxter, C, Carvalho, SF, Lavin, D, Mariappan, A, Radulescu, C, Singh, A, Tang, M, Morcrette, H, Bayzid, N, Cotic, M, Balcazar, CE, Gallagher, MD, Maloney, D, Stanton, TD, Williamson, KA, Manley, R, Michelsen, ML, Sambles, CM, Studholme, DJ, Warwick-Dugdale, J, Eccles, R, Gemmell, M, Gregory, R, Hughes, M, Nelson, C, Rainbow, L, Vamos, EE, Webster, HJ, Whitehead, M, Wierzbicki, C, Angyal, A, Green, LR, Whiteley, M, Bronner, IF, Farr, BW, Lensing, SV, McCarthy, SA, Quail, MA, Redshaw, NM, Thurston, SAJ, Rowe, W, Gaskin, A, Le-Viet, T, Birney, E, Volz, E, Funk, S, Martincorena, I, Barrett, JC, and Gerstung, M

Abstract

The evolution of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus leads to new variants that warrant timely epidemiological characterization. Here we use the dense genomic surveillance data generated by the COVID-19 Genomics UK Consortium to reconstruct the dynamics of 71 different lineages in each of 315 English local authorities between September 2020 and June 2021. This analysis reveals a series of subepidemics that peaked in early autumn 2020, followed by a jump in transmissibility of the B.1.1.7/Alpha lineage. The Alpha variant grew when other lineages declined during the second national lockdown and regionally tiered restrictions between November and December 2020. A third more stringent national lockdown suppressed the Alpha variant and eliminated nearly all other lineages in early 2021. Yet a series of variants (most of which contained the spike E484K mutation) defied these trends and persisted at moderately increasing proportions. However, by accounting for sustained introductions, we found that the transmissibility of these variants is unlikely to have exceeded the transmissibility of the Alpha variant. Finally, B.1.617.2/Delta was repeatedly introduced in England and grew rapidly in early summer 2021, constituting approximately 98% of sampled SARS-CoV-2 genomes on 26 June 2021.

Published
2021

12. Assessing the added value of group B Streptococcus maternal immunisation in preventing maternal infection and fetal harm: population surveillance study.

Author

Lamagni, T, Wloch, C, Broughton, K, Collin, SM, Chalker, V, Coelho, J, Ladhani, SN, Brown, CS, Shetty, N, and Johnson, AP

Subjects
STREPTOCOCCUS agalactiae, STILLBIRTH, SURGICAL site infections, CESAREAN section, IMMUNIZATION, PREGNANT women
Abstract

Objective: To assess the incidence of maternal group B Streptococcus (GBS) infection in England. Design: Population surveillance augmented through data linkage. Setting: England. Population: All pregnant women accessing the National Health Service (NHS) in England. Methods: Invasive GBS (iGBS) infections during pregnancy or within 6 weeks of childbirth were identified by linking Public Health England (PHE) national microbiology surveillance data for 2014 to NHS hospital admission records. Capsular serotypes of GBS were determined by reference laboratory typing of clinical isolates from women aged 15–44 years. Post‐caesarean section surgical site infection (SSI) caused by GBS was identified in 21 hospitals participating in PHE SSI surveillance (2009–2015). Main outcome measures: iGBS rate per 1000 maternities; risk of GBS SSI per 1000 caesarean sections. Results: Of 1601 patients diagnosed with iGBS infections in England in 2014, 185 (12%) were identified as maternal infections, a rate of 0.29 (95% CI 0.25–0.33) per 1000 maternities and representing 83% of all iGBS cases in women aged 18–44 years. Seven (3.8%) were associated with miscarriage. Fetal outcome identified excess rates of stillbirth (3.4 versus 0.5%) and extreme prematurity (<28 weeks of gestation, 3.7 versus 0.5%) compared with national averages (P < 0.001). Caesarean section surveillance in 27 860 women (21 hospitals) identified 47 cases of GBS SSI, with an estimated 4.24 (3.51–5.07) per 1000 caesarean sections, a median time‐to‐onset of 10 days (IQR 7–13 days) and ten infections that required readmission. Capsular serotype analysis identified a diverse array of strains with serotype III as the most common (43%). Conclusions: Our assessment of maternal GBS infection in England indicates the potential additional benefit of GBS vaccination in preventing adverse maternal and fetal outcomes. [ABSTRACT FROM AUTHOR]

Published
2022
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13. Emergence of dominant toxigenic M1T1 Streptococcus pyogenes clone during increased scarlet fever activity in England:a population-based molecular epidemiological study

Author

Lynskey, NN, Jauneikaite, E, Li, H-K, Zhi, X, Turner, CE, Mosavie, M, Pearson, M, Asai, M, Lobkowicz, L, Chow, JY, Parkhill, J, Lamagni, T, Chalker, V, Sriskandan, S, Parkhill, Julian [0000-0002-7069-5958], Apollo - University of Cambridge Repository, National Institute for Health Research, Wellcome Trust, Medical Research Council (MRC), and Imperial College Healthcare NHS Trust- BRC Funding

Subjects
Adult, Male, Canada, Adolescent, Genotype, Scarlet Fever, Streptococcus pyogenes, EPIDEMICS, Exotoxins, Bacteremia, TOXIN, Microbiology, Article, Young Adult, Bacterial Proteins, 1108 Medical Microbiology, Streptococcal Infections, Humans, Child, Aged, Aged, 80 and over, Antigens, Bacterial, Molecular Epidemiology, Science & Technology, PYROGENIC EXOTOXIN, Gene Expression Profiling, Incidence, Infant, Newborn, Infant, Membrane Proteins, 1103 Clinical Sciences, Middle Aged, GENE, United Kingdom, Epidemiologic Studies, Infectious Diseases, SOUTH-KOREA, England, Child, Preschool, VIRULENCE, ROFA, Female, Carrier Proteins, Life Sciences & Biomedicine, Bacterial Outer Membrane Proteins
Abstract

Background\ud \ud Since 2014, England has seen increased scarlet fever activity unprecedented in modern times. In 2016, England's scarlet fever seasonal rise coincided with an unexpected elevation in invasive Streptococcus pyogenes infections. We describe the molecular epidemiological investigation of these events.\ud \ud Methods\ud \ud We analysed changes in S pyogenes emm genotypes, and notifications of scarlet fever and invasive disease in 2014–16 using regional (northwest London) and national (England and Wales) data. Genomes of 135 non-invasive and 552 invasive emm1 isolates from 2009–16 were analysed and compared with 2800 global emm1 sequences. Transcript and protein expression of streptococcal pyrogenic exotoxin A (SpeA; also known as scarlet fever or erythrogenic toxin A) in sequenced, non-invasive emm1 isolates was quantified by real-time PCR and western blot analyses.\ud \ud Findings\ud \ud Coincident with national increases in scarlet fever and invasive disease notifications, emm1 S pyogenes upper respiratory tract isolates increased significantly in northwest London in the March to May period, from five (5%) of 96 isolates in 2014, to 28 (19%) of 147 isolates in 2015 (p=0·0021 vs 2014 values), to 47 (33%) of 144 in 2016 (p=0·0080 vs 2015 values). Similarly, invasive emm1 isolates collected nationally in the same period increased from 183 (31%) of 587 in 2015 to 267 (42%) of 637 in 2016 (p

Published
2019
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14. Congenital Cytomegalovirus Infection as a Cause of Sensorineural Hearing Loss in a Highly Immune Population

Author

Wang, K, Chalker, V, Bermingham, A, Harrison, T, Mant, D, and Harnden, A

Subjects
otorhinolaryngologic diseases
Abstract

Background: The burden of congenital cytomegalovirus (CMV)-associated sensorineural hearing loss (SNHL) in populations with CMV seroprevalence approaching 100% is unknown. The purpose of this study was to assess the rate, associated factors, and predictors of SNHL in CMV-infected infants identified by newborn screening in a highly seropositive maternal population. Methods: Newborns with positive saliva CMV-DNA that was confirmed by virus isolation in the first 2 weeks of life were enrolled in a prospective follow-up study to monitor hearing outcome. Results: Of 12,195 infants screened, 121 (1%) were infected with CMV and 12 (10%) had symptomatic infection at birth. Hearing function could be assessed in 102/121 children who underwent at least one auditory brainstem evoked response testing at a median age of 12 months. SNHL was observed in 10/102 (9.8%; 95% confidence interval: 5.1–16.7) children. Median age at the latest hearing evaluation was 47 months (12–84 months). Profound loss (>90 dB) was found in 4/5 children with bilateral SNHL while all 5 children with unilateral loss had moderate to severe deficit. The presence of symptomatic infection at birth (odds ratio, 38.1; 95% confidence interval: 1.6–916.7) was independently associated with SNHL after adjusting for intrauterine growth restriction, gestational age, gravidity, and maternal age. Among 10 infants with SNHL, 6 (60%) were born to mothers with nonprimary CMV infection. Conclusions: Even in populations with near universal immunity to CMV, congenital CMV infection is a significant cause of SNHL demonstrating the importance of CMV as a major cause of SNHL in children worldwide. As in other populations, SNHL is more frequently observed in symptomatic CMV infection.

Published
2019

15. Group B streptococcal disease in UK and Irish infants younger than 90 days, 2014–15: results from prospective surveillance

Author

O'Sullivan, C.P., Lamagni, T., Patel, D., Efstratiou, A., Cunney, R., Meehan, M., Ladhani, S., Reynolds, A.J., Campbell, R., Doherty, L., Boyle, M., Kapatai, G., Chalker, V., Lindsay, D., Smith, A., Davies, E., Jones, C.E., and Heath, P.T.

Abstract

BackgroundGroup B streptococcus is a leading cause of serious infection in young infants in many countries worldwide. We aimed to define the burden and clinical features of invasive group B streptococcal disease in infants younger than 90 days in the UK and Ireland, together with the characteristics of disease-causing isolates.MethodsProspective, active national surveillance of invasive group B streptococcal disease in infants younger than 90 days was done from April 1, 2014, to April 30, 2015, through the British Paediatric Surveillance Unit, microbiology reference laboratories, and national public health agencies in the UK and Ireland. Early onset was defined as disease in the first 6 days of life and late onset was defined as 7–89 days of life. Incidence was calculated using livebirths in 2014 (after adjustment for the 13-month surveillance period). Isolates were characterised by serotyping, multilocus sequence typing, and antimicrobial susceptibility testing.Findings856 cases of group B streptococcus were identified in 2014–15, an incidence of 0·94 per 1000 livebirths (95% CI 0·88–1·00). Incidence for early-onset disease (n=517) was 0·57 per 1000 livebirths (95% CI 0·52–0·62), and for late-onset disease (n=339) was 0·37 per 1000 livebirths (0·33–0·41). 53 infants died (case fatality rate 6·2%), of whom 27 had early-onset disease (case fatality rate 5·2%) and 26 had late-onset disease (case fatality rate 7·7%). The predominant serotypes were III (241 [60%] of 402 serotyped isolates) and Ia (69 [17%]); five serotypes (Ia, Ib, II, III, V) accounted for 377 (94%) of all serotyped isolates.InterpretationThe incidence of invasive infant group B streptococcal disease in the UK and Ireland has increased since a comparable study done in 2000–01. The burden of early-onset disease has not declined despite the introduction of national prevention guidelines. New strategies for prevention are required.FundingMeningitis Now.

Published
2019

18. Antibiotic susceptibility of Legionella pneumophila strains isolated in England and Wales 2007-17.

Author

Wilson, R E, Hill, R L R, Chalker, V J, Mentasti, M, and Ready, D

Subjects
LEGIONELLA pneumophila, ANTIBIOTICS, MICROBIAL sensitivity tests, PHARMACOLOGY, EPIDEMIOLOGY, COMPARATIVE studies, ERYTHROMYCIN, LEGIONELLA, LEGIONNAIRES' disease, RESEARCH methodology, MEDICAL cooperation, QUINOLONE antibacterial agents, RESEARCH, RIFAMPIN, EVALUATION research, PHARMACODYNAMICS
Abstract

Objectives: Antibiotic susceptibility of Legionella pneumophila is poorly understood, with treatment of Legionnaires' disease often based on empirical choice. The aim of this study was to determine the antibiotic susceptibility of L. pneumophila strains.Methods: Antibiotic susceptibility of 92 L. pneumophila strains isolated in England and Wales between 2007 and 2017 was determined using a microbroth dilution methodology for each agent tested. MICs and MBCs were determined and compared with published intracellular concentrations of each agent tested.Results: The MIC range of erythromycin was 0.06-1 mg/L, the MIC range of rifampicin was 0.0001 mg/L, the MIC range of ciprofloxacin was 0.004-0.25 mg/L and the MIC range of levofloxacin and moxifloxacin was 0.03-0.25 mg/L. The MBC range of erythromycin was 1-32 mg/L, but the MBC range of ciprofloxacin was the same as the MIC range. For levofloxacin and moxifloxacin the MBC range was elevated by one dilution and two dilutions, respectively. Typically, intracellular bronchial secretion concentrations of erythromycin might be expected to reach a suitable level to exceed the MIC range; however, 91 of 92 (98.9%) isolates had an MBC below the expected intracellular concentrations, which indicated erythromycin may have variable efficacy. MIC and MBC values of ciprofloxacin, levofloxacin and moxifloxacin were below achievable intracellular levels within bronchial secretions. Comparison of the MIC/MBC correlation showed very little clustering for erythromycin, but strong clustering for levofloxacin and to a lesser extent ciprofloxacin.Conclusions: Use of the MIC/MBC linkage analysis seems an appropriate way forward for antimicrobial susceptibility testing and supports current guidance recommending levofloxacin for the treatment of Legionnaires' disease. [ABSTRACT FROM AUTHOR]

Published
2018
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19. Have reducing tonsillectomy rates in England led to increasing incidence of invasive Group A Streptococcus infections in children?

Author

Banigo, A., Moinie, A., Bleach, N., Chand, M., Chalker, V., and Lamagni, T.

Subjects
TONSILLECTOMY complications, BACTERIAL diseases in children, STREPTOCOCCUS, CROSS-sectional method, BACTERICIDAL action, DIAGNOSIS
Abstract

Objectives: To determine whether there is a correlation between falling tonsillectomy numbers and increasing numbers of tonsillitis admissions and invasive Group A β‐haemolytic streptococcus (iGAS) infection in children aged 14 and under in England. Design: An observational cross‐sectional study was performed. Setting: The data extracted covered the period from 1991 until 2014. Participants: Hospital admissions for tonsillectomies, tonsillitis/pharyngitis and all diagnoses of iGAS in children aged 14 and under who had a tonsillectomy. Main outcome measures: Correlation between trends in tonsillectomies, tonsillitis/pharyngitis and iGAS. Results: Across all age groups, there was a dramatic reduction in the total number of tonsillectomies performed in England from 28 309 in 1990/1991, down to 6327 in 2013/2014 (77.7% reduction). The numbers of hospital admissions for management of acute tonsillitis and pharyngitis have risen dramatically. iGAS numbers have increased steadily over this time period and more than doubled in children aged 14 and under. There are significant negative correlations between the trend in iGAS infections and numbers of tonsillectomies in all ages. There are also strong positive correlations between the trend in numbers of tonsillitis episodes and the number of iGAS infections in all under 14‐year groups; the strongest correlation was seen in the 1‐ to 4‐year age group (+0.92 Pearson correlation coefficient). Conclusions: There appears to be a correlation between falling tonsillectomy numbers, increasing hospital admissions with tonsillitis and rising iGAS infection in England. Further studies are required to assess the aetiological role of tonsillitis in predisposing to iGAS infection and the potential societal benefit of tonsillectomies. [ABSTRACT FROM AUTHOR]

Published
2018
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21. Design and validation of a qPCR assay for accurate detection and initial serogrouping of Legionella pneumophila in clinical specimens by the ESCMID Study Group for Legionella Infections (ESGLI).

Author

David, S., Mentasti, M., Afshar, B., Harrison, T., Chalker, V., Kese, D., Echahidi, F., Uldum, S., Mrazek, J., and Mendonça, R.

Subjects
LEGIONELLA pneumophila, POLYMERASE chain reaction, DETECTION of microorganisms, SEROTYPES, LEGIONNAIRES' disease, PROTEIN genetics, DETECTION limit
Abstract

Prompt detection of Legionella pneumophila is essential for rapid investigation of legionellosis. Furthermore, as the majority of L. pneumophila infections are caused by serogroup 1 (sg1) strains, rapid identification of such strains can be critical in both routine and outbreak scenarios. The ESCMID Study Group for Legionella Infections (ESGLI) was established in 2012 and immediately identified as a priority the validation of a reliable, easy to perform and interpret, cost-effective qPCR assay to standardise the detection of L. pneumophila DNA amongst members. A novel L. pneumophila assay targeting the mip gene was designed and combined with previously published methodologies amplifying the sg1 marker ( wzm) and the green fluorescent protein gene ( gfp) internal process control. The resulting triplex assay was validated internationally on the three qPCR platforms used by the majority of European Legionella reference laboratories: ABI 7500 (Life Technologies), LightCycler 480 Instrument II (Roche) and Rotor-Gene Q (Qiagen). Clinical and EQA specimens were tested together with a large panel of strains (251 in total) to validate the assay. The assay proved to be 100 % specific for L. pneumophila and sg1 DNA both in silico and in vitro. Efficiency values for mip and wzm assays ranged between 91.97 and 97.69 %. Limit of detection values estimated with 95 % confidence were adopted for mip and wzm assays on all three qPCR platforms. Inhibition was not observed. This study describes a robust assay that could be widely implemented to standardise the molecular detection of L. pneumophila among ESGLI laboratories and beyond. [ABSTRACT FROM AUTHOR]

Published
2015
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22. Prevalence of Trichomonas vaginalis, Mycoplasma genitalium and Ureaplasma urealyticum in men with urethritis attending an urban sexual health clinic.

Author

Khatib, N, Bradbury, C, Chalker, V, Koh, GCKW, Smit, E, Wilson, S, and Watson, J

Subjects
TRICHOMONAS vaginalis, DISEASE prevalence, DISEASES in men, URETHRITIS, SEXUAL health, URBAN health, HEALTH policy, CLINICAL trials
Abstract

We conducted a study to determine the prevalence of Trichomonas vaginalis (TV), Mycoplasma genitalium (MG) and Ureaplasma urealyticum (UU) in men with urethritis, attending an urban sexual health clinic, in order to inform screening and treatment policies. Men attending an urban sexual health clinic between June 2011 and January 2012 were evaluated. Urine samples were collected from men with urethritis and tested for Chlamydia trachomatis (CT), Neisseria gonorrhoeae (GC) and TV using transcription-mediated amplification and for MG and UU using polymerase chain reaction. Eighty-three samples were analysed. The prevalence of CT was 33.7% (28/83), GC was 16.8% (14/83), TV was 3.6% (3/83), MG was 12.0% (10/83) and UU was 4.8% (4/83). Fifteen men had recurrent urethritis. Of these, three were found to have had TV, five to have had MG and none to have had UU, at initial presentation. Given the prevalence of MG in this study, there is an urgent need for further larger studies looking at optimal treatment regimens and screening strategies in urethritis. [ABSTRACT FROM AUTHOR]

Published
2015
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29. Population genomics of Streptococcus mitis in UK and Ireland bloodstream infection and infective endocarditis cases.

Author

Kalizang'oma A, Richard D, Kwambana-Adams B, Coelho J, Broughton K, Pichon B, Hopkins KL, Chalker V, Beleza S, Bentley SD, Chaguza C, and Heyderman RS

Subjects
Humans, United Kingdom epidemiology, Ireland epidemiology, Endocarditis microbiology, Endocarditis epidemiology, Genome, Bacterial genetics, Whole Genome Sequencing, Male, Female, Genetic Variation, Genomics, Aged, Phylogeny, Middle Aged, Drug Resistance, Bacterial genetics, Endocarditis, Bacterial microbiology, Endocarditis, Bacterial epidemiology, Adult, Virulence Factors genetics, Anti-Bacterial Agents pharmacology, Anti-Bacterial Agents therapeutic use, Virulence genetics, Streptococcus mitis genetics, Streptococcus mitis isolation & purification, Streptococcal Infections microbiology, Streptococcal Infections epidemiology, Bacteremia microbiology, Bacteremia epidemiology
Abstract

Streptococcus mitis is a leading cause of infective endocarditis (IE). However, our understanding of the genomic epidemiology and pathogenicity of IE-associated S. mitis is hampered by low IE incidence. Here we use whole genome sequencing of 129 S. mitis bloodstream infection (BSI) isolates collected between 2001-2016 from clinically diagnosed IE cases in the UK to investigate genetic diversity, antimicrobial resistance, and pathogenicity. We show high genetic diversity of IE-associated S. mitis with virtually all isolates belonging to distinct lineages indicating no predominance of specific lineages. Additionally, we find a highly variable distribution of known pneumococcal virulence genes among the isolates, some of which are overrepresented in disease when compared to carriage strains. Our findings suggest that S. mitis in patients with clinically diagnosed IE is not primarily caused by specific hypervirulent or antimicrobial resistant lineages, highlighting the accidental pathogenic nature of S. mitis in patients with clinically diagnosed IE., (© 2024. The Author(s).)

Published
2024
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30. A study on viruses and bacteria with particular interest on Mycoplasma pneumoniae in children with exacerbation of asthma from a tertiary care hospital in Sri Lanka.

Author

Wijesooriya LI, Chalker V, Perera P, and Sunil-Chandra NP

Abstract

Asthma is a significant public health concern, particularly in children with severe symptoms. Exacerbation of asthma (EOA) is life-threatening, and respiratory infections (RIs) play a crucial role. Though viruses play a significant role in EOA, patients are empirically treated with antibiotics, contributing to antibiotic resistance development. Although there are widely reported associations of EOA with viral or Mycoplasma pneumoniae infections, there are no published data for Sri Lanka. The present study aimed to identify the association of common respiratory viruses, typical respiratory bacterial pathogens and M. pneumoniae in children with EOA and relate them with the compatibility of antimicrobial use. A case-control study was conducted in the paediatric unit of North Colombo Teaching Hospital, Sri Lanka, involving two groups of children between 5 and 15 years of age. Group 1 is children with EOA and Group 2 is children with stable asthma (SA). Each group consisted of 100 children. Sputum/throat swabs were tested for common respiratory viruses using virus-specific fluorescein isothiocyanate-labelled monoclonal antibodies (MAbs), bacteria by routine culture, and M. pneumoniae by real-time polymerase chain reaction. Macrolide resistance in M. pneumoniae was detected using conventional PCR and sequencing specific genetic mutations in the 23S rRNA gene. M. pneumoniae was genotyped using nested multilocus sequence typing, which targeted eight housekeeping genes ( ppa , pgm , gyrB , gmk , glyA , atpA , arcC and adk ). There was no significant difference in age, gender, demographic or geographical location between the two groups. In children with EOA, antibiotics were used in 66 % (66/100) and macrolides in 42 % (42/100). Samples comprised 78 % (78/100) sputum and 22 % (22/100) throat swabs. Adenovirus was the most common virus identified, and it was significantly higher in children with EOA compared to those with SA. Still, the two groups had no significant difference in typical bacteria findings. M. pneumoniae was detected in one patient with EOA, but none was detected in the SA group. The M. pneumoniae was macrolide-sensitive and ST14 by multilocus sequence typing. This study showed that the empiric use of antibiotics in children with asthma might be better targeted with prior pathogen screening to inform appropriate treatment to minimize antibiotic resistance., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2024 The Authors.)

Published
2024
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31. Assessing the added value of group B Streptococcus maternal immunisation in preventing maternal infection and fetal harm: population surveillance study.

Author

Lamagni T, Wloch C, Broughton K, Collin SM, Chalker V, Coelho J, Ladhani SN, Brown CS, Shetty N, and Johnson AP

Subjects
Adolescent, Adult, England epidemiology, Female, Hospitalization, Humans, Infant, Newborn, Infant, Newborn, Diseases epidemiology, Infant, Newborn, Diseases etiology, Infant, Newborn, Diseases prevention & control, Medical Records, Population Surveillance, Pregnancy, Pregnancy Complications, Infectious etiology, Pregnancy Complications, Infectious prevention & control, State Medicine, Streptococcal Infections etiology, Streptococcal Infections prevention & control, Streptococcus agalactiae immunology, Vaccination, Young Adult, Pregnancy Complications, Infectious epidemiology, Prenatal Care, Streptococcal Infections epidemiology, Streptococcus agalactiae isolation & purification
Abstract

Objective: To assess the incidence of maternal group B Streptococcus (GBS) infection in England., Design: Population surveillance augmented through data linkage., Setting: England., Population: All pregnant women accessing the National Health Service (NHS) in England., Methods: Invasive GBS (iGBS) infections during pregnancy or within 6 weeks of childbirth were identified by linking Public Health England (PHE) national microbiology surveillance data for 2014 to NHS hospital admission records. Capsular serotypes of GBS were determined by reference laboratory typing of clinical isolates from women aged 15-44 years. Post-caesarean section surgical site infection (SSI) caused by GBS was identified in 21 hospitals participating in PHE SSI surveillance (2009-2015)., Main Outcome Measures: iGBS rate per 1000 maternities; risk of GBS SSI per 1000 caesarean sections., Results: Of 1601 patients diagnosed with iGBS infections in England in 2014, 185 (12%) were identified as maternal infections, a rate of 0.29 (95% CI 0.25-0.33) per 1000 maternities and representing 83% of all iGBS cases in women aged 18-44 years. Seven (3.8%) were associated with miscarriage. Fetal outcome identified excess rates of stillbirth (3.4 versus 0.5%) and extreme prematurity (<28 weeks of gestation, 3.7 versus 0.5%) compared with national averages (P < 0.001). Caesarean section surveillance in 27 860 women (21 hospitals) identified 47 cases of GBS SSI, with an estimated 4.24 (3.51-5.07) per 1000 caesarean sections, a median time-to-onset of 10 days (IQR 7-13 days) and ten infections that required readmission. Capsular serotype analysis identified a diverse array of strains with serotype III as the most common (43%)., Conclusions: Our assessment of maternal GBS infection in England indicates the potential additional benefit of GBS vaccination in preventing adverse maternal and fetal outcomes., (© 2021 Crown copyright. BJOG: An International Journal of Obstetrics and Gynaecology published by John Wiley & Sons Ltd. This article is published with the permission of the Controller of HMSO and the Queen's Printer for Scotland.)

Published
2022
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32. RAPD PCR detects co-colonisation of multiple group B streptococcus genotypes: A practical molecular technique for screening multiple colonies.

Author

To KN, Powell O, Jamrozy D, Kopunova R, Anastasiadou K, Faal A, Secka O, Chalker V, Le Doare K, and Jauneikaite E

Subjects
DNA, Bacterial, Female, Humans, Infant, Milk, Human microbiology, Nasopharynx microbiology, Polymorphism, Single Nucleotide, Rectum microbiology, Serogroup, Streptococcal Infections diagnosis, Streptococcal Infections microbiology, Vagina microbiology, Whole Genome Sequencing, Mass Screening methods, Polymerase Chain Reaction methods, Random Amplified Polymorphic DNA Technique methods, Streptococcus agalactiae genetics, Streptococcus agalactiae isolation & purification
Abstract

Group B Streptococcus (GBS) is a leading cause of neonatal meningitis, pneumonia, and sepsis. The biggest contributing factor of neonatal infections is due to vertical transmission from maternal colonisation of GBS in the genitourinary tract. Multiple serotype colonisation is often not investigated in epidemiological studies, but it is an important consideration for serotype-based vaccine development and implementation to ensure less abundant serotypes are not under-represented. In this study, we show that RAPD PCR is a quick tool useful in screening the presence of genetically different strains using multiple colony picks from a single patient swab. We observed a maximum of five different GBS strains colonising a single patient at a specific time., (Crown Copyright © 2021. Published by Elsevier B.V. All rights reserved.)

Published
2021
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33. Invasive Group B Streptococcus Disease With Recurrence and in Multiples: Towards a Better Understanding of GBS Late-Onset Sepsis.

Author

Freudenhammer M, Karampatsas K, Le Doare K, Lander F, Armann J, Acero Moreno D, Boyle M, Buxmann H, Campbell R, Chalker V, Cunney R, Doherty L, Davies E, Efstratiou A, Elling R, Endmann M, Essers J, Hentschel R, Jones CE, Kallsen S, Kapatai G, Krüger M, Ladhani S, Lamagni T, Lindsay D, Meehan M, O'Sullivan CP, Patel D, Reynolds AJ, Roll C, Schulzke S, Smith A, Stein A, von der Wense A, Voss E, Wieg C, Härtel C, Heath PT, and Henneke P

Subjects
Age of Onset, Anti-Bacterial Agents therapeutic use, Dysbiosis etiology, Europe epidemiology, Female, Humans, Infant, Newborn, Male, Microbiota, Pregnancy, Pregnancy Complications, Infectious, Recurrence, Retrospective Studies, Risk Factors, Triplets, Twins, Anti-Bacterial Agents adverse effects, Drug-Related Side Effects and Adverse Reactions epidemiology, Dysbiosis epidemiology, Sepsis epidemiology, Streptococcal Infections epidemiology, Streptococcus physiology
Abstract

Group B Streptococcus (GBS) is a common intestinal colonizer during the neonatal period, but also may cause late-onset sepsis or meningitis in up to 0.5% of otherwise healthy colonized infants after day 3 of life. Transmission routes and risk factors of this late-onset form of invasive GBS disease (iGBS) are not fully understood. Cases of iGBS with recurrence (n=25) and those occurring in parallel in twins/triplets (n=32) from the UK and Ireland (national surveillance study 2014/15) and from Germany and Switzerland (retrospective case collection) were analyzed to unravel shared (in affected multiples) or fixed (in recurrent disease) risk factors for GBS disease. The risk of iGBS among infants from multiple births was high (17%), if one infant had already developed GBS disease. The interval of onset of iGBS between siblings was 4.5 days and in recurrent cases 12.5 days. Disturbances of the individual microbiome, including persistence of infectious foci are suggested e.g. by high usage of perinatal antibiotics in mothers of affected multiples, and by the association of an increased risk of recurrence with a short term of antibiotics [aOR 4.2 (1.3-14.2), P=0.02]. Identical GBS serotypes in both recurrent infections and concurrently infected multiples might indicate a failed microbiome integration of GBS strains that are generally regarded as commensals in healthy infants. The dynamics of recurrent GBS infections or concurrent infections in multiples suggest individual patterns of exposure and fluctuations in host immunity, causing failure of natural niche occupation., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Freudenhammer, Karampatsas, Le Doare, Lander, Armann, Acero Moreno, Boyle, Buxmann, Campbell, Chalker, Cunney, Doherty, Davies, Efstratiou, Elling, Endmann, Essers, Hentschel, Jones, Kallsen, Kapatai, Krüger, Ladhani, Lamagni, Lindsay, Meehan, O’Sullivan, Patel, Reynolds, Roll, Schulzke, Smith, Stein, von der Wense, Voss, Wieg, Härtel, Heath and Henneke.)

Published
2021
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34. Uncovering Infant Group B Streptococcal (GBS) Disease Clusters in the United Kingdom and Ireland Through Genomic Analysis: A Population-based Epidemiological Study.

Author

Collin SM, Groves N, O'Sullivan C, Jauneikaite E, Patel D, Cunney R, Meehan M, Reynolds A, Smith A, Lindsay D, Doherty L, Davies E, Chalker V, Lamb P, Afshar B, Balasegaram S, Coelho J, Ready D, Brown CS, Efstratiou A, Le Doare K, Sriskandan S, Heath PT, and Lamagni T

Subjects
Disease Hotspot, Epidemiologic Studies, Genomics, Humans, Infant, Ireland epidemiology, United Kingdom epidemiology, Streptococcal Infections epidemiology, Streptococcus agalactiae genetics
Abstract

Background: The true frequency of hospital outbreaks of invasive group B streptococcal (iGBS; Streptococcus agalactiae) disease in infants is unknown. We used whole genome sequencing (WGS) of iGBS isolates collected during a period of enhanced surveillance of infant iGBS disease in the UK and Ireland to determine the number of clustered cases., Methods: Potentially linked iGBS cases from infants with early (<7 days of life) or late-onset (7-89 days) disease were identified from WGS data (HiSeq 2500 platform, Illumina) from clinical sterile site isolates collected between 04/2014 and 04/2015. We assessed time and place of cases to determine a single-nucleotide polymorphism (SNP) difference threshold for clustered cases. Case details were augmented through linkage to national hospital admission data and hospital record review by local microbiologists., Results: Analysis of sequences indicated a cutoff of ≤5 SNP differences to define iGBS clusters. Among 410 infant iGBS isolates, we identified 7 clusters (4 genetically identical pairs with 0 SNP differences, 1 pair with 3 SNP differences, 1 cluster of 4 cases with ≤1 SNP differences) of which 4 clusters were uncovered for the first time. The clusters comprised 16 cases, of which 15 were late-onset (of 192 late-onset cases with sequenced isolates) and 1 an early-onset index case. Serial intervals between cases ranged from 0 to 59 (median 12) days., Conclusions: Approximately 1 in 12 late-onset infant iGBS cases were part of a hospital cluster. Over half of the clusters were previously undetected, emphasizing the importance of routine submission of iGBS isolates to reference laboratories for cluster identification and genomic confirmation., (© Crown copyright 2020.)

Published
2021
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35. Detection of group B streptococcus colonisation in pregnant women: Comparison of two different culture methods and study of antimicrobial resistance patterns.

Author

Carreras-Abad C, To KN, Ramkhelawon L, Planche T, Monahan I, Djennad A, Chalker V, Heath PT, and Le Doare K

Subjects
Drug Resistance, Bacterial, Female, Hospitals, Humans, Pregnancy, Pregnant Women, Streptococcus agalactiae, Anti-Bacterial Agents pharmacology, Streptococcal Infections diagnosis, Streptococcal Infections drug therapy
Published
2021
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36. A real-time PCR for specific detection of the Legionella pneumophila serogroup 1 ST1 complex.

Author

Ginevra C, Chastang J, David S, Mentasti M, Yakunin E, Chalker VJ, Chalifa-Caspi V, Valinsky L, Jarraud S, and Moran-Gilad J

Subjects
Bacterial Proteins genetics, DNA Primers genetics, DNA Probes, Genome, Bacterial, Genomics, Genotype, Humans, Legionella pneumophila isolation & purification, Legionnaires' Disease microbiology, Molecular Typing methods, Sensitivity and Specificity, Sequence Analysis, DNA, Serogroup, Whole Genome Sequencing, Legionella pneumophila classification, Legionnaires' Disease diagnosis, Real-Time Polymerase Chain Reaction methods
Abstract

Objective: Legionella pneumophila serogroup 1 (Lp1) sequence type (ST) 1 is globally widespread in the environment and accounts for a significant proportion of Legionella infections, including nosocomial Legionnaires' disease (LD). This study aimed to design a sensitive and specific detection method for Lp ST1 that will underpin epidemiological investigations and risk assessment., Methods: A total of 628 Lp genomes (126 ST1s) were analyzed by comparative genomics. Interrogation of more than 900 accessory genes revealed seven candidate targets for specific ST1 detection and specific primers and hydrolysis probes were designed and evaluated. The analytical sensitivity and specificity of the seven primer and probe sets were evaluated on serially diluted DNA extracted from the reference strain CIP107629 and via qPCR applied on 200 characterized isolates. The diagnostic performance of the assay was evaluated on 142 culture-proven clinical samples from LD cases and a real-life investigation of a case cluster., Results: Of seven qPCR assays that underwent analytical validation, one PCR target (lpp1868) showed higher sensitivity and specificity for ST1 and ST1-like strains. The diagnostic performance of the assay using respiratory samples corresponded to a sensitivity of 95% (19/20) (95% CI (75.1-99.9)) and specificity of 100% (122/122) (95% CI (97-100)). The ST1 PCR assay could link two out of three culture-negative hospitalized LD cases to ST1 during a real-time investigation., Conclusion: Using whole genome sequencing (WGS) data, we developed and validated a sensitive and specific qPCR assay for the detection of Lp1 belonging to the ST1 clonal complex by amplification of the lpp1868 gene. The ST1 qPCR is expected to deliver an added value for Lp control and prevention, in conjunction with other recently developed molecular assays., (Copyright © 2019 European Society of Clinical Microbiology and Infectious Diseases. All rights reserved.)

Published
2020
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37. Genomic sequencing of a national emm66 group A streptococci (GAS) outbreak among people who inject drugs and the homeless community in England and Wales, January 2016-May 2017.

Author

Bubba L, Bundle N, Kapatai G, Daniel R, Balasegaram S, Anderson C, Chalker V, Lamagni T, Brown C, Ready D, Efstratiou A, and Coelho J

Subjects
Adult, Aged, Aged, 80 and over, Community-Acquired Infections microbiology, Drug Resistance, Bacterial, England epidemiology, Epidemiologic Methods, Female, Humans, Male, Middle Aged, Molecular Epidemiology, Streptococcal Infections microbiology, Streptococcus pyogenes drug effects, Streptococcus pyogenes genetics, Streptococcus pyogenes isolation & purification, Wales epidemiology, Whole Genome Sequencing, Antigens, Bacterial genetics, Bacterial Outer Membrane Proteins genetics, Carrier Proteins genetics, Community-Acquired Infections epidemiology, Disease Outbreaks, Ill-Housed Persons, Streptococcal Infections epidemiology, Streptococcus pyogenes classification, Substance Abuse, Intravenous complications
Abstract

An outbreak of an uncommon emm type (emm66.0) of group A streptococcus (GAS) occurred in England and Wales between January 2016 and May 2017, involving 52 individuals who were homeless or injecting drugs users. In order to investigate the outbreak, epidemiological and network analysis were performed; moreover 55 isolates (32 outbreak, 5 non-outbreak and 13 historical - 2005-2015) were tested with whole genome sequencing (WGS), antimicrobial resistance determination, Bayesian evolutionary analysis (BEAST). Forty one isolates (including 32 outbreak strains) belonged to a single emm66.0 clade (average SNP difference 6.6; range 0-16 SNPs) separate from the other isolates and two strains previously considered part of the outbreak (SNP average: 5876; range 93-8417 SNPs). Antibiotic resistance was not detected in the outbreak clone. No common source of infection was identified. WGS confirmed expansion of an emm66.0 clone in a hard-to-reach population and enabled refinement of the initial case definition., (Copyright © 2019. Published by Elsevier Ltd.)

Published
2019
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38. Recommended rejection of the names Malacoplasma gen. nov., Mesomycoplasma gen. nov., Metamycoplasma gen. nov., Metamycoplasmataceae fam. nov., Mycoplasmoidaceae fam. nov., Mycoplasmoidales ord. nov., Mycoplasmoides gen. nov., Mycoplasmopsis gen. nov. [Gupta, Sawnani, Adeolu, Alnajar and Oren 2018] and all proposed species comb. nov. placed therein.

Author

Balish M, Bertaccini A, Blanchard A, Brown D, Browning G, Chalker V, Frey J, Gasparich G, Hoelzle L, Knight T, Knox C, Kuo CH, Manso-Silván L, May M, Pollack JD, Ramírez AS, Spergser J, Taylor-Robinson D, Volokhov D, and Zhao Y

Subjects
Phylogeny, Terminology as Topic, Tenericutes classification
Abstract

The consensus of the members of the International Committee on Systematics of Prokaryotes' Subcommittee on the taxonomy of Mollicutes is that recently proposed sweeping changes to nomenclature of members of the Mycoplasmatales , specifically involving introduction of the names Malacoplasma gen. nov., Mesomycoplasma gen. nov., Metamycoplasma gen. nov., Metamycoplasmataceae fam. nov., Mycoplasmoidaceae fam. nov., Mycoplasmoidales ord. nov., Mycoplasmoides gen. nov., Mycoplasmopsis gen. nov., and all proposed species or subspecies comb. nov. placed therein, should be rejected because they violate one or more essential points of the International Code of Nomenclature of Prokaryotes.

Published
2019
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39. One hypervirulent clone, sequence type 283, accounts for a large proportion of invasive Streptococcus agalactiae isolated from humans and diseased tilapia in Southeast Asia.

Author

Barkham T, Zadoks RN, Azmai MNA, Baker S, Bich VTN, Chalker V, Chau ML, Dance D, Deepak RN, van Doorn HR, Gutierrez RA, Holmes MA, Huong LNP, Koh TH, Martins E, Mehershahi K, Newton P, Ng LC, Phuoc NN, Sangwichian O, Sawatwong P, Surin U, Tan TY, Tang WY, Thuy NV, Turner P, Vongsouvath M, Zhang D, Whistler T, and Chen SL

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Animals, Asia, Southeastern epidemiology, Child, Child, Preschool, Female, Foodborne Diseases epidemiology, Foodborne Diseases microbiology, Humans, Infant, Infant, Newborn, Male, Middle Aged, Molecular Epidemiology, Multilocus Sequence Typing, Phylogeny, Pregnancy, Streptococcal Infections microbiology, Streptococcus agalactiae pathogenicity, Tilapia, Whole Genome Sequencing, Young Adult, Fish Diseases epidemiology, Fish Diseases microbiology, Genotype, Streptococcal Infections epidemiology, Streptococcal Infections veterinary, Streptococcus agalactiae classification, Streptococcus agalactiae isolation & purification
Abstract

Background: In 2015, Singapore had the first and only reported foodborne outbreak of invasive disease caused by the group B Streptococcus (GBS; Streptococcus agalactiae). Disease, predominantly septic arthritis and meningitis, was associated with sequence type (ST)283, acquired from eating raw farmed freshwater fish. Although GBS sepsis is well-described in neonates and older adults with co-morbidities, this outbreak affected non-pregnant and younger adults with fewer co-morbidities, suggesting greater virulence. Before 2015 ST283 had only been reported from twenty humans in Hong Kong and two in France, and from one fish in Thailand. We hypothesised that ST283 was causing region-wide infection in Southeast Asia., Methodology/principal Findings: We performed a literature review, whole genome sequencing on 145 GBS isolates collected from six Southeast Asian countries, and phylogenetic analysis on 7,468 GBS sequences including 227 variants of ST283 from humans and animals. Although almost absent outside Asia, ST283 was found in all invasive Asian collections analysed, from 1995 to 2017. It accounted for 29/38 (76%) human isolates in Lao PDR, 102/139 (73%) in Thailand, 4/13 (31%) in Vietnam, and 167/739 (23%) in Singapore. ST283 and its variants were found in 62/62 (100%) tilapia from 14 outbreak sites in Malaysia and Vietnam, in seven fish species in Singapore markets, and a diseased frog in China., Conclusions: GBS ST283 is widespread in Southeast Asia, where it accounts for a large proportion of bacteraemic GBS, and causes disease and economic loss in aquaculture. If human ST283 is fishborne, as in the Singapore outbreak, then GBS sepsis in Thailand and Lao PDR is predominantly a foodborne disease. However, whether transmission is from aquaculture to humans, or vice versa, or involves an unidentified reservoir remains unknown. Creation of cross-border collaborations in human and animal health are needed to complete the epidemiological picture., Competing Interests: I have read the journal's policy and the authors of this manuscript have the following competing interests: SLC and TB are named applicants on a patent for the ST83-specific PCR test used in this study.

Published
2019
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40. Evaluation of matrix-assisted laser desorption ionisation time-of-flight mass spectrometry (MALDI-TOF MS) for the Identification of Group B Streptococcus.

Author

To KN, Cornwell E, Daniel R, Goonesekera S, Jauneikaite E, Chalker V, and Le Doare K

Subjects
Adult, Female, Humans, Infant, Newborn, Pregnancy, Sensitivity and Specificity, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization standards, Streptococcus agalactiae isolation & purification
Abstract

Objective: Group B Streptococcus (GBS) is a leading cause of neonatal meningitis and sepsis worldwide. Intrapartum antibiotics given to women carrying GBS are an effective means of reducing disease in the first week of life. Rapid and reliable tests are needed to accurately identify GBS from these women for timely intrapartum antibiotic administration to prevent neonatal disease. Many laboratories now use matrix-assisted laser desorption ionisation time-of-flight mass spectrometry (MALDI-TOF MS) by direct plating or cell lysis for the identification of GBS isolates. The cell lysis step increases time to results for clinical samples and is more complex to perform. Therefore, we seek to evaluate the sensitivity and specificity of the quicker and more rapid direct plating method in identifying GBS., Results: We directly compared swab isolates analysed by both direct plating and cell lysis method and demonstrated that direct plating has a sensitivity and specificity of 0.97 and 1, respectively, compared to an additional cell lysis step. We demonstrated that MALDI-TOF MS can be successfully used for batch processing by the direct plating method which saves time. These results are reassuring for laboratories worldwide who seek to identify GBS from swabs samples as quickly as possible.

Published
2019
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41. Positively interacting strains that co-circulate within a network structured population induce cycling epidemics of Mycoplasma pneumoniae.

Author

Zhang XS, Zhao H, Vynnycky E, and Chalker V

Subjects
Adult, Child, Coinfection epidemiology, Coinfection transmission, Community-Acquired Infections microbiology, Cross Reactions, Female, Humans, Incidence, Male, Models, Biological, Pneumonia, Mycoplasma microbiology, Prevalence, Serogroup, Community-Acquired Infections epidemiology, Community-Acquired Infections transmission, Epidemics, Mycoplasma pneumoniae immunology, Periodicity, Pneumonia, Mycoplasma epidemiology, Pneumonia, Mycoplasma transmission
Abstract

Mycoplasma pneumoniae (MP) is considered a common cause of pneumonia, causing about 15-20% of adult community-acquired pneumonia (CAP) and up to 40% of cases in children. It has often been observed that MP epidemics last approximately 1-2 years and occur every 3-7 years, with the dominant strains alternating between epidemics. However, the underlying mechanism by which these cycles and changes in the dominant strains occur remains unclear. The traditional models for the periodicity of MP epidemics neglected two phenomena: structured contact patterns among people and co-circulating strains of MP. We also believe that the two distinctive aspects of MP epidemics: prevalent serotype shifts among epidemics and incidence cycling of MP, are interconnected. We propose a network transmission model that assumes two strains of MP are transmitted within a network structured population and they can interact as secondary infections with primary infections. Our studies show that multiple strains that co-circulate within a network structured population and interact positively generate the observed patterns of recurrent epidemics of MP. Hence our study provides a possible mechanism for the cycling epidemics of MP, and could provide useful information for future vaccine design and vaccine evaluation/monitoring processes.

Published
2019
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42. Group B streptococcal disease in UK and Irish infants younger than 90 days, 2014-15: a prospective surveillance study.

Author

O'Sullivan CP, Lamagni T, Patel D, Efstratiou A, Cunney R, Meehan M, Ladhani S, Reynolds AJ, Campbell R, Doherty L, Boyle M, Kapatai G, Chalker V, Lindsay D, Smith A, Davies E, Jones CE, and Heath PT

Subjects
Antibiotic Prophylaxis, Female, Humans, Incidence, Infant, Infant, Newborn, Ireland epidemiology, Male, Microbial Sensitivity Tests, Multilocus Sequence Typing, Pregnancy, Prospective Studies, Risk Factors, Serogroup, Serotyping, Streptococcal Infections microbiology, Streptococcal Infections prevention & control, Streptococcus agalactiae isolation & purification, United Kingdom epidemiology, Streptococcal Infections epidemiology, Streptococcal Infections mortality, Streptococcus agalactiae genetics, Streptococcus agalactiae immunology
Abstract

Background: Group B streptococcus is a leading cause of serious infection in young infants in many countries worldwide. We aimed to define the burden and clinical features of invasive group B streptococcal disease in infants younger than 90 days in the UK and Ireland, together with the characteristics of disease-causing isolates., Methods: Prospective, active national surveillance of invasive group B streptococcal disease in infants younger than 90 days was done from April 1, 2014, to April 30, 2015, through the British Paediatric Surveillance Unit, microbiology reference laboratories, and national public health agencies in the UK and Ireland. Early onset was defined as disease in the first 6 days of life and late onset was defined as 7-89 days of life. Incidence was calculated using livebirths in 2014 (after adjustment for the 13-month surveillance period). Isolates were characterised by serotyping, multilocus sequence typing, and antimicrobial susceptibility testing., Findings: 856 cases of group B streptococcus were identified in 2014-15, an incidence of 0·94 per 1000 livebirths (95% CI 0·88-1·00). Incidence for early-onset disease (n=517) was 0·57 per 1000 livebirths (95% CI 0·52-0·62), and for late-onset disease (n=339) was 0·37 per 1000 livebirths (0·33-0·41). 53 infants died (case fatality rate 6·2%), of whom 27 had early-onset disease (case fatality rate 5·2%) and 26 had late-onset disease (case fatality rate 7·7%). The predominant serotypes were III (241 [60%] of 402 serotyped isolates) and Ia (69 [17%]); five serotypes (Ia, Ib, II, III, V) accounted for 377 (94%) of all serotyped isolates., Interpretation: The incidence of invasive infant group B streptococcal disease in the UK and Ireland has increased since a comparable study done in 2000-01. The burden of early-onset disease has not declined despite the introduction of national prevention guidelines. New strategies for prevention are required., Funding: Meningitis Now., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Published
2019
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43. Genomic sequence investigation Streptococcus pyogenes clusters in England (2010-2015).

Author

Coelho JM, Kapatai G, Jironkin A, Al-Shahib A, Daniel R, Dhami C, Laranjeira AM, Chambers T, Phillips S, Tewolde R, Underwood A, and Chalker VJ

Subjects
Cluster Analysis, Computational Biology, Cross Infection epidemiology, DNA, Bacterial genetics, England epidemiology, Genome, Bacterial, Genomics, Health Personnel, Humans, Phylogeny, Polymorphism, Single Nucleotide, Sequence Analysis, DNA, Streptococcal Infections microbiology, Streptococcus pyogenes isolation & purification, Disease Outbreaks statistics & numerical data, Homes for the Aged, Hospitals, Maternity, Nursing Homes, Streptococcal Infections epidemiology, Streptococcus pyogenes genetics
Abstract

Objectives: To analyse genomic sequence data of referred Streptococcus pyogenes isolates and those pertaining to selected elderly/nursing care or maternity clusters from 2010 to 2015 to ascertain genomic differences between epidemiologically related isolates and unrelated isolates from outbreaks of disease., Methods: The genomic sequences of 134 S. pyogenes isolates from 21 clusters of infection in elderly care or maternity settings from 2010 to 2015 were analysed using bioinformatics to ascertain genomic phylogeny, single nucleotide polymorphism (SNP) differences and statistical outliers from epidemiologically defined outbreaks. Analysis was undertaken within clusters and compared with sporadic isolates from geographically distinct outbreaks of S. pyogenes infection., Results: Genomic sequence analysis of 21 outbreaks of S. pyogenes infection ranged in size from a single patient (with colonized healthcare worker link) to 18 patient cases of group A streptococcus (GAS) infection in a single setting. Seventeen healthcare workers were identified in 8 of 21 outbreaks with the associated outbreak strain, with multiple staff in 2 of 21 outbreaks. Genomic sequences from epidemiologically linked isolates from patients, staff and healthcare environmental settings were highly conserved, differing by 0-1 SNP in some cases and mirrored geographical data. Four of 21 outbreaks had environmental contamination with the outbreak strain, indistinguishable or of limited SNP difference to the patient isolates. Genomic SNP analysis enabled exclusion of ten isolates from epidemiological outbreaks., Conclusions: Genomic discrimination can be applied to assist outbreak investigation. It enabled confirmation or exclusion of GAS cases from epidemiologically defined outbreaks. Colonization of healthcare workers and environmental contamination with the outbreak strain was demonstrated for several outbreaks., (Copyright © 2018 European Society of Clinical Microbiology and Infectious Diseases. Published by Elsevier Ltd. All rights reserved.)

Published
2019
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45. Low genomic diversity of Legionella pneumophila within clinical specimens.

Author

David S, Mentasti M, Parkhill J, and Chalker VJ

Subjects
Aged, Bacterial Typing Techniques, Female, Genome, Bacterial, Genotype, Humans, Legionella pneumophila isolation & purification, Male, Middle Aged, Molecular Typing, Whole Genome Sequencing, Legionella pneumophila genetics, Legionnaires' Disease microbiology, Polymorphism, Single Nucleotide
Abstract

Objectives: Legionella pneumophila is the leading cause of Legionnaires' disease, a severe form of pneumonia acquired from environmental sources. Investigations of both sporadic cases and outbreaks rely mostly on analysis of a single to a few colony pick(s) isolated from each patient. However, because of the lack of data describing diversity within single patients, the optimal number of picks is unknown. Here, we investigated diversity within individual patients using sequence-based typing (SBT) and whole-genome sequencing (WGS)., Methods: Ten isolates of L. pneumophila were obtained from each of ten epidemiologically unrelated patients. SBT and WGS were undertaken, and single-nucleotide polymorphisms (SNPs) were identified between isolates from the same patient., Results: The same sequence type (ST) was obtained for each set of ten isolates. Using genomic analysis, zero SNPs were identified between isolates from seven patients, a maximum of one SNP was found between isolates from two patients, and a maximum of two SNPs was found amongst isolates from one patient. Assuming that the full within-host diversity has been captured with ten isolates, statistical analyses showed that, on average, analysis of one isolate would yield a 70% chance of capturing all observed genotypes, and seven isolates would yield a 90% chance., Conclusions: SBT and WGS analyses of multiple colony picks obtained from ten patients showed no, or very low, within-host genomic diversity in L. pneumophila, suggesting that analysis of one colony pick per patient will often be sufficient to obtain reliable typing data to aid investigation of cases of Legionnaires' disease., (Copyright © 2018 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Published
2018
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46. Serial Clustering of Late-Onset Group B Streptococcal Infections in the Neonatal Unit: A Genomic Re-evaluation of Causality.

Author

Jauneikaite E, Kapatai G, Davies F, Gozar I, Coelho J, Bamford KB, Simone B, Begum L, Katiyo S, Patel B, Hoffman P, Lamagni T, Brannigan ET, Holmes AH, Kadhani T, Galletly T, Martin K, Lyall H, Chow Y, Godambe S, Chalker V, and Sriskandan S

Subjects
Bacteremia epidemiology, Cluster Analysis, Genomics, Humans, Incidence, Infant, Newborn, Neonatal Screening, Phylogeny, Prospective Studies, Risk Factors, Serogroup, Streptococcus agalactiae isolation & purification, United Kingdom epidemiology, Whole Genome Sequencing, Intensive Care Units, Neonatal, Streptococcal Infections complications, Streptococcal Infections epidemiology, Streptococcus agalactiae genetics
Abstract

Background: Invasive Group B streptococcus (GBS) is a major cause of serious neonatal infection. Current strategies to reduce early-onset GBS disease have no impact on late-onset disease (LOD). Although GBS LOD is viewed as a sporadic event in the community, LOD arising within the neonatal intensive care unit (ICU) raises questions about mode of acquisition., Methods: Following a cluster of 4 GBS LOD cases, enhanced surveillance for all GBS LOD was undertaken over 2 years in the neonatal ICU supported by neonatal rectal screening. GBS isolates were serotyped and genome-sequenced., Results: Twelve late -onset invasive GBS episodes were identified (incidence 0.6/1000 live births). Genomic analysis revealed that 11/12 GBS isolates (92%) were linked to at least one other LOD isolate. Isolates from the first cluster were serotype V, resistant to macrolides and lincosamides, and sequencing confirmed isolates were indistinguishable, or distinguishable by only one SNP difference, from each other. Rectal carriage was rare. Prospective surveillance identified three further clusters of LOD due to serotypes Ia (3 cases), Ib (2 cases), and III (2 cases), that would not have been identified without surveillance and genome sequencing, leading to a re-evaluation of interventions required to prevent GBS LOD., Conclusion: Acquisition routes for LOD GBS in the neonatal ICU are poorly understood; cases may not necessarily be sporadic. Within this neonatal ICU, our data suggest that a single case of LOD GBS sepsis should be considered a potential nosocomial transmission event warranting prompt investigation, heightened infection prevention vigilance and action where required.

Published
2018
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47. Resurgence of scarlet fever in England, 2014-16: a population-based surveillance study.

Author

Lamagni T, Guy R, Chand M, Henderson KL, Chalker V, Lewis J, Saliba V, Elliot AJ, Smith GE, Rushton S, Sheridan EA, Ramsay M, and Johnson AP

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Antigens, Bacterial analysis, Bacterial Outer Membrane Proteins analysis, Carrier Proteins analysis, Child, Child, Preschool, England epidemiology, Female, Hospitalization, Humans, Incidence, Infant, Infant, Newborn, Male, Middle Aged, Pharynx microbiology, Scarlet Fever microbiology, Streptococcus classification, Wales epidemiology, Young Adult, Communicable Diseases, Emerging epidemiology, Epidemiological Monitoring, Scarlet Fever epidemiology, Streptococcus isolation & purification
Abstract

Background: After decades of decreasing scarlet fever incidence, a dramatic increase was seen in England beginning in 2014. Investigations were launched to assess clinical and epidemiological patterns and identify potential causes., Methods: In this population-based surveillance study, we analysed statutory scarlet fever notifications held by Public Health England from 1911 to 2016 in England and Wales to identify periods of sudden escalation of scarlet fever. Characteristics of cases and outbreaks in England including frequency of complications and hospital admissions were assessed and compared with the pre-upsurge period. Isolates from throat swabs were obtained and were emm typed., Findings: Data were retrieved for our analysis between Jan 1, 1911, and Dec 31, 2016. Population rates of scarlet fever increased by a factor of three between 2013 and 2014 from 8·2 to 27·2 per 100 000 (rate ratio [RR] 3·34, 95% CI 3·23-3·45; p<0·0001); further increases were observed in 2015 (30·6 per 100 000) and in 2016 (33·2 per 100 000), which reached the highest number of cases (19 206) and rate of scarlet fever notifcation since 1967. The median age of cases in 2014 was 4 years (IQR 3-7) with an incidence of 186 per 100 000 children under age 10 years. All parts of England saw an increase in incidence, with 620 outbreaks reported in 2016. Hospital admissions for scarlet fever increased by 97% between 2013 and 2016; one in 40 cases were admitted for management of the condition or potential complications. Analysis of strains (n=303) identified a diversity of emm types with emm3 (43%), emm12 (15%), emm1 (11%), and emm4 (9%) being the most common. Longitudinal analysis identified 4-yearly periodicity in population incidence of scarlet fever but of consistently lower magnitude than the current escalation., Interpretation: England is experiencing an unprecedented rise in scarlet fever with the highest incidence for nearly 50 years. Reasons for this escalation are unclear and identifying these remains a public health priority., Funding: None., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Published
2018
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48. Genomic sequences of Streptococcus agalactiae with high-level gentamicin resistance, collected in the BSAC bacteraemia surveillance.

Author

Doumith M, Mushtaq S, Martin V, Chaudhry A, Adkin R, Coelho J, Chalker V, MacGowan A, Woodford N, and Livermore DM

Subjects
Bacteremia microbiology, DNA Transposable Elements, Epidemiological Monitoring, Genome, Bacterial, Genomics methods, Humans, Microbial Sensitivity Tests methods, Streptococcal Infections microbiology, Streptococcus agalactiae drug effects, Streptococcus agalactiae isolation & purification, Anti-Bacterial Agents pharmacology, Bacteremia epidemiology, Drug Resistance, Bacterial genetics, Gentamicins pharmacology, Sequence Analysis, DNA methods, Streptococcal Infections epidemiology, Streptococcus agalactiae genetics
Abstract

Background: Like other streptococci, Streptococcus agalactiae typically has intrinsic low-level aminoglycoside resistance. High-level gentamicin resistance was seen in 2 of 1125 isolates collected in the BSAC Bacteraemia Surveillance Programme between 2001 and 2014. These organisms, both isolated in 2014, were characterized., Methods: Identifications were by latex agglutination, MICs by BSAC agar dilution and sequencing by Illumina methodology., Results: Gentamicin MICs were >1024 mg/L versus a species mode of 8 mg/L; both isolates also were unusually ciprofloxacin resistant with MICs of 64 mg/L versus a species mode of 1 mg/L. They were distinct by sequence, but both belonged to the ST19 clone, which occurs globally. Both had aac(6')-aph(2″), carried by different transposons, explaining their gentamicin resistance, and had gyrA[81:S-L];parC[79:S-Y], accounting for ciprofloxacin resistance., Conclusions: These are the first multiresistant S. agalactiae with the bifunctional AAC(6')-APH(2″) enzyme to be reported in the UK for >10 years. Despite belonging to the same clonal complex, the two isolates and their resistance transposons were distinct. Both retained full susceptibility to penicillin, but any penicillin/gentamicin synergy is likely to be lost., (© The Author 2017. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Published
2017
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49. Multi-center evaluation of one commercial and 12 in-house real-time PCR assays for detection of Mycoplasma pneumoniae.

Author

Dumke R, Benitez AJ, Chalker V, Gullsby K, Henrich B, Hidalgo-Grass C, Hoogenboezem T, Kese D, Loens K, Maaskant J, Michael-Gayego A, Moses AE, Nir-Paz R, Pas SD, Pereyre S, Petersen RF, Rosenblatt M, van Rossum AMC, Uldum SA, Unger WWJ, Ursi D, Winchell JM, and Bebear C

Subjects
DNA, Bacterial genetics, Humans, Mycoplasma pneumoniae isolation & purification, Pneumonia, Mycoplasma microbiology, DNA, Bacterial analysis, Genome, Bacterial genetics, Mycoplasma pneumoniae genetics, Pneumonia, Mycoplasma diagnosis, Real-Time Polymerase Chain Reaction methods
Abstract

Detection of Mycoplasma pneumoniae by real-time PCR is not yet standardized across laboratories. We have implemented a standardization protocol to compare the performance of thirteen commercial and in-house approaches. Despite differences on threshold values of samples, all assays were able to detect at least 20M. pneumoniae genomes per reaction., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Published
2017
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50. Household transmission of invasive group A Streptococcus infections in England: a population-based study, 2009, 2011 to 2013.

Author

Mearkle R, Saavedra-Campos M, Lamagni T, Usdin M, Coelho J, Chalker V, Sriskandan S, Cordery R, Rawlings C, and Balasegaram S

Subjects
Adolescent, Disease Transmission, Infectious prevention & control, Disease Transmission, Infectious statistics & numerical data, England epidemiology, Family Characteristics, Female, Humans, Incidence, Infant, Newborn, Male, Middle Aged, Retrospective Studies, Streptococcal Infections epidemiology, Streptococcal Infections microbiology, Streptococcus pyogenes physiology, Virulence, Antibiotic Prophylaxis methods, Population Surveillance methods, Streptococcal Infections prevention & control, Streptococcal Infections transmission, Streptococcus pyogenes isolation & purification
Abstract

Invasive group A streptococcal infection has a 15% case fatality rate and a risk of secondary transmission. This retrospective study used two national data sources from England; enhanced surveillance (2009) and a case management system (2011-2013) to identify clusters of severe group A streptococcal disease. Twenty-four household pairs were identified. The median onset interval between cases was 2 days (range 0-28) with simultaneous onset in eight pairs. The attack rate during the 30 days after first exposure to a primary case was 4,520 per 100,000 person-years at risk (95% confidence interval (CI): 2,900-6,730) a 1,940 (95% CI: 1,240-2,880) fold elevation over the background incidence. The theoretical number needed to treat to prevent one secondary case using antibiotic prophylaxis was 271 overall (95% CI: 194-454), 50 for mother-neonate pairs (95% CI: 27-393) and 82 for couples aged 75 years and over (95% CI: 46-417). While a dramatically increased risk of infection was noted in all household contacts, increased risk was greatest for mother-neonate pairs and couples aged 75 and over, suggesting targeted prophylaxis could be considered. Offering prophylaxis is challenging due to the short time interval between cases emphasising the importance of immediate notification and assessment of contacts., (This article is copyright of The Authors, 2017.)

Published
2017
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