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2. The 2021 WHO catalogue of Mycobacterium tuberculosis complex mutations associated with drug resistance: a genotypic analysis

Author

Walker, Timothy M, Miotto, Paolo, Köser, Claudio U, Fowler, Philip W, Knaggs, Jeff, Iqbal, Zamin, Hunt, Martin, Chindelevitch, Leonid, Farhat, Maha R, Cirillo, Daniela Maria, Comas, Iñaki, Posey, James, Omar, Shaheed V, Peto, Timothy EA, Suresh, Anita, Uplekar, Swapna, Laurent, Sacha, Colman, Rebecca E, Nathanson, Carl-Michael, Zignol, Matteo, Walker, Ann Sarah, Crook, Derrick W, Ismail, Nazir, Rodwell, Timothy C, Consortium, the SeqTreat Consortium CRyPTIC, Walker, A Sarah, Steyn, Adrie JC, Lalvani, Ajit, Baulard, Alain, Christoffels, Alan, Mendoza-Ticona, Alberto, Trovato, Alberto, Skrahina, Alena, Lachapelle, Alexander S, Brankin, Alice, Piatek, Amy, Cruz, Ana Gibertoni, Koch, Anastasia, Cabibbe, Andrea Maurizio, Spitaleri, Andrea, Brandao, Angela P, Chaiprasert, Angkana, Barbova, Anna, Van Rie, Annelies, Ghodousi, Arash, Bainomugisa, Arnold, Mandal, Ayan, Roohi, Aysha, Javid, Babak, Zhu, Baoli, Letcher, Brice, Rodrigues, Camilla, Nimmo, Camus, NATHANSON, Carl-Michael, Duncan, Carla, Coulter, Christopher, Utpatel, Christian, Liu, Chunfa, Grazian, Clara, Kong, Clare, Wilson, Daniel J, Matias, Daniela, Jorgensen, Danielle, Zimenkov, Danila, Chetty, Darren, Moore, David AJ, Clifton, David A, van Soolingen, Dick, Liu, Dongxin, Kohlerschmidt, Donna, Barreira, Draurio, Ngcamu, Dumisani, Lazaro, Elias David Santos, Kelly, Ellis, Borroni, Emanuele, Roycroft, Emma, Andre, Emmanuel, Böttger, Erik C, Robinson, Esther, Menardo, Fabrizio, Mendes, Flavia F, Jamieson, Frances B, Coll, Francesc, Gao, George Fu, Kasule, George W, Rossolini, Gian Maria, Rodger, Gillian, Smith, E Grace, Meintjes, Graeme, Thwaites, Guy, Hoffmann, Harald, Albert, Heidi, Cox, Helen, Laurenson, Ian F, and Arandjelovic, Irena

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Microbiology, Clinical Sciences, Tuberculosis, Infectious Diseases, Rare Diseases, Antimicrobial Resistance, Orphan Drug, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Infection, Good Health and Well Being, Antitubercular Agents, Drug Resistance, Ethambutol, Microbial Sensitivity Tests, Mutation, Mycobacterium tuberculosis, World Health Organization, CRyPTIC Consortium, Seq&Treat Consortium, Immunology, Medical microbiology
Abstract

BackgroundMolecular diagnostics are considered the most promising route to achieving rapid, universal drug susceptibility testing for Mycobacterium tuberculosiscomplex (MTBC). We aimed to generate a WHO endorsed catalogue of mutations to serve as a global standard for interpreting molecular information for drug resistance prediction.MethodsA candidate gene approach was used to identify mutations as associated with resistance, or consistent with susceptibility, for 13 WHO endorsed anti-tuberculosis drugs. 38,215 MTBC isolates with paired whole-genome sequencing and phenotypic drug susceptibility testing data were amassed from 45 countries. For each mutation, a contingency table of binary phenotypes and presence or absence of the mutation computed positive predictive value, and Fisher's exact tests generated odds ratios and Benjamini-Hochberg corrected p-values. Mutations were graded as Associated with Resistance if present in at least 5 isolates, if the odds ratio was >1 with a statistically significant corrected p-value, and if the lower bound of the 95% confidence interval on the positive predictive value for phenotypic resistance was >25%. A series of expert rules were applied for final confidence grading of each mutation.Findings15,667 associations were computed for 13,211 unique mutations linked to one or more drugs. 1,149/15,667 (7·3%) mutations were classified as associated with phenotypic resistance and 107/15,667 (0·7%) were deemed consistent with susceptibility. For rifampicin, isoniazid, ethambutol, fluoroquinolones, and streptomycin, the mutations' pooled sensitivity was >80%. Specificity was over 95% for all drugs except ethionamide (91·4%), moxifloxacin (91·6%) and ethambutol (93·3%). Only two resistance mutations were classified for bedaquiline, delamanid, clofazimine, and linezolid as prevalence of phenotypic resistance was low for these drugs.InterpretationThis first WHO endorsed catalogue of molecular targets for MTBC drug susceptibility testing provides a global standard for resistance interpretation. Its existence should encourage the implementation of molecular diagnostics by National Tuberculosis Programmes.FundingUNITAID, Wellcome, MRC, BMGF.

Published
2022

3. Prediction of Susceptibility to First-Line Tuberculosis Drugs by DNA Sequencing

Author

Allix-Béguec, Caroline, Arandjelovic, Irena, Bi, Lijun, Beckert, Patrick, Bonnet, Maryline, Bradley, Phelim, Cabibbe, Andrea M, Cancino-Muñoz, Irving, Caulfield, Mark J, Chaiprasert, Angkana, Cirillo, Daniela, Clifton, David, Comas, Iñaki, Crook, Derrick W, De Filippo, Maria Rosaria, de Neeling, Han, Diel, Roland, Drobniewski, Francis A, Faksri, Kiatichai, Farhat, Maha R, Fleming, Joy, Fowler, Philip, Fowler, Tom A, Gao, Qian, Gardy, Jennifer, Gascoyne-Binzi, Deborah, Cruz, Ana Gibertoni, Gil-Brusola, Ana, Golubchik, Tanya, Gonzalo, Ximena, Grandjean, Louis, He, Guangxue, Guthrie, Jennifer L, Hoosdally, Sarah, Hunt, Martin, Iqbal, Zamin, Ismail, Nazir, Johnston, James, Khanzada, Faisal Masood, Khor, Chiea Chuen, Kohl, Thomas A, Kong, Clare, Lipworth, Sam, Liu, Qingyun, Maphalala, Gugu, Martinez, Elena, Mathys, Vanessa, Merker, Matthias, Miotto, Paolo, Mistry, Nerges, Moore, David, Murray, Megan, Niemann, Stefan, Ong, Rick Twee-Hee, Peto, Tim EA, Posey, James E, Prammananan, Therdsak, Pym, Alexander, Rodrigues, Camilla, Rodrigues, Mabel, Rodwell, Timothy, Rossolini, Gian Maria, Padilla, Elisabeth Sánchez, Schito, Marco, Shen, Xin, Shendure, Jay, Sintchenko, Vitali, Sloutsky, Alex, Smith, E Grace, Snyder, Matthew, Soetaert, Karine, Starks, Angela M, Supply, Philip, Suriyapol, Prapat, Tahseen, Sabira, Tang, Patrick, Teo, Yik-Ying, Thuong, Thuong Nguyen Thuy, Thwaites, Guy, Tortoli, Enrico, Omar, Shaheed Vally, van Soolingen, Dick, Walker, A Sarah, Walker, Timothy M, Wilcox, Mark, Wilson, Daniel J, Wyllie, David, Yang, Yang, Zhang, Hongtai, Zhao, Yanlin, and Zhu, Baoli

Subjects
Genetics, Human Genome, Tuberculosis, Clinical Research, Patient Safety, Prevention, Rare Diseases, Infectious Diseases, Antimicrobial Resistance, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Infection, Good Health and Well Being, Antitubercular Agents, Drug Resistance, Bacterial, Ethambutol, Genome, Bacterial, Genotype, Humans, Isoniazid, Microbial Sensitivity Tests, Mutation, Mycobacterium tuberculosis, Phenotype, Pyrazinamide, Rifampin, Whole Genome Sequencing, CRyPTIC Consortium and the 100, 000 Genomes Project, Medical and Health Sciences, General & Internal Medicine
Abstract

BackgroundThe World Health Organization recommends drug-susceptibility testing of Mycobacterium tuberculosis complex for all patients with tuberculosis to guide treatment decisions and improve outcomes. Whether DNA sequencing can be used to accurately predict profiles of susceptibility to first-line antituberculosis drugs has not been clear.MethodsWe obtained whole-genome sequences and associated phenotypes of resistance or susceptibility to the first-line antituberculosis drugs isoniazid, rifampin, ethambutol, and pyrazinamide for isolates from 16 countries across six continents. For each isolate, mutations associated with drug resistance and drug susceptibility were identified across nine genes, and individual phenotypes were predicted unless mutations of unknown association were also present. To identify how whole-genome sequencing might direct first-line drug therapy, complete susceptibility profiles were predicted. These profiles were predicted to be susceptible to all four drugs (i.e., pansusceptible) if they were predicted to be susceptible to isoniazid and to the other drugs or if they contained mutations of unknown association in genes that affect susceptibility to the other drugs. We simulated the way in which the negative predictive value changed with the prevalence of drug resistance.ResultsA total of 10,209 isolates were analyzed. The largest proportion of phenotypes was predicted for rifampin (9660 [95.4%] of 10,130) and the smallest was predicted for ethambutol (8794 [89.8%] of 9794). Resistance to isoniazid, rifampin, ethambutol, and pyrazinamide was correctly predicted with 97.1%, 97.5%, 94.6%, and 91.3% sensitivity, respectively, and susceptibility to these drugs was correctly predicted with 99.0%, 98.8%, 93.6%, and 96.8% specificity. Of the 7516 isolates with complete phenotypic drug-susceptibility profiles, 5865 (78.0%) had complete genotypic predictions, among which 5250 profiles (89.5%) were correctly predicted. Among the 4037 phenotypic profiles that were predicted to be pansusceptible, 3952 (97.9%) were correctly predicted.ConclusionsGenotypic predictions of the susceptibility of M. tuberculosis to first-line drugs were found to be correlated with phenotypic susceptibility to these drugs. (Funded by the Bill and Melinda Gates Foundation and others.).

Published
2018

4. Challenging the gold standard: the limitations of molecular assays for detection of Mycobacterium tuberculosis heteroresistance.

Author

Danchuk, Sarah N., Solomon, Ori E., Kohl, Thomas Andreas, Dreyer, Viola, Barilar, Ivan, Utpatel, Christian, Niemann, Stefan, van Soolingen, Dick, Anthony, Richard, van Ingen, Jakko, Michael, Joy S., and Behr, Marcel A.

Subjects
MYCOBACTERIUM tuberculosis, MYCOBACTERIA, MYCOPLASMA bovis, MICROBIAL sensitivity tests, RAPID diagnostic tests, WHOLE genome sequencing, MEDICAL microbiology
Published
2024
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5. Comparison of different treatments for isoniazid-resistant tuberculosis: an individual patient data meta-analysis

Author

Fregonese, Federica, Ahuja, Shama D, Akkerman, Onno W, Arakaki-Sanchez, Denise, Ayakaka, Irene, Baghaei, Parvaneh, Bang, Didi, Bastos, Mayara, Benedetti, Andrea, Bonnet, Maryline, Cattamanchi, Adithya, Cegielski, Peter, Chien, Jung-Yien, Cox, Helen, Dedicoat, Martin, Erkens, Connie, Escalante, Patricio, Falzon, Dennis, Garcia-Prats, Anthony J, Gegia, Medea, Gillespie, Stephen H, Glynn, Judith R, Goldberg, Stefan, Griffith, David, Jacobson, Karen R, Johnston, James C, Jones-López, Edward C, Khan, Awal, Koh, Won-Jung, Kritski, Afranio, Lan, Zhi Yi, Lee, Jae Ho, Li, Pei Zhi, Maciel, Ethel L, Galliez, Rafael Mello, Merle, Corinne SC, Munang, Melinda, Narendran, Gopalan, Nguyen, Viet Nhung, Nunn, Andrew, Ohkado, Akihiro, Park, Jong Sun, Phillips, Patrick PJ, Ponnuraja, Chinnaiyan, Reves, Randall, Romanowski, Kamila, Seung, Kwonjune, Schaaf, H Simon, Skrahina, Alena, van Soolingen, Dick, Tabarsi, Payam, Trajman, Anete, Trieu, Lisa, Banurekha, Velayutham V, Viiklepp, Piret, Wang, Jann-Yuan, Yoshiyama, Takashi, and Menzies, Dick

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Tuberculosis, Rare Diseases, Antimicrobial Resistance, Clinical Trials and Supportive Activities, Lung, Clinical Research, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Infection, Good Health and Well Being, Antibiotics, Antitubercular, Cohort Studies, Drug Administration Schedule, Drug Therapy, Combination, Ethambutol, Fluoroquinolones, Humans, Observational Studies as Topic, Outcome Assessment, Health Care, Pyrazinamide, Randomized Controlled Trials as Topic, Review Literature as Topic, Rifampin, Streptomycin, Tuberculosis, Multidrug-Resistant, Public Health and Health Services, Other Medical and Health Sciences, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundIsoniazid-resistant, rifampicin-susceptible (INH-R) tuberculosis is the most common form of drug resistance, and is associated with failure, relapse, and acquired rifampicin resistance if treated with first-line anti-tuberculosis drugs. The aim of the study was to compare success, mortality, and acquired rifampicin resistance in patients with INH-R pulmonary tuberculosis given different durations of rifampicin, ethambutol, and pyrazinamide (REZ); a fluoroquinolone plus 6 months or more of REZ; and streptomycin plus a core regimen of REZ.MethodsStudies with regimens and outcomes known for individual patients with INH-R tuberculosis were eligible, irrespective of the number of patients if randomised trials, or with at least 20 participants if a cohort study. Studies were identified from two relevant systematic reviews, an updated search of one of the systematic reviews (for papers published between April 1, 2015, and Feb 10, 2016), and personal communications. Individual patient data were obtained from authors of eligible studies. The individual patient data meta-analysis was performed with propensity score matched logistic regression to estimate adjusted odds ratios (aOR) and risk differences of treatment success (cure or treatment completion), death during treatment, and acquired rifampicin resistance. Outcomes were measured across different treatment regimens to assess the effects of: different durations of REZ (≤6 months vs >6 months); addition of a fluoroquinolone to REZ (fluoroquinolone plus 6 months or more of REZ vs 6 months or more of REZ); and addition of streptomycin to REZ (streptomycin plus 6 months of rifampicin and ethambutol and 1-3 months of pyrazinamide vs 6 months or more of REZ). The overall quality of the evidence was assessed using GRADE methodology.FindingsIndividual patient data were requested for 57 cohort studies and 17 randomised trials including 8089 patients with INH-R tuberculosis. We received 33 datasets with 6424 patients, of which 3923 patients in 23 studies received regimens related to the study objectives. Compared with a daily regimen of 6 months of (H)REZ (REZ with or without isoniazid), extending the duration to 8-9 months had similar outcomes; as such, 6 months or more of (H)REZ was used for subsequent comparisons. Addition of a fluoroquinolone to 6 months or more of (H)REZ was associated with significantly greater treatment success (aOR 2·8, 95% CI 1·1-7·3), but no significant effect on mortality (aOR 0·7, 0·4-1·1) or acquired rifampicin resistance (aOR 0·1, 0·0-1·2). Compared with 6 months or more of (H)REZ, the standardised retreatment regimen (2 months of streptomycin, 3 months of pyrazinamide, and 8 months of isoniazid, rifampicin, and ethambutol) was associated with significantly worse treatment success (aOR 0·4, 0·2-0·7). The quality of the evidence was very low for all outcomes and treatment regimens assessed, owing to the observational nature of most of the data, the diverse settings, and the imprecision of estimates.InterpretationIn patients with INH-R tuberculosis, compared with treatment with at least 6 months of daily REZ, addition of a fluoroquinolone was associated with better treatment success, whereas addition of streptomycin was associated with less treatment success; however, the quality of the evidence was very low. These results support the conduct of randomised trials to identify the optimum regimen for this important and common form of drug-resistant tuberculosis.FundingWorld Health Organization and Canadian Institutes of Health Research.

Published
2018

6. Phylogenomic and genomic analysis reveals unique and shared genetic signatures of Mycobacterium kansasii complex species

Author

Machado, Edson, primary, Vasconcellos, Sidra, additional, Gomes, Lia, additional, Catanho, Marcos, additional, Ramos, Jesus, additional, de Carvalho, Luciana, additional, Goldenberg, Telma, additional, Dalcolmo, Margareth, additional, Redner, Paulo, additional, Caldas, Paulo, additional, Campos, Carlos, additional, Lourenco, Maria Cristina, additional, Lasunskaia, Elena, additional, Mussi, Vinicius, additional, Spinasse, Lizania, additional, Vinhas, Solange, additional, Rigouts, Leen, additional, Cogneau, Sari, additional, de Rijk, Pim, additional, Utpatel, Christian, additional, Kaustova, Jarmila, additional, van der Laan, Tridia, additional, de Neeling, Han, additional, Rastogi, Nalin, additional, Levina, Klavdia, additional, Kutt, Marge, additional, Mokrousov, Igor, additional, Zhuravlev, Viacheslav, additional, Makhado, Ndivhu, additional, Zolnir-Dovc, Manca, additional, Jankovic, Vera, additional, de Waard, Jacobus, additional, Sisco, Maria, additional, van Soolingen, Dick, additional, Niemann, Stefan, additional, de Jong, Bouke C., additional, Meehan, Conor J, additional, and Suffys, Philip, additional

Published
2024
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10. SNP-IT Tool for Identifying Subspecies and Associated Lineages of Mycobacterium tuberculosis Complex

Author

Lipworth, Samuel, Jajou, Rana, de Neeling, Albert, Bradley, Phelim, van der Hoek, Wim, Maphalala, Gugu, Bonnet, Maryline, Sanchez-Padilla, Elizabeth, Diel, Roland, Niemann, Stefan, Iqbal, Zamin, Smith, Grace, Peto, Tim, Crook, Derrick, Walker, Timothy, and van Soolingen, Dick

Subjects
Genomes, Single nucleotide polymorphisms, Tuberculosis -- Genetic aspects, Genomics, Zoonoses, Genetic polymorphisms, Health
Abstract

Mycobacterium tuberculosis complex (MTBC) encompasses a group of organisms that cause tuberculosis (TB) in humans and animals. TB in humans is caused mainly by M. tuberculosis but also by other [...]

Published
2019
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11. Whole genome sequencing of Mycobacterium tuberculosis: current standards and open issues

Author

Meehan, Conor J., Goig, Galo A., Kohl, Thomas A., Verboven, Lennert, Dippenaar, Anzaan, Ezewudo, Matthew, Farhat, Maha R., Guthrie, Jennifer L., Laukens, Kris, Miotto, Paolo, Ofori-Anyinam, Boatema, Dreyer, Viola, Supply, Philip, Suresh, Anita, Utpatel, Christian, van Soolingen, Dick, Zhou, Yang, Ashton, Philip M., Brites, Daniela, Cabibbe, Andrea M., de Jong, Bouke C., de Vos, Margaretha, Menardo, Fabrizio, Gagneux, Sebastien, Gao, Qian, Heupink, Tim H., Liu, Qingyun, Loiseau, Chloé, Rigouts, Leen, Rodwell, Timothy C., Tagliani, Elisa, Walker, Timothy M., Warren, Robin M., Zhao, Yanlin, Zignol, Matteo, Schito, Marco, Gardy, Jennifer, Cirillo, Daniela M., Niemann, Stefan, Comas, Inaki, and Van Rie, Annelies

Published
2019
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14. The appearance of sugI mixed loci in three individuals during treatment for MDR-TB, supports the involvement of sugI in Mycobacterium tuberculosis d-cycloserine resistance in vivo.

Author

Anthony, Richard M, primary, Molemans, Marjan, additional, Akkwerman, Onno, additional, Sturkenboom, Marieke G.G., additional, Mulder, Arnout, additional, de Zwaan, Rina, additional, van Soolingen, Dick, additional, Alffenaar, Jan-Willem, additional, van Leth, Frank C.M., additional, Ghimire, Samiksha, additional, Yastskevich, Natalia, additional, Skrahina, Alena, additional, Ciobanu, Nelly, additional, Turcan, Nadia, additional, and Crudu, Valeriu, additional

Published
2023
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27. Host-pathogen co-adaptation shapes susceptibility to infection with Mycobacterium tuberculosis

Author

Gröschel, Matthias I, primary, Pérez-Llanos, Francy J., additional, Diel, Roland, additional, Vargas, Roger, additional, Escuyer, Vincent, additional, Musser, Kimberlee, additional, Trieu, Lisa, additional, Meissner, Jeanne Sullivan, additional, Knorr, Jillian, additional, Klinkenberg, Don, additional, Kouw, Peter, additional, Homolka, Susanne, additional, Samek, Wojciech, additional, Mathema, Barun, additional, van Soolingen, Dick, additional, Niemann, Stefan, additional, Ahuja, Shama, additional, and Farhat, Maha R, additional

Published
2022
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28. Treatment and Outcome of Culture-Confirmed Disease

Author

Hendrikx, Louise, van Hees, Colette L M, de Steenwinkel, Jurriaan E M, Bax, Hannelore I, Sprong, Tom, Mulder, Bert, Jansz, Arjan, van Griethuysen, Arjanne, Bosboom, Ron, Stemerding, Annette, Koetsier, Marjolein, van Coevorden, Marco, Mourik, Bas C, Quint, Koen D, Ott, Alewijn, van Soolingen, Dick, Kuipers, Saskia, van Crevel, Reinout, and van Ingen, Jakko

Subjects
nontuberculous mycobacteria, doxycycline, Mycobacterium marinum, epidemiology, fish tank finger
Abstract

Mycobacterium marinum is a nontuberculous mycobacterium that causes skin and soft tissue infections. Treatment consists of multiple antibiotics, sometimes combined with surgical debridement. There is little evidence for the choice of antibiotics, the duration of treatment, and the role of susceptibility testing.

Published
2022

32. Recurrent tuberculosis in the Netherlands - a 24-year follow-up study, 1993 to 2016

Author

Erkens, Connie, Tekeli, Betül, van Soolingen, Dick, Schimmel, Henrieke, and Verver, Suzanne

Subjects
reactivation, tuberculosis, recurrent TB, reinfection
Abstract

BackgroundNot all treated tuberculosis (TB) patients achieve long-term recovery and reactivation rates reflect effectiveness of TB treatment.AimWe aimed to estimate rates and risk factors of TB reactivation and reinfection in patients treated in the Netherlands, after completed or interrupted treatment.MethodsRetrospective cohort study of TB patients with available DNA fingerprint data, registered in the Netherlands Tuberculosis register (NTR) between 1993 and 2016. Reactivation was defined as an identical, and reinfection as a non-identical Mycobacterium tuberculosis strain in sequential episodes.ResultsReactivation rate was 55/100,000 person-years (py) for patients who completed, and 318/100,000 py for patients who interrupted treatment. The risk of reactivation was highest in the first 5 years after treatment in both groups. The incidence rate of reactivation was 228/100,000 py in the first 2 years and 57/100,000 py 2-5 years after completed treatment. The overall rate of reinfection was 16/100,000 py. Among those who completed treatment, patients with male sex, mono or poly rifampicin-resistant TB and a previous TB episode had significantly higher risk of reactivation. Extrapulmonary TB was associated with a lower risk. Among patients who interrupted treatment, directly observed treatment (DOT) and being an undocumented migrant or people experiencing homelessness were associated with a higher risk of reactivation.ConclusionsBoth patients who completed or interrupted TB treatment should be considered as risk groups for reactivation for at least 2-5 years after treatment. They patients should be monitored and guidelines should be in place to enhance early detection of recurrent TB.

Published
2022

33. Updating the approaches to define susceptibility and resistance to anti-tuberculosis agents: implications for diagnosis and treatment

Author

Antimycobacterial Susceptibility Testing Group, Georghiou, Sophia B., Rodwell, Timothy C., Korobitsyn, Alexei, Abbadi, Said H., Ajbani, Kanchan, Alffenaar, Jan-Willem, Alland, David, Alvarez, Nataly, Andres, Sönke, Ardizzoni, Elisa, Aubry, Alexandra, Baldan, Rossella, Ballif, Marie, Barilar, Ivan, Böttger, Erik C., Chakravorty, Soumitesh, Claxton, Pauline M., Cirillo, Daniela M., Comas, Iñaki, Coulter, Chris, Denkinger, Claudia M., Derendinger, Brigitta, Desmond, Edward P., Steenwinkel, Jurriaan E. M. de, Dheda, Keertan, Diacon, Andreas H., Dolinger, David L., Dooley, Kelly E., Egger, Matthias, Ehsani, Soudeh, Farhat, Maha R., Fattorini, Lanfranco, Finci, Iris, Fournier Le Ray, Laure, Furió, Victoria, Groenheit, Ramona, Gumbo, Tawanda, Heysell, Scott K., Hillemann, Doris, Hoffmann, Harald, Hsueh, Po-Ren, Hu, Yi, Huang, Hairong, Hussain, Alamdar, Ismail, Farzana, Izumi, Kiyohiko, Jagielski, Tomasz, Johnson, John L., Kambli, Priti, Kaniga, Koné, Karunaratne, G. H. R. Eranga, Sharma, Meenu Kaushal, Keller, Peter M., Kelly, Ellis C., Kholina, Margarita, Kohli, Mikashmi, Kranzer, Katharina, Laurenson, Ian F., Limberis, Jason, Lin, S-Y. Grace, Liu, Yongge, López-Gavín, Alexandre, Lyander, Anna, Machado, Diana, Martínez, Elena, Masood, Faisal, Mitarai, Satoshi, Mvelase, Nomonde R., Niemann, Stefan, Nikolayevskyy, Vladyslav, Maurer, Florian P., Merker, Matthias, Miotto, Paolo, Omar, Shaheed V., Otto-Knapp, Ralf, Palaci, Moisés, Palacios Gutiérrez, Juan José, Peacock, Sharon J., Peloquin, Charles A., Perera, Jennifer, Pierre-Audigier, Catherine, Pholwat, Suporn, Posey, James E., Prammananan, Therdsak, Rigouts, Leen, Robledo, Jaime, Rockwood, Neesha, Rodrigues, Camilla, Salfinger, Max, Schechter, Marcos C., Seifert, Marva, Sengstake, Sarah, Shinnick, Thomas, Shubladze, Natalia, Sintchenko, Vitali, Sirgel, Frederick, Somasundaram, Sulochana, Sterling, Timothy R., Spitaleri, Andrea, Streicher, Elizabeth, Supply, Philip, Svensson, Erik, Tagliani, Elisa, Tahseen, Sabira, Takaki, Akiko, Theron, Grant, Torrea, Gabriela, Van Deun, Armand, van Ingen, Jakko, Van Rie, Annelies, van Soolingen, Dick, Vargas Jr, Roger, Venter, Amour, Veziris, Nicolas, Villellas, Cristina, Viveiros, Miguel, Warren, Robin, Wen, Shu'an, Werngren, Jim, Wilkinson, Robert J., Yang, Caie, Yılmaz, F. Ferda, Zhang, Tingting, Zimenkov, Danila, Ismail, Nazir, Köser, Claudio U., Schön, Thomas, University of Zurich, Antimycobacterial Susceptibility Testing Group, Department of Genetics [Cambridge], University of Cambridge [UK] (CAM), Centre d'Immunologie et des Maladies Infectieuses (CIMI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre Médical de l'Institut Pasteur (CMIP), Institut Pasteur [Paris] (IP)-Université Paris Cité (UPCité), Institut de médecine et d'épidémiologie appliquée [AP-HP Hôpital Bichat-Claude Bernard] (IMEA), AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 (CIIL), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), As current or former employees or consultants for FIND, the work of R.B. Baldan, I. Comas, C.M. Denkinger, D.L. Dolinger, S.B. Georghiou, C.U. Köser and T.C. Rodwell on the systematic reviews, including this viewpoint, was supported by Unitaid (grant 2019-32-FIND MDR), BMGF (grant OPP1105925), the German Federal Ministry of Education and Research through KfW, the Dutch Ministry of Foreign Affairs, the Australian Department of Foreign Affairs and Trade, and UK aid from the British people. N. Alvarez and J. Robledo are funded by MinCiencias, Colombia (number 221389666216 CT-783-2018). A. Aubry and N. Veziris work at the Centre National de Reference des Mycobactéries, which receives an annual grant from Santé Publique France and have received research grants from Janssen for studies on bedaquiline. P. Claxton and I.F. Laurenson are funded through National Services Scotland. I. Comas was supported by PID2019-104477RB-I00 from the Spanish Science Ministry and by ERC (CoG 101001038). M. Egger is supported by the Swiss National Science Foundation (grant number 320030_153442 and 189498) and the US National Institutes of Health, National Institute of Allergy and Infectious Diseases, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the National Cancer Institute, the National Institute of Mental Health, the National Institute on Drug Abuse, the National Heart, Lung, and Blood Institute, the National Institute on Alcohol Abuse and Alcoholism, the National Institute of Diabetes and Digestive and Kidney Diseases, the Fogarty International Center, and the National Library of Medicine: Asia-Pacific, U01AI069907, CCASAnet, U01AI069923, Central Africa, U01AI096299, East Africa, U01AI069911, NA-ACCORD, U01AI069918, Southern Africa, U01AI069924, West Africa, U01AI069919. M.R. Farhat is supported by NIH NIAID R01AI155765. S.K. Heysell was funded by NIH NIAID grants R01 AI137080 and U01 AI150508. T. Jagielski was supported by a DAINA grant (number 2017/27/L/NZ6/03279) from the National Science Centre, Poland. J.L. Johnson was supported by contracts NO1-AI95383 and NO1-AI-70022 of the US National Institutes of Health. P.M. Keller was supported by Innosuisse 36198.1 IP-LS. C.U. Köser is a research associate at Wolfson College and visiting scientist at the Department of Genetics, University of Cambridge. The Federal Government of Germany supported C.U. Köser as part of his work for the European Laboratory Initiative, WHO Regional Office for Europe. C.U. Köser was further supported by the Royal Society of Tropical Medicine and Hygiene and the National Institute for Health Research Cambridge Biomedical Research Centre and received an observership by the European Society of Clinical Microbiology and Infectious Diseases to the EUCAST Development Laboratory for Bacteria (Växjö, Sweden), hosted by Gunnar Kahlmeter and Erika Matuschek. D. Machado and M. Viveiros are funded in part by Fundação para a Ciência e a Tecnologia, Portugal (PTDC/BIA-MIC/30692/2017, UID/Multi/04413/2020 and DL57/ CEECIND/0256/2017). S. Niemann is supported by the German Center for Infection Research, Excellenz Cluster Precision Medicine in Chronic Inflammation EXC 2167, Leibniz Science Campus Evolutionary Medicine of the LUNG (EvoLUNG). S.V. Omar has received funding to prepare and provide training for Janssen Pharmaceutica activities. L. Rigouts is supported by the Belgian Directorate General for Development. T.C. Rodwell was additionally funded in part by FIND and NIH NIAD, grants: P30 AI036214 and R21 AI135756. T. Schön is funded by the Swedish Heart and Lung Foundation and the Swedish Research Council. T.R. Sterling has received funding from the US National Institutes of Health and the Centers for Disease Control and Prevention. G. Theron and R. Warren are supported by baseline funding from the South African Medical Research Council. R.J. Wilkinson receives funding from the Wellcome Trust (203135) and from the Francis Crick Institute, which is supported by Cancer Research UK (FC0010218), UKRI (FC0010218) and the Wellcome Trust (FC0010218), Ministerio de Ciencia e Innovación (España), European Research Council, Comas, Iñaki, Comas, Iñaki [0000-0001-5504-9408], Antimycobacterial Susceptibility T, and Wellcome Trust

Subjects
[SDV]Life Sciences [q-bio], Respiratory System, Drug Resistance, Antitubercular Agents, Infektionsmedicin, Medical and Health Sciences, Drug Resistance, Multiple, Bacterial, Tuberculosis, Multidrug-Resistant, 11 Medical and Health Sciences, Human Biology & Physiology, MESH: Microbial Sensitivity Tests, 10179 Institute of Medical Microbiology, Bacterial, Multidrug-Resistant, Infectious Diseases, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Infection, Life Sciences & Biomedicine, Multiple, Model organisms, Pulmonary and Respiratory Medicine, Infectious Medicine, Immunology, Infectious Disease, 610 Medicine & health, Microbial Sensitivity Tests, Vaccine Related, Rare Diseases, Clinical Research, Biodefense, MESH: Drug Resistance, Bacterial, Drug Resistance, Bacterial, Tuberculosis, Humans, Science & Technology, MESH: Humans, Antimycobacterial Susceptibility Testing Group, FOS: Clinical medicine, Prevention, MESH: Drug Resistance, Multiple, Bacterial, Mycobacterium tuberculosis, Eucast, MESH: Antitubercular Agents, lnfectious Diseases and Global Health Radboud Institute for Health Sciences [Radboudumc 4], Orphan Drug, Emerging Infectious Diseases, Good Health and Well Being, 2740 Pulmonary and Respiratory Medicine, 570 Life sciences, biology, Human medicine, Antimicrobial Resistance, Model
Abstract

11 páginas, 2 figuras, 1 tabla, Inappropriately high breakpoints have resulted in systematic false-susceptible AST results to anti-TB drugs. MIC, PK/PD and clinical outcome data should be combined when setting breakpoints to minimise the emergence and spread of antimicrobial resistance., I. Comas was supported by PID2019-104477RB-I00 from the Spanish Science Ministry and by ERC (CoG 101001038)

Published
2022

36. Treatment and Outcome of Culture-Confirmed Mycobacterium marinum Disease

Author

Hendrikx, Louise, primary, van Hees, Colette L M, additional, de Steenwinkel, Jurriaan E M, additional, Bax, Hannelore I, additional, Sprong, Tom, additional, Mulder, Bert, additional, Jansz, Arjan, additional, van Griethuysen, Arjanne, additional, Bosboom, Ron, additional, Stemerding, Annette, additional, Koetsier, Marjolein, additional, van Coevorden, Marco, additional, Mourik, Bas C, additional, Quint, Koen D, additional, Ott, Alewijn, additional, van Soolingen, Dick, additional, Kuipers, Saskia, additional, van Crevel, Reinout, additional, and van Ingen, Jakko, additional

Published
2022
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37. Clinical Relevance of Rifampicin‐Moxifloxacin Interaction in Isoniazid-Resistant/Intolerant Tuberculosis Patients

Author

Vogensen, Vanessa B., primary, Bolhuis, Mathieu S., additional, Sturkenboom, Marieke G. G., additional, van der Werf, Tjip S., additional, de Lange, Wiel C. M., additional, Anthony, Richard M., additional, van Soolingen, Dick, additional, Alffenaar, Jan-Willem, additional, Kerstjens, Huib A. M., additional, and Akkerman, Onno W., additional

Published
2022
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42. A new nomenclature for the livestock-associated Mycobacterium tuberculosiscomplex based on phylogenomics

Author

Zwyer, Michaela, Çavusoglu, Cengiz, Ghielmetti, Giovanni, Pacciarini, Maria Lodovica, Scaltriti, Erika, Van Soolingen, Dick, Dötsch, Anna, Reinhard, Miriam, Gagneux, Sebastien, and Brites, Daniela

Subjects
phylogenetics, whole-genome sequencing, zoonotic tuberculosis, genetic diversity, mycobacterium tuberculosis complex
Abstract

Background The bacteria that compose the Mycobacterium tuberculosis complex (MTBC) cause tuberculosis (TB) in humans and in different animals, including livestock. Much progress has been made in understanding the population structure of the human-adapted members of the MTBC by combining phylogenetics with genomics. Accompanying the discovery of new genetic diversity, a body of operational nomenclature has evolved to assist comparative and molecular epidemiological studies of human TB. By contrast, for the livestock-associated MTBC members, Mycobacterium bovis, M. caprae and M. orygis, there has been a lack of comprehensive nomenclature to accommodate new genetic diversity uncovered by emerging phylogenomic studies. We propose to fill this gap by putting forward a new nomenclature covering the main phylogenetic groups within M. bovis, M. caprae and M. orygis. Methods We gathered a total of 8,736 whole-genome sequences (WGS) from public sources and 39 newly sequenced strains, and selected a subset of 829 WGS, representative of the worldwide diversity of M. bovis, M. caprae and M. orygis. We used phylogenetics and genetic diversity patterns inferred from WGS to define groups. Results We propose to divide M. bovis, M. caprae and M. orygis in three main phylogenetic lineages, which we named La1, La2 and La3, respectively. Within La1, we identified several monophyletic groups, which we propose to classify into eight sublineages (La1.1-La1.8). These sublineages differed in geographic distribution, with some being geographically restricted and others globally widespread, suggesting different expansion abilities. To ease molecular characterization of these MTBC groups by the community, we provide phylogenetically informed, single nucleotide polymorphisms that can be used as barcodes for genotyping. These markers were implemented in KvarQ and TB-Profiler, which are platform-independent, open-source tools. Conclusions Our results contribute to an improved classification of the genetic diversity within the livestock-associated MTBC, which will benefit future molecular epidemiological and evolutionary studies.

Published
2021

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