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472 results on '"Grosset, Jacques"'

1. Emerging Therapies

Author

Lamichhane, Gyanu, Grosset, Jacques H., Grosset, Jacques H., editor, and Chaisson, Richard E., editor

Published
2017
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6. Targeting DnaN for tuberculosis therapy using novel griselimycins

Author

Kling, Angela, Lukat, Peer, Almeida, Deepak V., Bauer, Armin, Fontaine, Evelyne, Sordello, Sylvie, Zaburannyi, Nestor, Herrmann, Jennifer, Wenzel, Silke C., König, Claudia, Ammerman, Nicole C., Barrio, María Belén, Borchers, Kai, Bordon-Pallier, Florence, Brönstrup, Mark, Courtemanche, Gilles, Gerlitz, Martin, Geslin, Michel, Hammann, Peter, Heinz, Dirk W., Hoffmann, Holger, Klieber, Sylvie, Kohlmann, Markus, Kurz, Michael, Lair, Christine, Matter, Hans, Nuermberger, Eric, Tyagi, Sandeep, Fraisse, Laurent, Grosset, Jacques H., Lagrange, Sophie, and Müller, Rolf

Published
2015

9. An enhanced regimen as post-exposure chemoprophylaxis for leprosy: PEP++

Author

Mieras, Liesbeth F, Taal, Anna T, van Brakel, Wim H, Cambau, Emmanuelle, Saunderson, Paul R, Smith, W Cairns S, Prakoeswa, Cita Rosita S, Astari, Linda, Scollard, David M, do Nascimento, Dejair Caitano, Grosset, Jacques, Kar, Hemanta K, Izumi, Shinzo, Gillini, Laura, Virmond, Marcos C L, and Sturkenboom, Marieke G G

Published
2018
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14. Benzothiazinones Kill Mycobacterium tuberculosis by Blocking Arabinan Synthesis

Author

Makarov, Vadim, Manina, Giulia, Mikusova, Katarina, Möllmann, Ute, Ryabova, Olga, Saint-Joanis, Brigitte, Dhar, Neeraj, Pasca, Maria Rosalia, Buroni, Silvia, Lucarelli, Anna Paola, Milano, Anna, De Rossi, Edda, Belanova, Martina, Bobovska, Adela, Dianiskova, Petronela, Kordulakova, Jana, Sala, Claudia, Fullam, Elizabeth, Schneider, Patricia, McKinney, John D., Brodin, Priscille, Christophe, Thierry, Waddell, Simon, Butcher, Philip, Albrethsen, Jakob, Rosenkrands, Ida, Brosch, Roland, Nandi, Vrinda, Bharath, Sowmya, Gaonkar, Sheshagiri, Shandil, Radha K., Balasubramanian, Venkataraman, Balganesh, Tanjore, Tyagi, Sandeep, Grosset, Jacques, Riccardi, Giovanna, and Cole, Stewart T.

Published
2009
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18. ANTIBIOTICS: Targeting DnaN for tuberculosis therapy using novel griselimycins

Author

Kling, Angela, Lukat, Peer, Almeida, Deepak V., Bauer, Armin, Fontaine, Evelyne, Sordello, Sylvie, Zaburannyi, Nestor, Herrmann, Jennifer, Wenzel, Silke C., König, Claudia, Ammerman, Nicole C., Barrio, María Belén, Borchers, Kai, Bordon-Pallier, Florence, Brönstrup, Mark, Courtemanche, Gilles, Gerlitz, Martin, Geslin, Michel, Hammann, Peter, Heinz, Dirk W., Hoffinann, Holger, Klieber, Sylvie, Kohknann, Markus, Kurz, Michael, Lair, Christine, Matter, Hans, Nuermberger, Eric, Tyagi, Sandeep, Fraisse, Laurent, Grosset, Jacques H., Lagrange, Sophie, and Müller, Rolf

Published
2015

24. Daily dosing of rifapentine cures tuberculosis in three months or less in the murine model

Author

Rosenthal, Ian M., Zhang, Ming, Williams, Kathy N., Peloquin, Charles A., Tyagi, Sandeep, Vernon, Andrew A., Bishai, William R., Chaisson, Richard E., Grosset, Jacques H., and Nuermberger, Eric L.

Abstract

Background Availability of an ultra-short-course drug regimen capable of curing patients with tuberculosis in 2 to 3 mo would significantly improve global control efforts. Because immediate prospects for novel treatment-shortening drugs remain uncertain, we examined whether better use of existing drugs could shorten the duration of treatment. Rifapentine is a long-lived rifamycin derivative currently recommended only in once-weekly continuation-phase regimens. Moxifloxacin is an 8-methoxyfluoroquinolone currently used in second-line regimens. Methods and Findings Using a well-established mouse model with a high bacterial burden and human-equivalent drug dosing, we compared the efficacy of rifapentine- and moxifloxacin-containing regimens with that of the standard daily short-course regimen based on rifampin, isoniazid, and pyrazinamide. Bactericidal activity was assessed by lung colony-forming unit counts, and sterilizing activity was assessed by the proportion of mice with culture-positive relapse after 2, 3, 4, and 6 mo of treatment. Here, we demonstrate that replacing rifampin with rifapentine and isoniazid with moxifloxacin dramatically increased the activity of the standard daily regimen. After just 2 mo of treatment, mice receiving rifapentine- and moxifloxacin-containing regimens were found to have negative lung cultures, while those given the standard regimen still harbored 3.17 [log.sub.10] colony-forming units in the lungs (p < 0.01). No relapse was observed after just 3 mo of treatment with daily and thrice-weekly administered rifapentine- and moxifloxacin-containing regimens, whereas the standard daily regimen required 6 mo to prevent relapse in all mice. Conclusions Rifapentine should no longer be viewed solely as a rifamycin for once-weekly administration. Our results suggest that treatment regimens based on daily and thrice-weekly administration of rifapentine and moxifloxacin may permit shortening the current 6 mo duration of treatment to 3 mo or less. Such regimens warrant urgent clinical investigation., Introduction The development of simplified treatment regimens is a major priority of the Global Plan to Stop TB [1]. Novel regimens that are substantially shorter than the current 6-mo regimen [...]

Published
2007

30. Fluoroquinolones, tuberculosis, and resistance

Author

Ginsburg, Amy Sarah, Grosset, Jacques H., and Bishai, William R.

Subjects
Tuberculosis, Drug resistance in microorganisms, Quinolone antibacterial agents, Quinolones, Antitubercular agents
Published
2003

39. Substitution of Moxifloxacin for Isoniazid during Intensive Phase Treatment of Pulmonary Tuberculosis

Author

Dorman, Susan E., Johnson, John L., Goldberg, Stefan, Muzanye, Grace, Padayatchi, Nesri, Bozeman, Lorna, Heilig, Charles M., Bernardo, John, Choudhri, Shurjeel, Grosset, Jacques H., Guy, Elizabeth, Guyadeen, Priya, Leus, Maria Corazon, Maltas, Gina, Menzies, Dick, Nuermberger, Eric L., Villarino, Margarita, Vernon, Andrew, and Chaisson, Richard E.

Published
2009
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50. Evolution of extensively drug-resistant tuberculosis over four decades: whole genome sequencing and dating analysis of Mycobacterium tuberculosis isolates from KwaZulu-Natal

Author

Cohen, Keira A., Abeel, Thomas, McGuire, Abigail Manson, Desjardins, Christopher A., Munsamy, Vanisha, Shea, Terrance P., Walker, Bruce J., Bantubani, Nonkqubela, Almeida, Deepak V., Alvarado, Lucia, Chapman, Sinead B., Mvelase, Nomonde R., Duffy, Eamon Y., Fitzgerald, Michael G., Govender, Pamla, Gujja, Sharvari, Hamilton, Susanna, Howarth, Clinton, Larimer, Jeffrey D., Maharaj, Kashmeel, Pearson, Matthew D., Priest, Margaret E., Zeng, Qiandong, Padayatchi, Nesri, Grosset, Jacques, Young, Sarah K., Wortman, Jennifer, Mlisana, Koleka P., O'Donnell, Max R., Birren, Bruce W., Bishai, William R., Pym, Alexander S., and Earl, Ashlee M.

Subjects
Nucleotide sequencing -- Methods -- Genetic aspects, Drug resistance in microorganisms -- Genetic aspects, DNA sequencing -- Methods -- Genetic aspects, Mycobacterium tuberculosis -- Genetic aspects -- Methods, Biological sciences
Abstract

Background The continued advance of antibiotic resistance threatens the treatment and control of many infectious diseases. This is exemplified by the largest global outbreak of extensively drug-resistant (XDR) tuberculosis (TB) identified in Tugela Ferry, KwaZulu-Natal, South Africa, in 2005 that continues today. It is unclear whether the emergence of XDR-TB in KwaZulu-Natal was due to recent inadequacies in TB control in conjunction with HIV or other factors. Understanding the origins of drug resistance in this fatal outbreak of XDR will inform the control and prevention of drug-resistant TB in other settings. In this study, we used whole genome sequencing and dating analysis to determine if XDR-TB had emerged recently or had ancient antecedents. Methods and Findings We performed whole genome sequencing and drug susceptibility testing on 337 clinical isolates of Mycobacterium tuberculosis collected in KwaZulu-Natal from 2008 to 2013, in addition to three historical isolates, collected from patients in the same province and including an isolate from the 2005 Tugela Ferry XDR outbreak, a multidrug-resistant (MDR) isolate from 1994, and a pansusceptible isolate from 1995. We utilized an array of whole genome comparative techniques to assess the relatedness among strains, to establish the order of acquisition of drug resistance mutations, including the timing of acquisitions leading to XDR-TB in the LAM4 spoligotype, and to calculate the number of independent evolutionary emergences of MDR and XDR. Our sequencing and analysis revealed a 50-member clone of XDR M. tuberculosis that was highly related to the Tugela Ferry XDR outbreak strain. We estimated that mutations conferring isoniazid and streptomycin resistance in this clone were acquired 50 y prior to the Tugela Ferry outbreak (katG S315T [isoniazid]; gidB 130 bp deletion [streptomycin]; 1957 [95% highest posterior density (HPD): 1937-1971]), with the subsequent emergence of MDR and XDR occurring 20 y (rpoB L452P [rifampicin]; pncA 1 bp insertion [pyrazinamide]; 1984 [95% HPD: 1974-1992]) and 10 y (rpoB D435G [rifampicin]; rrs 1400 [kanamycin]; gyrA A90V [ofloxacin]; 1995 [95% HPD: 1988-1999]) prior to the outbreak, respectively. We observed frequent de novo evolution of MDR and XDR, with 56 and nine independent evolutionary events, respectively. Isoniazid resistance evolved before rifampicin resistance 46 times, whereas rifampicin resistance evolved prior to isoniazid only twice. We identified additional putative compensatory mutations to rifampicin in this dataset. One major limitation of this study is that the conclusions with respect to ordering and timing of acquisition of mutations may not represent universal patterns of drug resistance emergence in other areas of the globe. Conclusions In the first whole genome-based analysis of the emergence of drug resistance among clinical isolates of M. tuberculosis, we show that the ancestral precursor of the LAM4 XDR outbreak strain in Tugela Ferry gained mutations to first-line drugs at the beginning of the antibiotic era. Subsequent accumulation of stepwise resistance mutations, occurring over decades and prior to the explosion of HIV in this region, yielded MDR and XDR, permitting the emergence of compensatory mutations. Our results suggest that drug-resistant strains circulating today reflect not only vulnerabilities of current TB control efforts but also those that date back 50 y. In drug-resistant TB, isoniazid resistance was overwhelmingly the initial resistance mutation to be acquired, which would not be detected by current rapid molecular diagnostics employed in South Africa that assess only rifampicin resistance., Introduction The global burden of tuberculosis (TB) remains high, with an estimated 9 million active disease cases and 1.5 million deaths in 2013 [1]. Multidrug-resistant (MDR) TB, defined as Mycobacterium [...]

Published
2015
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