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1 erm(41) genotype is a useful adjunct for M. abscessus.
2 table to test antibiotic activity against M. abscessus.
3 of inhibitors against TrmD in Mycobacterium abscessus.
4 showed promising in vivo activity against M. abscessus.
5 rium avium complex (MAC) and 69 (36%) for M. abscessus.
6 bserved in M. marinum and the smallest in M. abscessus.
7 ycobacteria including M. tuberculosis and M. abscessus.
8 topic shifts from incorporation of 15N in M. abscessus.
9 enum varied from those of M. chelonae and M. abscessus.
10 solates of M. chelonae and 25 isolates of M. abscessus.
11 t distinguish Mycobacterium chelonae from M. abscessus.
12 ne sequencing to identify M. chelonae and M. abscessus.
13 tiate M. immunogenum from M. chelonae and M. abscessus.
14 ting that this clone is a subgroup within M. abscessus.
15 erial species Mycobacterium fortuitum and M. abscessus.
16 The isolates were later identified as M. abscessus.
17 ers Mycobacterium smegmatis or Mycobacterium abscessus.
18 esence of global transmission networks of M. abscessus.
19 n reliably identify cross-transmission in M. abscessus.
20 and phylogenetically close to Mycobacterium abscessus.
21 life-threatening infections of Mycobacterium abscessus.
22 of a series of indolecarboxamides against M. abscessus.
23 bination works synergistically to inhibit M. abscessus.
24 occur during chronic lung infection with M. abscessus.
25 20% of U.S. isolates of M. abscessus subsp. abscessus.
26 which we propose the name "Para-streptomyces abscessus."
27 l isolates identified 2 clonal strains of M. abscessus; 1 clone was isolated from water sources at a
28 acterized clinical isolates comprising 29 M. abscessus, 15 M. massiliense, and 2 M. bolletii isolates
32 or rapidly growing mycobacteria (98% were M. abscessus), 78% (29 of 37) for M. kansasii, and 26% (9 o
35 iduals with cystic fibrosis (CF), in whom M. abscessus accelerates inflammatory lung damage, leading
36 the 2.9- angstrom resolution structure of M. abscessus AftD, determined by single-particle cryo-elect
37 strain, independent clinical isolates of M. abscessus also readily establish infection and prolifera
39 alues for 81 isolates of M. abscessus subsp. abscessus and 12 isolates of M. abscessus subsp. massili
40 identified 41 Mycobacterium abscessus subsp. abscessus and 13 M. abscessus subsp. massiliense isolate
45 of two clonal groups for M. abscessus subsp. abscessus and five clonal groups for M. abscesssus subsp
46 reviously identified as being M. chelonae/M. abscessus and identified M. massiliense from isolates fr
47 g of M. fortuitum against clarithromycin; M. abscessus and M. chelonae against the aminoglycosides; a
50 rculosis as well as against intracellular M. abscessus and M. leprae, indicating their potential as t
51 enome, regions that discriminated between M. abscessus and M. massiliense were identified through arr
52 d three pairs of closely related strains: M. abscessus and M. massiliense, M. mucogenicum and M. phoc
53 ounds exhibit activity against planktonic M. abscessus and M. tuberculosis as well as against intrace
57 olates were typed as M. abscessus subspecies abscessus and were clonally related within each patient.
58 oscopes and endoscopic cleaning machines (M. abscessus) and contaminated hospital water supplies (M.
60 tes of N. cyriacigeorgica, N. asteroides, N. abscessus, and N. otitidiscaviarum were susceptible to t
61 bmitted as M. chelonae were identified as M. abscessus, and one isolate submitted as M. abscessus was
62 cterium fortuitum group, three Mycobacterium abscessus, and three Mycobacterium chelonae isolates) we
63 rium fortuitum group, three of Mycobacterium abscessus, and three of Mycobacterium chelonae) were tes
65 bacterial infections caused by Mycobacterium abscessus are responsible for a range of disease manifes
66 metic mean = 1.5% of hsp65 sequences) and M. abscessus (arithmetic mean = 0.006% of hsp65 sequences).
67 he hflX gene in the pathogenic Mycobacterium abscessus, as well as the nonpathogenic Mycobacterium sm
70 We report the first series of Mycobacterium abscessus bacteremia after cytokine-induced killer cell
71 tibility breakpoints for M. abscessus subsp. abscessus be changed from </=2 to </=4 mug/ml and that i
72 ly effective at preventing infection with M. abscessus because it is a ubiquitous environmental sapro
73 the direct competitive inhibition of the M. abscessus beta-lactamase, Bla(Mab), using a novel assay,
75 ot be used to infer cross-transmission in M. abscessus but does provide enough information to replace
78 s demonstrates that the inability to type M. abscessus by PFGE is associated with a single clone of o
79 of using thiourea-containing buffer with M. abscessus by studying 69 isolates not previously typeabl
80 resistance in Mycobacterium abscessus subsp. abscessus, calling into question the usefulness of macro
82 ses (57%; odds ratio = 0.7, P < 0.05) and M. abscessus cases (51%; odds ratio = 0.5, P < 0.01) than i
84 tidolipid in the outermost portion of the M. abscessus cell wall masks underlying cell wall lipids in
86 cy of this combination against a panel of M. abscessus clinical isolates, revealing the therapeutic p
88 iability and showed enhanced effects on a M. abscessus clinical strain when combined with amikacin.
89 s provides an explanation whereby initial M. abscessus colonization of abnormal lung airways escapes
93 equencing (26 isolates of the M. chelonae-M. abscessus complex and 64 remaining isolates, including M
97 ceptibility by overexpressing Bla(Mab) in M. abscessus, demonstrating relebactam-Bla(Mab) target enga
99 t support this being a major mechanism for M abscessus dissemination at a national level in England.
101 ium avium complex and 120 with Mycobacterium abscessus enrolled in the US Bronchiectasis and NTM Rese
102 trophils treated with azithromycin killed M. abscessus equally as well as untreated neutrophils from
103 g susceptibility testing, all isolates of M. abscessus exhibited resistance to tobramycin (MIC of 8 t
106 s thought to be colonized with Mycobacterium abscessus for 13 yr prior to developing clinically appar
108 del to investigate pulmonary Mycobacteroides abscessus (formerly Mycobacterium abscessus) infection i
109 g were done on 168 consecutive isolates of M abscessus from 31 patients attending an adult cystic fib
113 cobacteria (RGM), particularly Mycobacterium abscessus, from individuals with cystic fibrosis (CF) is
114 is facilitated by biofilm formation, with M. abscessus glycopeptidolipids playing an important role.
118 e M. avium complex (MAC), the M. chelonae-M. abscessus group (MCAG), the M. fortuitum group (MFG), an
119 bscessus (M. abscessus sensu lato, or the M. abscessus group) comprises three closely related taxa wh
120 Mycobacterium massiliense (Mycobacterium abscessus group) is an emerging pathogen causing pulmona
121 e erm(41) and rrl genes in the Mycobacterium abscessus group, a multiplex real-time PCR assay for cla
123 iotin cofactor synthesis was required for M. abscessus growth due to increased intracellular biotin d
124 ugh colony morphology shift in Mycobacterium abscessus has been implicated in loss of glycopeptidolip
127 ncluding M. immunogenum, M. chelonae, and M. abscessus, have been associated with nosocomial infectio
128 ch is a major virulence factor that makes M. abscessus highly cytotoxic to mouse macrophages, and tha
129 tween the smooth and rough morphotypes of M. abscessus However, in cystic fibrosis neutrophils, wortm
130 t evidence of within-patient subclones of M. abscessus in adults with CF suggests the possibility tha
135 sphate (ABL/PI5P) were tested in vitro in M. abscessus-infected macrophages from PWCF as potential tr
136 cording in the in vivo physiopathology of M. abscessus infection and emphasizes cording as a mechanis
137 We developed a mouse model of pulmonary M. abscessus infection using the aerosolized route of infec
138 c fibrosis with a disseminated Mycobacterium abscessus infection was treated with a three-phage cockt
139 from nine non-CF patients with persistent M. abscessus infection were characterized by colony morphol
140 3 drugs usually combined for treatment of M. abscessus infection, cefoxitin was the most active becau
141 Alternative routes of acquisition of M. abscessus infection, in particular the environment, requ
142 a prospective advance in the treatment of M. abscessus infection; increasing the susceptibility of th
143 acteroides abscessus (formerly Mycobacterium abscessus) infection in an immunocompetent mouse strain,
144 ty, but the transplants did not clear the M. abscessus infections and both patients died as a result
145 al isolates, we show that the majority of M. abscessus infections are acquired through transmission,
146 eria-specific diagnostic to differentiate M. abscessus infections from underlying pulmonary disease i
147 Conventional imaging cannot distinguish M. abscessus infections from underlying pulmonary disease o
149 d chemical structure class active against M. abscessus infections with promising translational develo
157 e is still conflicting evidence as to how M. abscessus is acquired and whether cross-transmission occ
160 direct patient-to-patient transmission of M. abscessus is critically important in directing an infect
161 differentiation of these two species from M. abscessus is difficult and relies on the sequencing of o
163 sts healthcare-associated transmission of M. abscessus is rare and includes a report of potential hea
167 ink and a skin biopsy) and 11 Mycobacterium abscessus isolates (5 from the implicated bottle of gray
169 ed whole-genome sequencing of 11 clinical M. abscessus isolates derived from eight U.S. patients with
170 -genome sequencing data demonstrated that M. abscessus isolates from 16 patients were unrelated, diff
171 tively sequenced the whole genomes of 145 M. abscessus isolates from 62 patients, seen at 4 hospitals
173 Whole-genome sequencing was applied to 27 M. abscessus isolates from the 20 patients in this cohort t
174 liense and 15% to 20% of M. abscessus subsp. abscessus isolates renders these species intrinsically m
175 .S. and Western European M. abscessus subsp. abscessus isolates that are genetically distinct from ot
176 Previous population studies of clinical M. abscessus isolates utilized multilocus sequence typing o
177 and 145 clinical isolates (58 MAC and 87 M. abscessus isolates), including 54 clarithromycin- and/or
178 d to the unambiguous identification of 26 M. abscessus isolates, 7 M. massiliense isolates, and 2 M.
185 cal to the CLSI guidelines for Mycobacterium abscessus: </=16 mug/ml for susceptible, 32 mug/ml for i
186 bronchiectasis and refractory Mycobacterium abscessus lung disease was treated for 6 months with a t
190 ough, wild-type human clinical isolate of M. abscessus (M. abscessus-R) and a smooth, attenuated muta
191 PCR for straightforward identification of M. abscessus, M. massiliense, and M. bolletii and the asses
192 ion and typing of 42 clinical isolates of M. abscessus, M. massiliense, and M. bolletii from patients
194 ates with ambiguous species identities as M. abscessus-M. massiliense by rpoB, hsp65, and secA sequen
195 verscores resistance and that isolates of M. abscessus/M. chelonae from CF patients are more likely t
199 M. tuberculosis (MtMetX), Mycolicibacterium abscessus (MaMetX), and Mycolicibacterium hassiacum (MhM
201 tutions in their tail spike proteins, and M. abscessus mutants resistant to TPP-independent phages re
202 were characterized in a MIC assay against M. abscessus, Mycobacterium intracellulare, Mycobacterium s
203 also in few samples containing Mycobacterium abscessus,Mycobacterium gordonae, o rMycobacterium therm
204 acteria (41%), fungi (10%) and Mycobacterium abscessus, Mycoplasma hominis and Lactobacillus sp. (one
205 ubsp. bolletii (n = 24), M. abscessus subsp. abscessus (n = 6), Mycobacterium fortuitum (n = 3), Myco
206 re used to identify 75 isolates as either M. abscessus or M. chelonae that were originally submitted
207 antimicrobial activity against Mycobacterium abscessus or Pseudomonas aeruginosa could be detected.
208 o Mycobacterium avium, M. intracellulare, M. abscessus, or M. massiliense and three healthy controls
209 who presented with multifocal Mycobacterium abscessus osteomyelitis (patient 1) and disseminated CMV
211 ulous mycobacteria, especially Mycobacterium abscessus, post-transplantation survival has not been de
213 y (PET) was performed in a mouse model of M. abscessus pulmonary infection and in a patient with micr
214 s for initial proliferation and sustained M. abscessus pulmonary infection and permits evaluation of
215 ynamic (11)C-PABA PET in a mouse model of M. abscessus pulmonary infection rapidly distinguished infe
216 fibrosis and microbiologically confirmed M. abscessus pulmonary infection was safe and demonstrated
218 erved that the increased virulence of the M. abscessus R variant compared with the S variant correlat
219 ast-mycobacterium microcolony assay, with M. abscessus-R exhibiting growth characteristics similar to
220 phagocyte aggregates develop at sites of M. abscessus-R infection, but are absent with M. abscessus-
224 e human clinical isolate of M. abscessus (M. abscessus-R) and a smooth, attenuated mutant (M. abscess
228 reported for virulent M. tuberculosis and M. abscessus-S exhibiting growth characteristics similar to
232 clude that a mutation has occurred in the M. abscessus-S variant which has altered the ability of thi
233 essus-R) and a smooth, attenuated mutant (M. abscessus-S) which spontaneously dissociated from the cl
236 onomic statuses are under revision, i.e., M. abscessus sensu stricto, Mycobacterium bolletii, and Myc
237 cobacterium immunogenum, M. chelonae, and M. abscessus, showed various susceptibilities to the glutar
238 udy we demonstrate that rough variants of M. abscessus stimulate the human macrophage innate immune r
240 ives that efficiently kill the infectious M. abscessus strain were developed by genome engineering an
241 ern) occurs with almost 50% of Mycobacterium abscessus strains during pulsed-field gel electrophoresi
242 We found that patients acquired unique M. abscessus strains even after spending considerable time
243 xplores the genomic diversity of clinical M. abscessus strains from multiple continents and provides
244 om 3 confirmed infections grew Mycobacterium abscessus strains that were indistinguishable by pulsed-
245 PCR can be used for genetic comparison of M. abscessus strains, including strains which cannot be com
246 of a patient with disseminated Mycobacterium abscessus, Streptococcus viridians bacteremia, and cytom
248 urate approach for discriminating MAC and M. abscessus (sub)species and for detecting clarithromycin
254 erium abscessus subsp. bolletii (n = 24), M. abscessus subsp. abscessus (n = 6), Mycobacterium fortui
255 tedizolid MIC90 values for 81 isolates of M. abscessus subsp. abscessus and 12 isolates of M. abscess
256 bases accurately identified 41 Mycobacterium abscessus subsp. abscessus and 13 M. abscessus subsp. ma
257 ted the presence of two clonal groups for M. abscessus subsp. abscessus and five clonal groups for M.
258 ithromycin susceptibility breakpoints for M. abscessus subsp. abscessus be changed from </=2 to </=4
260 ssus subsp. massiliense and 15% to 20% of M. abscessus subsp. abscessus isolates renders these specie
261 closely related U.S. and Western European M. abscessus subsp. abscessus isolates that are genetically
263 ucible macrolide resistance in Mycobacterium abscessus subsp. abscessus, calling into question the us
265 The species identified were Mycobacterium abscessus subsp. bolletii (n = 24), M. abscessus subsp.
266 eregrinum and a nonfunctional erm gene in M. abscessus subsp. massiliense and 15% to 20% of M. absces
267 cterium abscessus subsp. abscessus and 13 M. abscessus subsp. massiliense isolates identified by whol
268 essus subsp. abscessus and 12 isolates of M. abscessus subsp. massiliense were 8 mug/ml and 4 mug/ml,
270 vium complex (MAC) species and Mycobacterium abscessus subspecies and for determining clarithromycin
271 utbreaks of near-identical isolates of the M abscessus subspecies massiliense (from 11 patients), dif
273 patient with a drug-resistant Mycobacterium abscessus suggests that phages may have considerable pot
274 eased cell envelope fluidity and promoted M. abscessus survival in the alkaline lung environment.
275 ients with genetically related strains of M. abscessus that had been previously typed by variable-num
276 genome sequencing (WGS) on 32 isolates of M. abscessus that were taken from multiple body sites of 2
277 monstrated for the fast grower Mycobacterium abscessus, the compound is potent in vitro and in vivo,
278 patients in this study have not acquired M. abscessus through direct patient-to-patient transmission
279 and spread of the environmental organism M. abscessus through the global cystic fibrosis population,
282 smear patterns were identical to those of M. abscessus type strain ATCC 19977, which had a nonsmear p
284 t respiratory epithelial cells respond to M. abscessus variants lacking GPL with expression of IL-8 a
285 ese studies increase our understanding of M. abscessus virulence and of neutrophil mycobactericidal m
291 s a significant resistance determinant in M. abscessus We demonstrate that mycobacterial HflX associa
292 Mycobacterium species -- M. smegmatis and M. abscessus -- we demonstrate a striking conservation of t
294 ncident NTM infections from either MAC or M. abscessus were less likely to have had chronic azithromy
296 Several bacterial species, including M. abscessus, were cultured from an opened multidose supple
298 uberculous mycobacterium (NTM) Mycobacterium abscessus, which causes progressive lung damage and is e
299 ncing of the erm gene of M. abscessus subsp. abscessus will predict inducible macrolide susceptibilit
300 ve not demonstrated cross-transmission of M. abscessus within our hospital, except between 1 sibling