reference strain m abscessus atcc 19977 t  (ATCC)

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Naftifine inhibits intracellular M. abscessus growth in a concentration- and time-dependent manner. THP-1 macrophages were infected with ( A ) ATCC 19977 T smooth variant, ( B ) ATCC 19977 T rough variant, and clinical isolates ( C ) 23-S-10, ( D ) 23-S-12, and ( E ) 23-S-13. The ATCC 19977 T strains are sensitive to both clarithromycin and amikacin, while the clinical isolates are resistant to both antibiotics. Following infection, cells were treated with increasing concentrations of naftifine (3–90 μM) or 10 μM clarithromycin as a control. Intracellular bacterial burden was quantified by CFU enumeration at 24, 48, and 72 hours post-treatment. Data represent mean ± SD from three independent experiments. Statistical significance was determined by two-way ANOVA with Tukey’s multiple comparisons test for comparisons between each naftifine concentration and the DMSO control at corresponding time points. ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: The reference strain M. abscessus ATCC 19977 T was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Concentration Assay, Infection, Variant Assay, Control

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Dose-dependent cytotoxicity analysis in uninfected and M. abscessus -infected cells. ( A ) Representative flow cytometry dot plots show Annexin V and 7-AAD staining patterns in uninfected (UI) and infected (IN) cells treated with increasing concentrations (0, 10, 30, and 90 μM) of the test compound. THP-1 cells were infected with M. abscessus ATCC 19977 T smooth variants and treated with naftifine for 3 days. Gated regions indicate dead cells (Annexin V + , including early and late apoptotic and necrotic populations). ( B and C ) Quantification of cell death shows the percentage of Annexin V + population (both 7-AAD + and 7-AAD⁻) in uninfected ( B ) and infected ( C ) cells. Data represent mean ± SEM from at least three independent experiments. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons against the control. ** P < 0.01 and **** P < 0.0001 compared to untreated control (0 μM).

Article Snippet: The reference strain M. abscessus ATCC 19977 T was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Infection, Flow Cytometry, Staining, Control

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Naftifine exhibits bacteriostatic activity against M. abscessus in axenic culture. Time-kill assays were performed to evaluate the antimicrobial activity of naftifine against different M. abscessus strains and morphological variants. ( A ) ATCC 19977 T smooth variant, ( B ) ATCC 19977 T rough variant, and clinical isolates ( C ) 23-S-10, ( D ) 23-S-12, and ( E ) 23-S-13. The ATCC 19977 T strains are sensitive to both clarithromycin and amikacin, while the clinical isolates are resistant to both antibiotics. Bacterial cultures in logarithmic growth phase were treated with naftifine at concentrations ranging from 2 to 64 µg/mL (equivalent to 6–198 μM) or DMSO vehicle control. Samples were collected at 24-hour intervals over a 96-hour incubation period, and bacterial viability was assessed by CFU enumeration following serial dilution plating. Data represent mean ± SEM from two independent experiments performed in triplicate. Statistical comparisons between naftifine-treated and DMSO control at each time point were performed using two-way ANOVA with Tukey’s multiple comparisons test. Statistical significance is indicated as * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: The reference strain M. abscessus ATCC 19977 T was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Activity Assay, Variant Assay, Control, Incubation, Serial Dilution

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Naftifine reduces M. abscessus burden in the lungs and spleens of immunosuppressed mice. BALB/c mice were immunosuppressed with dexamethasone and subsequently infected intranasally with 1,000 CFU of M. abscessus ATCC 19977 T rough variant. Treatment began 3 days post-infection and continued once daily for 14 days. Mice received either naftifine HCl (50 mg/kg of body weight, intraperitoneal), cefoxitin (200 mg/kg of body weight, subcutaneous, positive control), or PBS vehicle control (intraperitoneal). After the treatment period, mice were euthanized, and bacterial loads in the ( A ) lungs and ( B ) spleens were quantified by CFU enumeration and expressed as log 10 CFU per organ. Data represent individual mice with mean ± SEM. ( C ) Representative hematoxylin and eosin-stained lung sections from infected mice treated with PBS vehicle control (top panels) or naftifine (bottom panels) are shown at 4×, 10×, and 40× magnifications to illustrate histopathological changes. Statistical comparisons between treatment groups were performed with the Kruskal–Wallis test followed by Dunn’s multiple comparisons test. * P < 0.05; ** P < 0.01; *** P < 0.001 and ns, not significant.

Article Snippet: The reference strain M. abscessus ATCC 19977 T was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Infection, Variant Assay, Positive Control, Control, Staining

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Autophagy contributes to the intracellular efficacy of naftifine against M. abscessus . Intracellular bacterial survival (log 10 CFU) of ( A ) naftifine-sensitive M. abscessus ATCC 19977 T S (Mab S, blue) strain and naftifine-resistant M. abscessus strain (Mab-Naft R1, red) in wild-type RAW 264.7 macrophages (filled circles) or ( B ) ATG16L1 knockdown macrophages (open circles) treated with naftifine at 0, 5, 10, and 20 µM. Bacterial loads were quantified on days 1 (D1) and 2 (D2) post-infection. ( C and D ) Representative immunoblots showing LC3-I/LC3-II expression and β-actin (loading control) in macrophage lysates at day 1 post-infection with ( C ) Mab-Naft S or ( D ) Mab-Naft R1, treated with indicated naftifine concentrations (μM). Data represent mean ± SEM. Statistical significance was determined by two-way ANOVA. ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: The reference strain M. abscessus ATCC 19977 T was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Knockdown, Infection, Western Blot, Expressing, Control

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Synergistic interactions between naftifine and β-lactam antibiotics against M. abscessus . Checkerboard assays were performed to evaluate drug interactions between naftifine ( y -axis) and various antibiotics ( x -axis) against M. abscessus ATCC 19977 T smooth variant. Heat maps display the percentage of bacterial growth, with darker blue indicating greater growth. Twofold serial dilutions of each drug were tested in combination, and growth inhibition was assessed after incubation. Naftifine showed indifferent interactions with clarithromycin ( A ) and tigecycline ( E ), additive/partial synergistic effects with amikacin ( B ), but demonstrated synergistic effects when combined with the β-lactam antibiotics cefoxitin ( C ) and imipenem ( D ), particularly at sub-inhibitory concentrations. Synergy was defined as FICI ≤ 0.5, where the combined effect significantly exceeded the sum of individual drug activities. Data were analyzed and plotted using GraphPad Prism version 10.

Article Snippet: The reference strain M. abscessus ATCC 19977 T was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Variant Assay, Inhibition, Incubation

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Naftifine inhibits intracellular M. abscessus growth in a concentration- and time-dependent manner. THP-1 macrophages were infected with ( A ) ATCC 19977 T smooth variant, ( B ) ATCC 19977 T rough variant, and clinical isolates ( C ) 23-S-10, ( D ) 23-S-12, and ( E ) 23-S-13. The ATCC 19977 T strains are sensitive to both clarithromycin and amikacin, while the clinical isolates are resistant to both antibiotics. Following infection, cells were treated with increasing concentrations of naftifine (3–90 μM) or 10 μM clarithromycin as a control. Intracellular bacterial burden was quantified by CFU enumeration at 24, 48, and 72 hours post-treatment. Data represent mean ± SD from three independent experiments. Statistical significance was determined by two-way ANOVA with Tukey’s multiple comparisons test for comparisons between each naftifine concentration and the DMSO control at corresponding time points. ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: The tested strains included the reference ATCC 19977 T strain in both smooth and rough morphotypes and clinical isolates of M. abscessus subsp. abscessus harboring mutations that confer resistance to amikacin and clarithromycin ( ).

Techniques: Concentration Assay, Infection, Variant Assay, Control

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Dose-dependent cytotoxicity analysis in uninfected and M. abscessus -infected cells. ( A ) Representative flow cytometry dot plots show Annexin V and 7-AAD staining patterns in uninfected (UI) and infected (IN) cells treated with increasing concentrations (0, 10, 30, and 90 μM) of the test compound. THP-1 cells were infected with M. abscessus ATCC 19977 T smooth variants and treated with naftifine for 3 days. Gated regions indicate dead cells (Annexin V + , including early and late apoptotic and necrotic populations). ( B and C ) Quantification of cell death shows the percentage of Annexin V + population (both 7-AAD + and 7-AAD⁻) in uninfected ( B ) and infected ( C ) cells. Data represent mean ± SEM from at least three independent experiments. Statistical significance was determined by one-way ANOVA followed by Dunnett’s post hoc test for multiple comparisons against the control. ** P < 0.01 and **** P < 0.0001 compared to untreated control (0 μM).

Article Snippet: The tested strains included the reference ATCC 19977 T strain in both smooth and rough morphotypes and clinical isolates of M. abscessus subsp. abscessus harboring mutations that confer resistance to amikacin and clarithromycin ( ).

Techniques: Infection, Flow Cytometry, Staining, Control

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Naftifine exhibits bacteriostatic activity against M. abscessus in axenic culture. Time-kill assays were performed to evaluate the antimicrobial activity of naftifine against different M. abscessus strains and morphological variants. ( A ) ATCC 19977 T smooth variant, ( B ) ATCC 19977 T rough variant, and clinical isolates ( C ) 23-S-10, ( D ) 23-S-12, and ( E ) 23-S-13. The ATCC 19977 T strains are sensitive to both clarithromycin and amikacin, while the clinical isolates are resistant to both antibiotics. Bacterial cultures in logarithmic growth phase were treated with naftifine at concentrations ranging from 2 to 64 µg/mL (equivalent to 6–198 μM) or DMSO vehicle control. Samples were collected at 24-hour intervals over a 96-hour incubation period, and bacterial viability was assessed by CFU enumeration following serial dilution plating. Data represent mean ± SEM from two independent experiments performed in triplicate. Statistical comparisons between naftifine-treated and DMSO control at each time point were performed using two-way ANOVA with Tukey’s multiple comparisons test. Statistical significance is indicated as * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: The tested strains included the reference ATCC 19977 T strain in both smooth and rough morphotypes and clinical isolates of M. abscessus subsp. abscessus harboring mutations that confer resistance to amikacin and clarithromycin ( ).

Techniques: Activity Assay, Variant Assay, Control, Incubation, Serial Dilution

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Naftifine reduces M. abscessus burden in the lungs and spleens of immunosuppressed mice. BALB/c mice were immunosuppressed with dexamethasone and subsequently infected intranasally with 1,000 CFU of M. abscessus ATCC 19977 T rough variant. Treatment began 3 days post-infection and continued once daily for 14 days. Mice received either naftifine HCl (50 mg/kg of body weight, intraperitoneal), cefoxitin (200 mg/kg of body weight, subcutaneous, positive control), or PBS vehicle control (intraperitoneal). After the treatment period, mice were euthanized, and bacterial loads in the ( A ) lungs and ( B ) spleens were quantified by CFU enumeration and expressed as log 10 CFU per organ. Data represent individual mice with mean ± SEM. ( C ) Representative hematoxylin and eosin-stained lung sections from infected mice treated with PBS vehicle control (top panels) or naftifine (bottom panels) are shown at 4×, 10×, and 40× magnifications to illustrate histopathological changes. Statistical comparisons between treatment groups were performed with the Kruskal–Wallis test followed by Dunn’s multiple comparisons test. * P < 0.05; ** P < 0.01; *** P < 0.001 and ns, not significant.

Article Snippet: The tested strains included the reference ATCC 19977 T strain in both smooth and rough morphotypes and clinical isolates of M. abscessus subsp. abscessus harboring mutations that confer resistance to amikacin and clarithromycin ( ).

Techniques: Infection, Variant Assay, Positive Control, Control, Staining

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Autophagy contributes to the intracellular efficacy of naftifine against M. abscessus . Intracellular bacterial survival (log 10 CFU) of ( A ) naftifine-sensitive M. abscessus ATCC 19977 T S (Mab S, blue) strain and naftifine-resistant M. abscessus strain (Mab-Naft R1, red) in wild-type RAW 264.7 macrophages (filled circles) or ( B ) ATG16L1 knockdown macrophages (open circles) treated with naftifine at 0, 5, 10, and 20 µM. Bacterial loads were quantified on days 1 (D1) and 2 (D2) post-infection. ( C and D ) Representative immunoblots showing LC3-I/LC3-II expression and β-actin (loading control) in macrophage lysates at day 1 post-infection with ( C ) Mab-Naft S or ( D ) Mab-Naft R1, treated with indicated naftifine concentrations (μM). Data represent mean ± SEM. Statistical significance was determined by two-way ANOVA. ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: The tested strains included the reference ATCC 19977 T strain in both smooth and rough morphotypes and clinical isolates of M. abscessus subsp. abscessus harboring mutations that confer resistance to amikacin and clarithromycin ( ).

Techniques: Knockdown, Infection, Western Blot, Expressing, Control

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Protective mechanism of action of the antifungal drug naftifine against Mycobacterium abscessus infection

doi: 10.1128/aac.01105-25

Figure Lengend Snippet: Synergistic interactions between naftifine and β-lactam antibiotics against M. abscessus . Checkerboard assays were performed to evaluate drug interactions between naftifine ( y -axis) and various antibiotics ( x -axis) against M. abscessus ATCC 19977 T smooth variant. Heat maps display the percentage of bacterial growth, with darker blue indicating greater growth. Twofold serial dilutions of each drug were tested in combination, and growth inhibition was assessed after incubation. Naftifine showed indifferent interactions with clarithromycin ( A ) and tigecycline ( E ), additive/partial synergistic effects with amikacin ( B ), but demonstrated synergistic effects when combined with the β-lactam antibiotics cefoxitin ( C ) and imipenem ( D ), particularly at sub-inhibitory concentrations. Synergy was defined as FICI ≤ 0.5, where the combined effect significantly exceeded the sum of individual drug activities. Data were analyzed and plotted using GraphPad Prism version 10.

Article Snippet: The tested strains included the reference ATCC 19977 T strain in both smooth and rough morphotypes and clinical isolates of M. abscessus subsp. abscessus harboring mutations that confer resistance to amikacin and clarithromycin ( ).

Techniques: Variant Assay, Inhibition, Incubation

Journal: BMC Infectious Diseases

Article Title: A real-time PCR assay for rapid identification of inducible and acquired clarithromycin resistance in Mycobacterium abscessus

doi: 10.1186/s12879-020-05686-0

Figure Lengend Snippet: Clarithromycin Minimum Inhibitory Concentration (MIC) interpretations for M. abscessus isolates

Article Snippet: Reference strains Mycobacterium abscessus subsp. abscessus ATCC 19977 T , Mycobacterium abscessus subsp. bolletii CCUG 50184 T , and Mycobacterium abscessus subsp. massiliense CCUG 48898 T were used.

Techniques: Concentration Assay

Journal: BMC Infectious Diseases

Article Title: A real-time PCR assay for rapid identification of inducible and acquired clarithromycin resistance in Mycobacterium abscessus

doi: 10.1186/s12879-020-05686-0

Figure Lengend Snippet: Example of the amplification plot for a sample showing detection of a full-length erm (41) with the T allele and a wildtype rrl gene (Probe TRNC1 detects full-length erm (41) and allows us to determine if the gene is truncated or full-length, 16sabsc verifies M. abscessus identification and near neighbors, T28T and T28C detects the 2 alleles on position 28 of erm (41), and 2058Crrl and WTrrl for alleles on rrl )

Article Snippet: Reference strains Mycobacterium abscessus subsp. abscessus ATCC 19977 T , Mycobacterium abscessus subsp. bolletii CCUG 50184 T , and Mycobacterium abscessus subsp. massiliense CCUG 48898 T were used.

Techniques: Amplification

Journal: Emerging Infectious Diseases

Article Title: High-level Relatedness among Mycobacterium abscessus subsp. massiliense Strains from Widely Separated Outbreaks

doi: 10.3201/eid2003.131106

Figure Lengend Snippet: Twenty-four Mycobacterium abscessus group strain genomes analyzed for genetic relatedness*

Article Snippet: To replicate data from the Papworth cystic fibrosis outbreak clusters 1 and 2 ( ) by using a similar approach, we mapped sequencing reads from the subset of 6 Papworth isolates, together with reads with from the 3 Seattle cystic fibrosis isolates and soft tissue strain CRM-0020 from Brazil , onto the M. abscessus type strain ATCC 19977 T reference genome by using BWA software ( ).

Techniques:

Journal: Emerging Infectious Diseases

Article Title: High-level Relatedness among Mycobacterium abscessus subsp. massiliense Strains from Widely Separated Outbreaks

doi: 10.3201/eid2003.131106

Figure Lengend Snippet: Neighbor-joining phylogenetic tree based on whole-genome multiple alignment of 24 Mycobacterium abscessus group genomes. Genomes in were aligned by using Mugsy , core segments of the alignment were identified by using Phylomark , and resulting concatenated nucleotide sequences were used for construction of the midpoint-rooted neighbor-joining phylogenetic tree by using MEGA . Strains from an outbreak of M. abscessus subsp. massiliense infections at a cystic fibrosis center in Seattle, Washington, USA, are indicated in red; strains from an outbreak of M. abscessus subsp. massiliense infections at a cystic fibrosis center in Papworth, UK, are indicated in blue (cluster 1) and purple (cluster 2); strains from Brazil are indicated in magenta; and the M. abscessus subsp. massiliense type strain is indicated in green. Boostrap values obtained after 100 iterations were ≥97 for all nodes of the tree except 70 for the node separating strain M115 from the outbreak cluster and 40 and 41 for 2 nodes within the Papworth cluster 1 . SNPs, single-nucleotide polymorphisms.

Article Snippet: To replicate data from the Papworth cystic fibrosis outbreak clusters 1 and 2 ( ) by using a similar approach, we mapped sequencing reads from the subset of 6 Papworth isolates, together with reads with from the 3 Seattle cystic fibrosis isolates and soft tissue strain CRM-0020 from Brazil , onto the M. abscessus type strain ATCC 19977 T reference genome by using BWA software ( ).

Techniques:

Journal: Emerging Infectious Diseases

Article Title: High-level Relatedness among Mycobacterium abscessus subsp. massiliense Strains from Widely Separated Outbreaks

doi: 10.3201/eid2003.131106

Figure Lengend Snippet: Venn diagram of core single-nucleotide polymorphisms (SNPs) shared by outbreak localities. Core segments of the Mugsy alignment of the 20 Mycobacterium abscessus subsp. massiliense genomes were parsed for SNPs shared by different subsets of outbreak localities. Each field in the Venn diagram represents nucleotides that are identical among isolates of that field but different in other isolates represented on the diagram and non–outbreak-related M. abscessus subsp. massiliense strains 1S-151–0930, 5S-0817, M115, M139, M154, and the type strain CCUG 48898 T . Details on SNPs and genes they affect are shown in the .

Article Snippet: To replicate data from the Papworth cystic fibrosis outbreak clusters 1 and 2 ( ) by using a similar approach, we mapped sequencing reads from the subset of 6 Papworth isolates, together with reads with from the 3 Seattle cystic fibrosis isolates and soft tissue strain CRM-0020 from Brazil , onto the M. abscessus type strain ATCC 19977 T reference genome by using BWA software ( ).

Techniques:

Journal: Emerging Infectious Diseases

Article Title: High-level Relatedness among Mycobacterium abscessus subsp. massiliense Strains from Widely Separated Outbreaks

doi: 10.3201/eid2003.131106

Figure Lengend Snippet: Detection of rpoB and secA1 SNP signature in the Mycobacterium abscessus group and rapidly growing mycobacteria*

Article Snippet: To replicate data from the Papworth cystic fibrosis outbreak clusters 1 and 2 ( ) by using a similar approach, we mapped sequencing reads from the subset of 6 Papworth isolates, together with reads with from the 3 Seattle cystic fibrosis isolates and soft tissue strain CRM-0020 from Brazil , onto the M. abscessus type strain ATCC 19977 T reference genome by using BWA software ( ).

Techniques: In Silico

Journal: Emerging Infectious Diseases

Article Title: High-level Relatedness among Mycobacterium abscessus subsp. massiliense Strains from Widely Separated Outbreaks

doi: 10.3201/eid2003.131106

Figure Lengend Snippet: Neighbor-joining phylogenetic tree based on 13-target multilocus sequences types from 20 Mycobacterium abscessus subsp. massiliense genomes. Electronic PCR was performed on the M. abscessus subsp. massiliense genomes listed in by using primer pairs for 13 housekeeping genes ( cya , gdhA , argH , glpK , gnd , murC , pgm , pknA , pta , pur , rpoB , hsp65 , and secA1 ), including new primers designed as part of this study. Nucleotide sequences from each gene were concatenated for each genome and aligned by using ClustalW , and the core alignment was used for construction of a midpoint-rooted neighbor-joining phylogenetic tree by using MEGA . Strains from an outbreak of M. abscessus subsp. massiliense infections at a cystic fibrosis center in Seattle, Washington, USA, are indicated in red; strains from an outbreak of M. abscessus subsp. massiliense infections at a cystic fibrosis center in Papworth, UK, are indicated in blue (cluster 1) and purple (cluster 2); strains from Brazil are indicated in magenta; and the M. abscessus subsp. massiliense type strain is indicated in green. The longer branch length for Papworth isolate 12c was caused by low-quality nucleotides (single-nucleotide polymorphisms [SNPs]) located at the edge of Velvet contigs.

Article Snippet: To replicate data from the Papworth cystic fibrosis outbreak clusters 1 and 2 ( ) by using a similar approach, we mapped sequencing reads from the subset of 6 Papworth isolates, together with reads with from the 3 Seattle cystic fibrosis isolates and soft tissue strain CRM-0020 from Brazil , onto the M. abscessus type strain ATCC 19977 T reference genome by using BWA software ( ).

Techniques: