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1 genes essential for growth in Mycobacterium intracellulare.
2 induce killing of intracellular M. avium-M. intracellulare.
3 es, including M. smegmatis, M. avium, and M. intracellulare.
4 The third case was caused by Mycobacterium intracellulare.
5 nical relapse/reinfection than those with M. intracellulare.
6 bes), and 3 (7%) were M. avium; none were M. intracellulare.
7 cum and M. phocaicum, and M. chimaera and M. intracellulare.
8 confidence interval = 1.25 to 22.73) than M. intracellulare.
9 Most patients (77%) had M. intracellulare.
10 stigate the public health significance of M. intracellulare.
11 ly, 130 divergent ORFs were identified in M. intracellulare.
12 avium could invade more efficiently than M. intracellulare.
13 so observed in patients infected by M. avium-intracellulare.
14 isolates from HIV-negative patients were M. intracellulare.
15 pecies Micobacterium avium and Mycobacterium intracellulare.
16 within the 16S rRNA genes of M. avium and M. intracellulare.
17 echanism of host defense against M. avium-M. intracellulare.
18 ins genetically diverse from M. avium and M. intracellulare.
19 .82 degrees C (57.05 to 58.60 degrees C); M. intracellulare, 54.46 degrees C (53.69 to 55.23 degrees
20 ecies distribution, comprising 54 (81.8%) M. intracellulare, 6 (9.1%) M. avium, 5 (7.6%) M. colombien
21 wever, concentrations of Legionella spp., M. intracellulare, Acanthamoeba spp., and M. avium peaked d
22 A marked age trend for the isolation of M. intracellulare among women was noted: 0.27% (1-fold) for
25 ing, 49 (90.7%) respiratory isolates were M. intracellulare and 4 (7.4%) were Mycobacterium chimaera.
30 Furthermore, transformants of Mycobacterium intracellulare and Mycobacterium bovis BCG carrying the
34 cobacterium avium complex (MAC; M. avium, M. intracellulare, and "nonspecific or X" MAC) are emerging
35 s, 61% were M. avium, 37% were Mycobacterium intracellulare, and 2% were species nonspecific MAC.
40 % confidence interval [CI], 1.33-3.44) or M. intracellulare (AOR, 3.12; 95% CI, 1.62-5.99) were more
45 virus type 1-infected patients, M. avium-M. intracellulare can infect almost every tissue and organ.
47 requent NTM species were Mycobacterium avium-intracellulare complex (83.2%), M. kansasii (7.7%), and
48 e identified as belonging to the M. avium-M. intracellulare complex (but not M. paratuberculosis), an
49 he rapid diagnosis of Mycobacterium avium-M. intracellulare complex (MAC) bacteremia in patients with
51 Mycobacterium simiae and Mycobacterium avium-intracellulare complex but which possesses a distinct my
52 te that the currently identified M. avium-M. intracellulare complex includes strains genetically dive
53 rate the diagnosis of Mycobacterium avium-M. intracellulare complex infections, an immunomagnetic PCR
56 al differentiation of Mycobacterium avium-M. intracellulare complex strains into M. avium and M. intr
57 26 M. tuberculosis complex, 9 M. avium, 3 M. intracellulare complex, 3 M. kansasii, 4 M. gordonae, an
58 t samples were LiPA positive for M. avium-M. intracellulare complex, and all were identified as M. in
59 rongyloides stercoralis, Mycobacterium avium-intracellulare complex, and Cryptosporidium), distal sma
60 ntiates M. tuberculosis complex, M. avium-M. intracellulare complex, and the following mycobacterial
61 ium tuberculosis complex and the M. avium-M. intracellulare complex, as well as rapid- and slow-growi
62 oupled to magnetic beads with an M. avium-M. intracellulare complex-specific PCR protocol based on 16
66 ulosis than in patients with active M. avium-intracellulare disease or other nontuberculous pulmonary
67 fingerprinting of respiratory isolates of M. intracellulare from patients with underlying bronchiecta
68 trast, 41 of the 65 (63.1%) patients with M. intracellulare had probable to definite infection, a lev
69 determine if this is true for Mycobacterium intracellulare, household water sources for 36 patients
70 h of 10 clinical isolates of M. avium and M. intracellulare identified by conventional methods were a
74 cellulare was observed only when M. avium-M. intracellulare-infected cells were treated with 10 mM H2
75 h of intracellular mycobacteria, M. avium-M. intracellulare-infected human monocytes were treated wit
76 H2O2-induced apoptotic death of M. avium-M. intracellulare-infected monocytes and its association wi
77 nt study, a long-term culture of M. avium-M. intracellulare-infected monocytes was used to further ev
79 ts suggest that, among non-AIDS patients, M. intracellulare is more pathogenic and tends to infect wo
80 tic analysis revealed a high diversity of M. intracellulare isolates and their evolutionary relations
82 ed to characterize 32 Mycobacterium avium-M. intracellulare isolates, 4 Pseudomonas aeruginosa isolat
85 apy, seven of 13 patients with Mycobacterium intracellulare lung disease had an initial microbiologic
87 line shows potential for the treatment of M. intracellulare lung disease, but optimization of treatme
88 M-PD patients due to Mycobacterium avium, M. intracellulare, M. abscessus, or M. massiliense and thre
91 ollowing mycobacterial species: M. avium, M. intracellulare, M. kansasii, M. chelonae group, M. gordo
92 tuberculosis H37Rv (TBkatG) or Mycobacterium intracellulare (MACkatG) genes into M. tuberculosis H37R
96 inhibitory effect on Mycobacterium avium-M. intracellulare (MAI) when blood collected and processed
97 llulare complex strains into M. avium and M. intracellulare may provide a tool to better understand t
98 IC assay against M. abscessus, Mycobacterium intracellulare, Mycobacterium smegmatis, and Mycobacteri
100 MycoID as being M. avium (n = 98; 61.1%), M. intracellulare (n = 57; 35.8%), and mixed M. avium and M
105 gative with species-specific M. avium and M. intracellulare probes), and 3 (7%) were M. avium; none w
106 umophila, Mycobacterium avium, Mycobacterium intracellulare, Pseudmonas aeruginosa, or Acanthamoeba s
107 ynthesized: MAV and MIN, for M. avium and M. intracellulare, respectively, and MYCOB, for the slowly
108 oas abscess secondary to Mycobacterium avium-intracellulare, septic wrist, bacteremia, and septic tot
109 red in the distinct clades separated from M. intracellulare strains originating from other countries.
115 sis presented clade-specific proteins for M. intracellulare, such as PE and PPE protein families.
116 de probes that specifically detect either M. intracellulare, the two M. avium subspecies associated w
117 We compared the abilities of M. avium and M. intracellulare to tolerate the acidic conditions of the
118 n of pretreatment and relapse isolates of M. intracellulare uncovered mutations in a previously uncha
119 ntified functions essential for growth of M. intracellulare under conditions relevant to the host env
123 duction in CFU) of intracellular M. avium-M. intracellulare was observed only when M. avium-M. intrac
126 nce of Mycobacterium avium and Mycobacterium intracellulare were analyzed in a cohort of 7,472 patien
129 However, when strains of M. avium and M. intracellulare were examined for their ability to enter
132 at were present in M. avium but absent in M. intracellulare were identified, including some that may
133 cterium tuberculosis and Mycobacterium avium-intracellulare, were compared before and after vaccinati