ライフサイエンスコーパス: avium

1 atment, and contamination with Mycobacterium avium.

2 ed in B. pertussis, B. parapertussis, and B. avium.

3 to yet distinguishable from M. avium subsp. avium.

4 by reinfection with a separate isolate of M. avium.

5 from the 448 included patients, 54% were M. avium, 18% were M. intracellulare, and 28% were M. chima

6 cobacterium mucogenicum (52%), Mycobacterium avium (30%), and Mycobacterium gordonae (25%).

7 nd to be identical to S(1)-RNase from Prunus avium, a species that does not interbreed with P. tenell

8 atients whose isolates were identified as M. avium (adjusted odds ratio [AOR], 2.14; 95% confidence i

9 B. avium agglutinates guinea pig erythrocytes via an unknow

10 The region is unique for M. avium and is not present in M. tuberculosis or M. paratu

11 intracellulare (n = 57; 35.8%), and mixed M. avium and M. intracellulare (n = 2; 1.3%).

12 um-M. intracellulare complex strains into M. avium and M. intracellulare may provide a tool to better

13 probe but negative with species-specific M. avium and M. intracellulare probes), and 3 (7%) were M.

14 mycobacterial activity against Mycobacterium avium and Mycobacterium bovis Bacille Calmette-Guerin (B

15 cattle infected with either M. avium subsp. avium and Mycobacterium bovis were exposed to the array

16 , a major surface component of Mycobacterium avium and other non-tuberculosis mycobacteria, are ligan

17 is growing evidence that the incidence of M. avium and related nontuberculous species is increasing i

18 aused by Pneumocystis carinii, Mycobacterium avium, and Campylobacter coli that required euthanasia b

19 , E. casseliflavus, E. faecium, E. hirae, E. avium, and E. durans, respectively.

20 Legionella pneumophila, Mycobacterium avium, and Pseudomonas aeruginosa are opportunistic prem

21 ogens (Legionella pneumophila, Mycobacterium avium, and Pseudomonas aeruginosa), broader genera (Legi

22 dy we isolated different GPL species from M. avium, and using mass spectrometry and NMR analyses, cha

23 Patients treated for infections with M. avium (AOR, 5.64; 95% CI, 1.51-21.10) and M. chimaera (A

24 (-/-) mice are as resistant to Mycobacterium avium as Rag2(-/-) mice, whereas Rag2(-/-) mice lacking

25 nfection with a highly virulent strain of M. avium, but not with a low-virulence strain, led to a pro

26 Mycobacterium tuberculosis and Mycobacterium avium can complement lpqM donor mutants, suggesting that

27 Bordetella avium causes bordetellosis in birds, a disease similar t

28 Sequence of six M. avium clones identified one gene involved in glycopeptid

29 hat in self-incompatible species, such as P. avium, close neighbours may be pollinated by very differ

30 case of recurrent disseminated Mycobacterium avium complex (DMAC) disease with anti-gamma interferon

31 64%) were culture-positive for Mycobacterium avium complex (MAC) and 69 (36%) for M. abscessus.

32 A gene target for rapid identification of M. avium complex (MAC) and a region of the heat shock prote

33 drug used for the treatment of Mycobacterium avium complex (MAC) disease, but standard laboratory gui

34 pportunistic infections due to Mycobacterium avium complex (MAC) have been less common since the intr

35 Persistent growth of Mycobacterium avium complex (MAC) in the lungs indicates continuous in

36 The Mycobacterium avium complex (MAC) is an important group of opportunist

37 Lung disease caused by Mycobacterium avium complex (MAC) is increasing in prevalence.

38 r sources for 36 patients with Mycobacterium avium complex (MAC) lung disease were evaluated.

39 uate relapses in patients with Mycobacterium avium complex (MAC) lung disease, but the "gold standard

40 avitary nodular bronchiectatic Mycobacterium avium complex (MAC) lung disease, supporting data are li

41 Organisms within the Mycobacterium avium complex (MAC) may have differential virulence.

42 Mycobacterium avium complex (MAC) within macrophages undergoes a pheno

43 bacterium tuberculosis complex (MTC), the M. avium complex (MAC), the M. chelonae-M. abscessus group

44 cies, including members of the Mycobacterium avium complex (MAVC).

45 r syndrome, monocytopenia with Mycobacterium avium complex (MonoMAC), and MDS.

46 nontuberculous mycobacterial (Mycobacterium avium complex [MAC] or Mycobacterium abscessus) disease.

47 One hundred isolates of Mycobacterium avium complex and eight M. simiae isolates had tedizolid

48 These results suggest that members of the M. avium complex have a novel mechanism for activating cyto

49 V-infected patients, unmasking Mycobacterium avium complex infection after starting antiretroviral th

50 ycobacterium tuberculosis, M. leprae, and M. avium complex infections.

51 for susceptibility testing of Mycobacterium avium complex isolates against clarithromycin.

52 eem not to be risk factors for Mycobacterium avium complex lung disease in HIV-negative adults, but p

53 Mycobacterium avium complex lung disease is an increasingly common and

54 oing standard macrolide-based therapy for M. avium complex lung disease were monitored at standard fr

55 candidiasis, and disseminated Mycobacterium avium complex or Mycobacterium kansasii infection.

56 Ten of 639 MGIT cultures grew Mycobacterium avium complex or Mycobacterium kansasii, half of which w

57 y treated for tuberculosis and Mycobacterium avium complex predominated (27.7% [95% CI: 27.2-28.9%]).

58 Mycobacterium avium complex was concomitantly isolated in two cases, a

59 of positive cultures were for Mycobacterium avium complex, although this ranged by state, from 29% i

60 r Cryptococcus, 10% (1/10) for Mycobacterium avium complex, and 4% (3/72) for PCP.

61 acterium tuberculosis complex, Mycobacterium avium complex, and Mycobacterium spp. directly from clin

62 hold water/biofilm isolates of Mycobacterium avium could be matched by DNA fingerprinting.

63 this important receptor, and suggest that M. avium could potentially modify its GPL structure to limi

64 ly endemic varieties of sweet cherry (Prunus avium): cv. 'Spatbraune von Purbach', cv. 'Early Rivers'

65 Antiserum to HagB, but not HagA, blocked B. avium erythrocyte agglutination and explanted turkey tra

66 M. avium express glycopeptidolipids (GPLs) as a major cell

67 suggesting that released exosomes contain M. avium-expressed TLR ligands.

68 is activation is regulated in part by the M. avium fadD2 gene.

69 eumophila from recolonizing biofilms, but M. avium gene numbers increased by 0.14-0.76 logs in the bu

70 To identify M. avium genes and host cell pathways involved in the bacte

71 with 58% of G+C content versus 69% in the M. avium genome.

72 m a nonTB species of the genus Mycobacterium avium grown in liquid culture media.

73 ed Rag2(-/-)gammac(-/-) animals increased M. avium growth in the liver.

74 Studies with M. avium have shown that cytoskeletal rearrangement via act

75 tion induced by infection with Mycobacterium avium in human primary macrophages.

76 uted to decreased intracellular growth of M. avium in primary human macrophages that was reconstitute

77 RNA-mediated knockdown of Keap1 increased M. avium-induced expression of inflammatory cytokines and t

78 Interestingly, exosomes isolated from M. avium-infected but not from uninfected macrophages can s

79 the control of inflammatory signaling in M. avium-infected human primary macrophages.

80 In the present study we show that M. avium-infected macrophages release GPLs, which are traff

81 Here, we show that Mycobacterium avium-infected T cell-deficient mice injected with CD4 T

82 of experimentally inducible IRIS in which M. avium-infected T cell-deficient mice undergo a fatal inf

83 N-gamma and can confer protection against M. avium infection in immunocompromised mice.

84 years of age or older were more prone to M. avium infection than younger women or men of all ages we

85 term repopulating HSCs proliferate during M. avium infection, and that this response requires interfe

86 sing an in vivo mouse model of Mycobacterium avium infection, that an increased proportion of long-te

87 Using the mouse model of Mycobacterium avium infection, we show in this study that the producti

88 M. avium infects macrophages and actively interfere with th

89 ecies do cause human infections, and that M. avium infects mainly postmenopausal women.

90 d be facilitated growth of pathogens like M. avium inside macrophages.

91 To understand M. avium interaction with two evolutionarily distinct hosts

92 15.8%), M triplex in 1 patient (5.3%), and M avium intracellulare in 1 patient (5.3%).

93 Mycobacterium avium is a major opportunistic pathogen in HIV-positive

94 Mycobacterium avium is abundant in the environment.

95 M. avium isolates were significantly more likely to be asso

96 he development of SGS in wild cherry (Prunus avium L).

97 xidant capacities of 24 sweet cherry (Prunus avium L.) cultivars grown on the mountainsides of the Et

98 Fifteen sweet cherry (Prunus avium L.) old cultivars grown in the Czech Republic were

99 age/shipping quality of sweet cherry (Prunus avium L.), the effect of calcium chloride (CaCl2) added

100 f red-fleshed sweet cherry cultivars (Prunus avium; Lapins, Stella, Sweetheart and Staccato), with di

101 Mycobacterium avium (M. avium) subspecies vary widely in both pathogen

102 ma gondii (T. gondii, tg), and Mycobacterium avium (M. avium, ma) are the principal causes of morbidi

103 repeatedly positive for NTMs, the species M. avium, M. mucogenicum, and Mycobacterium abscessus were

104 better understand the role of Mycobacterium avium-M. intracellulare complex isolates in human diseas

105 The 159 Mycobacterium avium-M. intracellulare complex isolates were further id

106 Additional differentiation of Mycobacterium avium-M. intracellulare complex strains into M. avium an

107 (T. gondii, tg), and Mycobacterium avium (M. avium, ma) are the principal causes of morbidity and mor

108 cells was highly similar, suggesting that M. avium might have evolved mechanisms that are used to ent

109 M. avium mmpL4 proteins were found to bind to VDAC-1 protei

110 fferent mycobacterial strains (Mycobacterium avium, Mycobacterium bovis BCG or Mtb), were exposed to

111 6S rRNA gene A1408G mutation and included M. avium, Mycobacterium intracellulare, and Mycobacterium c

112 spp., Legionella pneumophila, Mycobacterium avium, Mycobacterium intracellulare, Pseudmonas aerugino

113 Mycobacterium avium, Mycobacterium tuberculosis, and Mycobacterium kan

114 d to the species level by MycoID as being M. avium (n = 98; 61.1%), M. intracellulare (n = 57; 35.8%)

115 To investigate whether M. avium needs to attach to the internal surface of the vac

116 . intracellulare probes), and 3 (7%) were M. avium; none were M. intracellulare.

117 M. avium or M. tuberculosis infection was markedly increase

118 Later, the mice received Mycobacterium avium or Mycobacterium tuberculosis I.T.

119 mus following dissemination of Mycobacterium avium or Mycobacterium tuberculosis.

120 s have led to speculation that Mycobacterium avium paratuberculosis (MAP) might be a causative agent

121 ggest that GPLs play an important role in M. avium pathogenesis.

122 When tested against Mycobacterium avium, PCIH was more effective than INH at inhibiting ba

123 ructural genomics protein from Mycobacterium avium (PDB ID 3q1t) has been reported to be an enoyl-CoA

124 M. intracellulare, Acanthamoeba spp., and M. avium peaked during the dry season.

125 d down for MR expression showed increased M. avium phagosome-lysosome fusion relative to control cell

126 of cross-reactivity with the M. avium subsp. avium proteins that was higher than the degree of cross-

127 annels in the transport of known secreted M. avium proteins, we demonstrated that the porin channels

128 n = 238, 92.6%), followed by M. avium subsp. avium serotype 1 (n = 12, 4.7%) and serotype 2, 3 (n = 7

129 is; the bird type, including M. avium subsp. avium serotype 1 and serotype 2, 3 (also M. avium subsp.

130 ts between those of P. tenella SFB(8) and P. avium SFB(1).

131 , a major surface component of Mycobacterium avium, showed limited acidification and delayed recruitm

132 distribution in Great Britain, Mycobacterium avium ssp. paratuberculosis (MAP) was detected in 115 of

133 . casei, M. tuberculosis H37Ra, and three M. avium strains and for cytotoxic activity against seven d

134 We determined the subspecies of 257 M. avium strains isolated from patients at the M.D. Anderso

135 Mycobacterium avium subsp hominissuis is associated with infection of

136 Johnes disease (JD), caused by Mycobacterium avium subsp paratuberculosis (MAP), occurs worldwide as

137 e (n = 3) and cattle infected with either M. avium subsp. avium and Mycobacterium bovis were exposed

138 ted a degree of cross-reactivity with the M. avium subsp. avium proteins that was higher than the deg

139 most common (n = 238, 92.6%), followed by M. avium subsp. avium serotype 1 (n = 12, 4.7%) and serotyp

140 sp. hominissuis; the bird type, including M. avium subsp. avium serotype 1 and serotype 2, 3 (also M.

141 very similar to yet distinguishable from M. avium subsp. avium.

142 lls (which have been shown to induce anti-M. avium subsp. hominissuis activity when added to THP-1 ce

143 ng that MBP-1 expression is important for M. avium subsp. hominissuis adherence to the host cell.

144 facilitates an improved understanding of M. avium subsp. hominissuis and how it establishes infectio

145 ar phagocytes cocultured with established M. avium subsp. hominissuis biofilm and surveyed various as

146 Our data collectively indicate that M. avium subsp. hominissuis biofilm induces TNF-alpha-drive

147 The reasoning behind how M. avium subsp. hominissuis biofilm is allowed to establish

148 g) assay determined that contact with the M. avium subsp. hominissuis biofilm led to early, widesprea

149 M. avium subsp. hominissuis biofilm triggered robust tumor

150 ring initial colonization of the airways, M. avium subsp. hominissuis forms microaggregates composed

151 no efficient approach to prevent or treat M. avium subsp. hominissuis infection in the lungs.

152 BP-1 immune serum significantly inhibited M. avium subsp. hominissuis infection throughout the respir

153 s not seen until much later in planktonic M. avium subsp. hominissuis infection.

154 Mycobacterium avium subsp. hominissuis is an opportunistic human patho

155 We therefore conclude that M. avium subsp. hominissuis is the dominant M. avium subspe

156 Results showed M. avium subsp. hominissuis to be most common (n = 238, 92.

157 erizes a pathogenic mechanism utilized by M. avium subsp. hominissuis to bind and invade the host res

158 "Mycobacterium avium subsp. hominissuis" is a robust and pervasive envi

159 "Mycobacterium avium subsp. hominissuis" is an opportunistic environmen

160 d to THP-1 cells infected with planktonic M. avium subsp. hominissuis).

161 Of the 238 patients with M. avium subsp. hominissuis, 65 (27.3%) showed evidence of

162 um subsp. paratuberculosis and Mycobacterium avium subsp. hominissuis, a pathogen known to interact w

163 teins exposed at the bacterial surface of M. avium subsp. hominissuis.

164 racterize the surface-exposed proteome of M. avium subsp. hominissuis.

165 ntly less efficient at dissemination than M. avium subsp. hominissuis.

166 ptosis but did not lead to elimination of M. avium subsp. hominissuis.

167 f three types: the human or porcine type, M. avium subsp. hominissuis; the bird type, including M. av

168 f Ag85A, Ag85B, and Ag85C from Mycobacterium avium subsp. paratuberculosis (MAP) (K(D) values were de

169 optimized for the isolation of Mycobacterium avium subsp. paratuberculosis (MAP) from milk and colost

170 vailable diagnostic assays for Mycobacterium avium subsp. paratuberculosis (MAP) have poor sensitivit

171 Johne's disease is caused by Mycobacterium avium subsp. paratuberculosis (MAP) infection and result

172 echanisms of host responses to Mycobacterium avium subsp. paratuberculosis (MAP) infection during the

173 ate the stochastic dynamics of Mycobacterium avium subsp. paratuberculosis (MAP) infection on US dair

174 solates with the sequenced bovine isolate M. avium subsp. paratuberculosis (MAP) K-10.

175 Total lipids from an M. avium subsp. paratuberculosis (Map) ovine strain (S-type

176 cterium kansasii (n = 10), and Mycobacterium avium subsp. paratuberculosis (n = 10), cases exposed to

177 ll as cattle experimentally infected with M. avium subsp. paratuberculosis (n = 3) were used to probe

178 d Western blot analysis indicated that wt M. avium subsp. paratuberculosis activates Cdc42 and RhoA p

179 We now know that M. avium subsp. paratuberculosis activates the epithelial l

180 The invasion of the intestinal mucosa by M. avium subsp. paratuberculosis and Mycobacterium avium su

181 ity, and oxidative stress were similar in M. avium subsp. paratuberculosis and Mycobacterium tubercul

182 ncluded were previously reported or known M. avium subsp. paratuberculosis antigens to serve as a fra

183 Monitoring cellular markers, only live M. avium subsp. paratuberculosis bacilli were able to preve

184 e's disease, allowing the transmission of M. avium subsp. paratuberculosis between animals.

185 with the Cdc42 of cells infected with wt M. avium subsp. paratuberculosis but not with the deltaOx m

186 ted for the presence of viable Mycobacterium avium subsp. paratuberculosis by a novel peptide-mediate

187 cols to ensure that low concentrations of M. avium subsp. paratuberculosis can be detected.

188 Mycobacterium avium subsp. paratuberculosis causes an enteric infectio

189 Infection with Mycobacterium avium subsp. paratuberculosis causes Johne's disease in

190 Mycobacterium avium subsp. paratuberculosis causes Johne's disease in

191 Mycobacterium avium subsp. paratuberculosis causes Johne's disease, an

192 resulted in a greater recovery of viable M. avium subsp. paratuberculosis cells from milk than from

193 reatment decreased the recovery of viable M. avium subsp. paratuberculosis cells more than treatment

194 Counts of viable M. avium subsp. paratuberculosis cells ranging from 1 to 11

195 e wild-type strain and a mutant strain of M. avium subsp. paratuberculosis deficient in tissue coloni

196 We interrogated an M. avium subsp. paratuberculosis DeltasigL mutant against a

197 months following intestinal deposition of M. avium subsp. paratuberculosis despite a lack of fecal sh

198 ociated with transcriptional responses of M. avium subsp. paratuberculosis during macrophage infectio

199 's patches, were used to demonstrate that M. avium subsp. paratuberculosis enters the intestinal muco

200 novel signaling pathway activated during M. avium subsp. paratuberculosis entry that links the produ

201 acterizing the gene expression profile of M. avium subsp. paratuberculosis exposed to different stres

202 chnique, we found 15 different strains of M. avium subsp. paratuberculosis from a total of 142 isolat

203 the three evaluated for the isolation of M. avium subsp. paratuberculosis from milk, as it achieved

204 To identify M. avium subsp. paratuberculosis genes associated with the

205 On the transcriptional level, over 300 M. avium subsp. paratuberculosis genes were significantly a

206 In addition, the results indicated that M. avium subsp. paratuberculosis had equal abilities to cro

207 We hypothesized that M. avium subsp. paratuberculosis harnesses host responses t

208 The infection biology of Mycobacterium avium subsp. paratuberculosis has recently crystallized,

209 actions between epithelium and Mycobacterium avium subsp. paratuberculosis have not been intensively

210 n optimized protocol for the isolation of M. avium subsp. paratuberculosis in milk.

211 We show that M. avium subsp. paratuberculosis infection led to phagosome

212 Mycobacterium avium subsp. paratuberculosis infection of cattle takes

213 sigL in the pathogenesis and immunity of M. avium subsp. paratuberculosis infection, a potential rol

214 were culture positive, indicating a true M. avium subsp. paratuberculosis infection.

215 A number of studies have suggested that M. avium subsp. paratuberculosis interacts with M cells in

216 In summary, M. avium subsp. paratuberculosis interacts with the intesti

217 steps to further elucidate the process of M. avium subsp. paratuberculosis invasion.

218 Johne's disease suggests that Mycobacterium avium subsp. paratuberculosis is a causative agent.

219 Thus, M. avium subsp. paratuberculosis is an opportunist that tak

220 Once inside the cell, M. avium subsp. paratuberculosis is known to survive harsh

221 Mycobacterium avium subsp. paratuberculosis is shed into the milk and

222 M. avium subsp. paratuberculosis isolates from bovine fecal

223 of the genetic relatedness of Mycobacterium avium subsp. paratuberculosis isolates harvested from bo

224 The M. avium subsp. paratuberculosis isolates were obtained fro

225 on scheme (tissue-associated versus fecal M. avium subsp. paratuberculosis isolates).

226 rase recognition in the tissue-associated M. avium subsp. paratuberculosis isolates.

227 nserved membrane protein homologue to the M. avium subsp. paratuberculosis MAP2446c gene and four oth

228 quently, we analyzed the virulence of six M. avium subsp. paratuberculosis mutants with inactivation

229 In this report, the stress response of M. avium subsp. paratuberculosis on a genome-wide level (st

230 ulated with 10(2) to 10(8) CFU/ml of live M. avium subsp. paratuberculosis organisms.

231 To improve our understanding of M. avium subsp. paratuberculosis pathogenesis, we examined

232 ter decipher the role of sigma factors in M. avium subsp. paratuberculosis pathogenesis, we targeted

233 To determine whether an M. avium subsp. paratuberculosis protein delivered to the h

234 is that it enables a direct comparison of M. avium subsp. paratuberculosis proteins to each other in

235 ogical significance of such regulators in M. avium subsp. paratuberculosis rremains elusive.

236 lation of a wild-type strain and a mutant M. avium subsp. paratuberculosis strain (with an inactivate

237 The results of M. avium subsp. paratuberculosis strain typing and observed

238 e media determined differential growth of M. avium subsp. paratuberculosis strains and that this shou

239 nd lead to a discrepancy in the growth of M. avium subsp. paratuberculosis strains.

240 nt methods on the selection of Mycobacterium avium subsp. paratuberculosis subtypes.

241 For this evaluation, M. avium subsp. paratuberculosis subtyping was based on the

242 (sigH) that was shown to be important for M. avium subsp. paratuberculosis survival inside gamma inte

243 low-shedding cows are truly infected with M. avium subsp. paratuberculosis than are passively sheddin

244 a analysis revealed unique gene groups of M. avium subsp. paratuberculosis that were regulated under

245 =597), suggesting the high sensitivity of M. avium subsp. paratuberculosis to acidic environments.

246 ted macrophage recruitment in response to M. avium subsp. paratuberculosis using a MAC-T bovine macro

247 suggested a substantial role for sigL in M. avium subsp. paratuberculosis virulence, as indicated by

248 tal strain, suggesting a role for sigH in M. avium subsp. paratuberculosis virulence.

249 M. avium subsp. paratuberculosis was also shown to interact

250 M. avium subsp. paratuberculosis was capable of invading th

251 To our surprise, strains of M. avium subsp. paratuberculosis were able to traverse the

252 No strains of M. avium subsp. paratuberculosis were found.

253 Several mutants of M. avium subsp. paratuberculosis were identified which inva

254 cows that were low shedders of Mycobacterium avium subsp. paratuberculosis were passively shedding or

255 pon translocation, dendritic cells ingest M. avium subsp. paratuberculosis, but this process does not

256 Mycobacterium avium subsp. paratuberculosis, the agent of Johne's dise

257 tion of the cell communication pathway by M. avium subsp. paratuberculosis, which loosens the integri

258 tigated whether it is possible that these M. avium subsp. paratuberculosis-infected animals could hav

259 o seroreactivity against M. kansasii- and M. avium subsp. paratuberculosis-infected animals.

260 us colitis displayed significantly higher M. avium subsp. paratuberculosis-specific immunoglobulin G2

261 5 to 2.0% did not affect the viability of M. avium subsp. paratuberculosis.

262 een infected by environmental exposure of M. avium subsp. paratuberculosis.

263 atuberculosis than are passively shedding M. avium subsp. paratuberculosis.

264 passively shedding or truly infected with M. avium subsp. paratuberculosis.

265 ication of previously unknown antigens of M. avium subsp. paratuberculosis.

266 ells less efficiently than wild-type (wt) M. avium subsp. paratuberculosis.

267 early stages of infection of calves with M. avium subsp. paratuberculosis.

268 equence polymorphisms present uniquely in M. avium subsp. paratuberculosis.

269 our understanding of the pathogenesis of M. avium subsp. paratuberculosis.

270 ubsp. silvaticum); and the ruminant type, M. avium subsp. paratuberculosis.

271 Shedding levels (CFU of M. avium subsp. paratuberculosis/g of feces) for the animal

272 M. avium subsp. silvaticum isolates were observed to have a

273 avium serotype 1 and serotype 2, 3 (also M. avium subsp. silvaticum); and the ruminant type, M. aviu

274 Genome diversity in M. avium subspecies appears to be mediated by large sequenc

275 avium subsp. hominissuis is the dominant M. avium subspecies clinically, that the two bird-type subs

276 entify large sequence polymorphisms among M. avium subspecies obtained from a variety of host animals

277 ed by slow replicating bacilli Mycobacterium avium subspecies paratuberculosis (MAP) infecting macrop

278 In a prospective study, M. avium subspecies paratuberculosis detection in early Cro

279 By the analysis of 14 SNPs Mycobacterium avium subspecies paratuberculosis isolates can be charac

280 genome sequence data from 133 Mycobacterium avium subspecies paratuberculosis isolates with differen

281 e large-scale global typing of Mycobacterium avium subspecies paratuberculosis isolates.

282 oA carboxylase holoenzyme from Mycobacterium avium subspecies paratuberculosis revealed an architectu

283 Typing of Mycobacterium avium subspecies paratuberculosis strains presents a cha

284 intestinal pathogens including Mycobacterium avium subspecies paratuberculosis, adherent-invasive Esc

285 es for the characterization of Mycobacterium avium subspecies paratuberculosis, and whole-genome sequ

286 uberculosis are both caused by Mycobacterium avium subspecies paratuberculosis.

287 5P), yet both lipids are present in other M. avium subspecies.

288 Mycobacterium avium (M. avium) subspecies vary widely in both pathogenicity and

289 or siRNA lead to significant decrease of M. avium survival.

290 n the cytoplasm of HEp-2 cells exposed to M. avium, the recombinant protein was shown to be potential

291 within a single subspecies of Mycobacterium avium these lipids can differ.

292 rial uptake by macrophages, we screened a M. avium transposon mutant library for the inability to ent

293 s (VDAC) were identified as components of M. avium vacuoles in macrophages.

294 bed in macrophages infected by Mycobacterium avium was not observed in our model, which presented a d

295 While Mycobacterium avium was once regarded as innocuous, its high frequency

296 In comparison, M. avium was recovered from 141 water/biofilm samples.

297 M. avium was recovered more frequently from sterile sites t

298 Subspecies and host adapted isolates of M. avium were distinguishable by the presence or absence of

299 ized the six SDSs, but L. pneumophila and M. avium were not detected.

300 athogens Toxoplasma gondii and Mycobacterium avium when administered via the i.p. or i.v. route, resp

301 rlying thymic atrophy during infection by M. avium with the participation of locally produced NO, end