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 , TNF-alpha has a protective role against M. avium.

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

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

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

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

9 ide polymorphisms (SNPs), suggesting that M. avium accumulates mutations at higher rates during persi

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

11 B. avium agglutinates guinea pig erythrocytes via an unknow

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

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

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

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

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

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

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

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

20 e, polymorphic SNPs for sweet cherry and the avium and the fruticosa subgenomes of sour cherry, respe

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

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

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

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

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

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

27 ia (NTM), some of which-namely Mycobacterium avium-are important opportunistic pathogens.

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

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

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

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

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

33 obacterium abscessus (34%) and Mycobacterium avium complex (83%) were the most common nontuberculous

34 M. abscessus (34%) and M. avium complex (83%) were the most commonly isolated nont

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

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

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

38 Members of the Mycobacterium avium complex (MAC) are characterized as nontuberculosis

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

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

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

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

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

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

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

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

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

48 ne probe assay for identifying Mycobacterium avium complex (MAC) species and Mycobacterium abscessus

49 Total mycobacteria and Mycobacterium avium complex (MAC) were quantified by qPCR targeting, r

50 Mycobacterium avium complex (MAC) were the dominant species isolated f

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

52 culous mycobacteria (NTM), and Mycobacterium avium complex (MAC), however, were widespread.

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

54 lmonary disease are members of Mycobacterium avium complex (MAC).

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

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

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

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

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

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

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

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

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

64 Mycobacterium avium complex lung disease is an increasingly common and

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

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

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

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

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

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

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

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

73 t common NTM pathogens such as Mycobacterium avium complex, Mycobacterium kansasii, and Mycobacterium

74 10.8%); 45.7% of isolates were Mycobacterium avium complex.

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

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

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

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

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

80 ate microbial identification of Enterococcus avium from metagenomic samples with FDA-ARGOS reference

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

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

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

84 ing, respectively, 11.0 and 2.4 Mb of the P. avium genome.

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

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

87 cies Mycobacterium marinum and Mycobacterium avium harboring insertions in the orthologous gene whose

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

89 y revealed the rapid genetic evolution of M. avium in chronically infected patients, accompanied by c

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

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

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

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

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

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

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

97 e used a model of disseminated Mycobacterium avium infection in mice to investigate the mechanisms of

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

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

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

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

102 re required for granuloma assembly during M. avium infections in mice.

103 M. avium infects macrophages and actively interfere with th

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

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

106 15.8%), M triplex in 1 patient (5.3%), and M avium intracellulare in 1 patient (5.3%).

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

108 Mycobacterium avium is abundant in the environment.

109 o characterize the genomic changes within M. avium isolates collected from single patients over time

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

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

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

113 Sweet cherry (Prunus avium L.) trees are both economically important fruit cr

114 market driven trait in sweet cherry (Prunus avium L.) where the desirable increase in fruit firmness

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

116 ork, three Spanish local varieties of Prunus avium (L.), as well as two foreign varieties were studie

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

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

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

120 from 12 NTM-PD patients due to Mycobacterium avium, M. intracellulare, M. abscessus, or M. massiliens

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

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

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

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

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

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

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

128 6S rRNA gene A1408G mutation and included M. avium, Mycobacterium intracellulare, and Mycobacterium c

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

130 Mycobacterium avium, Mycobacterium tuberculosis, and Mycobacterium kan

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

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

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

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

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

136 mus following dissemination of Mycobacterium avium or Mycobacterium tuberculosis.

137 obial VOCs and (2) apply it to Mycobacterium avium paratuberculosis; the vaccine strain of M. bovis B

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

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

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

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

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

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

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

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

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

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

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

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

150 of inflammatory cytokines by host-adapted M. avium strains.

151 Mycobacterium avium subsp hominissuis is associated with infection of

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

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

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

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

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

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

158 Mycobacterium avium subsp. hominissuis (MAH) is increasingly recognize

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

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

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

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

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

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

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

166 M. avium subsp. hominissuis biofilm triggered robust tumor

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

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

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

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

171 Mycobacterium avium subsp. hominissuis is an opportunistic human patho

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 inflammatory disease caused by Mycobacterium avium subsp. paratuberculosis (MAP) in cattle and other

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 Mycobacterium avium subsp. paratuberculosis causes an enteric infectio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 Mycobacterium avium subsp. paratuberculosis infection of cattle takes

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

226 ination of immune responses occurs during M. avium subsp. paratuberculosis infection, with these resp

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

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

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

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

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

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

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

234 M. avium subsp. paratuberculosis isolates from bovine fecal

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

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

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

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

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

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

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

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

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

244 Infection of the host with Mycobacterium avium subsp. paratuberculosis results in chronic and pro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

264 5 to 2.0% did not affect the viability of M. avium subsp. paratuberculosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

282 Typing of Mycobacterium avium subspecies paratuberculosis strains presents a cha

283 bp fragment of genomic DNA of Mycobacterium avium subspecies paratuberculosis through real-time PCR

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