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1                                              M. bovis bacillus Calmette-Guerin-primed sanroque T cell
2                                              M. bovis BCG Ag84 was able to form oligomers in vitro, p
3                                              M. bovis BCG growth on both solid and liquid media was i
4                                              M. bovis infections generated cavitary CFU counts of 10(
5                                              M. bovis is also associated with other clinical presenta
6 ected as low as 1 to 5 M. bovis cells and 10 M. bovis cells, respectively, per 1.5 ml of trunk wash u
7  the experimentally defined peptides from 10 M. bovis antigens that were recognized by bovine T cells
8 2 pools of overlapping peptides spanning 119 M. bovis secreted and potentially secreted proteins were
9 d and applied to the characterization of 137 M. bovis isolates from diverse geographical origins, obt
10                     In the current study, 16 M. bovis proteins were discovered in the blood serum pro
11 rains (13 were PZA-resistant strains) and 21 M. bovis strains (8 were BCG strains).
12  and found 57 M. tuberculosis isolates and 3 M. bovis BCG isolates from patients who had received int
13 ing the sequences of these four genes in 455 M. bovis strains isolated from cattle in the aforementio
14 ble discrimination was achieved, with the 47 M. bovis isolates resolved into 14 unique profiles, whil
15 R and TSEP methods detected as low as 1 to 5 M. bovis cells and 10 M. bovis cells, respectively, per
16 adgers shedding between 1 x 10(3)- 4 x 10(5) M. bovis cells g(-1) of faeces, creating a substantial a
17 filtration method detected as low as 5 to 50 M. bovis cells per 1.5 ml of trunk wash.
18 rait-allele associations, we interrogated 75 M. bovis and 61 M. tuberculosis genomes for single nucle
19 ycobacterium bovis Ravenel, M. bovis AF2122, M. bovis BCG, M. tuberculosis H37Rv, M. tuberculosis CDC
20 d by enzyme-linked immunosorbent assay after M. bovis challenge, but not the frequency of responding
21  CD4(+) T cells at an early time point after M. bovis BCG vaccination, but CD4(+) T cells were found
22 development of disease as an end point after M. bovis challenge.
23 IFN-gamma test) can detect cattle soon after M. bovis infection regardless of the dose.
24 displayed antimycobacterial activity against M. bovis bacillus Calmette-Guerin.
25 3 is involved in protective immunity against M. bovis infection in cattle and are in accordance with
26                             In contrast, all M. bovis isolates generated a double-peak pattern when m
27                           This method allows M. bovis infections in badger populations to be monitore
28  Guerin (BCG) vaccine strain selected for an M. bovis PK+ mutant, a finding that explains the alterat
29 roscopy-dissected lymph node lesions from an M. bovis-infected animal.
30 FU/ml) was evaluated by IMS combined with an M. bovis-specific touchdown PCR.
31 ulosis from the closely related M. bovis and M. bovis BCG.
32 virulent wild-type M. tuberculosis H37Rv and M. bovis do not increase THP-1 apoptosis over baseline.
33 nalysis was undertaken for selected host and M. bovis proteins using a cattle serum repository contai
34 ogenic mycobacteria, including M. leprae and M. bovis, suggesting that a core of basic in vivo surviv
35 ication in PNAS reported that M. marinum and M. bovis bacillus Calmette-Guerin produce a type of spor
36 H stimulated cAMP production in both Mtb and M. bovis BCG, but broadly affected cAIG regulation only
37 this regulation required cmr in both Mtb and M. bovis BCG.
38 ders of bacteria (including M. smegmatis and M. bovis BCG) can be produced.
39 ution mutation in all tested BCG strains and M. bovis in comparison to the M. tuberculosis sequence.
40  clones of M. tuberculosis sensu stricto and M. bovis are distinct, deeply branching genotypic comple
41 ant mycobacteria such as M. tuberculosis and M. bovis Bacille-Calmette-Guerin.
42  CD4 T cell responses to M. tuberculosis and M. bovis bacillus Calmette-Guerin (BCG) Pasteur in vivo
43    We herein report that M. tuberculosis and M. bovis bacillus Calmette-Guerin infection down-regulat
44 ccelerated the growth of M. tuberculosis and M. bovis BCG crp mutants in mycomedium, but not within m
45 slow-growth phenotype of M. tuberculosis and M. bovis BCG crp mutants in vitro.
46 oth genes was reduced in M. tuberculosis and M. bovis BCG crp mutants.
47 dstream dissemination of M. tuberculosis and M. bovis BCG is uncommon in HIV-infected children vaccin
48 on of serC and Rv0885 in M. tuberculosis and M. bovis BCG, using site-specific mutagenesis, promoter
49 able from both wild-type M. tuberculosis and M. bovis isolates.
50 y to distinguish between M. tuberculosis and M. bovis.
51  clinical specimens previously identified as M. bovis by spoligotyping revealed an isolate of M. tube
52 but not in slow-growing mycobacteria such as M. bovis BCG or M. tuberculosis.
53 cobacterium bovis (along with the attenuated M. bovis bacillus Calmette-Guerin [BCG]), and Mycobacter
54 sed by virulent mycobacteria since avirulent M. bovis bacillus Calmette-Guerin (BCG) fails to trigger
55 s that badger-to-cattle and cattle-to-badger M. bovis transmission may typically occur through contam
56 RP(Mt) regulon members also differed between M. bovis BCG and M. tuberculosis.
57 velop GEAs capable of distinguishing between M. bovis-infected and uninfected warthogs.
58 for analysis of MAs in Mycobacterium bovis ( M. bovis) and M. tuberculosis lipid extracts.
59 ) transcriptome, due to Mycobacterium bovis (M. bovis) infection, has been well documented; however,
60 nd IL-17A production in Mycobacterium bovis (M. bovis)-infected cattle compared to non-infected contr
61 nitively identify M. tuberculosis, M. bovis, M. bovis BCG, and other members of the complex.
62 ifferentiation of M. tuberculosis, M. bovis, M. bovis BCG, M. africanum, M. microti, and M. canettii
63 btype II), M. africanum subtype I, M. bovis, M. bovis BCG, M. caprae, M. microti, or "M. canettii" or
64 d females are disproportionately affected by M. bovis, which was independently associated with extrap
65 nsic changes of gammadelta T cells caused by M. bovis BCG vaccination rather than being due solely to
66 epidemiology of human tuberculosis caused by M. bovis in the United States and validate previous find
67 e oncology patients with infection caused by M. bovis-BCG were studied.
68 ber 2015, searching for infections caused by M. bovis-BCG.
69 ell subset in acquired immunity conferred by M. bovis BCG vaccination.
70 s at early ages are functionally enhanced by M. bovis BCG vaccination and suggests an important role
71 rial antigens were significantly enhanced by M. bovis BCG vaccination.
72 ed to CD4(+) T cells, in immunity induced by M. bovis BCG vaccination, 4-week-old specific-pathogen-f
73 protein and compared to responses induced by M. bovis-derived purified protein derivative.
74 scribes for the first time that FLA carrying M. bovis can transmit TB.
75                                  Circulating M. bovis proteins, specifically polyketide synthetase 5,
76 4 novel small RNAs (sRNAs) in the TB-complex M. bovis BCG, using a combination of experimental and co
77 s using a cattle serum repository containing M. bovis (n = 128), Mycobacterium kansasii (n = 10), and
78 ecifically polyketide synthetase 5, detected M. bovis-infected cattle with little to no seroreactivit
79  assays (GEAs) may be valuable for detecting M. bovis-infection, as shown in numerous African wildlif
80 ermine the performance of tests in detecting M. bovis in badger feces for the Department for Environm
81 apid, and cost-effective means of diagnosing M. bovis infection in cattle and badgers.
82 -4 responses were observed for the different M. bovis doses, suggesting that diagnostic assays (tuber
83 of pathology were observed for the different M. bovis doses.
84 he niacin test that clinically distinguishes M. bovis from M. tuberculosis.
85                   African 1 was the dominant M. bovis clonal complex, with 97 unique genotypes includ
86 actor, KLF4, to the promoter of CIITA during M. bovis BCG infection of macrophages was essential to o
87            Host-pathogen interactions during M. bovis infection are poorly understood, especially ear
88 s loss, which is the case for an exceptional M. bovis human outbreak strain from Spain.
89 amples of sera collected from experimentally M. bovis-infected cattle and deer revealed that ESAT6-p-
90                   Two hundred and fifty-five M. bovis were isolated, identified and genotyped using d
91                                    Following M. bovis infection, the comparative tuberculin skin test
92 s with greatest immunocapture capability for M. bovis in broth were those coated simultaneously with
93 nsitive and 93% specific against culture for M. bovis (n = 1,464) at necropsy.
94 yping (MLST) schemes have been developed for M. bovis, with one serving as the PubMLST reference meth
95 to 15.6 CFU/ml for humans, while the LOD for M. bovis SB0121 was 30 CFU/ml compared to 143.4 CFU/ml f
96 1 was 30 CFU/ml compared to 143.4 CFU/ml for M. bovis BCG in humans.
97 the greatest sensitivity and specificity for M. bovis detection.
98                        Analysis of cDNA from M. bovis BCG shows that during in vitro growth all the g
99 P10, peripheral blood mononuclear cells from M. bovis-infected cattle were stimulated in vitro with a
100 ted epitopes were recognized by T cells from M. bovis-infected cattle.
101 eptides that were recognized by T cells from M. bovis-infected cattle.
102 nthesis pathway (nadABC) can be deleted from M. bovis, demonstrating a functioning salvage pathway.
103 cobacterial glycoprotein, antigen MPB83 from M. bovis.
104              They were also used to generate M. bovis-specific peptide ligands by phage display biopa
105  CDC1551) into 5 major "SNP cluster groups." M. bovis isolates clustered into three major lineages ba
106 me that antigen vectored by the slow-growing M. bovis BCG but not that vectored by fast-growing, read
107 ular growth of M. smegmatis and slow-growing M. bovis BCG.
108 Mycobacterium smegmatis and the slow-growing M. bovis M. bovis BCG, were engineered to express a mode
109 (aPR, 2.0 [95% CI, 1.7-2.4]) also had higher M. bovis prevalences.
110  novel spoligotypes representing the highest M. bovis genetic diversity observed in Africa to date.
111                            It is unclear how M. bovis is able to survive in the environment for long
112 ricanum subtype II), M. africanum subtype I, M. bovis, M. bovis BCG, M. caprae, M. microti, or "M. ca
113                                           In M. bovis BCG, the fadD28 and mas promoters were function
114                                           In M. bovis-infected animals, PPDB specific IL-22 and IL-17
115 sion was significantly higher (P = 0.003) in M. bovis culture-positive cows (n = 12) than in culture-
116  quantify the roles of badgers and cattle in M. bovis infection dynamics in the presence of data bias
117 lation by the cAMP-responsive protein CRP in M. bovis BCG as a model for tuberculosis (TB)-complex ba
118 but broadly affected cAIG regulation only in M. bovis BCG.
119 the nat gene caused an extended lag phase in M. bovis BCG and a cell morphology associated with an al
120 lence regulation system PhoP/PhoR (PhoPR) in M. bovis and in the closely linked Mycobacterium african
121 red the early steps of biofilm production in M. bovis BCG, to distinguish intercellular aggregation f
122 otein with an in vivo DNA binding profile in M. bovis BCG similar to that of CRP(Mt) in M. tuberculos
123 , granuloma formation was more pronounced in M. bovis BCG-infected CG/NE-deficient mice in comparison
124 n of increased IL-22 and IL-17A responses in M. bovis-infected animals to the level of protein produc
125 ell proliferation and IFN-gamma secretion in M. bovis infection, with nonprotein antigens inducing si
126 rget genes were significantly upregulated in M. bovis-infected warthogs with the greatest upregulatio
127 RP(BCG) and CRP(Mt) in vitro and in vivo, in M. bovis BCG and M. tuberculosis, to evaluate CRP(BCG)'s
128 tudies using mycobacterial models, including M. bovis BCG, M. marinum, and M. smegmatis have signific
129         Mice lacking IRAK-4 showed increased M. bovis burden in spleen, liver, and lungs and smaller
130                                   Initially, M. bovis capture from Middlebrook 7H9 broth suspensions
131 lted in fewer tubercles than did intradermal M. bovis BCG vaccination.
132 firmed the clonal nature of the investigated M. bovis population, based on MLST data.
133                                  Not only is M. bovis unable to use glycerol as a sole carbon source
134        In livestock, the dominant species is M. bovis causing bovine tuberculosis (bTB), a disease of
135 was possible to follow the migration of live M. bovis Bacille Calmette-Guerin (BCG) and to observe in
136 s persists in lungs of immunocompetent mice, M. bovis BCG is cleared, and clearance is T cell depende
137                                In our model, M. bovis would be taken up by amoebal trophozoites, whic
138                                    Moreover, M. bovis BCG-induced upregulation of C-type lectin Mincl
139  counts of 10(6) to 10(9) bacilli, while non-M. bovis species and BCG yielded CFU counts that ranged
140                       Sera from noninfected, M. bovis-infected, or M. avium subsp. paratuberculosis-i
141 ella; neither Mycobacterium tuberculosis nor M. bovis was isolated.
142 data regarding the identification of a novel M. bovis phylogenetic clade responsible for ongoing tran
143 oximately 30%), whereas the adenylylation of M. bovis BCG GS does not change.
144        Targeted and whole-genome analysis of M. bovis isolates indicated the emergences of a predomin
145 uberculosis, 20 M. africanum and one case of M. bovis) and 69 (15%) were due to infection with NTM.
146 e-half of the animals infected with 1 CFU of M. bovis developed pulmonary pathology typical of bovine
147 cheal route with 1,000, 100, 10, or 1 CFU of M. bovis.
148            In addition, 40% of all clones of M. bovis BCG had lost the hyg resistance cassette after
149                           Complementation of M. bovis with the pykA gene from M. tuberculosis H37Rv r
150 s were spiked with various concentrations of M. bovis cells and subjected to the described treatment
151 ogical and histopathological confirmation of M. bovis infection.
152 e of interleukin-2 (IL-2), in the context of M. bovis infection.
153  times allowed highly sensitive detection of M. bovis BCG.
154             The sensitivity for detection of M. bovis is lowered to 82% when only PZA-monoresistant i
155  field sampling of latrines and detection of M. bovis with quantitative PCR tests, the results of whi
156 -mortem diagnostic tool for the detection of M. bovis-infected warthogs.
157  In this report, we examined the dynamics of M. bovis transmission among dairy cattle in the Nile Del
158 cing (WGBS) was used to assess the effect of M. bovis infection on the bAM DNA methylome.
159                          However, effects of M. bovis infection on adhesion molecule expression have
160            Understanding the epidemiology of M. bovis in badger populations is essential for directin
161 no important role during the early events of M. bovis infection.
162             We further show that exposure of M. bovis-infected trophozoites and cysts to Balb/c mice
163 ural PIMs identified from a lipid extract of M. bovis BCG.
164 resence of the putative virulence factors of M. bovis.
165 tation diminished inflammation and growth of M. bovis BCG via enhanced reactive oxygen species produc
166 e from the characteristic dysgonic growth of M. bovis to eugonic growth, an appearance normally assoc
167  novel function of P27 in the interaction of M. bovis with its natural host cell, the bovine macropha
168 lity as a rapid test to confirm isolation of M. bovis and M. caprae from veterinary specimens followi
169 re has the potential to improve isolation of M. bovis from lymph nodes and hence the diagnosis of bov
170 erial Ags and accumulating in the lesions of M. bovis-infected animals.
171 ld be recognized by T cells from a number of M. bovis-infected hosts, we tested whether a virtual-mat
172 the diffusion of phosphates across the OM of M. bovis BCG and Mycobacterium tuberculosis are unknown.
173 comprise respectively 59% and 49% of ORFs of M. bovis BCG Pasteur and M. smegmatis mc(2) 155.
174 chanisms of the virulence and persistence of M. bovis and Mycobacterium tuberculosis Here, we describ
175 he wide host range and disease phenotypes of M. bovis.
176        The approach was to widen the pool of M. bovis antigens that could be used as DIVA targets, by
177  were associated with a higher prevalence of M. bovis disease.
178  is associated with increasing prevalence of M. bovis infection in badgers, especially where landscap
179 h a widespread increase in the prevalence of M. bovis infection in badgers.
180                       The high prevalence of M. bovis is of public health concern and limits the pote
181          The minimum estimated prevalence of M. bovis was 2.8% (1.9-3.9), 7.7% (6.1-9.6), 21.3% (15.2
182 [95% CI, 3.1-5.3]) had higher prevalences of M. bovis disease.
183 hibition of TLR9-induced cross processing of M. bovis bacillus Calmette-Guerin expressing OVA could b
184 eta effectively enhanced cross processing of M. bovis bacillus Calmette-Guerin expressing OVA, bypass
185 he p27-p55 operon impairs the replication of M. bovis in bovine macrophages.
186 e badger's role as a persistent reservoir of M. bovis.
187 nd water, may act as long-term reservoirs of M. bovis in the environment.
188 Unlike significant wild animal reservoirs of M. bovis that are considered pests in other countries, s
189 ce of monitoring environmental reservoirs of M. bovis which may constitute a component of disease spr
190 jor secreted immunogenic protein (rMPB70) of M. bovis were used in an enzyme-linked immunosorbent ass
191          Exosomes isolated from the serum of M. bovis bacillus Calmette-Guerin-infected mice could al
192 specifically increased in the blood serum of M. bovis-infected animals).
193 specifically increased in the blood serum of M. bovis-infected animals).
194 d has been proposed as a potential source of M. bovis BCG's attenuation.
195  CG and NE into the bronchoalveolar space of M. bovis BCG-infected mice.
196                      Certain spoligotypes of M. bovis and M. caprae were not detected by the LFD in S
197 vium paratuberculosis; the vaccine strain of M. bovis Bacillus Calmette-Guerin; and M. kansasii to de
198  derivatives and increases susceptibility of M. bovis BCG to antibiotics that permeate the cell wall.
199 il, demonstrates that recent transmission of M. bovis is ongoing at distinct sites.
200       Indeed, human-to-human transmission of M. bovis strains and other members of the animal lineage
201 ut little evidence of recent transmission of M. bovis was more common in Adamawa compared to the Nort
202 ovide valuable tools for molecular typing of M. bovis.
203 he decreased infectivity and/or virulence of M. bovis relative to M. tuberculosis in humans.
204                                         Only M. bovis DNA was amplified, indicating 100% analytical s
205 tic cell lines by Mycobacterium smegmatis or M. bovis BCG harboring a plasmid encoding the fluorescen
206 crophages with Mycobacterium tuberculosis or M. bovis strain BCG enhances MHC-II release in synergy w
207 re now genetically differentiated from other M. bovis clades.
208                                As predicted, M. bovis BCG cell lysates metabolized the BphC substrate
209  antigens of such cells were used to produce M. bovis-specific polyclonal and monoclonal antibodies i
210 umulate in the lungs during murine pulmonary M. bovis BCG and M. tb.
211 vities by using Mycobacterium bovis Ravenel, M. bovis AF2122, M. bovis BCG, M. tuberculosis H37Rv, M.
212                                  Recombinant M. bovis BCG but not recombinant M. smegmatis conferred
213        In contrast, antigen from recombinant M. bovis BCG was presented by all three dendritic cell t
214 f dendritic cell maturation than recombinant M. bovis BCG infection.
215 ate M. tuberculosis from the closely related M. bovis and M. bovis BCG.
216 s-reactivity with the more distantly related M. bovis proteins.
217                        Infected badgers shed M. bovis in their feces.
218 d secondary lesions at intrapulmonary sites, M. bovis infections led to the most apparent gross patho
219 uberculosis challenge compared with standard M. bovis bacille Calmette-Guerin vaccination.
220 rium tuberculosis but not the vaccine strain M. bovis bacille Calmette-Guerin (BCG).
221 losis (MTB), missing from the vaccine strain M. bovis BCG, and its importance to virulence has been e
222 o 10 CFU/ml of the M. tuberculosis surrogate M. bovis BCG.
223        We observed robust local and systemic M. bovis-specific IFN-gamma and IL-17 production by both
224 91; P < 0.0001), with the added benefit that M. bovis was differentiated from another MTBC species in
225                    Furthermore, we show that M. bovis infection in cattle induces robust IL-17A prote
226 g-term epidemiological data, suggesting that M. bovis and related phoPR-mutated strains pose a lower
227 Importantly, we show for the first time that M. bovis arrests phagosome maturation in a process that
228                                          The M. bovis isolates from badgers tended to be similar to t
229     Polyclonal antibodies raised against the M. bovis hemolysin-cytotoxin also recognized a protein o
230 riant SNPs, while 84 SNPs differentiated the M. bovis BCG lineage from the virulent isolates.
231 f which considered as robust markers for the M. bovis Marajo strain.
232                    In the first instance the M. bovis-derived protein ESAT-6 was used as a model anti
233                                Moreover, the M. bovis epidemiology in this setting is herein found to
234 potato slices used for the derivation of the M. bovis bacillus Calmette and Guerin (BCG) vaccine stra
235 ds target small hypervariable regions of the M. bovis genome and provide anonymous biallelic informat
236 accination with the attenuated strain of the M. bovis pathogen, BCG, is not used to control bovine tu
237 quence was identified in most genomes of the M. bovis strains collected in all three countries.
238 ermissive to M. bovis infection and that the M. bovis bacilli may survive within the cysts of four of
239 Cluster 1 (WC1), and we demonstrate that the M. bovis-specific gammadelta T cell response is composed
240 sis probe and a single-peak pattern with the M. bovis probe.
241 sis probe and a double-peak pattern with the M. bovis probe.
242 rovide an intracellular niche allowing their M. bovis cargo to persist for extended periods of time.
243                One M. tuberculosis and three M. bovis strains were recovered from non-lesioned animal
244 ntages of tuberculosis cases attributable to M. bovis remained consistent nationally (range, 1.3%-1.6
245         Surprisingly, 2 isolates belonged to M. bovis BCG group, which are not allowed for animal vac
246  Mincle expression on lung sentinel cells to M. bovis BCG infection.
247                               In contrast to M. bovis RNAP, Escherichia coli RNAP efficiently forms R
248                Disseminated infection due to M. bovis is otherwise uncommon.
249  paratuberculosis (n = 10), cases exposed to M. bovis (n = 424), and negative controls (n = 38).
250 ated with an IRAK-4 inhibitor and exposed to M. bovis showed reduced TNF-alpha and IL-12, suggesting
251 Dictyostellium discoideum) are permissive to M. bovis infection and that the M. bovis bacilli may sur
252 ncreased lung bacterial loads in response to M. bovis BCG infection.
253  cells play a role in the immune response to M. bovis in cattle by contributing to the IFN-gamma resp
254 en developed that detect immune responses to M. bovis antigens absent in BCG; but these are too expen
255 gs were found to mount Th1-like responses to M. bovis BCG vaccination as determined by immunoprolifer
256 an serve as reliable biomarkers for tracking M. bovis infection in animal populations.
257 ns to definitively identify M. tuberculosis, M. bovis, M. bovis BCG, and other members of the complex
258  for the differentiation of M. tuberculosis, M. bovis, M. bovis BCG, M. africanum, M. microti, and M.
259 s were culture-positive for M. tuberculosis; M. bovis was not isolated.
260 aboratories, which detects antibodies to two M. bovis proteins, MPB70 and MPB83.
261            Proteomic comparison of wild-type M. bovis BCG with a Rv1675c (cmr) knockout strain showed
262 t attenuated BCG, but not virulent wild-type M. bovis or M. tuberculosis.
263 from wild-type M. tuberculosis and wild-type M. bovis, optimization of the column temperature, increa
264 tor responses and leukocyte recruitment upon M. bovis BCG challenge, and they demonstrated increased
265 nst tuberculosis than the currently utilized M. bovis BCG vaccine.
266                     In contrast, the vaccine M. bovis bacillus Calmette-Guerin (BCG) does not stimula
267  optimized IMS method was applied to various M. bovis-spiked lymph node matrices, it demonstrated exc
268 madelta T cell biology and, because virulent M. bovis infection of cattle represents an excellent mod
269 ll BCG substrains, was deleted from virulent M. bovis and Mycobacterium tuberculosis strains, and the
270 report that gammadelta T cells from virulent M. bovis-infected cattle respond specifically and direct
271 he rest of isolates belonged to the virulent M. bovis clonal complex European 2 present in Latin Amer
272 ps of calves were infected with the virulent M. bovis strain AF2122/97.
273 ith M. bovis BCG and challenge with virulent M. bovis and (ii) infection with M. bovis and treatment
274  had PZA resistance; 465 of 925 (50.3%) were M. bovis.
275                       Gamma-irradiated whole M. bovis AF2122/97 cells and ethanol-extracted surface a
276 haracteristics independently associated with M. bovis disease using adjusted prevalence ratios (aPRs)
277 diagnose infection of cattle or badgers with M. bovis, using a serum sample.
278 emains endemic and vaccination at birth with M. bovis bacille Calmette-Guerin (BCG) is widely used.
279 at, following natural infection of cows with M. bovis, as the stage of granuloma increases from stage
280                             Experiments with M. bovis and M. tuberculosis revealed the general releva
281 /MurA(+) lysis plasmid and immunization with M. bovis BCG, demonstrating that RASV strains displaying
282 ed in cattle experimentally co-infected with M. bovis and F. hepatica.
283 rately enriched with iron were infected with M. bovis BCG expressing green fluorescent protein.
284  in guinea pigs experimentally infected with M. bovis by aerosol and found to be equivalent to wild-t
285 e that had been experimentally infected with M. bovis despite the fact that the antigens were recogni
286 xclusively noted among rabbits infected with M. bovis Ravenel and AF2122.
287          The methylomes of bAM infected with M. bovis were compared to those of non-infected bAM 24 h
288 onses in cattle experimentally infected with M. bovis.
289 th virulent M. bovis and (ii) infection with M. bovis and treatment with isoniazid (INH) prior to rec
290 aired pathogen elimination to infection with M. bovis BCG in comparison to wild-type mice.
291 nt a spill-over host in which infection with M. bovis is not self-maintaining.
292 is cleared over time, whereas infection with M. bovis results in chronic, progressive, cavitary disea
293 ols as early as 3 weeks after infection with M. bovis, the earliest time point examined postchallenge
294 ble protective effect against infection with M. bovis.
295 y acquired, catheter-related infections with M. bovis-BCG in patients with indwelling catheters.
296  disease, a phenotype usually seen only with M. bovis infection.
297 ific-pathogen-free pigs were vaccinated with M. bovis BCG and monitored by following the gammadelta T
298 ce of guinea pigs previously vaccinated with M. bovis BCG.
299 st Mycobacterium bovis: (i) vaccination with M. bovis BCG and challenge with virulent M. bovis and (i
300 es resolved the genotypic differences within M. bovis strains and differentiated these strains from M

 
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