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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 otypes were discriminated in the panel of 47 M. bovis isolates.
15 ble discrimination was achieved, with the 47 M. bovis isolates resolved into 14 unique profiles, whil
16 R and TSEP methods detected as low as 1 to 5 M. bovis cells and 10 M. bovis cells, respectively, per
17 adgers shedding between 1 x 10(3)- 4 x 10(5) M. bovis cells g(-1) of faeces, creating a substantial a
18 filtration method detected as low as 5 to 50 M. bovis cells per 1.5 ml of trunk wash.
19 rait-allele associations, we interrogated 75 M. bovis and 61 M. tuberculosis genomes for single nucle
20 gs challenged with a low dose of aerosolized M. bovis.
21 ycobacterium bovis Ravenel, M. bovis AF2122, M. bovis BCG, M. tuberculosis H37Rv, M. tuberculosis CDC
22 d by enzyme-linked immunosorbent assay after M. bovis challenge, but not the frequency of responding
23  CD4(+) T cells at an early time point after M. bovis BCG vaccination, but CD4(+) T cells were found
24 development of disease as an end point after M. bovis challenge.
25 IFN-gamma test) can detect cattle soon after M. bovis infection regardless of the dose.
26 displayed antimycobacterial activity against M. bovis bacillus Calmette-Guerin.
27 3 is involved in protective immunity against M. bovis infection in cattle and are in accordance with
28                             In contrast, all M. bovis isolates generated a double-peak pattern when m
29                           This method allows M. bovis infections in badger populations to be monitore
30                              In contrast, an M. bovis whiB3 deletion mutant was completely attenuated
31  Guerin (BCG) vaccine strain selected for an M. bovis PK+ mutant, a finding that explains the alterat
32 roscopy-dissected lymph node lesions from an M. bovis-infected animal.
33                        Complementation of an M. bovis FbiC(-) mutant with fbiC restored the F(420) ph
34 FU/ml) was evaluated by IMS combined with an M. bovis-specific touchdown PCR.
35 ulosis from the closely related M. bovis and M. bovis BCG.
36 anum, M. canettii, M. microti, M. bovis, and M. bovis BCG), commercially available molecular assays c
37 sis, M. africanum, M. microti, M. bovis, and M. bovis BCG.
38 virulent wild-type M. tuberculosis H37Rv and M. bovis do not increase THP-1 apoptosis over baseline.
39 nalysis was undertaken for selected host and M. bovis proteins using a cattle serum repository contai
40 ogenic mycobacteria, including M. leprae and M. bovis, suggesting that a core of basic in vivo surviv
41 ication in PNAS reported that M. marinum and M. bovis bacillus Calmette-Guerin produce a type of spor
42 H stimulated cAMP production in both Mtb and M. bovis BCG, but broadly affected cAIG regulation only
43 this regulation required cmr in both Mtb and M. bovis BCG.
44 ainst M. luteus, Mycobacterium smegmatis and M. bovis (BCG).
45 ders of bacteria (including M. smegmatis and M. bovis BCG) can be produced.
46 cherichia coli, Mycobacterium smegmatis, and M. bovis BCG.
47 ution mutation in all tested BCG strains and M. bovis in comparison to the M. tuberculosis sequence.
48  clones of M. tuberculosis sensu stricto and M. bovis are distinct, deeply branching genotypic comple
49 ant mycobacteria such as M. tuberculosis and M. bovis Bacille-Calmette-Guerin.
50  CD4 T cell responses to M. tuberculosis and M. bovis bacillus Calmette-Guerin (BCG) Pasteur in vivo
51    We herein report that M. tuberculosis and M. bovis bacillus Calmette-Guerin infection down-regulat
52 ccelerated the growth of M. tuberculosis and M. bovis BCG crp mutants in mycomedium, but not within m
53 slow-growth phenotype of M. tuberculosis and M. bovis BCG crp mutants in vitro.
54 oth genes was reduced in M. tuberculosis and M. bovis BCG crp mutants.
55 dstream dissemination of M. tuberculosis and M. bovis BCG is uncommon in HIV-infected children vaccin
56 on of serC and Rv0885 in M. tuberculosis and M. bovis BCG, using site-specific mutagenesis, promoter
57 able from both wild-type M. tuberculosis and M. bovis isolates.
58 y to distinguish between M. tuberculosis and M. bovis.
59  as M. bovis, and 13 (2%) were identified as M. bovis BCG.
60  clinical specimens previously identified as M. bovis by spoligotyping revealed an isolate of M. tube
61 d as M. africanum, 8 (1%) were identified as M. bovis, and 13 (2%) were identified as M. bovis BCG.
62 but not in slow-growing mycobacteria such as M. bovis BCG or M. tuberculosis.
63 0 mRNA, whereas live virulent and attenuated M. bovis organisms increased the gene expression almost
64 cobacterium bovis (along with the attenuated M. bovis bacillus Calmette-Guerin [BCG]), and Mycobacter
65 sed by virulent mycobacteria since avirulent M. bovis bacillus Calmette-Guerin (BCG) fails to trigger
66 s that badger-to-cattle and cattle-to-badger M. bovis transmission may typically occur through contam
67 on-generated Mycobacterium bovis strain BCG (M. bovis) mutants that could not make coenzyme F(420) we
68 RP(Mt) regulon members also differed between M. bovis BCG and M. tuberculosis.
69 nd IL-17A production in Mycobacterium bovis (M. bovis)-infected cattle compared to non-infected contr
70 nitively identify M. tuberculosis, M. bovis, M. bovis BCG, and other members of the complex.
71 ifferentiation of M. tuberculosis, M. bovis, M. bovis BCG, M. africanum, M. microti, and M. canettii
72 btype II), M. africanum subtype I, M. bovis, M. bovis BCG, M. caprae, M. microti, or "M. canettii" or
73 d females are disproportionately affected by M. bovis, which was independently associated with extrap
74 nsic changes of gammadelta T cells caused by M. bovis BCG vaccination rather than being due solely to
75 epidemiology of human tuberculosis caused by M. bovis in the United States and validate previous find
76 e oncology patients with infection caused by M. bovis-BCG were studied.
77 ber 2015, searching for infections caused by M. bovis-BCG.
78 ell subset in acquired immunity conferred by M. bovis BCG vaccination.
79 s at early ages are functionally enhanced by M. bovis BCG vaccination and suggests an important role
80 rial antigens were significantly enhanced by M. bovis BCG vaccination.
81 ed to CD4(+) T cells, in immunity induced by M. bovis BCG vaccination, 4-week-old specific-pathogen-f
82 protein and compared to responses induced by M. bovis-derived purified protein derivative.
83 scribes for the first time that FLA carrying M. bovis can transmit TB.
84                                  Circulating M. bovis proteins, specifically polyketide synthetase 5,
85 4 novel small RNAs (sRNAs) in the TB-complex M. bovis BCG, using a combination of experimental and co
86 s using a cattle serum repository containing M. bovis (n = 128), Mycobacterium kansasii (n = 10), and
87 ecifically polyketide synthetase 5, detected M. bovis-infected cattle with little to no seroreactivit
88 apid, and cost-effective means of diagnosing M. bovis infection in cattle and badgers.
89 -4 responses were observed for the different M. bovis doses, suggesting that diagnostic assays (tuber
90 of pathology were observed for the different M. bovis doses.
91 he niacin test that clinically distinguishes M. bovis from M. tuberculosis.
92                   African 1 was the dominant M. bovis clonal complex, with 97 unique genotypes includ
93 actor, KLF4, to the promoter of CIITA during M. bovis BCG infection of macrophages was essential to o
94 ifferentiation of members of TBC, especially M. bovis and M. tuberculosis, when it is important to di
95 s loss, which is the case for an exceptional M. bovis human outbreak strain from Spain.
96 amples of sera collected from experimentally M. bovis-infected cattle and deer revealed that ESAT6-p-
97                   Two hundred and fifty-five M. bovis were isolated, identified and genotyped using d
98                                    Following M. bovis infection, the comparative tuberculin skin test
99 lysis of cellular immune responses following M. bovis challenge demonstrated that proliferative T-cel
100 s with greatest immunocapture capability for M. bovis in broth were those coated simultaneously with
101 nsitive and 93% specific against culture for M. bovis (n = 1,464) at necropsy.
102      They also indicate a different role for M. bovis and M. tuberculosis whiB3 genes in pathogenesis
103 the greatest sensitivity and specificity for M. bovis detection.
104                        Analysis of cDNA from M. bovis BCG shows that during in vitro growth all the g
105 P10, peripheral blood mononuclear cells from M. bovis-infected cattle were stimulated in vitro with a
106 ges, peripheral blood mononuclear cells from M. bovis-infected cattle were stimulated with M. bovis p
107 ted epitopes were recognized by T cells from M. bovis-infected cattle.
108 eptides that were recognized by T cells from M. bovis-infected cattle.
109 nthesis pathway (nadABC) can be deleted from M. bovis, demonstrating a functioning salvage pathway.
110 cobacterial glycoprotein, antigen MPB83 from M. bovis.
111              They were also used to generate M. bovis-specific peptide ligands by phage display biopa
112  CDC1551) into 5 major "SNP cluster groups." M. bovis isolates clustered into three major lineages ba
113 me that antigen vectored by the slow-growing M. bovis BCG but not that vectored by fast-growing, read
114 ular growth of M. smegmatis and slow-growing M. bovis BCG.
115 Mycobacterium smegmatis and the slow-growing M. bovis M. bovis BCG, were engineered to express a mode
116 (aPR, 2.0 [95% CI, 1.7-2.4]) also had higher M. bovis prevalences.
117  novel spoligotypes representing the highest M. bovis genetic diversity observed in Africa to date.
118                            It is unclear how M. bovis is able to survive in the environment for long
119 ricanum subtype II), M. africanum subtype I, M. bovis, M. bovis BCG, M. caprae, M. microti, or "M. ca
120                                           In M. bovis BCG, the fadD28 and mas promoters were function
121                                           In M. bovis-infected animals, PPDB specific IL-22 and IL-17
122 sts that upregulation of thymosin beta-10 in M. bovis-infected macrophages is linked with increased c
123 lation by the cAMP-responsive protein CRP in M. bovis BCG as a model for tuberculosis (TB)-complex ba
124 ession of thymosin beta-10 was identified in M. bovis-infected bovine macrophages by differential dis
125 but broadly affected cAIG regulation only in M. bovis BCG.
126 the nat gene caused an extended lag phase in M. bovis BCG and a cell morphology associated with an al
127 lence regulation system PhoP/PhoR (PhoPR) in M. bovis and in the closely linked Mycobacterium african
128 otein with an in vivo DNA binding profile in M. bovis BCG similar to that of CRP(Mt) in M. tuberculos
129 , granuloma formation was more pronounced in M. bovis BCG-infected CG/NE-deficient mice in comparison
130 n of increased IL-22 and IL-17A responses in M. bovis-infected animals to the level of protein produc
131 ell proliferation and IFN-gamma secretion in M. bovis infection, with nonprotein antigens inducing si
132 RP(BCG) and CRP(Mt) in vitro and in vivo, in M. bovis BCG and M. tuberculosis, to evaluate CRP(BCG)'s
133                             Heat-inactivated M. bovis induced a slight increase in thymosin beta-10 m
134 tudies using mycobacterial models, including M. bovis BCG, M. marinum, and M. smegmatis have signific
135         Mice lacking IRAK-4 showed increased M. bovis burden in spleen, liver, and lungs and smaller
136                                   Initially, M. bovis capture from Middlebrook 7H9 broth suspensions
137 lted in fewer tubercles than did intradermal M. bovis BCG vaccination.
138 firmed the clonal nature of the investigated M. bovis population, based on MLST data.
139                                  Not only is M. bovis unable to use glycerol as a sole carbon source
140        In livestock, the dominant species is M. bovis causing bovine tuberculosis (bTB), a disease of
141 s persists in lungs of immunocompetent mice, M. bovis BCG is cleared, and clearance is T cell depende
142 osis, M. africanum, M. canettii, M. microti, M. bovis, and M. bovis BCG), commercially available mole
143 f M. tuberculosis, M. africanum, M. microti, M. bovis, and M. bovis BCG.
144                                In our model, M. bovis would be taken up by amoebal trophozoites, whic
145                                    Moreover, M. bovis BCG-induced upregulation of C-type lectin Mincl
146  counts of 10(6) to 10(9) bacilli, while non-M. bovis species and BCG yielded CFU counts that ranged
147                       Sera from noninfected, M. bovis-infected, or M. avium subsp. paratuberculosis-i
148 ella; neither Mycobacterium tuberculosis nor M. bovis was isolated.
149 oximately 30%), whereas the adenylylation of M. bovis BCG GS does not change.
150 uberculosis, 20 M. africanum and one case of M. bovis) and 69 (15%) were due to infection with NTM.
151 e-half of the animals infected with 1 CFU of M. bovis developed pulmonary pathology typical of bovine
152 cheal route with 1,000, 100, 10, or 1 CFU of M. bovis.
153            In addition, 40% of all clones of M. bovis BCG had lost the hyg resistance cassette after
154                           Complementation of M. bovis with the pykA gene from M. tuberculosis H37Rv r
155 s were spiked with various concentrations of M. bovis cells and subjected to the described treatment
156 ogical and histopathological confirmation of M. bovis infection.
157 e of interleukin-2 (IL-2), in the context of M. bovis infection.
158  times allowed highly sensitive detection of M. bovis BCG.
159             The sensitivity for detection of M. bovis is lowered to 82% when only PZA-monoresistant i
160  field sampling of latrines and detection of M. bovis with quantitative PCR tests, the results of whi
161                          However, effects of M. bovis infection on adhesion molecule expression have
162            Understanding the epidemiology of M. bovis in badger populations is essential for directin
163 no important role during the early events of M. bovis infection.
164             We further show that exposure of M. bovis-infected trophozoites and cysts to Balb/c mice
165 ural PIMs identified from a lipid extract of M. bovis BCG.
166 resence of the putative virulence factors of M. bovis.
167 tation diminished inflammation and growth of M. bovis BCG via enhanced reactive oxygen species produc
168 e from the characteristic dysgonic growth of M. bovis to eugonic growth, an appearance normally assoc
169  novel function of P27 in the interaction of M. bovis with its natural host cell, the bovine macropha
170 lity as a rapid test to confirm isolation of M. bovis and M. caprae from veterinary specimens followi
171 re has the potential to improve isolation of M. bovis from lymph nodes and hence the diagnosis of bov
172 erial Ags and accumulating in the lesions of M. bovis-infected animals.
173           Lymphocytes obtained from lungs of M. bovis-infected cattle also had reduced expression of
174 ld be recognized by T cells from a number of M. bovis-infected hosts, we tested whether a virtual-mat
175 the diffusion of phosphates across the OM of M. bovis BCG and Mycobacterium tuberculosis are unknown.
176 comprise respectively 59% and 49% of ORFs of M. bovis BCG Pasteur and M. smegmatis mc(2) 155.
177 chanisms of the virulence and persistence of M. bovis and Mycobacterium tuberculosis Here, we describ
178 he wide host range and disease phenotypes of M. bovis.
179  were associated with a higher prevalence of M. bovis disease.
180  is associated with increasing prevalence of M. bovis infection in badgers, especially where landscap
181 h a widespread increase in the prevalence of M. bovis infection in badgers.
182                       The high prevalence of M. bovis is of public health concern and limits the pote
183          The minimum estimated prevalence of M. bovis was 2.8% (1.9-3.9), 7.7% (6.1-9.6), 21.3% (15.2
184 [95% CI, 3.1-5.3]) had higher prevalences of M. bovis disease.
185 hibition of TLR9-induced cross processing of M. bovis bacillus Calmette-Guerin expressing OVA could b
186 eta effectively enhanced cross processing of M. bovis bacillus Calmette-Guerin expressing OVA, bypass
187 he p27-p55 operon impairs the replication of M. bovis in bovine macrophages.
188 e badger's role as a persistent reservoir of M. bovis.
189 nd water, may act as long-term reservoirs of M. bovis in the environment.
190 Unlike significant wild animal reservoirs of M. bovis that are considered pests in other countries, s
191 ce of monitoring environmental reservoirs of M. bovis which may constitute a component of disease spr
192 jor secreted immunogenic protein (rMPB70) of M. bovis were used in an enzyme-linked immunosorbent ass
193          Exosomes isolated from the serum of M. bovis bacillus Calmette-Guerin-infected mice could al
194 specifically increased in the blood serum of M. bovis-infected animals).
195 specifically increased in the blood serum of M. bovis-infected animals).
196 d has been proposed as a potential source of M. bovis BCG's attenuation.
197  CG and NE into the bronchoalveolar space of M. bovis BCG-infected mice.
198                      Certain spoligotypes of M. bovis and M. caprae were not detected by the LFD in S
199  derivatives and increases susceptibility of M. bovis BCG to antibiotics that permeate the cell wall.
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  discrimination possible in strain typing of M. bovis, with the added benefit of an intuitive digital
203 ovide valuable tools for molecular typing of M. bovis.
204 he decreased infectivity and/or virulence of M. bovis relative to M. tuberculosis in humans.
205                                          One M. bovis and 66 M. tuberculosis isolates were identified
206                                         Only M. bovis DNA was amplified, indicating 100% analytical s
207 tic cell lines by Mycobacterium smegmatis or M. bovis BCG harboring a plasmid encoding the fluorescen
208 crophages with Mycobacterium tuberculosis or M. bovis strain BCG enhances MHC-II release in synergy w
209                                As predicted, M. bovis BCG cell lysates metabolized the BphC substrate
210  antigens of such cells were used to produce M. bovis-specific polyclonal and monoclonal antibodies i
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 as assessed by histopathology, and resembled M. bovis BCG vaccination in this respect.
218 d secondary lesions at intrapulmonary sites, M. bovis infections led to the most apparent gross patho
219 fers INH and ETH resistance to M. smegmatis, M. bovis BCG and M. tuberculosis.
220 uberculosis challenge compared with standard M. bovis bacille Calmette-Guerin vaccination.
221 rium tuberculosis but not the vaccine strain M. bovis bacille Calmette-Guerin (BCG).
222 losis (MTB), missing from the vaccine strain M. bovis BCG, and its importance to virulence has been e
223  the murine model compared with subcutaneous M. bovis BCG Pasteur vaccination.
224 o 10 CFU/ml of the M. tuberculosis surrogate M. bovis BCG.
225 91; P < 0.0001), with the added benefit that M. bovis was differentiated from another MTBC species in
226                    Furthermore, we show that M. bovis infection in cattle induces robust IL-17A prote
227 g-term epidemiological data, suggesting that M. bovis and related phoPR-mutated strains pose a lower
228 thymosin beta-10 expression, suggesting that M. bovis or mycobacterial products are essential in the
229 Importantly, we show for the first time that M. bovis arrests phagosome maturation in a process that
230     Polyclonal antibodies raised against the M. bovis hemolysin-cytotoxin also recognized a protein o
231 riant SNPs, while 84 SNPs differentiated the M. bovis BCG lineage from the virulent isolates.
232 ein of the molecular mass predicted from the M. bovis BCG sequence (approximately 95,000 Da), as well
233 utants contained transposons inserted in the M. bovis homologue of the Mycobacterium tuberculosis gen
234                    In the first instance the M. bovis-derived protein ESAT-6 was used as a model anti
235 potato slices used for the derivation of the M. bovis bacillus Calmette and Guerin (BCG) vaccine stra
236 ins homologous over the entire length of the M. bovis FbiC, but in seven microorganisms two separate
237 the N-terminal or C-terminal portions of the M. bovis FbiC.
238 ds target small hypervariable regions of the M. bovis genome and provide anonymous biallelic informat
239 quence was identified in most genomes of the M. bovis strains collected in all three countries.
240 ermissive to M. bovis infection and that the M. bovis bacilli may survive within the cysts of four of
241 Cluster 1 (WC1), and we demonstrate that the M. bovis-specific gammadelta T cell response is composed
242 interferon (IFN-gamma) responses towards the M. bovis-specific antigen ESAT-6, whose gene is absent f
243 sis probe and a single-peak pattern with the M. bovis probe.
244 sis probe and a double-peak pattern with the M. bovis probe.
245 rovide an intracellular niche allowing their M. bovis cargo to persist for extended periods of time.
246                One M. tuberculosis and three M. bovis strains were recovered from non-lesioned animal
247 ntages of tuberculosis cases attributable to M. bovis remained consistent nationally (range, 1.3%-1.6
248  Mincle expression on lung sentinel cells to M. bovis BCG infection.
249                               In contrast to M. bovis RNAP, Escherichia coli RNAP efficiently forms R
250                Disseminated infection due to M. bovis is otherwise uncommon.
251  paratuberculosis (n = 10), cases exposed to M. bovis (n = 424), and negative controls (n = 38).
252 ated with an IRAK-4 inhibitor and exposed to M. bovis showed reduced TNF-alpha and IL-12, suggesting
253 Dictyostellium discoideum) are permissive to M. bovis infection and that the M. bovis bacilli may sur
254 ncreased lung bacterial loads in response to M. bovis BCG infection.
255  cells play a role in the immune response to M. bovis in cattle by contributing to the IFN-gamma resp
256 gs were found to mount Th1-like responses to M. bovis BCG vaccination as determined by immunoprolifer
257 vis-infected cattle are highly responsive to M. bovis sonic extract (MBSE).
258 an serve as reliable biomarkers for tracking M. bovis infection in animal populations.
259 ns to definitively identify M. tuberculosis, M. bovis, M. bovis BCG, and other members of the complex
260  for the differentiation of M. tuberculosis, M. bovis, M. bovis BCG, M. africanum, M. microti, and M.
261 aboratories, which detects antibodies to two M. bovis proteins, MPB70 and MPB83.
262            Proteomic comparison of wild-type M. bovis BCG with a Rv1675c (cmr) knockout strain showed
263                       In contrast, wild-type M. bovis infection failed to activate any caspases in TH
264 from wild-type M. tuberculosis and wild-type M. bovis, optimization of the column temperature, increa
265 tor responses and leukocyte recruitment upon M. bovis BCG challenge, and they demonstrated increased
266 nst tuberculosis than the currently utilized M. bovis BCG vaccine.
267                     In contrast, the vaccine M. bovis bacillus Calmette-Guerin (BCG) does not stimula
268  optimized IMS method was applied to various M. bovis-spiked lymph node matrices, it demonstrated exc
269 madelta T cell biology and, because virulent M. bovis infection of cattle represents an excellent mod
270 ll BCG substrains, was deleted from virulent M. bovis and Mycobacterium tuberculosis strains, and the
271 report that gammadelta T cells from virulent M. bovis-infected cattle respond specifically and direct
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 (BCG) and were then challenged with virulent M. bovis.
275  had PZA resistance; 465 of 925 (50.3%) were M. bovis.
276 seeding of the organism to organs from which M. bovis could be excreted.
277                       Gamma-irradiated whole M. bovis AF2122/97 cells and ethanol-extracted surface a
278 haracteristics independently associated with M. bovis disease using adjusted prevalence ratios (aPRs)
279 diagnose infection of cattle or badgers with M. bovis, using a serum sample.
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 CG-vaccinated guinea pigs were infected with M. bovis BCG, Mycobacterium avium, the attenuated Mycoba
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 onses in cattle experimentally infected with M. bovis.
288 th virulent M. bovis and (ii) infection with M. bovis and treatment with isoniazid (INH) prior to rec
289 aired pathogen elimination to infection with M. bovis BCG in comparison to wild-type mice.
290 nt a spill-over host in which infection with M. bovis is not self-maintaining.
291 is cleared over time, whereas infection with M. bovis results in chronic, progressive, cavitary disea
292 ols as early as 3 weeks after infection with M. bovis, the earliest time point examined postchallenge
293 ble protective effect against infection with M. bovis.
294 y acquired, catheter-related infections with M. bovis-BCG in patients with indwelling catheters.
295  disease, a phenotype usually seen only with M. bovis infection.
296 . bovis-infected cattle were stimulated with M. bovis purified protein derivative (PPD) or pokeweed m
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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