Journal articles: 'Mycobacterium bovis infection'

1

Holdiness, Mack R. "Mycobacterium bovis Infection." Archives of Internal Medicine 145, no. 10 (October 1, 1985): 1930. http://dx.doi.org/10.1001/archinte.1985.00360100204047.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Holdiness, M. R. "Mycobacterium bovis infection." Archives of Internal Medicine 145, no. 10 (October 1, 1985): 1930b—1930. http://dx.doi.org/10.1001/archinte.145.10.1930b.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Stern, Rebecca, Clay Roscoe, and Elizabeth A. Misch. "<i>Mycobacterium bovis</i> BCG osteoarticular infection complicating immune therapy for bladder cancer: a case report." Journal of Bone and Joint Infection 6, no. 4 (February 22, 2021): 107–10. http://dx.doi.org/10.5194/jbji-6-107-2021.

Full text

Abstract:

Abstract. Osteoarticular infection with Mycobacterium bovis (M. bovis) is a rare complication of bladder cancer treatment with intravesical Bacillus Calmette–Guèrin (BCG). We describe a case of disseminated Mycobacterium bovis BCG infection masquerading as a chronic prosthetic joint infection in a patient with several risk factors for progressive mycobacterial infection.

APA, Harvard, Vancouver, ISO, and other styles

4

Waters, W. R., A. O. Whelan, K. P. Lyashchenko, R. Greenwald, M. V. Palmer, B. N. Harris, R. G. Hewinson, and H. M. Vordermeier. "Immune Responses in Cattle Inoculated with Mycobacterium bovis, Mycobacterium tuberculosis, or Mycobacterium kansasii." Clinical and Vaccine Immunology 17, no. 2 (December 9, 2009): 247–52. http://dx.doi.org/10.1128/cvi.00442-09.

Full text

Abstract:

ABSTRACT Cattle were inoculated with Mycobacterium bovis, Mycobacterium tuberculosis, or Mycobacterium kansasii to compare the antigen-specific immune responses to various patterns of mycobacterial disease. Disease expression ranged from colonization with associated pathology (M. bovis infection) and colonization without pathology (M. tuberculosis infection) to no colonization or pathology (M. kansasii infection). Delayed-type hypersensitivity and gamma interferon responses were elicited by each mycobacterial inoculation; however, the responses by the M. bovis- and M. tuberculosis-inoculated animals exceeded those of the M. kansasii-inoculated animals. Specific antibody responses were detected in all M. tuberculosis- and M. bovis-inoculated cattle 3 weeks after inoculation. From 6 to 16 weeks after M. tuberculosis inoculation, the antibody responses waned, whereas the responses persisted with M. bovis infection. With M. kansasii inoculation, initial early antibody responses waned by 10 weeks after inoculation and then increased 2 weeks after the injection of purified protein derivative for the skin test at 18 weeks after challenge. These findings indicate that antibody responses are associated with the antigen burden rather than the pathology, cellular immune responses to tuberculin correlate with infection but not necessarily with the pathology or bacterial burden, and exposure to mycobacterial antigens may elicit an antibody response in a presensitized animal.

APA, Harvard, Vancouver, ISO, and other styles

5

Nau, Gerard J., Lucy Liaw, Geoffrey L. Chupp, Jeffrey S. Berman, Brigid L. M. Hogan, and Richard A. Young. "Attenuated Host Resistance againstMycobacterium bovis BCG Infection in Mice Lacking Osteopontin." Infection and Immunity 67, no. 8 (August 1, 1999): 4223–30. http://dx.doi.org/10.1128/iai.67.8.4223-4230.1999.

Full text

Abstract:

ABSTRACT Expression of the cytokine osteopontin (OPN) is elevated in granulomas caused by Mycobacterium tuberculosis. We tested the hypothesis that OPN contributes to host protection in a mouse model of mycobacterial infection. When infected with Mycobacterium bovis BCG, mice lacking a functional OPN gene had more severe infections characterized by heavier bacterial loads and a delayed clearance of the bacteria. The OPN-null mice had greater granuloma burdens consistent with the elevated bacterial load. The ability of osteopontin to facilitate the clearance of mycobacteria was most pronounced early after infection and appeared to be independent of known mediators of resistance to infection by mycobacteria: antigen-specific T-cell immunity, gamma interferon production, and nitric oxide production. BCG grew more rapidly in macrophages derived from OPN-null mice than in those from wild-type mice, demonstrating that the null phenotype was due to an intrinsic macrophage defect. These results indicate that osteopontin augments the host response against a mycobacterial infection and that it acts independently from other antimycobacterial resistance mechanisms.

APA, Harvard, Vancouver, ISO, and other styles

6

Erb, Klaus J., Claudia Trujillo, Mike Fugate, and Heidrun Moll. "Infection with the Helminth Nippostrongylus brasiliensis Does Not Interfere with Efficient Elimination of Mycobacterium bovis BCG from the Lungs of Mice." Clinical and Vaccine Immunology 9, no. 3 (May 2002): 727–30. http://dx.doi.org/10.1128/cdli.9.3.727-730.2002.

Full text

Abstract:

ABSTRACT Infection with Mycobacterium tuberculosis continues to be one of the major global health threats. Strong mycobacterium-specific Th1 immune responses correlate with protection, and decreased Th1 responses correlate with disease progression. In contrast, the impact of Th2 responses on the development of protective immune responses to mycobacteria remains unclear. To analyze whether ongoing Th2 responses present in the lung influence the development of a protective Th1 immune response to mycobacteria, we coinfected mice with the helminth Nippostrongylus brasiliensis and Mycobacterium bovis BCG. We found that the T cells from the lymph nodes of coinfected mice secreted significantly less gamma interferon than did the T cells from mice infected with M. bovis BCG after in vitro stimulation with purified protein from M. tuberculosis when 108 CFU of M. bovis BCG were used for the infection. This result indicates that the helminth infection reduced the Th1 immune response to the mycobacteria in the lung. However, mycobacterial clearance was not delayed in the coinfected animals. Importantly, the infection with BCG after the helminth infection did not reduce the helminth-induced Th2 response in the lung, ruling out the possibility that the lack of a reduction in bacterial clearance in the coinfected mice was due to a downmodulation of the helminth-induced Th2 response. Taken together, our results suggest that ongoing Th2 responses in the lung do not necessarily lead to increased susceptibility to mycobacterial infection.

APA, Harvard, Vancouver, ISO, and other styles

7

Aldwell, Frank E., Bridget L. Dicker, Fernanda M. Da Silva Tatley, Martin F. Cross, Simon Liggett, Colin G. Mackintosh, and J. Frank T. Griffin. "Mycobacterium bovis-Infected Cervine Alveolar Macrophages Secrete Lymphoreactive Lipid Antigens." Infection and Immunity 68, no. 12 (December 1, 2000): 7003–9. http://dx.doi.org/10.1128/iai.68.12.7003-7009.2000.

Full text

Abstract:

ABSTRACT Tuberculosis is caused by intracellular bacteria belonging to the genus Mycobacterium, including M. tuberculosisand M. bovis. Alveolar macrophages (AMs) are the primary host cell for inhaled mycobacteria. However, little is known about the mechanisms by which infected AMs can process and present mycobacterial antigens to primed lymphocytes and how these responses may affect ensuing protection in the host. In the present study, we sought to determine whether AMs from a naturally susceptible host forMycobacterium bovis (red deer) could produce and secrete soluble immunoreactive antigens following mycobacterial infection in vitro. Confluent monolayers of deer AMs were infected with either heat-killed or live virulent M. bovis or M. bovis BCG at a multiplicity of infection of 5:1 and cultured for 48 h. Culture supernatants were collected, concentrated, and tested for the presence of mycobacterial antigens in a lymphocyte proliferation assay by using peripheral blood mononuclear cells fromM. bovis-sensitized or naive deer. Supernatants derived from macrophages which had been infected with live bacilli stimulated the proliferation of antigen-sensitized, but not naive, lymphocytes. Supernatants derived from uninoculated AMs or AMs inoculated with heat-killed bacilli failed to stimulate lymphocyte proliferation. The lymphoproliferative activity was retained following lipid extraction of the supernatants, which were free of amino groups as determined by thin-layer chromatography. These results demonstrate that mycobacteria which are actively growing within AMs produce lipids which are secreted into the extracellular milieu and that these lipids are recognized by lymphocytes from mycobacterium-primed hosts. We suggest that mycobacterial lipids are released from AMs following aerosol infection in vivo and that they play an important role in the early immune response to tuberculosis.

APA, Harvard, Vancouver, ISO, and other styles

8

Thoen, Charles O., William J. Quinn, Lyle D. Miller, Larry L. Stackhouse, Bradford F. Newcomb, and James M. Ferrell. "Mycobacterium Bovis Infection in North American Elk (Cervus Elaphus)." Journal of Veterinary Diagnostic Investigation 4, no. 4 (October 1992): 423–27. http://dx.doi.org/10.1177/104063879200400410.

Full text

Abstract:

A naturally occurring outbreak of Mycobacterium bovid infection in captive wild elk (wapiti) in Montana was confirmed by mycobacteriologic examination. Twenty-eight of 143 elk responded to M. bovis purified protein derivative (PPD) tuberculin injected intradermally in the cervical region (SCT). The results of comparative cervical tuberculin skin tests conducted within 9 days of SCT revealed greater responses to M. bovis PPD tuberculin than to M. avium PPD tuberculin in 23 of 28 elk responding. At necropsy, several grossly visible tuberculous lesions were observed in the parenchyma of the lung, thoracic lymph nodes, and submandibular lymph nodes. Microscopic examination of appropriately stained tissue sections revealed the presence of granulomatous lesions containing acid-fast bacilli. An enzyme-linked immunosorbent assay (ELISA) was developed using a sarkosyl extract of M. bovis (antigen) and peroxidase-labeled protein G (conjugate); reactions were detected in the sera of 8 of 9 elk responding to M. bovis PPD tuberculin. Lymphocyte blastogenic assay responses were detected using M. bovis antigens in 7 of 9 elk positive on skin tests using M. bovis PPD.

APA, Harvard, Vancouver, ISO, and other styles

9

Naughton, James F., Katrina L. Mealey, K. Jane Wardrop, J. Lindsay Oaks, and Daniel S. Bradway. "Systemic Mycobacterium avium Infection in a Dog Diagnosed by Polymerase Chain Reaction Analysis of Buffy Coat." Journal of the American Animal Hospital Association 41, no. 2 (March 1, 2005): 128–32. http://dx.doi.org/10.5326/0410128.

Full text

Abstract:

Dogs may be infected by Mycobacterium (M.) tuberculosis, M. bovis, and M. avium complex, and the clinical signs associated with each of these infections may be indistinguishable. Rapid speciation of the infecting organism is desirable because of the public health concerns associated with M. bovis and M. tuberculosis infections. A mycobacterial infection was suspected in the dog of this report based on acid-fast staining of organisms in macrophages obtained from liver aspirates and buffy-coat preparations. Polymerase chain reaction (PCR) analysis of a buffy-coat preparation identified M. avium.

APA, Harvard, Vancouver, ISO, and other styles

10

Waters, W. R., B. J. Nonnecke, M. V. Palmer, S. Robbe-Austermann, J. P. Bannantine, J. R. Stabel, D. L. Whipple, et al. "Use of Recombinant ESAT-6:CFP-10 Fusion Protein for Differentiation of Infections of Cattle by Mycobacterium bovis and by M. avium subsp. avium and M. avium subsp. paratuberculosis." Clinical Diagnostic Laboratory Immunology 11, no. 4 (July 2004): 729–35. http://dx.doi.org/10.1128/cdli.11.4.729-735.2004.

Full text

Abstract:

ABSTRACT Immunological diagnosis of Mycobacterium bovis infection of cattle is often confounded by cross-reactive responses resulting from exposure to other mycobacterial species, especially Mycobacterium avium. Early secretory antigenic target 6 (ESAT-6) and culture filtrate protein 10 (CFP-10) are dominant gamma interferon (IFN-γ)-inducing antigens of tuberculous mycobacteria, and they are absent from many environmental nontuberculous mycobacteria. Because M. avium exposure is the primary confounding factor in the diagnosis of M. bovis-infected animals, in vitro responses to a recombinant ESAT-6:CFP-10 (rESAT-6:CFP-10) fusion protein by blood leukocytes from cattle naturally exposed to M. avium or experimentally challenged with Mycobacterium avium subsp. avium or Mycobacterium avium subsp. paratuberculosis were compared to responses by M. bovis-infected cattle. Responses to heterogeneous mycobacterial antigens (i.e., purified protein derivatives [PPDs] and whole-cell sonicates [WCSs]) were also evaluated. Tumor necrosis factor alpha (TNF-α), IFN-γ, and nitric oxide responses by M. bovis-infected cattle to rESAT-6:CFP-10 exceeded (P < 0.05) the corresponding responses by cattle naturally sensitized to M. avium. Experimental infection with M. bovis, M. avium, or M. avium subsp. paratuberculosis induced significant (P < 0.05) IFN-γ and nitric oxide production to WCS and PPD antigens, regardless of the mycobacterial species used for the preparation of the antigen. Responses to homologous crude antigens generally exceeded responses to heterologous antigens. Nitric oxide and IFN-γ responses to rESAT-6:CFP-10 by blood leukocytes from M. bovis-infected calves exceeded (P < 0.05) the corresponding responses of noninfected, M. avium-infected, and M. avium subsp. paratuberculosis-infected calves. Despite the reported potential for secretion of immunogenic ESAT-6 and CFP-10 proteins by M. avium and M. avium subsp. paratuberculosis, it appears that use of the rESAT-6:CFP-10 fusion protein will be useful for the detection of tuberculous cattle in herds with pre-existing sensitization to M. avium and/or M. avium subsp. paratuberculosis.

APA, Harvard, Vancouver, ISO, and other styles

11

Langlois, M. E., F. Ader, O. Dumistrescu, E. Servien, J. Saison, T. Ferry, C. Chidiac, and F. Valour. "Mycobacterium bovis prosthetic joint infection." Médecine et Maladies Infectieuses 46, no. 8 (December 2016): 445–48. http://dx.doi.org/10.1016/j.medmal.2016.07.005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Costa, F??bio F., Gabriela Castro, Jacy Andrade, Am??lia de Ribeiro Jesus, Roque Pacheco de Almeida, and Cristiana M. Nascimento-Carvalho. "Resistant Mycobacterium bovis Disseminated Infection." Pediatric Infectious Disease Journal 25, no. 2 (February 2006): 190. http://dx.doi.org/10.1097/01.inf.0000200103.69932.4c.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

van der Burgt, G. M., T. Crawshaw, A. P. Foster, D. J. B. Denny, and A. Schock. "Mycobacterium bovis infection in dogs." Veterinary Record 165, no. 21 (November 21, 2009): 634. http://dx.doi.org/10.1136/vr.165.21.634.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Nicolle, Delphine, Cécile Fremond, Xavier Pichon, André Bouchot, Isabelle Maillet, Bernhard Ryffel, and Valerie J. F. Quesniaux. "Long-Term Control of Mycobacterium bovis BCG Infection in the Absence of Toll-Like Receptors (TLRs): Investigation of TLR2-, TLR6-, or TLR2-TLR4-Deficient Mice." Infection and Immunity 72, no. 12 (December 2004): 6994–7004. http://dx.doi.org/10.1128/iai.72.12.6994-7004.2004.

Full text

Abstract:

ABSTRACT Live mycobacteria have been reported to signal through both Toll-like receptor 2 (TLR2) and TLR4 in vitro. Here, we investigated the role of TLR2 in the long-term control of the infection by the attenuated Mycobacterium, Mycobacterium bovis BCG, in vivo. We sought to determine whether the reported initial defect of bacterial control (K. A. Heldwein et al., J. Leukoc. Biol. 74:277-286, 2003) resolved in the chronic phase of BCG infection. Here we show that TLR2-deficient mice survived a 6-month infection period with M. bovis BCG and were able to control bacterial growth. Granuloma formation, T-cell and macrophage recruitment, and activation were normal. Furthermore, the TLR2 coreceptor, TLR6, is also not required since TLR6-deficient mice were able to control chronic BCG infection. Finally, TLR2-TLR4-deficient mice infected with BCG survived the 8-month observation period. Interestingly, the adaptive response of TLR2- and/or TLR4-deficient mice seemed essentially normal on day 14 or 56 after infection, since T cells responded normally to soluble BCG antigens. In conclusion, our data demonstrate that TLR2, TLR4, or TLR6 are redundant for the control of M. bovis BCG mycobacterial infection.

APA, Harvard, Vancouver, ISO, and other styles

15

Jordao, L., M. Simoes, C. Bleck, G. Griffiths, and E. Anes. "Characterization of Mycobacterium bovis Phagosome." Microscopy and Microanalysis 14, S3 (September 2008): 124–25. http://dx.doi.org/10.1017/s1431927608089629.

Full text

Abstract:

Mycobacterium tuberculosis complex are among the most successful pathogens. Their success resides in the ability to interfere with intracellular traffic avoiding natural pathways of the phagosome maturation. Recently, mycobacteria escape from the phagosome to the cytosol was investigated as an alternative survival strategy. In this context we decided to determine the exact intracellular location of Mycobacterium bovis in different host macrophages and characterize the pathogen intracellular niche for survival. The main goal here was to characterize live vs dead M. bovis spp phagosome in different host macrophages. Macrophages infection, fluorescence and EM procedures were carried out as described previously.

APA, Harvard, Vancouver, ISO, and other styles

16

Paarwater, Brandon A., Jomien M. Mouton, Samantha L. Sampson, Stephanus T. Malherbe, Jane A. Shaw, Gerhard Walzl, Leigh A. Kotze, and Nelita du Plessis. "Inhaled particulate matter affects immune responsiveness of human lung phagocytes to mycobacteria." American Journal of Physiology-Lung Cellular and Molecular Physiology 321, no. 3 (September 1, 2021): L566—L575. http://dx.doi.org/10.1152/ajplung.00014.2021.

Full text

Abstract:

The influence of smoke-derived or air pollution-derived cytoplasmic particulate matter (PM) can be detrimental and can lead to failed lung immunity. We investigated mycobacterial uptake, intracellular replication, and soluble immune-mediator responses of human bronchoalveolar lavage cells (BALCs) loaded with/without PM, to infection with mycobacterial strains. We observed that only BALCs containing PM display an ex vivo phenotypic profile dominated by spontaneous interleukin (IL)-10 production. PM-loaded BALCs retained the ability to phagocytose both Mycobacterium bovis Bacille Calmette Guérin (BCG) and Mycobacterium tuberculosis ( M.tb) ΔleuDΔpanCD at equal efficacy as clear non-PM-loaded BALCs. However, immune responsiveness, such as the production of IL-6 ( P = 0.015) and tumor necrosis factor-α (TNF)-α ( P = 0.0172) immediately post M. bovis BCG infection, were dramatically lower in black BALCs loaded with PM versus clear non-PM-loaded BALCs. By 24 h post infection, differential immune responses to M. bovis BCG between black versus clear BALC waned, and instead, production of IL-6 ( P = 0.03) and IL-1α ( P = 0.04) by black BALCs was lower versus clear BALCs following M.tb ΔleuDΔpanCD infection. Considering that TNF-α and IL-6 are characterized as critical to host protection against mycobacteria, our findings suggest that BALCs loaded with inhaled PM, display lower levels of antimycobacterial mediators and that the response magnitude differs according to infective mycobacterial strain. Even though this did not translate into altered mycobacterial killing at early time points post infection, the long-term impact of such changes remains to be established.

APA, Harvard, Vancouver, ISO, and other styles

17

Da Silva Pedroso, Silvia Cristina, Karla Valéria Batista Lima, Ismari Perini Furlaneto, Yan Corrêa Rodrigues, Darlene Kássia Saraiva Queiroz Pantoja, Alex Junior Souza de Souza, and Washington Luiz Assunção Pereira. "Bovine tuberculosis due to Mycobacterium bovis and other mycobacteria among water buffalo (Bubalus bubalis) from the Brazilian Amazon." Journal of Infection in Developing Countries 15, no. 05 (May 31, 2021): 736–41. http://dx.doi.org/10.3855/jidc.13558.

Full text

Abstract:

Introduction: Zoonotic tuberculosis is a disease of public health importance worldwide, especially in developing countries. The present study aimed to investigate the role played by Mycobacterium bovis and other mycobacteria as etiologic agents of bubaline tuberculosis (TB) in the Brazilian Amazon region. Methodology: Granulomatous lesions suggestive of TB obtained from 109 buffaloes (n =109) during sanitary inspection at slaughter were subjected to histopathological evaluation, immunohistochemical (IHC) detection of Mycobacterium antigens, and to molecular tests (PCR) to detect hsp65, IS6110 and RD4 genes, which are specific to Mycobacterium spp., Mycobacterium tuberculosis Complex (MTBC) and M. bovis, respectively. Results: PCR results indicated Mycobacterium infection in 87.2% of the cases, of which 69.5% were positive for M. bovis, 27.4% belonged to MTBC, and 3.1% were probably non-TB mycobacteria. There was good agreement between the genus-specific molecular technique and the histopathological analysis. This high frequency of TB cases caused by non-M. bovis suggests a diversified scenario of mycobacteria associated with bubaline TB in the Brazilian Amazon region. Conclusions: The results reinforce the need of discussing the inclusion of more accurate techniques in examinations carried out by Inspection Services in Brazil.

APA, Harvard, Vancouver, ISO, and other styles

18

Riendeau, Carrie J., and Hardy Kornfeld. "THP-1 Cell Apoptosis in Response to Mycobacterial Infection." Infection and Immunity 71, no. 1 (January 2003): 254–59. http://dx.doi.org/10.1128/iai.71.1.254-259.2003.

Full text

Abstract:

ABSTRACT We previously reported that Mycobacterium tuberculosis infection primes human alveolar macrophages (HAM) for tumor necrosis factor alpha (TNF-α)-mediated apoptosis and that macrophage apoptosis is associated with killing internalized bacilli. Virulent mycobacterial strains elicit much less apoptosis than attenuated strains, implying that apoptosis is a defense against intracellular infection. The present study evaluated the potential for phorbol myristate acetate-differentiated THP-1 cells to mimic this response of primary macrophages. Consistent with the behavior of alveolar macrophages, attenuated M. tuberculosis H37Ra and Mycobacterium bovis BCG strongly induce THP-1 apoptosis, which requires endogenous TNF. THP-1 apoptosis is associated with reduced viability of infecting BCG. In contrast, virulent wild-type M. tuberculosis H37Rv and M. bovis do not increase THP-1 apoptosis over baseline. BCG induced early activation of caspase 10 and 9, followed by caspase 3. In contrast, wild-type M. bovis infection failed to activate any caspases in THP-1 cells. BCG-induced THP-1 apoptosis is blocked by retroviral transduction with vectors expressing crmA but not bcl-2. We conclude that differentiated THP-1 cells faithfully model the apoptosis response of HAM. Analysis of the THP-1 cell response to infection with virulent mycobacteria suggests that TNF death signals are blocked proximal to initiator caspase activation, at the level of TNF receptor 1 or its associated intracytoplasmic adaptor complex. Interference with TNF death signaling may be a virulence mechanism that allows M. tuberculosis to circumvent innate defenses leading to apoptosis of infected host cells.

APA, Harvard, Vancouver, ISO, and other styles

19

Gooding, Travis M., Paul D. R. Johnson, Dianne E. Campbell, John A. Hayman, Elizabeth L. Hartland, Andrew S. Kemp, and Roy M. Robins-Browne. "Immune Response to Infection withMycobacterium ulcerans." Infection and Immunity 69, no. 3 (March 1, 2001): 1704–7. http://dx.doi.org/10.1128/iai.69.3.1704-1707.2001.

Full text

Abstract:

ABSTRACT Mycobacterium ulcerans is a slow-growing, acid-fast bacillus that causes chronic necrotizing skin ulcers known as Buruli ulcers. Previously reported information on immunity to this mycobacterium is limited. We examined immune responses to M. ulcerans and M. bovis BCG in patients with M. ulcerans disease and in 20 healthy control subjects (10 tuberculin test positive and 10 tuberculin test negative). Cell-mediated immunity was assessed by stimulating peripheral blood mononuclear cells (PBMC) with whole mycobacteria and then measuring PBMC proliferation and the production of gamma interferon (IFN-γ). Humoral immunity was assessed by immunoblotting. PBMC from all subjects showed significantly greater proliferation and IFN-γ production in response to stimulation with living mycobacteria compared with killed cells. However, PBMC from subjects with past or current M. ulcerans disease showed significantly reduced proliferation and production of IFN-γ in response to stimulation with live M. ulcerans or M. bovis than PBMC from healthy, tuberculin test-positive subjects (P < 0.001) and showed results in these assays comparable to those of tuberculin test-negative subjects (P > 0.2). Serum from 9 of 11 patients with M. ulcerans disease, but no control subject, contained antibodies to M. ulcerans. The results indicate that patients with M. ulcerans infection mount an immune response to M. ulcerans as evidenced by antibody production, but they demonstrate profound systemic T-cell anergy to mycobacterial antigens. These findings may explain some of the distinct clinical and pathological features of M. ulcerans-induced disease.

APA, Harvard, Vancouver, ISO, and other styles

20

Cheadle, Eleanor J., Dearbhaile O'Donnell, Peter J. Selby, and Andrew M. Jackson. "Closely Related Mycobacterial Strains Demonstrate Contrasting Levels of Efficacy as Antitumor Vaccines and Are Processed for Major Histocompatibility Complex Class I Presentation by Multiple Routes in Dendritic Cells." Infection and Immunity 73, no. 2 (February 2005): 784–94. http://dx.doi.org/10.1128/iai.73.2.784-794.2005.

Full text

Abstract:

ABSTRACT Mycobacteria expressing recombinant antigens are already being developed as vaccines against both infections and tumors. Little is known about how dendritic cells might process such antigens. Two different mycobacterial species, the fast-growing Mycobacterium smegmatis and the slow-growing M. bovis M. bovis BCG, were engineered to express a model tumor antigen, the Kb-restricted dominant cytotoxic T-lymphocyte epitope OVA257-264. Recombinant M. bovis BCG but not recombinant M. smegmatis conferred protection to mice challenged with the B16-OVA tumor cell line. We went on to investigate whether the contrast in antitumor efficacy could be due to differences in how dendritic cells process antigen from the two mycobacterial strains for class I presentation. Both strains of mycobacteria caused phenotypic maturation of dendritic cells, but recombinant M. smegmatis infection led to a greater degree of dendritic cell maturation than recombinant M. bovis BCG infection. Antigen from recombinant M. smegmatis was processed and presented as OVA257-264 on Kb molecules by the dendritic cell line DC2.4 but not by bone marrow-derived dendritic cells (BMDC) or splenic dendritic cells. In contrast, antigen from recombinant M. bovis BCG was presented by all three dendritic cell types as long as the mycobacteria were viable. Such presentation was dependent on proteasome function and nascent major histocompatibility complex (MHC) class I molecules in DC2.4 cells but independent of the proteasome and transporter associated with antigen processings (TAP) in BMDC and splenic dendritic cells. These data demonstrate for the first time that antigen vectored by the slow-growing M. bovis BCG but not that vectored by fast-growing, readily destroyed M. smegmatis is processed and presented on MHC class I by in vitro-generated dendritic cells, which has implications for recombinant microbial vaccine development.

APA, Harvard, Vancouver, ISO, and other styles

21

Yates, Joseph R., Patrick J. Lillie, Emma Helbren, and Annette D. Samson. "Mycobacterium bovis infection mimicking pancreatic cancer." Lancet Infectious Diseases 20, no. 9 (September 2020): 1099. http://dx.doi.org/10.1016/s1473-3099(19)30560-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Grange, J. M. "Mycobacterium bovis infection in human beings." Tuberculosis 81, no. 1-2 (February 2001): 71–77. http://dx.doi.org/10.1054/tube.2000.0263.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

COUSINS, DV, BR FRANCIS, R. CASEY, and C. MAYBERRY. "Mycobacterium bovis infection in a goat." Australian Veterinary Journal 70, no. 7 (March 10, 2008): 262–63. http://dx.doi.org/10.1111/j.1751-0813.1993.tb08045.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Ellis, M. D., S. Davies, I. A. P. McCandlish, R. Monies, K. Jahans, and R. de la Rua-Domenech. "Mycobacterium bovis infection in a dog." Veterinary Record 159, no. 2 (July 8, 2006): 46–48. http://dx.doi.org/10.1136/vr.159.2.46.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

O’Halloran, Conor, Jayne Hope, and Danielle Gunn-Moore. "Mycobacterium bovis infection in working foxhounds." Veterinary Record 183, no. 11 (September 20, 2018): 356.2–356. http://dx.doi.org/10.1136/vr.k3955.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Zhu, Jian-guo, and Yuan Lin. "Surveillance of infection by Mycobacterium bovis." Reviews in Medical Microbiology 22, no. 2 (April 2011): 17–21. http://dx.doi.org/10.1097/mrm.0b013e3283467179.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Grange, John M., and Malcolm D. Yates. "Zoonotic aspects of Mycobacterium bovis infection." Veterinary Microbiology 40, no. 1-2 (May 1994): 137–51. http://dx.doi.org/10.1016/0378-1135(94)90052-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Bryan, J., P. den Boon, J. McGuirk, G. Madigan, and U. Fogarty. "Mycobacterium bovis Infection in a Donkey." Journal of Comparative Pathology 148, no. 1 (January 2013): 80. http://dx.doi.org/10.1016/j.jcpa.2012.11.138.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Vinnerås, Björn, Göran Bölske, Helene Wahlström, and Ann Albihn. "Survival of Mycobacterium tuberculosis and Mycobacterium bovis in human urine." Water Science and Technology 63, no. 6 (March 1, 2011): 1075–80. http://dx.doi.org/10.2166/wst.2011.344.

Full text

Abstract:

Tuberculosis is a zoonotic disease that mainly causes respiratory infection. However, it can also infect other organs such as the kidneys and bladder, which can lead to high counts of the organisms in the urine. Introducing urine diversion systems and reuse of the urine in agriculture may introduce new transmission routes for infection, increasing the risk of spread. This study evaluated the inactivation rate of mycobacteria in human urine for ensuring safe reuse in agriculture and examined whether current World Health Organization recommendations on storage time are sufficient for inactivating Mycobacterium tuberculosis and Mycobacterium bovis. In this study, a decimal reduction in M. tuberculosis and M. bovis in human urine containing 7 and 3 g NH3-N L−1, respectively, was obtained in just over 10 days at 4°C and below three days at 22°C. This is considerably faster than previously reported reduction rates of mycobacteria in animal slurry at similar temperatures. Based on the present results, a storage time of five weeks at temperatures below 20°C or of two weeks at temperatures above 20°C is sufficient to prevent transmission of mycobacteria when recycling human urine. These values lie within the WHO recommended storage period.

APA, Harvard, Vancouver, ISO, and other styles

30

Fritz, Christian, Silvia Maass, Andreas Kreft, and Franz-Christoph Bange. "Dependence of Mycobacterium bovis BCG on Anaerobic Nitrate Reductase for Persistence Is Tissue Specific." Infection and Immunity 70, no. 1 (January 2002): 286–91. http://dx.doi.org/10.1128/iai.70.1.286-291.2002.

Full text

Abstract:

ABSTRACT Mycobacterium bovis BCG, the only presently available vaccine against tuberculosis, was obtained from virulent M. bovis after serial passages in vitro. The vaccine strain retained at least some of its original virulence, as it persists in immune-competent hosts and occasionally may cause fatal disease in immune-deficient hosts. Mycobacterial persistence in vivo is thought to depend on anaerobic metabolism, an apparent paradox since all mycobacteria are obligate aerobes. Here we report that M. bovis BCG lacking anaerobic nitrate reductase (NarGHJI), an enzyme essential for nitrate respiration, failed to persist in the lungs, liver, and kidneys of immune-competent (BALB/c) mice. In immune-deficient (SCID) mice, however, bacilli caused chronic infection despite disruption of narG, even if growth of the mutant was severely impaired in lungs, liver, and kidneys. Persistence and growth of BCG in the spleens of either mouse strain appeared largely unaffected by lack of anaerobic nitrate reductase, indicating that the role of the enzyme in pathogenesis is tissue specific. These data suggest first that anaerobic nitrate reduction is essential for metabolism of M. bovis BCG in immune-competent but not immune-deficient mice and second that its role in mycobacterial disease is tissue specific, both of which are observations with important implications for pathogenesis of mycobacteria and vaccine development.

APA, Harvard, Vancouver, ISO, and other styles

31

Flesch, I. E., J. H. Hess, S. Huang, M. Aguet, J. Rothe, H. Bluethmann, and S. H. Kaufmann. "Early interleukin 12 production by macrophages in response to mycobacterial infection depends on interferon gamma and tumor necrosis factor alpha." Journal of Experimental Medicine 181, no. 5 (May 1, 1995): 1615–21. http://dx.doi.org/10.1084/jem.181.5.1615.

Full text

Abstract:

Interleukin 12 (IL-12) produced by macrophages immediately after infection is considered essential for activation of a protective immune response against intracellular pathogens. In the murine Mycobacterium bovis Bacillus Calmette-Guérin (BCG) model we assessed whether early IL-12 production by macrophages depends on other cytokines. In vitro, murine bone marrow-derived macrophages produced IL-12 after infection with viable M. bovis BCG or stimulation with LPS, however, priming with recombinant interferon gamma (rIFN-gamma) was necessary. In addition, IL-12 production by these macrophages was blocked by specific anti-tumor necrosis factor alpha (TNF-alpha) antiserum. Macrophages from gene deletion mutant mice lacking either the IFN-gamma receptor or the TNF receptor 1 (p55) failed to produce IL-12 in vitro after stimulation with rIFN-gamma and mycobacterial infection. In vivo, IL-12 production was induced in spleens of immunocompetent mice early during M. bovis BCG infection but not in those of mutant mice lacking the receptors for IFN-gamma or TNF. Our results show that IL-12 production by macrophages in response to mycobacterial infection depends on IFN-gamma and TNF. Hence, IL-12 is not the first cytokine produced in mycobacterial infections.

APA, Harvard, Vancouver, ISO, and other styles

32

Nedeltchev, Gueno G., Tirumalai R. Raghunand, Mandeep S. Jassal, Shichun Lun, Qi-Jian Cheng, and William R. Bishai. "Extrapulmonary Dissemination of Mycobacterium bovis but Not Mycobacterium tuberculosis in a Bronchoscopic Rabbit Model of Cavitary Tuberculosis." Infection and Immunity 77, no. 2 (December 8, 2008): 598–603. http://dx.doi.org/10.1128/iai.01132-08.

Full text

Abstract:

ABSTRACT The rabbit model of tuberculosis is attractive because of its pathophysiologic resemblance to the disease in humans. Rabbits are naturally resistant to infection but may manifest cavitary lung lesions. We describe here a novel approach that utilizes presensitization and bronchoscopic inoculation to reliably produce cavities in the rabbit model. With a fixed inoculum of bacilli, we were able to reproducibly generate cavities by using Mycobacterium bovis Ravenel, M. bovis AF2122, M. bovis BCG, M. tuberculosis H37Rv, M. tuberculosis CDC1551, and the M. tuberculosis CDC1551 ΔsigC mutant. M. bovis infections generated cavitary CFU counts of 106 to 109 bacilli, while non-M. bovis species and BCG yielded CFU counts that ranged from 104 to 108 bacilli. Extrapulmonary dissemination was almost exclusively noted among rabbits infected with M. bovis Ravenel and AF2122. Though all of the species yielded secondary lesions at intrapulmonary sites, M. bovis infections led to the most apparent gross pathology. Using the M. tuberculosis icl and dosR gene expression patterns as molecular sentinels, we demonstrated that both the cavity wall and cavity lumen are microenvironments associated with hypoxia, upregulation of the bacterial dormancy program, and the use of host lipids for bacterial catabolism. This unique cavitary model provides a reliable animal model to study cavity pathogenesis and extrapulmonary dissemination.

APA, Harvard, Vancouver, ISO, and other styles

33

Michelet, Lorraine, Céline Richomme, Edouard Réveillaud, Krystel De Cruz, Jean-Louis Moyen, and Maria Laura Boschiroli. "Mycobacterium microti Infection in Red Foxes in France." Microorganisms 9, no. 6 (June 9, 2021): 1257. http://dx.doi.org/10.3390/microorganisms9061257.

Full text

Abstract:

Mycobacterium microti, member of the Mycobacterium tuberculosis, complex is known to interfere in the screening and diagnosis of bovine tuberculosis. This pathogen is increasingly detected in the frame of surveillance programs for tuberculosis in livestock and wildlife. Recently, red foxes (Vulpes vulpes) were found infected by Mycobacterium bovis in four French endemic areas. M. microti infection was concomitantly found during this investigation. Rates of infection by M. microti and M. bovis are not different except in one of the four areas (lower prevalence for M. microti in Charente). As for M. bovis infection, none of the infected foxes presented gross TB-like lesions. Infection of red foxes by M. microti seems to occur by ingestion of contaminated food, as mesenteric lymph nodes are mostly infected albeit no fecal excretion could be detected. Red foxes appear to be susceptible to Mycobacterium microti infection but seem to play a role of dead-end host for the transmission of this bacillus.

APA, Harvard, Vancouver, ISO, and other styles

34

Waters, W. R., M. V. Palmer, T. C. Thacker, J. B. Payeur, N. B. Harris, F. C. Minion, R. Greenwald, et al. "Immune Responses to Defined Antigens of Mycobacterium bovis in Cattle Experimentally Infected with Mycobacterium kansasii." Clinical and Vaccine Immunology 13, no. 6 (June 2006): 611–19. http://dx.doi.org/10.1128/cvi.00054-06.

Full text

Abstract:

ABSTRACT Cross-reactive responses elicited by exposure to nontuberculous mycobacteria often confound the interpretation of antemortem tests for Mycobacterium bovis infection of cattle. The use of specific proteins (e.g., ESAT-6, CFP-10, and MPB83), however, generally enhances the specificity of bovine tuberculosis tests. While genes for these proteins are absent from many nontuberculous mycobacteria, they are present in M. kansasii. Instillation of M. kansasii into the tonsillar crypts of calves elicited delayed-type hypersensitivity and in vitro gamma interferon and nitrite concentration responses of leukocytes to M. avium and M. bovis purified protein derivatives (PPDs). While the responses of M. kansasii-inoculated calves to M. avium and M. bovis PPDs were approximately equivalent, the responses of M. bovis-inoculated calves to M. bovis PPD exceeded their respective responses to M. avium PPD. The gamma interferon and nitrite responses of M. kansasii-inoculated calves to recombinant ESAT-6-CFP-10 (rESAT-6-CFP-10) exceeded corresponding responses of noninoculated calves as early as 15 and 30 days after inoculation, respectively, and persisted throughout the study. The gamma interferon and nitrite responses of M. bovis-inoculated calves to rESAT-6-CFP-10 exceeded the corresponding responses of M. kansasii-inoculated calves beginning 30 days after inoculation. By using a lipoarabinomannan-based enzyme-linked immunosorbent assay, specific serum antibodies were detected as early as 50 days after challenge with M. kansasii. By a multiantigen print immunoassay and immunoblotting, serum antibodies to MPB83, but not ESAT-6 or CFP-10, were detected in M. kansasii-inoculated calves; however, responses to MPB83 were notably weaker than those elicited by M. bovis infection. These findings indicate that M. kansasii infection of calves elicits specific responses that may confound the interpretation of bovine tuberculosis tests.

APA, Harvard, Vancouver, ISO, and other styles

35

Pal, Mahendra, Nigusa Zenebe, and Md Tanvir Rahman. "Growing Significance of Mycobacterium bovis in Human Health." Microbes and Health 3, no. 1 (August 1, 2014): 29–34. http://dx.doi.org/10.3329/mh.v3i1.19779.

Full text

Abstract:

Tuberculosis is one of the most wide spread highly infectious bacterial zoonotic diseases, and is responsible for high morbidity and mortality in the world particularly in the developing nations. Mycobacterium bovis and closely associated acid fast bacilli cause disease in humans and animals. Humans can be infected with M. bovis where cattle act as the principal reservoir. Air borne infections continue to occur among the persons working in the meat industry, slaughterhouses, and in persons living in close physical contact with infected animals.M. bovis infection is recognized as an occupational hazard to abattoir workers, livestock handlers and veterinarians. The main cause of concern related to M. bovis in industrialized counties are epizootics nature of the disease in domesticated and wild animals. In addition, latent infection in immigrants particularly in HIV infected patients are also a big issue in developed world, since those people could be the potential source of TB for other people. The reemergence of M. bovis infection in captive and free-ranging wild animals, with subsequent transmission to domestic animals, is of concern to livestock producers and regulatory officials. As wild animals represent major reservoir of tuberculosis bacilli, it is imperative to investigate the role of wild animals in transmission dynamics of M. bovis infection. Further studies on the molecular epidemiology and development of safe, cheap and potent drugs to mitigate tuberculosis in highly susceptible population particularly in HIV/AIDS patients is emphasized. In addition, multidisciplinary approaches such as One Health that comprise professionals from medical science, veterinary medicine and wildlife etc. are essential to take measures to control this devastating bacterial zoonosis. DOI: http://dx.doi.org/10.3329/mh.v3i1.19779 Microbes and Health, June 2014. 3(1): 29-34

APA, Harvard, Vancouver, ISO, and other styles

36

O’Halloran, Conor, Olympia Ioannidi, Nicki Reed, Kevin Murtagh, Eili Dettemering, Stefaan Van Poucke, John Gale, et al. "Tuberculosis due to Mycobacterium bovis in pet cats associated with feeding a commercial raw food diet." Journal of Feline Medicine and Surgery 21, no. 8 (May 13, 2019): 667–81. http://dx.doi.org/10.1177/1098612x19848455.

Full text

Abstract:

Objectives Mycobacterium bovis, a member of the Mycobacterium tuberculosis complex, can infect cats and has proven zoonotic risks for owners. Infected cats typically present with a history of outdoor lifestyle and hunting behaviour, and cutaneous granulomas are most commonly observed. The aim of this study is to describe an outbreak of tuberculous disease commencing with six young cats, living exclusively indoors in five different households across England, being presented to separate veterinarians across the UK with a variety of clinical signs. Methods Investigations into the pyogranulomatous lesions, lymphadenopathy and/or pulmonary disease of these cases consistently identified infection with M bovis. Infection was confirmed by PCR, where possible, or was indicated with a positive interferon-gamma release assay (IGRA), where material for PCR was unavailable. In-contact, cohabiting cats were screened by IGRA and follow-up testing was undertaken/advised where results were positive. A lifestyle investigation was undertaken to identify the source of infection. Results Six clinically sick cats and seven in-contact cats were identified with evidence of M bovis infection. Five clinical cases were either too sick to treat or deteriorated despite therapy, giving a mortality rate of 83%. Lifestyle investigations revealed the common factors between clusters to be that affected cats had mycobacterial infections speciated to M bovis, were exclusively indoor cats and were fed a commercially available raw food product produced by a single manufacturer. The Food Standards Agency, Animal & Plant Health Agency, Public Health England and the food manufacturer concerned have been notified/informed. Other possible sources of exposure for these cats to M bovis were explored and were excluded, including wildlife contact, access to raw milk, the presence of rodent populations inside the buildings in which the cats lived and exposure to known infectious humans. Conclusions and relevance Upon investigations, our results provide compelling, if circumstantial, evidence of an association between the commercial raw diet of these cats and their M bovis infections.

APA, Harvard, Vancouver, ISO, and other styles

37

Michelet, Lorraine, Krystel De Cruz, Sylvie Hénault, Jennifer Tambosco, Céline Richomme, Édouard Réveillaud, Hélène Gares, Jean-Louis Moyen, and María Laura Boschiroli. "Mycobacterium bovis Infection of Red Fox, France." Emerging Infectious Diseases 24, no. 6 (June 2018): 1150–53. http://dx.doi.org/10.3201/eid2406.180094.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Cassidy, J. P. "Mycobacterium bovis infection: Everything but the cow." Veterinary Journal 198, no. 2 (November 2013): 303–4. http://dx.doi.org/10.1016/j.tvjl.2013.09.014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Güner, Mehmet Derviş, Umut Bektaş, Ramazan Akmeşe, Haldun Onuralp Kamburoğlu, Mehmet Armangil, and Şadan Ay. "Wrist Tenosynovitis due to Mycobacterium bovis Infection." Plastic and Reconstructive Surgery Global Open 2, no. 12 (December 2014): e262. http://dx.doi.org/10.1097/gox.0000000000000238.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Adams, Garry. "Mycobacterium bovis infection in animals and humans." Preventive Veterinary Medicine 26, no. 3-4 (April 1996): 353–54. http://dx.doi.org/10.1016/0167-5877(96)80486-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Neill, S. D., J. M. Pollock, D. B. Bryson, and J. Hanna. "Pathogenesis of Mycobacterium bovis infection in cattle." Veterinary Microbiology 40, no. 1-2 (May 1994): 41–52. http://dx.doi.org/10.1016/0378-1135(94)90045-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Geijtenbeek, Teunis B. H., Sandra J. van Vliet, Estella A. Koppel, Marta Sanchez-Hernandez, Christine M. J. E. Vandenbroucke-Grauls, Ben Appelmelk, and Yvette van Kooyk. "Mycobacteria Target DC-SIGN to Suppress Dendritic Cell Function." Journal of Experimental Medicine 197, no. 1 (December 23, 2002): 7–17. http://dx.doi.org/10.1084/jem.20021229.

Full text

Abstract:

Mycobacterium tuberculosis represents a world-wide health risk and immunosuppression is a particular problem in M. tuberculosis infections. Although macrophages are primarily infected, dendritic cells (DCs) are important in inducing cellular immune responses against M. tuberculosis. We hypothesized that DCs represent a target for M. tuberculosis and that the observed immuno-suppression results from modulation of DC functions. We demonstrate that the DC-specific C-type lectin DC-SIGN is an important receptor on DCs that captures and internalizes intact Mycobacterium bovis bacillus Calmette-Guérin (BCG) through the mycobacterial cell wall component ManLAM. Antibodies against DC-SIGN block M. bovis BCG infection of DCs. ManLAM is also secreted by M. tuberculosis–infected macrophages and has been implicated as a virulence factor. Strikingly, ManLAM binding to DC-SIGN prevents mycobacteria- or LPS-induced DC maturation. Both mycobacteria and LPS induce DC maturation through Toll-like receptor (TLR) signaling, suggesting that DC-SIGN, upon binding of ManLAM, interferes with TLR-mediated signals. Blocking antibodies against DC-SIGN reverse the ManLAM-mediated immunosuppressive effects. Our results suggest that M. tuberculosis targets DC-SIGN both to infect DCs and to down-regulate DC-mediated immune responses. Moreover, we demonstrate that DC-SIGN has a broader pathogen recognition profile than previously shown, suggesting that DC-SIGN may represent a molecular target for clinical intervention in infections other than HIV-1.

APA, Harvard, Vancouver, ISO, and other styles

43

ÇAVUŞOĞLU, Cengiz, and Fethiye Ferda YILMAZ. "Ege Bölgesi’nde İnsan Mycobacterium bovis Enfeksiyonlarının Moleküler Epidemiyolojisi." Mikrobiyoloji Bulteni 51, no. 2 (April 15, 2017): 165–70. http://dx.doi.org/10.5578/mb.53963.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Chambers, Mark A., Ann Williams, Graham Hatch, Dolores Gavier-Widén, Graham Hall, Kris Huygen, Douglas Lowrie, Philip D. Marsh, and R. Glyn Hewinson. "Vaccination of Guinea Pigs with DNA Encoding the Mycobacterial Antigen MPB83 Influences Pulmonary Pathology but Not Hematogenous Spread following Aerogenic Infection with Mycobacterium bovis." Infection and Immunity 70, no. 4 (April 2002): 2159–65. http://dx.doi.org/10.1128/iai.70.4.2159-2165.2002.

Full text

Abstract:

ABSTRACT Protection of cattle against bovine tuberculosis by vaccination could be an important control strategy in countries where there is persistent Mycobacterium bovis infection in wildlife and in developing countries where it is not economical to implement a tuberculin test and slaughter control program. The main aim of such a vaccination strategy would be to reduce transmission of infection by reducing the lung pathology caused by infection and preventing seeding of the organism to organs from which M. bovis could be excreted. Recent reports of successful DNA vaccination against Mycobacterium tuberculosis in small-animal models have suggested that DNA vaccines act by reducing lung pathology without sensitizing animals to tuberculin testing. We therefore evaluated the ability of vaccines consisting of DNA encoding the mycobacterial antigens MPB83 and 85A to reduce lung pathology and prevent hematogenous spread in guinea pigs challenged with a low dose of aerosolized M. bovis. Vaccination with MPB83 DNA reduced the severity of pulmonary lesions, as assessed by histopathology, and resembled M. bovis BCG vaccination in this respect. However, unlike BCG vaccination, MPB83 DNA vaccination did not protect challenged guinea pigs from hematogenous spread of organisms to the spleen. In contrast, vaccination with antigen 85A DNA, a promising DNA vaccine for human tuberculosis, had no measurable protective effect against infection with M. bovis.

APA, Harvard, Vancouver, ISO, and other styles

45

Fulton, S. A., S. M. Reba, T. D. Martin, and W. H. Boom. "Neutrophil-Mediated Mycobacteriocidal Immunity in the Lung during Mycobacterium bovis BCG Infection in C57BL/6 Mice." Infection and Immunity 70, no. 9 (September 2002): 5322–27. http://dx.doi.org/10.1128/iai.70.9.5322-5327.2002.

Full text

Abstract:

ABSTRACT Although neutrophils have been identified as sources of inflammatory cytokines and chemokines, little is known about their immunologic function during mycobacterial infection in the lungs. In this study, we examined the growth of Mycobacterium bovis BCG in the lungs under experimental conditions that altered neutrophil recruitment to the lungs. Depletion and recruitment of neutrophils was associated with respective increases and decreases in M. bovis BCG growth. Thus, neutrophils may enhance mycobacteriocidal immunity in the lungs.

APA, Harvard, Vancouver, ISO, and other styles

46

Waters, W. R., M. V. Palmer, T. C. Thacker, J. P. Bannantine, H. M. Vordermeier, R. G. Hewinson, R. Greenwald, et al. "Early Antibody Responses to Experimental Mycobacterium bovis Infection of Cattle." Clinical and Vaccine Immunology 13, no. 6 (June 2006): 648–54. http://dx.doi.org/10.1128/cvi.00061-06.

Full text

Abstract:

ABSTRACT Bovine tuberculosis persists as a costly zoonotic disease in numerous countries despite extensive eradication and control efforts. Sequential serum samples obtained from Mycobacterium bovis-infected cattle were evaluated for seroreactivity to mycobacterial antigens. Animals received M. bovis by aerosol, intratonsil, intranasal, or intratracheal inoculation. Assays included the multiantigen print immunoassay for determination of antigen recognition patterns, immunoblot analysis for sensitive kinetic studies, and the VetTB STAT-PAK test, a novel, rapid test based on lateral-flow technology. Responses to MPB83 were detected for all M. bovis-infected animals regardless of the route or strain of M. bovis used for inoculation. Other less commonly recognized antigens included ESAT-6, CFP-10, and MPB70. Responses to MPB83 were detectable as early as 4 weeks after inoculation, were boosted upon injection of purified protein derivatives for skin testing, and persisted throughout the course of each of the four challenge studies. MPB83-specific immunoglobulin M (IgM) was detected prior to MPB83-specific IgG detection; however, early IgM responses rapidly waned, suggesting a benefit of tests that detect both IgM- and IgG-specific antibodies. The VetTB STAT-PAK test detected responses in sera from 60% (15/25) of the animals by 7 weeks after challenge and detected responses in 96% (24/25) of the animals by 18 weeks. These findings demonstrate the potential for new-generation antibody-based tests for the early detection of M. bovis infection in cattle.

APA, Harvard, Vancouver, ISO, and other styles

47

Hestvik, Anne Lise K., Zakaria Hmama, and Yossef Av-Gay. "Kinome Analysis of Host Response to Mycobacterial Infection: a Novel Technique in Proteomics." Infection and Immunity 71, no. 10 (October 2003): 5514–22. http://dx.doi.org/10.1128/iai.71.10.5514-5522.2003.

Full text

Abstract:

ABSTRACT An array of mammalian phospho-specific antibodies was used to screen for a host response upon mycobacterial infection, reflected as changes in host protein phosphorylation. Changes in the phosphorylation state of 31 known signaling molecules were tracked after infection with live or heat killed Mycobacterium bovis BCG or after incubation with the mycobacterial cell wall component lipoarabinomannan (LAM). Mycobacterial infection triggers a signaling cascade leading to activation of stress-activated protein kinase and its subsequent downstream target, c-Jun. Mycobacteria were also shown to inhibit the activation of protein kinase C ε and to induce phosphorylation of proteins not yet known to be involved in mycobacterial infection, such as the cytoskeletal protein α-adducin, glycogen synthase kinase 3β, and a receptor subunit involved in regulation of intracellular Ca2+ levels. The mycobacterial cell wall component LAM has been identified as a trigger for some of these modulation events.

APA, Harvard, Vancouver, ISO, and other styles

48

Hussain, Zhao, Shah, Sabir, Wang, Liao, Song, et al. "PP2Ac Modulates AMPK-Mediated Induction of Autophagy in Mycobacterium bovis—Infected Macrophages." International Journal of Molecular Sciences 20, no. 23 (November 29, 2019): 6030. http://dx.doi.org/10.3390/ijms20236030.

Full text

Abstract:

Mycobacterium bovis (M. bovis) is the causative agent of bovine tuberculosis in cattle population across the world. Human beings are at equal risk of developing tuberculosis beside a wide range of M. bovis infections in animal species. Autophagic sequestration and degradation of intracellular pathogens is a major innate immune defense mechanism adopted by host cells for the control of intracellular infections. It has been reported previously that the catalytic subunit of protein phosphatase 2A (PP2Ac) is crucial for regulating AMP-activated protein kinase (AMPK)-mediated autophagic signaling pathways, yet its role in tuberculosis is still unclear. Here, we demonstrated that M. bovis infection increased PP2Ac expression in murine macrophages, while nilotinib a tyrosine kinase inhibitor (TKI) significantly suppressed PP2Ac expression. In addition, we observed that TKI-induced AMPK activation was dependent on PP2Ac regulation, indicating the contributory role of PP2Ac towards autophagy induction. Furthermore, we found that the activation of AMPK signaling is vital for the regulating autophagy during M. bovis infection. Finally, the transient inhibition of PP2Ac expression enhanced the inhibitory effect of TKI-nilotinib on intracellular survival and multiplication of M. bovis in macrophages by regulating the host’s immune responses. Based on these observations, we suggest that PP2Ac should be exploited as a promising molecular target to intervene in host–pathogen interactions for the development of new therapeutic strategies towards the control of M. bovis infections in humans and animals.

APA, Harvard, Vancouver, ISO, and other styles

49

Storandt, Michael, and Avish Nagpal. "Prosthetic joint infection: an extremely rare complication of intravesicular BCG therapy." BMJ Case Reports 12, no. 12 (December 2019): e232809. http://dx.doi.org/10.1136/bcr-2019-232809.

Full text

Abstract:

A 66-year-old man was seen in clinic due to concerns of tuberculosis of the right hip. He had a history of urothelial bladder carcinoma, which was treated via transurethral resection followed by intravesicular instillations of Mycobacterium bovis BCG (BCG). A few months later, he developed slowly worsening pain over his prosthetic right hip, and it was recommended he undergo surgical revision. During surgery, joint effusion was noted and synovial fluid was sent for bacterial and mycobacterial cultures, growing an acid-fast bacillus after 3 weeks, identified as Mycobacterium tuberculosis complex via nucleic acid probe. Susceptibility testing revealed resistance to pyrazinamide, which is typically seen in M. bovis. PCR confirmed the diagnosis of BCG infection. The patient was treated with isoniazid, rifampin and ethambutol, which he tolerated well. This case highlights the challenges associated with diagnosis and management of this rare complication of a commonly used therapy.

APA, Harvard, Vancouver, ISO, and other styles

50

Xing, Zhou, Jun Wang, Kenneth Croitoru, and Julia Wakeham. "Protection by CD4 or CD8 T Cells against PulmonaryMycobacterium bovis Bacillus Calmette-Guérin Infection." Infection and Immunity 66, no. 11 (November 1, 1998): 5537–42. http://dx.doi.org/10.1128/iai.66.11.5537-5542.1998.

Full text

Abstract:

ABSTRACT Mice deficient in CD8 T cells demonstrated levels of Th1 cytokines and granulomatous responses in the lungs very similar to those demonstrated by normal control mice and were fully capable of controlling pulmonary mycobacterial infection by Mycobacterium bovis BCG as assessed at day 37 postinfection. In comparison, mice deficient in CD4 T cells had similar levels of interleukin-12 (IL-12) and tumor necrosis factor alpha but lower levels of gamma interferon in the lungs and were still able to mount tissue granulomatous responses and control pulmonary mycobacterial infection. In contrast, IL-12−/− mice with impaired CD4 and CD8 T-cell responses had a markedly weakened control of infection, whereas SCID mice deficient in all T cells succumbed to such pulmonary mycobacterial infections.

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Mycobacterium bovis infection'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles