An evaluation of factors associated with taking and responding positive to the tuberculin skin test in individuals with HIV/AIDS

<p>Abstract</p> <p>Background</p> <p>The tuberculin skin test (TST) is still the standard test for detecting latent infection by <it>M tuberculosis </it>(LTBI). Given that the Brazilian Health Ministry recommends that the treatment of latent tuberculosis (LTBI) should be guided by the TST results, the present study sets out to describe the coverage of administering the TST in people living with HIV at two referral health centers in the city of Recife, where TST is offered to all patients. In addition, factors associated with the non-application of the test and with positive TST results were also analyzed.</p> <p>Methods</p> <p>A cross-sectional study was carried out with HIV patients, aged 18 years or over, attending outpatient clinics at the Correia Picanço Hospital/SES/PE and the Oswaldo Cruz/UPE University Hospital, who had been recommended to take the TST, in the period between November 2007 and February 2010. Univariate and multivariate logistic regression analyses were carried out to establish associations between the dependent variable - taking the TST (yes/no), at a first stage analysis, and the independent variables, followed by a second stage analysis considering a positive TST as the dependent variable. The odds ratio was calculated as the measure of association and the confidence interval (CI) at 95% as the measure of accuracy of the estimate.</p> <p>Results</p> <p>Of the 2,290 patients recruited, 1087 (47.5%) took the TST. Of the 1,087 patients who took the tuberculin skin test, the prevalence of TST ≥ 5 mm was 21.6% among patients with CD4 ≥ 200 and 9.49% among those with CD4 < 200 (p = 0.002). The patients most likely not to take the test were: men, people aged under 39 years, people with low educational levels and crack users. The risk for not taking the TST was statiscally different for health service. Patients who presented better immunity (CD4 ≥ 200) were more than two and a half times more likely to test positive that those with higher levels of immunodeficiency (CD4 < 200).</p> <p>Conclusions</p> <p>Considering that the TST is recommended by the Brazilian health authorities, coverage for taking the test was very low. The most serious implication of this is that LTBI treatment was not carried out for the unidentified TST-positive patients, who may consequently go on to develop TB and eventually die.</p

Pre-harvest calcium sulfate applications affect vase life and severity of gray mold in cut roses

Gray mold, caused by Botrytis cinerea Pers. Fr., is a major disease in roses. The effect of spraying rose (Cultivar ‘Kiss’) buds with calcium sulfate on the intensity of gray mold was evaluated. Calcium sulfate was sprayed on the buds at different schedules and concentrations before harvest. Thereafter, the buds were harvested and either inoculated or not with B. cinerea. The treatments reduced both the progress and severity of gray mold and increased vase life of the flowers. Good results were achieved with 10 and 20 mM calcium sulfate, applied 24 h before harvest. In the uninoculated assay, the maximum percentages of reduction of the area under the disease progress curve (AUDPC) and of severity were 86% and 86%, respectively, and in the inoculated assay, 68% and 76%, respectively. Vase life of the flowers was increased at least 30% in the assay without inoculation and 20% in the assay with inoculation. Spraying roses with calcium sulfate at 10 mM or 20 mM one day before harvest is recommended to control gray mold after harvest

Mycobacterium leprae-induced Insulin-like Growth Factor I attenuates antimicrobial mechanisms, promoting bacterial survival in macrophages

Submitted by sandra infurna ([email protected]) on 2016-07-02T23:45:33Z No. of bitstreams: 1 katherine_mattos_etal_IOC_2016.pdf: 1295630 bytes, checksum: f98c045639477298b4060493549ed5f8 (MD5)Approved for entry into archive by sandra infurna ([email protected]) on 2016-07-03T00:00:26Z (GMT) No. of bitstreams: 1 katherine_mattos_etal_IOC_2016.pdf: 1295630 bytes, checksum: f98c045639477298b4060493549ed5f8 (MD5)Made available in DSpace on 2016-07-03T00:00:26Z (GMT). No. of bitstreams: 1 katherine_mattos_etal_IOC_2016.pdf: 1295630 bytes, checksum: f98c045639477298b4060493549ed5f8 (MD5) Previous issue date: 2016Submitted by Angelo Silva ([email protected]) on 2016-07-07T11:16:57Z No. of bitstreams: 3 katherine_mattos_etal_IOC_2016.pdf.txt: 65894 bytes, checksum: e5afd9deb877b4e5fae199967e48b1f7 (MD5) katherine_mattos_etal_IOC_2016.pdf: 1295630 bytes, checksum: f98c045639477298b4060493549ed5f8 (MD5) license.txt: 2991 bytes, checksum: 5a560609d32a3863062d77ff32785d58 (MD5)Approved for entry into archive by sandra infurna ([email protected]) on 2016-07-07T12:20:07Z (GMT) No. of bitstreams: 3 license.txt: 2991 bytes, checksum: 5a560609d32a3863062d77ff32785d58 (MD5) katherine_mattos_etal_IOC_2016.pdf: 1295630 bytes, checksum: f98c045639477298b4060493549ed5f8 (MD5) katherine_mattos_etal_IOC_2016.pdf.txt: 65894 bytes, checksum: e5afd9deb877b4e5fae199967e48b1f7 (MD5)Made available in DSpace on 2016-07-07T12:20:07Z (GMT). No. of bitstreams: 3 license.txt: 2991 bytes, checksum: 5a560609d32a3863062d77ff32785d58 (MD5) katherine_mattos_etal_IOC_2016.pdf: 1295630 bytes, checksum: f98c045639477298b4060493549ed5f8 (MD5) katherine_mattos_etal_IOC_2016.pdf.txt: 65894 bytes, checksum: e5afd9deb877b4e5fae199967e48b1f7 (MD5) Previous issue date: 2016Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Microbiologia Celular. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Microbiologia Celular. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Instituto Carlos Chagas Filho. Laboratório de Parasitologia Molecular. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Microbiologia Celular. Rio de Janeiro, RJ, BrasilFundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Microbiologia Celular. Rio de Janeiro, RJ, BrasilInstituto Lauro de Souza Lima. Bauru, SP, Brasil.Instituto Lauro de Souza Lima. Bauru, SP, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Microbiologia Celular. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Instituto Carlos Chagas Filho. Laboratório de Parasitologia Molecular. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Microbiologia Celular. Rio de Janeiro, RJ, Brasil.Mycobacterium leprae (ML), the etiologic agent of leprosy, can subvert macrophage antimicrobial activity by mechanisms that remain only partially understood. In the present study, the participation of hormone insulin-like growth factor I (IGF-I) in this phenomenum was investigated. Macrophages from the dermal lesions of the disseminated multibacillary lepromatous form (LL) of leprosy expressed higher levels of IGF-I than those from the self-limited paucibacillary tuberculoid form (BT). Higher levels of IGF-I secretion by ML-infected macrophages were confirmed in ex vivo and in vitro studies. Of note, the dampening of IGF-I signaling reverted the capacity of ML-infected human and murine macrophages to produce antimicrobial molecules and promoted bacterial killing. Moreover, IGF-I was shown to inhibit the JAK/STAT1-dependent signaling pathways triggered by both mycobacteria and IFN-γ most probably through its capacity to induce the suppressor of cytokine signaling-3 (SOCS3). Finally, these in vitro findings were corroborated by in vivo observations in which higher SOCS3 expression and lower phosphorylation of STAT1 levels were found in LL versus BT dermal lesions. Altogether, our data strongly suggest that IGF-I contributes to the maintenance of a functional program in infected macrophages that suits ML persistence in the host, reinforcing a key role for IGF-I in leprosy pathogenesis