Browsing by Subject "Infectious Disease"
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Item Doctors, Patients, and Adherence to HIV Medication: Findings of the Communication, Communities, and Health Study(2008-05-01) Seater, Margaret; Kimberly Fulda; Kathryn CardarelliThis study is about whether doctors have the potential to influence adherence by forming a solid patient-doctor relationship. This study is also about health disparities; specifically, if racialized life experiences have any association with either adherence or the formation of a solid patient-doctor relationship. Self-reported racial discrimination was shown to be a risk factor for non-adherence (OR 4.725, p-value [less than] 0.05), while compassionate behavior on the part of the clinician predicted adherence (OR 0.062, p-value [less than] 0.1 trend). Future directions include applying for extramural funding to conduct a clinical trial emphasizing communication as a way to eliminate health disparities. In the long term, the goal of medical educators should be to recruit more non-white physicians in order to further eliminate health disparities.Item Epidemiologic Assessment of a Targeted Tuberulosis Screening and Treatment Program Based on Geographic and Molecular Clustering(2005-08-01) Moonan, Patrick KevinMoonan, Patrick K., Epidemiologic Assessment of a Targeted Tuberculosis Screening and Treatment Program Based on Geographic and Molecular Clustering. Doctor of Public Health (Disease Prevention and Control), August 2005, 93 pp., 12 tables, 7 illustrations, bibliography, 148 tables. One of the primary goals of the tuberculosis elimination strategy is to interrupt the transmission of mycobacterium tuberculosis (TB). The most effective way to accomplish this goal is to identify and treat individuals who have active tuberculosis. However, even in highly effected tuberculosis control programs, M. tuberculosis continues to be transmitted to others, largely because most transmission occurs before diagnosis and initiation of therapy. Under the current recommendations, testing should be targeted at specific high-risk populations. While a strategy of targeted testing and treatment of persons most likely to develop tuberculosis is attractive, it is uncertain how best to accomplish this goal. This is the first study to assess the use of geographic and molecular surveillance in guiding a targeted tuberculosis screening and treatment of active tuberculosis and latent tuberculosis infection that monitors potential transmission in a defined high risk geographic area. The results of this geographically targeted program demonstrate significant yield for discovering active cases, latent tuberculosis infection, and recent transmission (TST converters). In this setting, geographically targeted screening identified as many as 19.8 tuberculosis cases per 1,000 persons screened and as many as 292.4 latent tuberculosis infections per 1,000 persons screened. Additionally, successful treatment of these individuals reduced the number of both cases and latent infection identified. Over a three-year period the case detection rate, latent infection detection rate, and TST conversion rate was reduced by 335%, 171% and 285% respectively.Item Factors Associated with Multi-Drug Resistance among Patients with Streptoccus pneumoniae Ear Infections(2004-05-01) Mendoza, Belinda A.; Francisco Soto Mas; Chiehwen Ed Hsu; Antonio ReneMendoza, Belinda A., Factors Associated with Multi-Drug Resistance among Patients with Streptoccus pneumoniae Ear Infections. Master of Public Health (Social and Behavioral Sciences), May 2004, 27 pp., 6 tables, 1 figure, references, 9 titles. Clinical trials play an important role in the development of new medical treatments. The purpose of this study is to describe patients participating in a clinical trial and at analyze the socio-demographic characteristics of patients with susceptible and multi-drug resistant Streptococcus pneumoniae ear infections. At the conclusion of this study, a socio-demographic description of clinical trial participants was obtained and the results were slightly younger than patients with susceptible S. pneumoniae ear infections and were more likely to attend day care.Item Interleukin-8: Baculovirus Expression and the Receptor Signal Transduction Pathway(1994-06-01) Kang, Xiaoqiang; Stephen R. Grant; Rafael Alvarez; Paula SumstomXiaoqiang, Kang., Interleukin-8: Baculovirus Expression and the Receptor Signal Transduction Pathway. Doctor of Philosophy (Biomedical Sciences), June, 1994, 150 pp., 4 tables, 36 illustrations, bibliography, 212 titles. The cDNA for human interleukin-8 (IL8) was subcloned from a bacterial source into the eukaryotic baculoviral vector expression system. Recombinant human IL-8 (rhIL-8) was synthesized and secreted from SF9 cells following infection of a recombinant virus harboring the full-length IL-8 structural gene. Recombinant human interleukin-8 was purified ([greater than] 600 fold) to homogeneity using preparative HPLC. The rhIL-8 preparation retained all of the physical, immunological, and biochemical properties of the natural product (monocyte-derived IL-8). Baculovirus vector expression coupled to preparative HPLC proved to be a very efficient method for large-scale recombinant interleukin production. Biochemical mechanisms that mediate IL-8 receptor-stimulated activities are poorly understood. In this study, I have explored the intracellular mechanism(s) induced by IL-8 in differentiated HL-60 cells. IL-8 induced a rapid and transient activation of phospholipase A2 in differentiated HL-60 cells. A consequence of phospholipase A2 activation was the release of arachidonic acid and the generation of lysophospholipids from membrane phospholipids. The IL-8 stimulated-arachidonic acid release was pertussis toxin and phospholipase A2 inhibitor sensitive, and protein kinase C independent. In contrast to another neutrophil chemotactic factor, fMLP, IL-8 did not stimulate the activation of phospholipase C and phospholipase D. When comparing the phosphorylation events induced by IL-8 and fMLP, I found that these two chemotactic factors triggered different protein phosphorylation profiles. Tyrosine phosphorylation of proteins was not detected following IL-8 stimulation in HL-60 cells. However, IL-8 stimulated the rapid autophosphorylation of calcium/calmodulin-dependent protein kinase II (CaM kinase II). These results strongly suggest that the IL-8 receptor is closely coupled to the activation of PLA2 and that CaM kinase II is an integral component of IL-8 receptor signal pathway.Item North Texas Health & Science - 2011, Issue 2(University of North Texas Health Science Center at Fort Worth, 2011-01-01)Item Synergy 2011: Annual Research Report(2011-01-01)Item T-Helper Cell Responses in Lungs After Immunization and Chronic Respiratory Disease; And Their Association With Pulmonary Inflammation(2001-05-01) Jones, Harlan P.; Simecka, Jerry; Dimitrijevich, S. Dan; Goldfarb, Ronald H.The purpose of these studies was to characterize T helper cell responses in the lungs of mice after immunization and chronic respiratory infection. CD4+ T cells were the major population of T cells resident in the lung in comparison to CD8+ T cells. Polyclonal activation of resident CD4+T cells produced abundant levels of IL-4 in comparison to IFN-γ, indicating that Th2 cells were the major sub-population of CD4+ T cells. In contrast, resident CD8+ T cells were the sole producer of IFN-γ by naïve T lymphocytes. Furthermore, the distribution of T cells was similar between BALB/c, C3H/HeN, C57BL/6 and DBA/2N strains of mice. However differences in the distribution of CD8+T cells, as well as the levels of IL-4 and IFN-y production produced by resident T cells were found between C57 and the other strains of mice tested. These results demonstrate that host genetic factors may be involved in determining host susceptibility to respiratory disease. Differences in the intensity of antigenic stimulation provoke changes in the type of T cell response generated. Intranasal immunization with influenza (FLU) vaccine antigen alone initiated solely an antigen-specific Th2-like response. In contrast, the addition of the potent mucosal adjuvant cholera toxin (CT) in combination with FLU antigen induced not only resident Th2 responses, but also induced antigen-specific Th1-like responses. This change corresponded with a dramatic increase in the number of CD4+ T cells in the lung. Thus, intense immunization of respiratory T cells enhanced resident T helper cell responses, but also promoted the activation of Th1 responses. Chronic respiratory infection also elicited changes in the resident population of T cells consistent with pulmonary inflammatory immune responses. At early stages of infection, CD4+, but not CD8+ T cells increased in number within inductive respiratory lymphoid tissues (lower respiratory nodes [LRNs]). Between day 7 and 14 however, there was a dramatic increase in the number of CD4+ T cells in the lung. Interestingly, CD8+ T cells also increased in the lungs, suggesting their activation along mucosal sites during mycoplasma infection. Mycoplasma-specific IL-4 and IFN-γ production also increased in a tissue-specific/time-dependent manner. IL-4 production was initially observed in the LRNs, whereas significant levels of IL-4 and IFN-γ was produced in both tissues 14 days after infection. In comparison, IFN-γ was the predominate cytokine, produce at 14 days coinciding with pulmonary inflammation. Suggesting that intense activation promoted changes in the resident pulmonary Th2 environment, and possible is a major component of pulmonary inflammatory immune responses. Both CD4+ and CD8= T cells were shown to have a role in modulation of disease severity during mycoplasma disease. Observation of gross pulmonary lesions reveal that mycoplasma infected mice treated with anti-CD8 antibody showed increase clinical signs of disease and pronounced gross pulmonary lesions. Additionally the number of total mononuclear cells increased dramatically in the absence of CD8+ T cells. Thus, CD8+ T cells may have a regulatory role in controlling resident CD4+ T cells that increased 14 days after infection. Chemokine production is known to mediate the recruitment of lymphocytes to enhance the initiation of immunity as well as be responsible for modulating inflammatory responses. We find that mycoplasma increase the number of dendritic cells in the lung 14 days after infection, and stimulated the production of dendritic cell-derived ABCD-1 chemokine. Also, β-chemokine MIP-1α and MIB-1β production was observed during intense immunization as well as during mycoplasma infection. These results provide evidence for a potential mechanism through which changes in resident pulmonary T cell responses occur given the intensity of the immune response generated.Item The Effect of CsrA on Biofilm Development in Escherichia coli(2001-05-01) Jackson, Debra White; Julian Borejdo; Richard Easom; Jerry SimeckaJackson, Debra W., The Effect of CsrA on Biofilm Development in Escherichia coli. Doctor of Philosophy (Biomedical Sciences), May 2001, 127 pp., 2 tables, 15 illustrations, bibliography, 138 titles. CsrA, carbon storage regulator, is a small RNA-binding protein that acts as a global regulator and modulates specific mRNA stability in Escherichia coli. CsrA regulates central carbon metabolism in addition to flagella biogenesis. In this study, the phylogenetic distribution of csrA and its role in Escherichia coli biofilm development were examined. CsrA homologs were examined using Southern hybridization experiment and by analyzing existing sequencing data and was found to be widespread among eubacteria. CsrA was shown to be capable of acting as a genetic switch for biofilm formation and dispersal. A csrA mutant of E. coli was shown to increase biofilm formation and exhibit apparent pillars and channels characteristic of a mature biofilm. Over-expression of csrA completely inhibited biofilm formation in E. coli K-12 and decreased biofilm formation in related enteric pathogens. Induction of csrA expression from a multicopy plasmid caused dispersal of a pre-formed biofilm. Gene expression studies revealed that csrA expression is dynamically regulated during biofilm formation. Several outer-membrane factors and global regulators that have been implicated in biofilm formation were examined for effects on biofilm formation in a csrA mutant. Crystal violet adherence assays revealed that flagella and type I pili affect biofilm formation in a scrA mutant strain; however, colonic acid and curli fimbriae did not exhibit quantitative effects on biofilm formation in the csrA mutant, but the stationary phase sigma factor, RpoS, had no quantitative effect on csrA mutant biofilm formation. Therefore, a csrA mutant will form a biofilm in the absence of each of these outer-membrane factors and global regulatory factors of biofilm formation. The effects of csrA on biofilm formation were found to be mediated in part through its effects on intracellular glycogen metabolism. Thus the redirection of carbon flux, in response to environmental and/or physiological cues, is important for biofilm development.Item TRICHOSPORON ASAHII DISSEMINATED INFECTION IN A NEUTROPENIC PEDIATRIC PATIENT WITH HIGH-RISK ACUTE LYMPHOBLASTIC LEUKEMIA(2013-04-12) Ryan, KatherinePurpose: The purpose of this study is to report a fatal case of infection caused by Trichosporon asahii in a pediatric patient with acute lymphoblastic leukemia (ALL) and to present an update on systemic trichosporonosis in neutropenic patients with special reference to the treatment and diagnosis of Amphotericin B resistant infections. Methods: A 4-year-old girl was admitted to the hospital with recurrent fevers, bone pain, malaise, and pancytopenia. She was diagnosed with B precursor ALL and a history of asthma and prior corticosteroid treatment. She was started on a an ALL treatment protocol (AALL 1131) as high risk due to prior treatment with steroids. At day 15 of her remission induction therapy, her management was complicated by her left arm suddenly becoming painful and edematous, and she spiked a fever (T-max 40.4° C). Blood cultures Trichosporon yeast species and her absolute neutrophil count (ANC) was 0. She was started on amphotericin B and her CVC was removed. The organism was identified as Trichosporon asahii, a fungal species known for multi-drug resistance. She was then started on voriconazole and continued Amphotericin B and Cefepime for fungal and broad-spectrum bacterial coverage. As her infection persisted, T. asahii was repeatedly demonstrated in blood cultures. Results: In the days following, she developed an oxygen requirement, her abdomen became distended and firm, there was a significant decrease in urine output, and a sonogram showed pyelonephritis. Both lower extremities became edematous and scattered red papules developed on her abdomen, chest, face, and back. She was moved to the PICU 17 days from admission. On day 18, she required intubation and pressor support, G-CSF was started, and the first signs of multi-organ failure were evident. On the 23rd day from her admission, life-supporting measures were discontinued at the request of the family and she died at 1:10am. Post-mortem it was determined that the strain of T. asahii grown from her blood cultures was resistant to amphotericin B and micafungin, but sensitive to voriconazole. Conclusions: With greater awareness of etiologic significance of T. asahii and its drug resistance, future cases of trichosporonosis are more likely to be identified early, based on culture sensitivity, and evaluated for innovative antifungal therapy.