Browsing by Subject "Influenza Virus Vaccines"
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Item Individual child and parental factors that influence influenza vaccination in children 6 months to 59 months of age(2011-12-01) Offutt-Powell, Tabatha; Kathryn CardarelliInfluenza illness is a vaccine-preventable disease, yet seasonal outbreaks occur yearly and vaccination coverage rates remain suboptimal. Given that childhood vaccination is dependent on parental decision-making processes, parental beliefs about influenza vaccination are important for elucidating the underlying factors contributing to suboptimal influenza vaccination coverage rates of young children. Furthermore, the 2009 H1N1 influenza pandemic was well-publicized in the media, yet the lack of increased vaccination coverage among pediatric populations during the pandemic may reflect insufficient concern regarding the threat of influenza. Our study aimed to evaluate the effect of social and behavioral factors that may influence parental decision making and subsequently influenza vaccination of children attending daycare during the 2010 – 2011 influenza season in Tarrant County, Texas. Our study involved the administration of a one-time self-administered paper survey to parents of children aged 6 months to 59 months attending home- or center-based daycare. One hundred sixty six parents from twenty-three daycares completed the survey. Logistic regression was used to estimate odds ratios for total associations and corresponding 95% confidence limits (CL) of each factor on influenza vaccine uptake. Our results suggest that physician recommendation (OR=16.4, 95% CL: 5.5, 48.6) and parents with high levels of preventive behaviors (High: OR=7.1, 95% CL: 1.9, 26.4; Moderate: OR=1.4, 95% CL: 0.4, 5.3) influence influenza vaccination of children in daycare. Parents with a high perceived threat of the 2009 H1N1 pandemic influenza strain had greater odds of vaccinating their children than parents with high perceived threat of influenza illness compared to parents with a low perceived threat of influenza illness (High: OR=3.3, 95% CL: 2.1, 5.1; Moderate: OR=1.2, 95% CL: 0.8, 1.8) and this association varied by race/ethnicity. Although preliminary, our findings suggest the potential relation of physician recommendation and parental preventive behaviors, with limited effect of the 2009 H1N1 influenza pandemic, as influential factors in the relation between health beliefs and behaviors and vaccination decision-making for children attending daycare. Future research may benefit from continued exploration of social and behavioral factors that influence influenza vaccination of children in pediatric populations with consideration of the measurement of social and health behavior constructs.Item Parental Intent to Vaccinate Young Children Against the Flu(2013-12-01) Komatz, Stephani; Suhasini Ramisetty-MiklerBackground: Influenza is a preventable respiratory condition that affects over 3 million people every year. Young children are especially susceptible to complications from influenza. Daycare settings are highly vulnerable for infectious disease transmission. The objective of the study is to examine parental, child, and demographic factors that are associated with intent to vaccinate and whether intention determines parental vaccinating behavior. Methods: Parents of children 6 years and younger from 23 daycare centers in Tarrant County participated in a survey. Data on parental intent to vaccinate, education on flu vaccination, access to and utilization of health care, and health status of the child were collected. Analyses included bivariate and multivariate techniques to assess associations between predictors and outcomes. Results: Predictive factors associated with parental intent to vaccinate include physician discussion of benefits of flu vaccines (OR = 2.91, 95% CI (1.75, 4.83), p Conclusions: The study indicates that physician discussion of benefits of the flu vaccine, access to and utilization of health care, the child’s health status are important factors that may help in increasing parental intention to vaccinate their child against the flu. These factors can be utilized to improve the efficacy of outreach programs and vaccination success rates.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.