DISTINCT TEMPORALITIES IN THE BREAST CANCER DISEASE PROCESS

Comprehensive approach study aimed understanding the reflections and contrasts between personal time and medical therapy protocol time in the life of a young woman with breast cancer. Addressed as a situational study and grounded in Beth’s life story about getting sick and dying of cancer at age 34, the study’s data collection process employed interviews, observation and medical record analysis. The construction of the analytic-synthetic box based on the chronology of Beth’s clinical progression, treatment phases and temporal perception of occurrences enabled us to point out a linear medical therapy protocol time identified by the diagnosis and treatment sequencing process. On the other hand, Beth’s experienced time was marked by simultaneous and non-linear events that generated suffering resulting from the disease. Such comprehension highlights the need for healthcare professionals to take into account the time experienced by the patient, thus providing an indispensable cancer therapeutic protocol with a personal character

HIV infection disrupts the sympatric host-pathogen relationship in human tuberculosis

The phylogeographic population structure of Mycobacterium tuberculosis suggests local adaptation to sympatric human populations. We hypothesized that HIV infection, which induces immunodeficiency, will alter the sympatric relationship between M. tuberculosis and its human host. To test this hypothesis, we performed a nine-year nation-wide molecular-epidemiological study of HIV-infected and HIV-negative patients with tuberculosis (TB) between 2000 and 2008 in Switzerland. We analyzed 518 TB patients of whom 112 (21.6%) were HIV-infected and 233 (45.0%) were born in Europe. We found that among European-born TB patients, recent transmission was more likely to occur in sympatric compared to allopatric host-pathogen combinations (adjusted odds ratio [OR] 7.5, 95% confidence interval [95% CI] 1.21-infinity, p = 0.03). HIV infection was significantly associated with TB caused by an allopatric (as opposed to sympatric) M. tuberculosis lineage (OR 7.0, 95% CI 2.5-19.1, p<0.0001). This association remained when adjusting for frequent travelling, contact with foreigners, age, sex, and country of birth (adjusted OR 5.6, 95% CI 1.5-20.8, p = 0.01). Moreover, it became stronger with greater immunosuppression as defined by CD4 T-cell depletion and was not the result of increased social mixing in HIV-infected patients. Our observation was replicated in a second independent panel of 440 M. tuberculosis strains collected during a population-based study in the Canton of Bern between 1991 and 2011. In summary, these findings support a model for TB in which the stable relationship between the human host and its locally adapted M. tuberculosis is disrupted by HIV infection