The lung in the immunocompromised patient. Infectious complications Part 1. (17/4196)

Pulmonary infections are a major cause of morbidity and mortality in the immunosuppressed patient. Among the infections encountered are Pneumocystis carinii, mycobacterial, fungal, and bacterial infection. In this review, we will discuss these various possible infections, their frequency of occurrence, and their clinical presentation in the various immunosuppressed groups.  (+info)

Clinical evaluation of the enhanced Gen-Probe Amplified Mycobacterium Tuberculosis Direct Test for rapid diagnosis of tuberculosis in prison inmates. (18/4196)

The reliability of the enhanced Amplified Mycobacterium Tuberculosis Direct Test (E-MTD; Gen-Probe, Inc., San Diego, Calif.) for rapid diagnosis of pulmonary tuberculosis (TB) was evaluated by testing 1, 004 respiratory specimens from 489 Texas prison inmates. Results were compared to those of mycobacterial culture (BACTEC TB 460 and Middlebrook 7H11 biplates), smear for acid-fast bacilli (AFB; auramine O), and clinical course. After chart review, three patients (nine specimens) who were on antituberculosis therapy before the study began were excluded from final analysis. Of the remaining 995 specimens, 21 were AFB smear positive: 13 grew Mycobacterium tuberculosis complex (MTBC), 6 grew nontuberculous mycobacteria, and 2 (from two patients diagnosed with TB and started on therapy after the study began) were culture negative. Twenty-eight specimens (20 patients) were positive for MTBC by culture and E-MTD. Seven specimens (seven patients) were positive by culture alone; three were from patients who had other E-MTD-positive specimens, two were false-positive cultures, and two were false-negative E-MTD results. Eight specimens were positive by E-MTD only; four specimens (four patients) were false-positive E-MTD results, and four specimens were from two patients with earlier E-MTD-positive specimens that grew MTBC. Thus, there were 22 patients with TB (10 smear positive and 12 smear negative). The sensitivity and specificity of the AFB smear for diagnosis of TB, by patient, were 45.5 and 98.9%, respectively. After resolving discrepancies, these same values for E-MTD were 90.9 and 99.1% overall, 100 and 100% for the smear-positive patients, and 83.3 and 99.1% for the smear-negative patients. Excluding the one smear-negative patient whose E-MTD-negative, MTBC culture-positive specimen contained inhibitory substances, the sensitivity of E-MTD was 95.2% overall and 90.9% in smear-negative patients. The specificity and positive predictive value of E-MTD can be improved, without altering other performance characteristics, by modifying the equivocal zone recommended by the manufacturer. These data suggest that E-MTD is a reliable method for rapid diagnosis of pulmonary TB, irrespective of the AFB smear result. Guidelines for the most appropriate use of E-MTD with smear-negative patients are needed.  (+info)

Childhood tuberculosis in an urban population in South Africa: burden and risk factor. (19/4196)

AIM: To study the epidemiology of childhood tuberculosis (TB) in a developing country. SETTING: Two urban communities of Cape Town, South Africa with a TB case notification rate of 1149/100 000. DESIGN: Retrospective descriptive study using the national population census (1991), 10 year official TB notification records, and a geographical information system. RESULTS: The case notification rate of TB in children 0-5 years old was 3588 cases/100 000 children aged 0-5 years, 3.5 times the case notification rate in adults. Children (0-14 years) accounted for 39% of the total case load. Childhood TB case notification rate correlated with parental education (r = -0.64), annual household income (r = -0.6), and crowding (r = 0.32). CONCLUSION: Children, especially those living in poor socioeconomic conditions, form an important epidemiological group and account for a notable proportion of the morbidity caused by TB. Efforts to improve TB control must therefore not only target adults (case detection and cure of infectious cases) but also children (screening of child contacts of adult cases) and the socioeconomic living conditions.  (+info)

Mycobacterium tuberculosis infection masquerading as diffuse alveolar hemorrhage after autologous stem cell transplant. (20/4196)

We report a fatal case of pulmonary tuberculosis masquerading as diffuse alveolar hemorrhage after autologous stem cell transplant.  (+info)

Impaired interleukin-8-induced degranulation of polymorphonuclear neutrophils from human immunodeficiency virus type 1-infected individuals. (21/4196)

Degranulation of peripheral blood polymorphonuclear leukocytes (PMNLs) was monitored in human immunodeficiency virus (HIV) type 1 (HIV-1)-infected individuals with or without pulmonary tuberculosis (HIV/TB and HIV groups, respectively) by measuring the release of beta-glucuronidase induced by interleukin-8 (IL-8). This was increased in a dose-dependent manner in the control groups consisting of healthy blood donors and patients with pulmonary tuberculosis. In contrast, PMNLs from the HIV and HIV/TB groups responded reciprocally in the same assay; that is, higher IL-8 input concentrations resulted in the release of less enzyme than lower IL-8 input concentrations. The degranulation response of PMNLs from HIV-1-infected individuals was similarly altered for another agonist, N-formyl-methionyl-leucyl-phenylalanine, suggesting that impairment of the nonoxidative armature of PMNL was a more generalized phenomenon. However, impaired IL-8-induced degranulation was found to be associated with the reduced expression of both IL-8 receptors, A and B, on whole-blood PMNLs from HIV-1-infected patients compared with that on whole-blood PMNLs from healthy persons. The density of IL-8RA, in particular, was most reduced on the surfaces of PMNLs from those patients with the poorest degranulation in response to IL-8. Inefficient agonist-induced degranulation may contribute to the increased susceptibility of HIV-1-infected persons to secondary microbial infections, this being further exacerbated in HIV/TB patients who, in addition, display defects in phagocytosis and oxidative burst.  (+info)

Role of interleukin-18 (IL-18) in mycobacterial infection in IL-18-gene-disrupted mice. (22/4196)

Immunity to mycobacterial infection is closely linked to the emergence of T cells that secrete cytokines, gamma interferon (IFN-gamma), interleukin-12 (IL-12), and tumor necrosis factor alpha (TNF-alpha), resulting in macrophage activation and recruitment of circulating monocytes to initiate chronic granuloma formation. The cytokine that mediates macrophage activation is IFN-gamma, and, like IL-12, IL-18 was shown to activate Th1 cells and induce IFN-gamma production by these cells. In order to investigate the role of IL-18 in mycobacterial infection, IL-18-deficient mice were infected with Mycobacterium tuberculosis and Mycobacterium bovis BCG Pasteur, and their capacities to control bacterial growth, granuloma formation, cytokine secretion, and NO production were examined. These mice developed marked granulomatous, but not necrotic, lesions in their lungs and spleens. Compared with the levels in wild-type mice, the splenic IFN-gamma levels were low but the IL-12 levels were normal in IL-18-deficient mice. The reduced IFN-gamma production was not secondary to reduced induction of IL-12 production. The levels of NO production by peritoneal macrophages of IL-18-deficient and wild-type mice did not differ significantly. Granulomatous lesion development by IL-18-deficient mice was inhibited significantly by treatment with exogenous recombinant IL-18. Therefore, IL-18 is important for the generation of protective immunity to mycobacteria, and its main function is the induction of IFN-gamma expression.  (+info)

IL-18 promotes type 1 cytokine production from NK cells and T cells in human intracellular infection. (23/4196)

We investigated the role of IL-18 in leprosy, a disease characterized by polar cytokine responses that correlate with clinical disease. In vivo, IL-18 mRNA expression was higher in lesions from resistant tuberculoid as compared with susceptible lepromatous patients, and, in vitro, monocytes produced IL-18 in response to Mycobacterium leprae. rIL-18 augmented M. leprae-induced IFN-gamma in tuberculoid patients, but not lepromatous patients, while IL-4 production was not induced by IL-18. Anti-IL-12 partially inhibited M. leprae-induced release of IFN-gamma in the presence of IL-18, suggesting a combined effect of IL-12 and IL-18 in promoting M. leprae-specific type 1 responses. IL-18 enhanced M. leprae-induced IFN-gamma production rapidly (24 h) by NK cells and in a more sustained manner (5 days) by T cells. Finally, IL-18 directly induced IFN-gamma production from mycobacteria-reactive T cell clones. These results suggest that IL-18 induces type 1 cytokine responses in the host defense against intracellular infection.  (+info)

Social factors associated with increases in tuberculosis notifications. (24/4196)

This study assessed the contribution of immigration and deprivation to the changes in tuberculosis notifications in Liverpool over the last 20 yrs. Ethnic origin was retrospectively assigned to all named cases from 1974 to 1995. Average tuberculosis rates were calculated for the 33 council wards in Liverpool for 1981-1985 and 1991-1995. Multiple regression was used to determine the independent effects of socioeconomic and population measures from the 1981 and 1991 censuses in explaining these ward-based rates. Since 1974, there has been a steady increase in the percentage of non-Caucasian cases of tuberculosis, from 8.7% in 1975-1977, 15.1% in 1981-1983, 17.5% in 1987-1989 to 28.0% in 1993-1995. Multiple regression analysis showed that in 1981 only unemployment had a significant independent relationship with tuberculosis rates, but in 1991 two indices of deprivation and ethnicity had a significant influence. The increasing proportion of non-Caucasian tuberculosis cases, both while the number of notifications was declining before 1987 and increasing afterwards, is not necessarily consistent with the concept that immigration has influenced the recent increase. However, the fact that ethnicity now independently explains some of the council ward variations but did not in the early 1980s suggests that immigration does influence the distribution of disease within the city.  (+info)