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Tuberculin conversion among health care workers was strongly associated with inadequate ventilation in general patient rooms and with type and duration of work, but not with ventilation of respiratory isolation rooms.

Delayed diagnosis of active pulmonary tuberculosis (TB) among hospitalized patients is common and believed to contribute significantly to nosocomial transmission. This study was conducted to define the occurrence, associated patient risk factors, and outcomes among patients and exposed workers of delayed diagnosis of active pulmonary TB. Among 429 patients newly diagnosed to have active pulmonary TB between June 1992 and June 1995 in 17 acute-care hospitals in four Canadian cities, initiation of appropriate treatment was delayed 1 week or more in 127 (30%). This was associated with atypical clinical and demographic patient characteristics, and after adjustment for these characteristics, with admission to hospitals with low TB admission rate of 0.2-3.3 per 10,000 admissions (odds ratio [OR]: 7.4; 95% confidence interval [CI]: 3.2,17.5) or intermediate TB admissions of 3.4-9.9/10,000 (OR: 2.3; CI: 1.6,3.2) as well as potentially preventable (late) intensive care unit admission (OR: 16.8; CI: 2.0,144) and death (OR: 3.3; CI: 1.7,6.5]). In hospitals with low TB admission rates, initially missed diagnosis, smear-positive patients undergoing bronchoscopy, late intensive care unit admission (OR: 2.3; CI: 0.1,56), and death (OR: 3.8; CI: 1.2,12.1) were more common than in hospitals with high TB admissions (> 10/ 10,000); a similar trend was seen in hospitals with intermediate TB admissions. Even after adjustment for workers' characteristics and ventilation in patients' rooms tuberculin conversions were disproportionately high in hospitals with low and intermediate TB admission rates and significantly higher in hospitals with overall TB mortality rate above 10% (OR: 2.5; CI: 1.6,3.7). In the hospitals studied, as the rate of TB admissions decreased, the likelihood of poor outcomes and risk of transmission of TB infection per hospitalized patient with TB increased. Institutional risk of TB transmission was poorly correlated with number of patients with TB and better correlated with indicators of patient care such as delayed diagnosis and treatment and overall TB-related patient mortality.

In animal cells, myo-inositol is an important regulatory molecule in several physiological and biochemical processes, including signal transduction and membrane biogenesis. However, the fundamental biological functions of myo-inositol are still far from clear in plants. Here, we report the genetic characterization of three Arabidopsis thaliana genes encoding D-myo-inositol-3-phosphate synthase (MIPS), which catalyzes the rate-limiting step in de novo synthesis of myo-inositol. Each of the three MIPS genes rescued the yeast ino1 mutant, which is defective in yeast MIPS gene INO1, and they had different dynamic expression patterns during Arabidopsis embryo development. Although single mips mutants showed no obvious phenotypes, the mips1 mips2 double mutant and the mips1 mips2 mips3 triple mutant were embryo lethal, whereas the mips1 mips3 and mips1 mips2 +/2 double mutants had abnormal embryos. The mips phenotypes resembled those of auxin mutants. Indeed, the double and triple mips mutants displayed abnormal expression patterns of DR5:green fluorescent protein, an auxin-responsive fusion protein, and they had altered PIN1 subcellular localization. Also, membrane trafficking was affected in mips1 mips3. Interestingly, overexpression of PHOSPHATIDYLINOSITOL SYNTHASE2, which converts myoinositol to membrane phosphatidylinositol (PtdIns), largely rescued the cotyledon and endomembrane defects in mips1 mips3. We conclude that myo-inositol serves as the main substrate for synthesizing PtdIns and phosphatidylinositides, which are essential for endomembrane structure and trafficking and thus for auxin-regulated embryogenesis.

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