Background: Although the use of antiretroviral therapy has led to dramatic declines in AIDS-associated mortality, Pneumocystis pneumonia (PCP) remains a leading cause of death in HIV-infected patients. Objectives: To measure mortality, identify predictors of mortality at time of illness presentation and derive a PCP mortality prediction rule that stratifies patients by risk for mortality. Methods: An observational cohort study with case note review of all HIV-infected persons with a laboratory diagnosis of PCP at San Francisco General Hospital from 1997 to 2006. Results: 451 patients were diagnosed with PCP on 524 occasions. In-hospital mortality was 10.3%. Multivariate analysis identified five significant predictors of mortality: age (adjusted odds ratio (AOR) per 10-year increase, 1.69; 95% CI 1.08 to 2.65; p = 0.02); recent injection drug use (AOR 2.86; 95% CI 1.28 to 6.42; p = 0.01); total bilirubin .0.6 mg/dl (AOR 2.59; 95% CI 1.19 to 5.62; p = 0.02); serum albumin ,3 g/dl (AOR 3.63; 95% CI 1.72-7.66; p = 0.001); and alveolar-arterial oxygen gradient >50 mm Hg (AOR 3.02; 95% CI 1.41 to 6.47; p = 0.004). Using these five predictors, a six-point PCP mortality prediction rule was derived that stratifies patients according to increasing risk of mortality: score 0-1, 4%; score 2-3, 12%; score 4-5, 48%. Conclusions: The PCP mortality prediction rule stratifies patients by mortality risk at the time of illness presentation and should be validated as a clinical tool.

This study identifies both climatological and air pollution constituents as independent risk factors for hospitalization of HIV-positive patients with PcP in San Francisco. Thus, the environmental effects on PcP are more likely complex than previously thought. Further studies are needed to understand how these factors exert their effects and to determine if these factors are associated with PcP in other geographic locations.

The DNA downstream of the lux structural genes in the Vibrio fischeri lux operon has been sequenced and a new lux gene (luxG) has been identified. A hairpin loop that begins with a poly(A) region and ends with a poly(T) region and thus can function as a bidirectional termination site for luxG and a convergent gene is located immediately downstream of luxG. 3' S1 nuclease mapping has demonstrated that the luxG mRNA was induced in a cell-density-dependent fashion consistent with it being part of the lux system and that the lux mRNA terminated immediately after the hairpin loop. The mRNA coded by an open reading frame convergent to luxG on the complementary strand was also shown by S1 nuclease mapping to overlap the lux mRNA for at least 20 nucleotides before termination. Expression of DNA containing the hairpin loop, placed between a strong promoter and a reporter gene and transferred by conjugation into luminescent bacteria, demonstrated the very high efficiency of termination by this hairpin loop oriented in either direction. These results also demonstrate that the organization of the genes at the 3' ends of the lux operons of V. fischeri and V. harveyi has clearly diverged.The Vibrio fischeri luminescence system is the most well characterized of the bacterial lux systems. Two operons encompassing seven lux genes (luxABCDE, luxI, and luxR) are sufficient for expression and regulation of luminescence on transformation into Escherichia coli (7,8). The right operon contains the lux structural genes in the or/der luxCDABE preceded by the regulatory gene, luxI. The left operon, immediately upstream of luxI, contains a second regulatory gene, luxR, transcribed in the opposite direction. It has been proposed that luxI specifies a product responsible for synthesis of an autoinducer that on binding with a receptor produced by luxR is responsible for the growthdependent induction of luminescence (6, 7). The V. fischeri lux structural genes are composed of two genes (luxA and -B) coding for the a and P subunits of luciferase and three genes (luxC, -D, and -E) that code for polypeptides that catalyze the formation of the aldehyde substrate for the luminescent reaction (2).Transposon mutagenesis of the V. fischeri lux system has shown that all transposon insertions that block luminescence were located within the two regulatory and five structural lux genes (7,8). Based on this genetic analysis of the V. fischeri luminescence system, it would appear that the complete lux system had been defined.The organization of the lux systems from V. harveyi and Photobacterium phosphoreum have at least partially been determined (12,14). In contrast to the V. fischeri lux system, regulatory genes are not located immediately upstream of the structural genes in the V. harveyi lux system. Instead, the DNA upstream is very rich in AT residues and contains numerous stop codons in all reading frames extending for >600 nucleotides (15). The order of the lux structural genes is the same in these two systems as in the V. fischeri lux system exce...

Results: 68% (117/172) of all patients were colonised with Pneumocystis. No strong associations with colonisation were identified for any demographic factors. Among clinical factors, having a CD4+ T cell count (50 cells/ml (unadjusted OR 2.4, 95% CI 1.09 to 5.48; p = 0.031) and using PCP prophylaxis (unadjusted OR 0.55, 95% CI 0.29 to 1.07; p = 0.077) were associated with Pneumocystis colonisation, although the latter association may have been due to chance. After adjustment for CD4+ T cell count, use of PCP prophylaxis was associated with a decreased odds of colonisation (adjusted OR 0.45, 95% CI 0.21 to 0.98; p = 0.045). 11 patients who were colonised were subsequently readmitted for evaluation of a second episode of pneumonia; three were found to be colonised again, but none had PCP. Conclusions: The majority of hospitalised HIV infected patients with non-PCP pneumonia are colonised with Pneumocystis. Failure to use co-trimoxazole prophylaxis and severe immunosuppression are associated with an increase in the odds of colonisation. Pneumocystis colonisation among hospitalised patients does not commonly lead to PCP.