Laboratory-based evaluation of legionellosis epidemiology in Ontario, Canada, 1978 to 2006

BACKGROUND: Legionellosis is a common cause of severe community acquired pneumonia and respiratory disease outbreaks. The Ontario Public Health Laboratory (OPHL) has conducted most testing for Legionella species in the Canadian province of Ontario since 1978, and represents a multi-decade repository of population-based data on legionellosis epidemiology. We sought to provide a laboratory-based review of the epidemiology of legionellosis in Ontario over the past 3 decades, with a focus on changing rates of disease and species associated with legionellosis during that time period. METHODS: We analyzed cases that were submitted and tested positive for legionellosis from 1978 to 2006 using Poisson regression models incorporating temporal, spatial, and demographic covariates. Predictors of infection with culture-confirmed L. pneumophila serogroup 1 (LP1) were evaluated with logistic regression models. Results: 1,401 cases of legionellosis tested positive from 1978 to 2006. As in other studies, we found a late summer to early autumn seasonality in disease occurrence with disease risk increasing with age and in males. In contrast to other studies, we found a decreasing trend in cases in the recent decade (IRR 0.93, 95% CI 0.91 to 0.95, P-value = 0.001); only 66% of culture-confirmed isolates were found to be LP1. CONCLUSION: Despite similarities with disease epidemiology in other regions, legionellosis appears to have declined in the past decade in Ontario, in contrast to trends observed in the United States and parts of Europe. Furthermore, a different range of Legionella species is responsible for illness, suggesting a distinctive legionellosis epidemiology in this North American region

Repeated measures of cerebral and cerebellar volume analyzed by total percentage of growth from p18 to p30.

<p><b>A)</b> There were no significant differences in cerebral growth amongst groups. <b>B)</b> Cerebellar growth in male mice was not different between treatment groups. Female TH treated mice had significantly increased cerebellar growth when compared to control female mice (*p = 0.048). Controls n = 4 males and females, NT n = 4 males and females, TH n = 6 males and 5 females.</p

GFAP immunohistochemistry at p18.

<p>Cortex and white matter injury showing GFAP positive areas and paucity of stain in control. Hippocampal injury with glial staining and lack of staining in control mouse. Striatal injury with widespread GFAP staining indicating glial activation and lack of staining in control, other than normal white matter staining.</p

Representative MRI and gross histopathology at p18 and p30.

<p><b>A)</b> Representative T2—weighted MR imaging animals at each time point, treatment, and sex. Images at p18 and p30 are from the same animal. The trend of mild to moderate, variable injury and neuroprotection particularly in females is demonstrated. <b>B)</b> Low power views H&E stained anterior and posterior sections from p30 male mice.</p

Cerebral and cerebellar volumes on MRI at p18 and p30.

<p><b>A)</b> Residual cerebral volumes at p18 are lower in NT compared to controls (* p<0.001) and to TH (# p<0.001). By p30, both NT and TH cerebral volumes are less than controls (* p = 0.003 and ^ p<0.001). <b>B)</b> Residual cerebral volumes stratified by sex. Male mouse residual cerebral volume at p18 was smaller in NT vs. TH and controls (*p<0.001 and # p = 0.002). At p30, differences persisted in males between NT and controls (*p<0.001). No differences were found between female groups. <b>C)</b> Cerebellar volumes stratified by sex. At p18, cerebellar volume in TH males was smaller than controls (*p = 0.01). No differences between groups were found in female cerebellar volume. p18 males: control n = 6, NT n = 9, TH n = 12; females: control n = 6, NT n = 11, TH n = 10. p30 males: control n = 7, NT n = 9, TH n = 12; females: control n = 5, NT n = 11, TH n = 11.</p