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Background: Lyme disease (LD) is a multisystem infection that can affect the skin, heart, joints and nervous system. In Canada, the incidence of LD cases has increased over the past decade making this a disease of public health concern. The objective of this study is to summarize the epidemiology of LD cases reported in Canada from 2009 through 2019. Methods: Incidence over time, case classification (confirmed and probable), seasonal and geographic distribution, demographic and clinical characteristics of reported LD cases were determined. Logistic regression was used to explore potential demographic risk factors for the occurrence of LD. Results: During 2009-2019, a total of 10,150 LD cases were reported by the provinces to the Public Health Agency of Canada, of which 7,242 (71.3%) were confirmed and 2,908 (28.7%) were probable cases. The annual count increased from 144 in 2009 to 2,634 in 2019, mainly due to an increase in locally acquired infections, from 65.3% to 93.6%, respectively. The majority of cases (92.1%) were reported from three provinces: Ontario (46.0%); Nova Scotia (28.0%); and Québec (18.1%). Most of the locally acquired cases (74.0%) were reported in the summer months of June (20.0%), July (35.4%) and August (18.6%). The highest incidence rates (cases per 100,000 population) were in children aged 5-9 years (45.0) and in adults aged 65-69 years (74.3), with 57.3% of all reported cases occurring among males. The most common presenting symptoms were single erythema migrans rash (75.1%) and arthritis (34.1%). The frequency of reported clinical manifestations varied among age groups and seasons with erythema migrans and arthritis at presentation reported more frequently in children than older patients. Conclusion: The results of this report highlight the continued emergence of LD in Canada and the need for further development and implementation of targeted awareness campaigns designed to minimize the burden of LD.
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RATIONALE: Discoidin domain receptor 1 (DDR1) is a tyrosine kinase activated by native collagens. Based on previous findings showing increased DDR1 expression in bronchoalveolar lavage cells from patients with idiopathic pulmonary fibrosis, we hypothesized that DDR1 mediates disease progression after lung injury. OBJECTIVES: To investigate the inflammatory and fibrotic responses of DDR1 knockout and wild-type mice to bleomycin-induced lung injury. METHODS: Age- and sex-matched DDR1 knockout and wild-type C57BL/6 mice received a single intratracheal instillation of 2 U/kg bleomycin or saline, respectively. After 2 wk, lung inflammation and fibrosis were assessed using immunohistochemistry, real-time polymerase chain reaction, TUNEL assay, ELISA, fluorescence-activated cell sorting, and Western blot analysis. MEASUREMENTS AND MAIN RESULTS: Compared with wild-type animals, DDR1-null mice were largely protected against bleomycin-induced injury. Bleomycin-induced increases in collagen protein levels and tenascin-C mRNA levels were abrogated in knockout animals. Furthermore, myofibroblast expansion and apoptosis were much lower in these animals compared with their wild-type counterparts. Absence of inflammation in knockout mice was confirmed by lavage cell count and a cytokine ELISA. Western blot analysis of injured lung tissue revealed that DDR1-null mice failed to respond to the bleomycin insult with p38 MAPK activation, which was readily observed in wild-type mice. CONCLUSIONS: DDR1 expression is a prerequisite for the development of lung inflammation and fibrosis. Blockade of DDR1 may therefore be a novel therapeutic intervention in patients with pulmonary fibrosis.
