Murine model of pneumonia caused by Parachlamydia acanthamoebae

The role of Parachlamydia acanthamoebae as an agent of pneumonia is suggested by sero-epidemiological studies, molecular surveys and by the permissivity of macrophages, lung fibroblasts and pneumocytes to this obligate intracellular bacteria. We thus developed a murine model of pneumonia due to Parachlamydia. Mice were inoculated intratracheally with Parachlamydia acanthamoebae. Pneumonia-associated mortality was of 50% 5 days post-inoculation. Lungs histopathology was characterized by purulent and interstitial pneumonia. The presence of Parachlamydia in the lesions was demonstrated by PCR, immunohistochemistry and electron microscopy. Moreover, living Parachlamydia could be recovered from the lungs of infected mice using amoebal co-culture. All control mice inoculated with heat-inactivated bacteria were free of symptoms and survived. Thus, we demonstrated that Parachlamydia induce a severe pneumonia in mice. This animal model, which confirms the third and fourth Koch postulates, may be suitable to test in vivo efficient therapeutic regimens against Parachlamydia.

Low C-reactive protein values at admission predict mortality in patients with severe community-acquired pneumonia caused by Streptococcus pneumoniae that require intensive care management.

PURPOSE: To identify risk factors associated with mortality in patients with severe community-acquired pneumonia (CAP) caused by S. pneumoniae who require intensive care unit (ICU) management, and to assess the prognostic values of these risk factors at the time of admission. METHODS: Retrospective analysis of all consecutive patients with CAP caused by S. pneumoniae who were admitted to the 32-bed medico-surgical ICU of a community and referral university hospital between 2002 and 2011. Univariate and multivariate analyses were performed on variables available at admission. RESULTS: Among the 77 adult patients with severe CAP caused by S. pneumoniae who required ICU management, 12 patients died (observed mortality rate 15.6 %). Univariate analysis indicated that septic shock and low C-reactive protein (CRP) values at admission were associated with an increased risk of death. In a multivariate model, after adjustment for age and gender, septic shock [odds ratio (OR), confidence interval 95 %; 4.96, 1.11-22.25; p = 0.036], and CRP (OR 0.99, 0.98-0.99 p = 0.034) remained significantly associated with death. Finally, we assessed the discriminative ability of CRP to predict mortality by computing its receiver operating characteristic curve. The CRP value cut-off for the best sensitivity and specificity was 169.5 mg/L to predict hospital mortality with an area under the curve of 0.72 (0.55-0.89). CONCLUSIONS: The mortality of patients with S. pneumoniae CAP requiring ICU management was much lower than predicted by severity scores. The presence of septic shock and a CRP value at admission <169.5 mg/L predicted a fatal outcome.