Respiratory virosis and invasive bacterial superinfections - The case for influenza and meningococcal diseases
Unité des Neisseria, département de médecine moléculaire, Institut Pasteur, centre national de référence des méningocoques, 25-28, rue du Docteur-Roux, 75724 cedex 15 Paris, France.Archives de Pédiatrie (Impact Factor: 0.41). 12/2003; 10(11):1013-5. DOI: 10.1016/S0929-693X(03)00491-3
The pathophysiology of bacterial superinfections of influenza, including meningococcal diseases, remains obscure. Mice, normally resistant to the meningococcus, become susceptible after previous influenza A virus infection. This immunosuppressive effect is transitory and is associated with the peak of the inflammatory anti-virus reaction. These results underline the importance of preventing bacterial superinfections of influenza by the surveillance of any relapse of fever after improvement of the influenza syndrome. At the community level, influenza vaccine, beside its specific effects, might also prevent many cases of invasive superinfections, including meningococcal diseases.
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ABSTRACT: Despite the use of antimicrobial prophylaxis, cytomegalovirus (CMV) and Pneumocystis carinii (PC) pneumonia (PCP) are both leading causes of morbidity and mortality in immunocompromised patients. It has previously been reported that CMV infection modulates host immune responses with a variety of mechanisms which include the suppression of helper T cell functions and antigen presenting cell (APC) functions, both of which are critical for PCP resolution. However, the mechanisms of these interactions and other possible immune regulatory effects are not clearly understood. In this study, we investigated the impact of murine CMV (MCMV) induced immunomodulation on the progression of PCP in a co-infection model. Initial results show that dually infected mice had evidence of more severe PC disease, which include a greater loss of body weight, an excess lung PC burden and delayed clearance of PC from lungs, compared to mice with PC infection alone. At day 7 post-infection, dually infected mice had reduced numbers of MHC-II expressing cells in the lung interstitium and lymph nodes and reduced migration of CD11c+ cells to both the tracheobronchial lymph nodes and alveolar spaces. Dual infected mice showed elevated numbers of specific CD8 responses concomitant with a decrease in activated CD4+ T cells in both the lymph nodes and in alveolar spaces when compared to mice infected with MCMV alone. These data suggest that MCMV infection inhibits the immune responses generated against PC which contribute to the delayed clearance of the organism.Virus Research 01/2006; 114(1-2):35-44. DOI:10.1016/j.virusres.2005.05.008 · 2.32 Impact Factor
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ABSTRACT: To evaluate risk factors for meningococcal carriage and carriage acquisition in the African meningitis belt, comparing epidemic serogroup A (NmA) to non-epidemic serogroups. During the non-epidemic meningitis season of 2003, pharyngeal swabs were taken at five monthly visits in a representative population sample (N = 488) of Bobo-Dioulasso, Burkina Faso (age 4-29 years) and analysed by culture. Standardized questionnaires were administered. In 2006, a similar study was performed in 624 individuals (age 1-39 years) during an NmA meningitis epidemic. We evaluated serogroup-specific risk factors for carriage, carriage acquisition and clearance using multivariate logistic and Poisson regression, and a Cox proportional hazard model. The prevalence of NmA carriage (current or recent pharyngitis or rhinitis) was 16% (31%) vs. 0% (9%) in the epidemic vs. the hyperendemic setting. During the epidemic situation, NmA carriage was significantly associated with recent sore throat (adjusted odds ratio (OR), 3.41) and current rhinitis (OR 2.65). During the non-epidemic meningitis season in 2003, air humidity (20-39% and >or=40%, compared to <20%) during the month before swabbing was significantly and positively associated with carriage acquisition of non-groupable meningococci (OR 2.18 and 1.55) and inversely with carriage clearance (hazard ratio 0.61 and 0.27, respectively). Respiratory tract infections may increase meningococcal carriage, and thus contribute to epidemic risk, in addition to seasonality in the meningitis belt. Humid climate may favour carriage of unencapsulated meningococci. These findings may help identifying interventions against epidemic and hyperendemic meningococcal meningitis due to non-vaccine serogroups.Tropical Medicine & International Health 11/2008; 13(12):1543-52. DOI:10.1111/j.1365-3156.2008.02165.x · 2.33 Impact Factor
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ABSTRACT: Despite much progress in surveillance and biological research, no explanation exists to date for the epidemic pattern of meningitis in the African meningitis belt, which is required to mathematically model the impact of vaccine strategies or to predict epidemics. This paper presents a hypothetical explanatory model for epidemic meningococcal meningitis. Four incidence patterns are defined as model states, including endemic incidence during the rainy season, ubiquitous hyperendemicity during the dry season, occasional localized epidemics, and-at the regional level-regular epidemic waves spanning over communities or years. While the transition from endemic to hyperendemic situation in a community is caused by an increase in risk of meningitis given colonization by a virulent meningococcus (due to damage of the pharyngeal mucosa by dry climate), the transition from hyperendemic to epidemic situation involves increased pharyngeal colonization and transmission (possibly caused by viral respiratory infection epidemics). The described mechanisms are sufficient to explain the 10- to 100-fold incidence increase that both transitions usually imply. Epidemic waves occur if new meningococcal strains which escape pre-existing immunity, enter the population. Future research should include the impact of viral co-infection on bacterial colonization and invasion.International journal of infectious diseases: IJID: official publication of the International Society for Infectious Diseases 12/2009; 14(7):e553-9. DOI:10.1016/j.ijid.2009.08.013 · 1.86 Impact Factor
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