J Bacteriol 2006,188(11):3748–3756 PubMedCrossRef Authors’ contri

J Bacteriol 2006,188(11):3748–3756.PubMedCrossRef Authors’ contributions MO participated in the design of the study, carried out the experimental work, image and statistical analyzes, analyzed and interpreted data, and wrote the manuscript.

HH conceived the study, participated in the design of the study and data interpretation, and helped to write the manuscript. IFN conceived the study, participated in the design of the study and corrected the manuscript. All authors have read and approved the manuscript.”
“Background An appreciation of the immunological mechanisms that affect the interaction between the host and its pathogens is crucial for an understanding of the epidemiology of infection [1–4]. By linking within-host immunological processes to the between-host dynamics of infection it is possible to explain,

and ultimately prevent, the conditions that allow for the invasion and survival of a pathogen within a MLN2238 nmr host and the consequences check details for transmission. Fundamental to this is the knowledge of how the immune response affects pathogen replication and clearance as well as the intensity and duration of shedding and, thus, transmission. Chronic bacteria infections can pose a challenge to the study of host infectiousness and associated immune response in that bacteria can either persist in the host, despite an acute inflammatory phase and active immunity, or colonize and persist without causing any apparent clinical or symptomatic effects [5–7]. Bacteria

can activate their pathogenicity at a later time by triggering serious P-type ATPase disease and high infectiousness or can increase their transmission rate in response to changes in host susceptibility [8–12]. These findings suggest that immune-compromised and chronically infected hosts can act either as life-long bacteria shedders or shed bacteria for a restricted period, usually coinciding with the acute phase of infection. To understand the dynamics of chronic infections, we need to identify not only the key immunological processes that affect long term pathogen persistence but also how pathogen replication, intensity and duration of bacteria shedding is associated with the immune response. Here, we investigated the relationship between immune response and shedding rate in a chronic bacteria infection using the Bordetella bronchiseptica-rabbit system. Our recent work on the epidemiology of B. bronchiseptica in a free living population of rabbits (Oryctolagus cuniculus) showed that this is a common and persistent infection: annual prevalence ranged between 88% and 97% and by 2 months of age, 65% of the individuals had already seroconverted [13]. A model for bacteria infection was find more suggested where the annual recruitment of new infected individuals was associated with the onset of the host breeding season and the availability of new naïve offspring.

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