ABSTRACT
A cluster of time-linked cases and the identification of a clonal strain suggest the occurrence of an outbreak of listeriosis in Belgium in 2011, presumably due to the consumption of hard cheese made with pasteurised milk and produced by a Belgium manufacturer. The outbreak clone was identified as Listeria monocytogenes serovar 1/2a, sensitive to arsenic and cadmium and of multilocus sequence typing MLST-type 37. Food investigation of this outbreak was facilitated by the European Epidemic Intelligence Information System and data exchanged between French and Belgium listeriosis surveillance systems.
Subject(s)
Disease Outbreaks/prevention & control , Information Dissemination , Listeria monocytogenes/isolation & purification , Listeriosis/diagnosis , Listeriosis/epidemiology , Population Surveillance/methods , Aged , Aged, 80 and over , Arsenites/immunology , Bacterial Typing Techniques , Belgium/epidemiology , Cadmium Chloride/immunology , Cluster Analysis , Disease Outbreaks/statistics & numerical data , Drug Resistance, Microbial , Electrophoresis, Gel, Pulsed-Field , Europe , Female , Foodborne Diseases/diagnosis , Foodborne Diseases/epidemiology , Foodborne Diseases/prevention & control , Geographic Information Systems , Hospitalization/statistics & numerical data , Hospitalization/trends , Humans , Listeria monocytogenes/immunology , Listeriosis/microbiology , Listeriosis/prevention & control , Male , Microbial Sensitivity Tests , Middle Aged , Molecular Sequence DataABSTRACT
Immunotoxic effects of heavy metals, as a typical environmental agent, and their mechanisms are reviewed based on our findings on autoimmune response induced by exposure to cadmium (Cd) as CdCl(2). Adverse immune effects of chemicals, defined as immunotoxicity, have been used as a sensitive biomarker for assessing health effects of environmental chemicals. My initial research focused on renal toxicity of heavy metals was developed to elucidate characteristics and mechanisms for immune-mediated nephritis induced by heavy metals. In our studies the most interesting finding was autoantibody production enhanced by the oral exposure to Cd at environmental levels. It was observed simultaneously with enhancement of non-specific antibody production and suppression of primed-antigen specific antibody production. Immunostimulation including induction of autoantibodies was found to be the primary immunotoxic effect of Cd, because of the dose-sensitivity, and to be associated with polyclonal B cell activation (PBA). Further mechanism studies on the PBA induced by Cd in vitro showed that it was mediated by T cells, via cytokines, dominantly Type-2 cytokines, and recognition of MHC-II antigens of cell surface. The similarity among PBAs induced by inorganic salts of Cd, mercury and lead suggests that it would be the common effect among the metals to be involved in their pathogenesis of nephritis. Finally possible health significance of chemical-induced PBA is discussed associated with an increasing trend of autoimmune diseases in industrialized countries.
