The goal of this chapter is to describe the pathogenesis of Brucella
reporting, the host-pathogen and the cell/macrophage Brucella
interactions, and the major virulence factors of this bacteria genus. The
epithelium of the respiratory, digestive and reproductive tracts are the
most important ports of bacterium entry in the host. The mechanisms by
which Brucella enters the cells and evades the host immune system
remains poorly understood. However, in the past decade, the mechanisms
of Brucella pathogenesis and host immunity have been extensively
investigated. Brucella has the ability to survive and replicate
intracellularly in mononuclear phagocytes and to control host immune
responses. This pathogen developed several strategies to evade the host s
immune defense mechanisms preventing inflammatory responses at the
site of entrance in the host and maintain the infection. Brucella bacterium
is internalized by macrophages and dendritic cells, and invades the
bloodstream and lymphatics causing an eventual transitory bacteremia.
Inside phagocytic cells, few bacteria can survive. Brucella also shows a
strong tissue tropism to monocytes in the liver, spleen, lymph nodes,
bone marrow and trophoblasts. All these target cells lead to clinical
manifestations, characterized by infection in lymphoid tissues and
inflammatory lesions in the reproductive tract of pregnant females.
Unlike other bacteria, Brucella lacks classical bacterial virulence factors
such as exotoxins, capsules, secreted proteases, fimbriae, flagella,
virulence plasmids, resistant strains and phage-encoded toxins. Other
virulence factors have been implicated in the pathogenesis as the type IV
secretion system, the BvrR/BvrS two component regulatory system, the
Brucella intact lipopolysaccharide O-antigen in smooth strains, and cyclic
-1,2-glucans. Toll-like receptors are single-pass type I transmembranespanning
of proteins that play a key role in the innate immune system.
Future perspectives include new genomics and omics technologies and
software tools to analyze virulent genes associated with a Brucella
infection. This information will provide a better knowledge of infection
and Brucella-host relations that are necessary for vaccine production and
strategies to prevent and control brucellosis in small ruminants.
