Brucella suis

Preferred Scientific Name

• Brucella suis Huddleston

• Domain: Bacteria
•     Phylum: Proteobacteria
•         Class: Alphaproteobacteria
•             Order: Rhizobiales
•                 Family: Brucellaceae
•                     Genus: Brucella
•                         Species: Brucella suis

The survival of Brucella under environmental conditions is a relatively important factor in the transmission of disease. The survival rate of Brucella is similar to other non-sporing Gram-negative bacteria and as such is extremely variable depending on prevailing conditions. Experimental evidence indicates that B. suis is readily killed by pasteurisation, 2-4 hours of direct sunlight, and the most commonly used disinfectants. Brucella can survive in organic matter at freezing or near-freezing temperatures in excess of 2 years. Consequently, efforts to eliminate brucellosis from pig farms must include an effective sanitation program (Luchsinger et al., 1965).

The understanding of the pathogenesis of brucellosis has increased substantially in recent years (for reviews see Poester et al., 2013; Olsen et al., 2014; de Figueiredo et al., 2015) although there remain significant gaps in knowledge. Brucella can invade through epithelial cells of its host and once invaded through the digestive or respiratory tract is capable of surviving intracellularly within phagocytic or non-phagocytic host cells. The mechanisms of cell invasion are not clear and specific host receptors have not been identified but invasion through the digestive tract elicits no host inflammatory response so Brucella invade silently unnoticed by the innate immune response of the host. Brucellae lack classical virulence factors, but lipopolysaccharide (LPS) plays a major role as it prevents complement mediated bacterial killing and provides resistance against antimicrobial peptides such as defensins and lactoferrin. Brucella LPS has weak endotoxic properties compared to other bacteria, allowing the organism to escape detection by Toll-like receptors of the innate immune system. Brucella interact with cholesterol-rich microdomains (lipid rafts) within the plasma membrane mediating internalisation into host cells.

Once Brucella have entered cells they interfere with intracellular trafficking preventing fusion of the Brucella containing vacuole (BCV) with lysosome markers and directing the BCV towards a rough endoplasmic reticulum (RER) containing compartment highly permissive to intracellular replication of Brucella and the establishment of chronic infection. One of a number of systems known to be important for virulence is the BvrR/BvrS two component regulator which is required for modulation of host cell cytoskeleton on Brucella invasion. Cylic β-1,2 glucans are constituents of the bacterial periplasm with osmoregulatory and cholesterol sequestering activity required for intracellular survival. They prevent phagosome maturation by interfering with lipid rafts and preventing fusion of lysosomes with the BCV. Brucella also express a type IV secretion system encoded by the virB operon that is induced intracellularly in macrophages (Boschiroli et al., 2002) and is crucial for intracellular survival and virulence of B. suis .B. suis virB mutants cannot survive and multiply in macrophages or epithelial cells (O’Callaghan et al., 1999).