Brucella

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Chapter 199 Brucella

Gordon E. Schutze, Richard F. Jacobs

Human brucellosis, caused by organisms of the genus Brucella, continues to be a major public health problem worldwide. Humans are accidental hosts and acquire this zoonotic disease from direct contact with an infected animal or consumption of products of an infected animal. Although brucellosis is widely recognized as an occupational risk among adults working with livestock, much of the brucellosis in children is food-borne and is associated with consumption of unpasteurized milk products. It is also a potential agent of bioterrorism (Chapter 704).

Etiology

Brucella abortus (cattle), B. melitensis (goat/sheep), B. suis (swine), and B. canis (dog) are the most common organisms responsible for human disease. These organisms are small, aerobic, non–spore-forming, nonmotile, gram-negative coccobacillary bacteria that are fastidious in their growth but can be grown on various laboratory media including blood and chocolate agars.

Epidemiology

Because of improved sanitation, brucellosis has become rare in industrialized countries. Brucellosis exists worldwide and is especially prevalent in the Mediterranean basin, Arabian Gulf, Indian subcontinent, and parts of Mexico and Central and South America. In industrialized countries, recreational or occupational exposure to infected animals is a major risk factor for the development of disease. In the USA, 50% of cases occur in California and Texas. Among children, geographic locations that are endemic for B. melitensis remain areas of increased risk for the development of infection. In such locations, unpasteurized milk from goats or camels may be used to feed children, thus leading to the development of brucellosis. A history of travel to endemic regions or consumption of exotic food or unpasteurized dairy or dairy products may be an important clue to the diagnosis of human brucellosis.

Pathogenesis

Routes of infection for these organisms include inoculation through cuts or abrasions in the skin, inoculation of the conjunctival sac of the eye, inhalation of infectious aerosols, or ingestion of contaminated meat or dairy products. The risk for infection depends on the nutritional and immune status of the host, the route of inoculum, and the species of Brucella. For reasons that remain unclear, B. melitensis and B. suis tend to be more virulent than B. abortus or B. canis.

The major virulence factor for Brucella appears to be its cell wall lipopolysaccharide. Strains containing smooth lipopolysaccharide have been demonstrated to have greater virulence and are more resistant to killing by polymorphonuclear leukocytes. These organisms are facultative intracellular pathogens that can survive and replicate within the mononuclear phagocytic cells (monocytes, macrophages) of the reticuloendothelial system. Even though Brucella are chemotactic for entry of leukocytes into the body, the leukocytes are less efficient at killing these organisms than other bacteria despite the assistance of serum factors such as complement.

Organisms that are not phagocytosed by the leukocytes are ingested by the macrophages and become localized within the reticuloendothelial system. Specifically, they reside within the liver, spleen, lymph nodes, and bone marrow and result in granuloma formation. Antibodies are produced against the lipopolysaccharide and other cell wall antigens. This provides a means of diagnosis and probably has a role in long-term immunity. The major factor in recovery from infection appears to be development of a cell-mediated response resulting in macrophage activation and enhanced intracellular killing. Specifically, sensitized T lymphocytes release cytokines (e.g., interferon-γ and tumor necrosis factor-α), which activate the macrophages and enhance their intracellular killing capacity.

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