brucellosis of Pathophysiology
Brucellae are aerobic gram-negative coccobacilli that possess a unique capacity to invade each phagocytic and nonphagocytic cells and to survive within the intracellular environment by locating ways to avoid the immune system. This ability helps explain why brucellosis is a systemic disease and can involve nearly every organ system.
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Brucella can gain entry into the human body through breaks in the skin, mucous membranes, conjunctivae, and respiratory and gastrointestinal (GI) tracts. Sexual transmission has not been convincingly documented. Ingestion usually occurs by way of unpasteurized milk; meat products often have a low bacterial load. In the United States, percutaneous needlestick exposure, conjunctival exposure through eye splash, and inhalation are the most common routes of entry.
as soon as in the bloodstream, the organisms quickly emerge as intracellular pathogens contained within circulating polymorphonuclear cells (PMNs) and macrophages, using numerous mechanisms to keep away from or suppress bactericidal responses. Animal records suggest that the lipopolysaccharide (LPS) coat (easy in B melitensis, B abortus, and B suis; rough in B canis) is likely to play a role in intracellular survival, perhaps due to adenine and guanine monophosphate production, which inhibits phagosomal fusion and oxidative burst activity.
In addition, Brucella species have relatively low virulence, toxicity, and pyrogenicity, making them poor inducers of some inflammatory cytokines, such as tumor necrosis factor (TNF) and interferons. Furthermore, the bacteria do not activate the alternative complement system. Finally, they are thought to inhibit programmed cell death.
After ingestion via phagocytes, about 15-30% of brucellae survive. Susceptibility to intracellular killing differs amongst species, with B abortus conveniently killed and B melitensis hardly ever affected; these variations might give an explanation for the differences in pathogenicity and medical manifestations in human cases of brucellosis.
Brucellae that live on are transported into the lymphatic system and might reflect there locally; additionally they may replicate within the kidney, liver, spleen, breast tissue, or joints, causing both localized and systemic infection. Any organ system may be involved (eg, central nervous system [CNS], heart, joints, genitourinary system, pulmonary system, and skin); localization of the process may cause focal signs and symptoms or findings. After replication within the endoplasmic reticulum, the brucellae are released with the help of hemolysins and precipitated cell necrosis.
Development of cell-mediated immunity is the principal mechanism of recovery. The host response to infection with B abortus is characterized by the development of tissue granulomas indistinguishable from those of sarcoidosis. In contrast, infection with the more virulent species (B melitensis and B suis) more commonly results in visceral microabscesses.
even though Brucella infection is ordinarily controlled via cell-mediated immunity as opposed to antibody activity, a few immunity to reinfection is provided by means of serum immunoglobulin (Ig). initially, IgM levels rise, followed by IgG titers. IgM may stay in the serum in low levels for several months, whereas IgG sooner or later declines. constantly elevated IgG titers or 2nd rises in IgG usually imply persistent or relapsed infection. IgA antibodies are elaborated late and also may also persist for extremely long intervals.
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