Infectious disease of humans and domestic animals. It is characterized by gradual onset of fever, chills, sweats, weakness, and aches, and it usually ends within six months. It is named after the British physician David Bruce (b. 1855—d. 1931), who first identified (1887) the causative bacteria. Three main species in the genus Brucella commonly cause the disease in humans, who contract it from infected animals (goats, sheep, pigs, cattle). Brucellosis is rarely transmitted between humans but spreads rapidly in animals, causing severe economic losses. Drug therapy is not practical for animal brucellosis, but vaccination of young animals is useful. Infected animals must be removed from herds. Antibiotics are effective against acute disease in humans, in whom it can cause liver and heart problems if untreated.
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There appears to be an increase in the risk for developing particular vasculitis-related diseases (e.g. Henoch-Schönlein purpura), spondylarthropathy, prolonged arthritis of certain joints and protracted myalgia.
A genetic test is also available now that the disease has been linked to mutations in the MEFV gene. Sequencing of exons 2, 3, 5, and 10 of this gene detects an estimated 97% of all known mutations.
The function of pyrin has not been completely elucidated, but it appears to be a suppressor of the activation of caspase 1, the enzyme that stimulates production of interleukin 1β, a cytokine central to the process of inflammation. It is not conclusively known what exactly sets off the attacks, and why overproduction of IL-1 would lead to particular symptoms in particular organs (e.g. joints or the peritoneal cavity).
The MEFV gene is located on the short arm of chromosome 16 (16p13). The disease inherits in an autosomal recessive fashion. Therefore, two asymptomatic carrier parents have a 25% chance of a child with the disorder. FMF patients who marry a carrier or another FMF patient have a 50% and 100% chance, respectively, in having a child with FMF.
Since the 1970s, colchicine, a drug otherwise mainly used in gout, has been shown to decrease attack frequency in FMF patients. The exact way in which colchicine suppresses attacks is unclear. While this agent is not without side-effects (such as abdominal pain and muscle pains), it may markedly improve quality of life in patients. The dosage is typically 1-2 mg a day. Development of amyloidosis is delayed with colchicine treatment. Interferon is being studied as a therapeutic modality.
Studies in the area of familial mediterranean fever therapy reported from Ondokuz Mayis University, Department of Periodontology.(Clinical report)
Jun 03, 2009; New investigation results, 'Periodontal disease in patients with familial Mediterranean fever: from inflammation to amyloidosis,'...
Studies Conducted at University of California Medical Center on Familial Mediterranean Fever Recently Published.
Apr 16, 2011; Researchers detail in 'Diagnosis and management of familial Mediterranean fever: integrating medical genetics in a dedicated...
Research from Kecioren Training and Research Hospital Provides New Data about Familial Mediterranean Fever.(Report)
Apr 07, 2012; New investigation results, "Assessment of cardiac functions using tissue Doppler imaging in children with familial Mediterranean...