Pathogenic bacteria survive in iron-limited host environments by using several iron acquisition mechanisms. Acinetobacter baumannii, causing serious infections in compromised patients, produces an iron-chelating molecule, called acinetobactin, which is composed of equimolar quantities of 2,3-dihydroxybenzoic acid (DHBA), L-threonine, and N-hydroxyhistamine, to compete with host cells for iron. Genes that are involved in the production and transport of acinetobactin are clustered within the genome of A. baumannii. A recent study showed that entA, located outside of the acinetobactin gene cluster, plays important roles in the biosynthesis of the acinetobactin precursor DHBA and in bacterial pathogenesis. Therefore, understanding the genes that are associated with the biosynthesis and transport of acinetobactin in the bacterial genome is required. This review is intended to provide a general overview of the genes in the genome of A. baumannii that are required for acinetobactin biosynthesis and transport.
Acinetobacter baumannii* ; Bacteria ; Genome ; Genome, Bacterial ; Humans ; Iron ; Multigene Family ; Siderophores ; Threonine

Toxoplasmosis is a disease caused by the protozoan Toxoplasma gondii, which occurs worldwide in mammals and birds. Brain is the primary target organ because Toxoplasma gondii is a ubiquitous intracellular parasite that causes most frequently life-threatening encephalitis in immunocompromised patients. Relation of tissue cysts number, histopathology score and acute phase proteins were investigated. In this study, 36 mice are infected with Me49 strain of Toxoplasma gondii. The control group has 6 healthy mice. After inoculation of Toxoplasma gondii, at 10., 15., 20., 30., 45., 60. days, 6 each mice euthanized after collection of blood samples. Hemopexin, haptoglobulin, macroglobulin, serum amyloid A and clusterin levels are determined by ELISA. Then, brain tissues were investigated histopathologically and lesions were scored. The average cyst numbers were determined by counting three samples (25 µl each) of each brain homogenate under light microscopy. Inflammatory reaction was observed on day 10 days after inoculation (d.a.i.) The lesions were characterized by perivascular mononuclear cell infiltration, focal mononuclear cell infiltration in the meninges, and glial proliferation. Tissue cysts were observed in all Toxoplasma gondii-infected groups. The highest lesion score was observed at 60 d.a.i. And the most tissue cyst number were on day 30. d.a.i. Serum levels of hemopexin, haptoglobulin, macroglobulin, serum amyloid A and clusterin were significantly higher than the control group on day 10–20., 10., 10–30., 10.,10–45 d.a.i., respectively. High level of acute phase proteins in mice on certain days infected with Toxoplasma gondii was exhibited a relationship between brain lesions and tissue cysts.