Brucellosis is a highly contagious zoonosis that affects the public health and economic performance of endemic as well as non-endemic countries. In developing nations, brucellosis is often a very common but neglected disease. The purpose of this review is to provide insight about brucellosis in animal populations in Egypt and help to understand the situation from 1986 to 2013. A total of 67 national and international scientific publications on serological investigations, isolation, and biotyping studies from 1986 to 2013 were reviewed to verify the current status of brucellosis in animal populations in Egypt. Serological investigations within the national surveillance program give indirect proof for the presence of brucellosis in cattle, buffaloes, sheep, goats, and camels in Egypt. Serologic testing for brucellosis is a wellestablished procedure in Egypt, but most of the corresponding studies do not follow the scientific standards. B. melitensis biovar (bv) 3, B. abortus bv 1, and B. suis bv 1 have been isolated from farm animals and Nile catfish. Brucellosis is prevalent nationwide in many farm animal species. There is an obvious discrepancy between official seroprevalence data and data from scientific publications. The need for a nationwide survey to genotype circulating Brucellae is obvious. The epidemiologic situation of brucellosis in Egypt is unresolved and needs clarification.

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Copper is required for aerobic respiration by Mycobacterium tuberculosis and its human host, but this essential element is toxic in abundance. Copper nutritional immunity refers to host processes that modulate levels of free copper to alternately starve and intoxicate invading microbes. Bacteria engulfed by macrophages are initially contained within copper-limited phagosomes, which fuse with ATP7A vesicles that pump in toxic levels of copper. In this report, we examine how CtpB, a P-type ATPase in M. tuberculosis, aids in response to nutritional immunity. In vitro, the induced expression of ctpB in copper-replete medium inhibited mycobacterial growth, while deletion of the gene impaired growth only in copper-starved medium and within copper-limited host cells, suggesting a role for CtpB in copper acquisition or export to the copper-dependent respiration supercomplex. Unexpectedly, the absence of ctpB resulted in hypervirulence in the DBA/2 mouse infection model. As ctpB null strains exhibit diminished growth only in copper-starved conditions, reduced copper transport may have enabled the mutant to acquire a “Goldilocks” amount of the metal during transit through copper-intoxicating environments within this model system. This work reveals CtpB as a component of the M. tuberculosis toolkit to counter host nutritional immunity and underscores the importance of elucidating copper-uptake mechanisms in pathogenic mycobacteria.