Complete DNA sequence of a serogroup A strain of Neisseria meningitidis Z2491

Neisseria meningitidis causes bacterial meningitis and is therefore responsible for considerable morbidity and mortality in both the developed and the developing world. Meningococci are opportunistic pathogens that colonize the nasopharynges and oropharynges of asymptomatic carriers. For reasons that are still mostly unknown, they occasionally gain access to the blood, and subsequently to the cerebrospinal fluid, to cause septicaemia and meningitis. N. meningitidis strains are divided into a number of serogroups on the basis of the immunochemistry of their capsular polysaccharides; serogroup A strains are responsible for major epidemics and pandemics of meningococcal disease, and therefore most of the morbidity and mortality associated with this disease. Here we have determined the complete genome sequence of a serogroup A strain of Neisseria meningitidis, Z2491. The sequence is 2,184,406 base pairs in length, with an overall G+C content of 51.8%, and contains 2,121 predicted coding sequences. The most notable feature of the genome is the presence of many hundreds of repetitive elements, ranging from short repeats, positioned either singly or in large multiple arrays, to insertion sequences and gene duplications of one kilobase or more. Many of these repeats appear to be involved in genome fluidity and antigenic variation in this important human pathogen.     

How Cooper pairs vanish approaching the Mott insulator in Bi2Sr2CaCu2O8+delta

The antiferromagnetic ground state of copper oxide Mott insulators is achieved by localizing an electron at each copper atom in real space (r-space). Removing a small fraction of these electrons (hole doping) transforms this system into a superconducting fluid of delocalized Cooper pairs in momentum space (k-space). During this transformation, two distinctive classes of electronic excitations appear. At high energies, the mysterious 'pseudogap' excitations are found, whereas, at lower energies, Bogoliubov quasi-particles-the excitations resulting from the breaking of Cooper pairs-should exist. To explore this transformation, and to identify the two excitation types, we have imaged the electronic structure of Bi(2)Sr(2)CaCu(2)O(8+delta) in r-space and k-space simultaneously. We find that although the low-energy excitations are indeed Bogoliubov quasi-particles, they occupy only a restricted region of k-space that shrinks rapidly with diminishing hole density. Concomitantly, spectral weight is transferred to higher energy r-space states that lack the characteristics of excitations from delocalized Cooper pairs. Instead, these states break translational and rotational symmetries locally at the atomic scale in an energy-independent way. We demonstrate that these unusual r-space excitations are, in fact, the pseudogap states. Thus, as the Mott insulating state is approached by decreasing the hole density, the delocalized Cooper pairs vanish from k-space, to be replaced by locally translational- and rotational-symmetry-breaking pseudogap states in r-space.     

The abundance threshold for plague as a critical percolation phenomenon

Percolation theory is most commonly associated with the slow flow of liquid through a porous medium, with applications to the physical sciences. Epidemiological applications have been anticipated for disease systems where the host is a plant or volume of soil, and hence is fixed in space. However, no natural examples have been reported. The central question of interest in percolation theory, the possibility of an infinite connected cluster, corresponds in infectious disease to a positive probability of an epidemic. Archived records of plague (infection with Yersinia pestis) in populations of great gerbils (Rhombomys opimus) in Kazakhstan have been used to show that epizootics only occur when more than about 0.33 of the burrow systems built by the host are occupied by family groups. The underlying mechanism for this abundance threshold is unknown. Here we present evidence that it is a percolation threshold, which arises from the difference in scale between the movements that transport infectious fleas between family groups and the vast size of contiguous landscapes colonized by gerbils. Conventional theory predicts that abundance thresholds for the spread of infectious disease arise when transmission between hosts is density dependent such that the basic reproduction number (R(0)) increases with abundance, attaining 1 at the threshold. Percolation thresholds, however, are separate, spatially explicit thresholds that indicate long-range connectivity in a system and do not coincide with R(0) = 1. Abundance thresholds are the theoretical basis for attempts to manage infectious disease by reducing the abundance of susceptibles, including vaccination and the culling of wildlife. This first natural example of a percolation threshold in a disease system invites a re-appraisal of other invasion thresholds, such as those for epidemic viral infections in African lions (Panthera leo), and of other disease systems such as bovine tuberculosis (caused by Mycobacterium bovis) in badgers (Meles meles).