Pregnant women with low levels of vitamin D may be more likely to suffer from bacterial vaginosis (BV) – a common vaginal infection that increases a woman's risk for preterm delivery, according to a University of Pittsburgh study. Available online and published in the June issue of the Journal of Nutrition, the study may explain why African-American women, who often lack adequate vitamin D, are three times more likely than white women to develop BV. "Bacterial vaginosis affects nearly one in three reproductive-aged women, so there is great need to understand how it can be prevented," said Lisa M. Bodnar, Ph.D., M.P.H., R.D., assistant professor of epidemiology, obstetrics and gynecology, University of Pittsburgh. "It is not only associated with a number of gynecologic conditions, but also may contribute to premature delivery – the leading cause of neonatal mortality – making it of particular concern to pregnant women." The study, which included 469 pregnant women, sought to determine whether poor vitamin D status played a role in predisposing women, especially African-Americans, to BV. Dr. Bodnar and colleagues at Magee-Womens Research Institute found that 41 percent of the study participants had BV and of these, 93 percent had insufficient levels of vitamin D. They also found that the prevalence of BV decreased as vitamin D levels rose. Vitamin D may play a role in BV by regulating the production and function of antimicrobial molecules, which in turn may help the immune system prevent and control bacterial infection. However, only about one in four Americans gets enough vitamin D. Vitamin D deficiency may be more common in African-Americans because dark pigmentation limits the amount of vitamin D that can be made in the skin through casual exposure to sunlight. African-American women also are less likely to meet dietary recommendations of vitamin D.

Although there has been great progress in treating human immunodeficiency virus 1 (HIV-1) infection1, preventing transmission has thus far proven an elusive goal. Indeed, recent trials of a candidate vaccine and microbicide have been disappointing, both for want of efficacy and concerns about increased rates of transmission2, 3, 4. Nonetheless, studies of vaginal transmission in the simian immunodeficiency virus (SIV)–rhesus macaque (Macacca mulatta) model point to opportunities at the earliest stages of infection in which a vaccine or microbicide might be protective, by limiting the expansion of infected founder populations at the portal of entry5, 6. Here we show in this SIV–macaque model, that an outside-in endocervical mucosal signalling system, involving MIP-3alpha (also known as CCL20), plasmacytoid dendritic cells and CCR5+ cell-attracting chemokines produced by these cells, in combination with the innate immune and inflammatory responses to infection in both cervix and vagina, recruits CD4+ T cells to fuel this obligate expansion. We then show that glycerol monolaurate—a widely used antimicrobial compound7 with inhibitory activity against the production of MIP-3alpha and other proinflammatory cytokines8—can inhibit mucosal signalling and the innate and inflammatory response to HIV-1 and SIV in vitro, and in vivo it can protect rhesus macaques from acute infection despite repeated intra-vaginal exposure to high doses of SIV. This new approach, plausibly linked to interfering with innate host responses that recruit the target cells necessary to establish systemic infection, opens a promising new avenue for the development of effective interventions to block HIV-1 mucosal transmission.

Developed more than 200 years ago and found in households around the world, chlorine bleach is among the most widely used disinfectants, yet scientists never have understood exactly how the familiar product kills bacteria. New research from the University of Michigan, however, reveals key details in the process by which bleach works its antimicrobial magic. In a study published in the Nov. 14 issue of the journal Cell, a team led by molecular biologist Ursula Jakob describes a mechanism by which hypochlorite, the active ingredient of household bleach, attacks essential bacterial proteins, ultimately killing the bugs ... Jakob and her team were studying a bacterial protein known as heat shock protein 33 (Hsp33), which is classified as a molecular chaperone. The main job of chaperones is to protect proteins from unfavorable interactions, a function that's particularly important when cells are under conditions of stress, such as the high temperatures that result from fever ... Jakob and her research team figured out that bleach and high temperatures have very similar effects on proteins. Just like heat, the hypochlorite in bleach causes proteins to lose their structure and form large aggregates.

Ten years ago, European officials, experts and other stakeholders met in Copenhagen, Denmark, at the invitation of the Danish Ministry of Health and the Danish Ministry of Food, Agriculture and Fisheries. This European conference on "The Microbial Threat" due to antimicrobial resistance resulted in the publication of "Copenhagen Recommendations" calling for action to limit the emerging problem of antimicrobial-resistant microorganisms [1]. Following the conference, the European Commission prepared a comprehensive Community strategy against antimicrobial resistance, which was published in 2001 [2] and presented in Eurosurveillance [3]. Later the same year, European Union (EU) Health Ministers adopted a Council Recommendation on the prudent use of antimicrobial agents in human medicine with a series of specific measures aimed at containing the spread of antimicrobial resistance by prudent use of antimicrobial agents [4]. A review article published in this journal in 2001 showed that only six European countries had a national action plan to contain antimicrobial resistance [5]. An evaluation of implementation of the Council Recommendation performed by the European Commission showed that, by 2003, 16 countries had developed a national strategy to contain antimicrobial resistance and nine countries had an action plan [6,7]. The European Commission is currently performing another evaluation of the implementation of the Council Recommendation and its results will be available in 2009.

Dramatic increases in the prevalence of multidrug-resistant bacteria have put the spotlight on the lack of new antibacterials coming through the pipeline. How might regulatory guidance for clinical trials of antibacterials help tackle this shortfall?

If cleanliness is next to godliness, modern America is the land of the faithful -- fighting the good fight against today's so-called superbugs with sparkling countertops and well-washed hands. Our culture's cleanliness obsession has been fed by a booming business in household products that promise the virtue of sterility. According to estimates by the Environmental Protection Agency, our antimicrobial crusade has us spending almost $1 billion annually on soaps and detergents, toys and cutting boards, bedsheets and toothbrushes, all of them treated with chemical compounds designed to kill the germs that cling to them. At the forefront of this product niche is the antimicrobial hand wash, commonly fortified with the bug-battling chemical triclosan.

The "resistance movement" founded by bacteria to combat antibiotics may be losing ground. By combining key properties of two different types of weapons used by the innate defense systems of organisms, a team of scientists at the Weizmann Institute of Science has managed to design a more powerful weapon, hoping that this will provide a basis for novel and more effective antibiotics. The first is a "magnetic" weapon – a natural antibiotic produced by all organisms. Because these antimicrobial peptides (AMPs) are positively charged, they are attracted to the bacteria's negatively charged surface like a magnet, where they can then exert their antibacterial effects. The second, "detergent-like" weapon – called a lipopeptide – is produced only by bacteria and fungi which, due to a negative charge, target mainly fungi. This weapon contains a fatty acid chain that, like similar chains in soap which dissolve dirt and oils, breaks down the fatty membranes of the fungi.