What is this odd rash on my arm?

Question by Kells: What is this odd rash on my arm?
I got some odd rashes developing on my wrist and also on my elbow. They’re patterned.

Best answer:

Answer by Bag Addict
Poison?

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New antibiotics research progress?

Question by sunshouqing1314: New antibiotics research progress?

Best answer:

Answer by kriemheld1001
Other molecules are also showing promised as future antibiotics. Osterhelt and colleagues showed in October 2005 in Nature Medicine that molecules called acyldepsipeptides prevent the growth on Petri plates of antibiotic resistant bacteria including S. aureus. The molecules also helped 80% of mice infected with staph survive.

Further studies revealed that the molecules hone in on a bacterial protease, a new target for antibiotics. The molecules unhinder the protease, and the unrestrained protease activity somehow halts cell division. It’s unclear whether molecules such as these will develop into full-fledged antibiotics, but discovering entirely new kinds of antibiotics will be crucial to keep up with the spread of antibiotic resistant bacteria.

Most antibiotics are derived from naturally occurring anti-bacterial compounds. Scientists have thoroughly searched the soil bacteria that produce most of the known antibiotics, but they are still finding new leads. For instance, Wang and colleagues in Nature (2006) and PNAS (2007) have described related natural products that inhibit fatty acid production and block growth in bacteria, including antibiotic-resistant strains.

Still other groups are gaining an improved understanding of how existing antibiotics work to get clues about how to improve them. In the March 9, 2007 issue of Science, Lovering and colleagues used x-ray crystallography to get a 3-dimensional picture of a pencillin-related antibiotic called moenomycin clinging to a staph protein called PBP2. This protein helps the bacterium make its cell wall; moenomycin and related antibiotics block this protein from making normal cell walls. Moenomycin is used in animal feed to help livestock grow and has thus bacteria seem to have not developed resistance. Understanding this structure could help researchers develop new antibiotics for humans that similarly evade the development of resistance.

Other groups are probing new ways of treating infections once they develop. Buonpane and colleagues, reporting in the June 2007 issue of Nature Medicine, are developing an antidote to one S. aureus toxin, Staphylococcus enterotoxin B (SEB). SEB causes toxic shock syndrome by binding to T cells through T-cell receptors and over activating the immune system throughout the body. The researchers are developing small, free-floating versions of the T cell receptor; in this strategy, these receptor mimics soak up the toxin and prevent it from binding to the receptors on T cells, thereby preventing an immune response. They’ve developed one such molecule and have shown that it protects rabbits exposed to toxin.

To be successful, the molecule would need to be combined with one or two other molecules that bind to other toxins. Once the team has identified other molecules, they intend to test animals against infections by whole bacteria. Because it interferes with the host immune response rather than killing the bacteria, this strategy would be most useful for treating patients that have already gone into sepsis. It might complement human intravenous immunoglobulin, the last resort for patients in septic shock.

Researchers are also delving into ways that S. aureus evades the immune system. For instance, Staphylococcus forms biofilms, organized communities of bacteria growing together in a molecular matrix. This organization is especially important for the growth of bacteria on medical devices, such as catheters or breathing tubes, or in the lungs of cystic fibrosis patients. In the April 23, 2007 issue of PNAS, Rice and colleagues show that staph do not form biofilms when they have a mutation in a gene called cid, which is involved in a bacterial cell death pathway. They further showed that cells that die release DNA, which forms an important component of the biofilm’s matrix. Normal biofilms disintegrated when treated with a DNA-dissolving enzyme, supporting the idea.

As the prevalence of antibiotic resistance grows, so does interest in vaccines that prevent infections from taking hold. Despite some promising findings in animals, however, human testing of staph vaccines has foundered. Testing is risky, because researchers must show that vaccines protect healthy people, rather than treat sick ones. That means that trials need more people enrolled to be able to show statistically significant protection.

And two trials of staph vaccines have failed recently. In 2005, clinical trial data showed that StaphVAX, a vaccine developed by Nabi Biopharmaceutical, failed to protect kidney dialysis patients from staph infections. The vaccine contained fragments of sugars found on the surface of bacteria. The company has since stopped work on the vaccine. Veronate, under testing by Inhbitex, Inc., appeared to protect low-birthweight babies from staph infections in Phase II trials, but that initial finding didn’t emerge from Phase III trials, the company announced in 2006. Veronate contains antibodies that bind to adhesion molecules carried on the surface of bacteria.

Despite these failures, additional vaccine targets are in the offing. In the October 30, 2006 issue of PNAS, Schneewind and colleagues immunized mice with four staph surface proteins that they found were similary among many staph strains. Each of the proteins provide some degree of protection to mice from kidney infections, but when combined, the proteins protected against kidney disease to an even greater extent. In addition, they saved mice exposed to a lethal dose of S. aureus. Mice vaccinated with only one of the four proteins did not survive the lethal dose.

Other promising targets for vaccines include a molecule called RAP. This protein activates a regulatory RNA molecule called RNAIII, which in turn turns on genes that help staph attach to and invade host tissue. Another possible candidate is a surface sugar called PNAG, which apparently encourages S. aureus to form organized biofilms. Vaccinating mice with PNAG protects them from S. aureus infection. But despite numerous leads and tantalizing findings in animals, the road to an effective, approved vaccine is long.

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