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This should actually not be surprising, because for some time now, just one class of drug has been able to successfully treat the infection.

Now researchers in Sweden and Japan identified a new variant of Neisseria gonorrhoeae, the bug that causes gonorrhea, that can survive that last remaining drug, the cephalosporin-class antibiotics. Researchers isolated the strain from the throat of a sex worker in Japan, the Los Angeles Times reports.

“This is both an alarming and a predictable discovery,” said Dr. Magnus Unemo, of the Swedish Reference Laboratory for Pathogenic Neisseria, in a statement. The bacteria has been evolving to resist antibiotics since they became the standard treatment for the infection in the 1940s, during World War II.

The researchers were able to pinpoint four new genetic mutations that enable the bacteria’s resistance. Even worse, it readily passes on this resistance to other strains, increasing their resistance 500-fold, the Times says.

Gonorrhea is a particularly troubling and interesting bug. It is one of the only diseases that is unique to our species, and it’s one of the oldest known human pathogens. Earlier this year, researchers found a fragment of human DNA in the genome of Neisseria gonorrhoeae, evidence that it has adapted to its hosts quite well. The bacterium apparently picks up a genetic sequence from the host it’s infecting, according to that research, which was published in February. This may lend N. gonorrhoeae the ability to develop different strains of itself — and can explain why it has been so effective at morphing to evade antibiotics’ assaults.

The first treatments against gonorrhea used sulfonamides, but the bacteria evolved to resist it; later treatments used penicillin, which also no longer works; tetracyclines and fluoroquinolines like Cipro don’t either, the L.A. Times notes.

It’s too early to tell whether this new super-STD is already spreading, but it’s likely to do so unless new therapies are developed, Unemo said.

Gonorrhea impacts about 700,000 Americans every year, according to the Centers for Disease Control and Prevention. If untreated, it can lead to serious health complications in both genders, the CDC says. It can lead to infertility in women and especially men, and it increases the risk of transmitting other STDs, like HIV. Babies born to infected mothers are at high risk of developing serious infections and blindness. About 3 to 4 percent of the time, it can spread to the skin, blood, heart and joints in infected adults.

The report on this new strain was presented Sunday at a Quebec City meeting of the International Society for Sexually Transmitted Disease Research. Just last Thursday, the CDC reported growing numbers of gonorrhea infections that require unusually high doses of cephalosporins to cure them, the LA Times said. For now, treatment should include cephalosporins and the antibiotic azithromycin, while the CDC and National Institutes of Health work on new drugs.

[Eurekalert]

Scientists say the research is a major step forward for gene therapy, which has long promised to cure disease by editing genetic sequences.

The therapy is based on enzymes called zinc-finger nucleases, which serve as a sort of genetic scissors. The enzymes are engineered to match a specific gene location on a chromosome, where they snip through DNA’s double helix.

In this case, researchers led by Katherine A. High, a hematologist and gene therapy expert at The Children’s Hospital of Philadelphia, used ZFN proteins that were engineered to snip through the location of a genetic mutation that causes hemophilia. Hemophiliacs lack a blood-clotting factor made by the liver that helps stanch bleeding, so their blood cannot clot, meaning minor injuries can be life-threatening.

High and colleagues had to take another step in their research, because hemophilic mice have a different genetic mutation than humans. They engineered mice to express the faulty human sequence, located on the F9 gene, and they designed ZFNs to cut through it. Then they engineered a virus that targets the liver (where the blood clotting factor is made) to carry the normal, unmutated version of F9.

As a result, the mutated section was removed, and the unmutated gene was inserted instead. Then the DNA molecule is stimulated to repair itself, sewing the new gene in place.

This is an improvement over other genetic editing techniques that use viruses to cut and paste the new genes. Although they have been shown to work, viral therapy has some inherent problems, including unpredictable chromosomal insertion, which can induce unwanted mutations. But the ZFN is designed to home in on a precise location of mutated DNA.

After this treatment, the animals’ blood clotted in 44 seconds, compared with more than a minute for hemophiliac mice, according to Nature.

The study shows that zinc finger proteins and replacement genes can be used to induce changes in living animals, which is promising for a wide range of therapies. For instance, other researchers are using ZFNs to disrupt a gene that makes a receptor used by the AIDS virus, as the New York Times reports. People without that gene, CCR5, are naturally immune to HIV.

The mouse study is reported in this week's issue of the journal Nature.

[via Science Daily]

Destruction of the smallpox virus, which was eradicated in the 1970s, has been mulled since 1980, but World Health Organization officials renewed debate about the matter earlier this year and will decide the viruses’ fate at an upcoming meeting.

Two labs possess the last known live samples of the variola virus — the Centers for Disease Control and Prevention in Atlanta, and a Russian facility in Siberia. Officials in developing nations, where smallpox is more likely to spread should it resurface, have been pushing for their destruction since 1980. The World Health Assembly decided to kill the samples in 1996, but they have been granted stays of execution in the decade and a half since, with the United States, Russia and others arguing the virus samples could seed new vaccines and potential treatments for infected patients.

In January, WHO officials again started discussions about whether to destroy the samples. The World Health Assembly will decide in May. LiveScience reviews the controversy here.

Epidemiologists believe smallpox has killed about one-third of those it has infected throughout history, accounting for hundreds of millions of victims dating back to ancient Egypt. A decade-long global vaccination effort eliminated the virus from human populations; the last natural case was found in October 1977 in Somalia. The elimination of Rinderpest, a cattle plague, will be only the second such disease eradication story in human history.

Officials in the U.S. and Russia have said they will fight efforts to set a destruction date, arguing the viruses are needed for research and to guard against bioterrorism. Some fear nations like North Korea or Iran may possess secret samples, although those countries deny it.

[LiveScience]

[via Gizmodo]

The UN will formally announce the triumph this summer

But this summer, the Food and Agriculture Organization of the United Nations plans to formally announce rinderpest’s eradication, making it the second scourge, after smallpox, to be intentionally wiped off the face of the Earth.

Rinderpest arrived alongside the domestication of cattle, in the Indus River valley about 10,000 years ago. It traveled west out of Asia with the Huns and Mongols. With the growth of the railroad, rinderpest spread so quickly that Europe was nearly cow-free in the 1870s.

Epidemics continued among Africa’s cattle and wildlife—including buffalo, antelopes and giraffes—well into the 20th century. Then, in 1950, an English veterinary pathologist named Walter Plowright started working in labs in Kenya and Nigeria. Soon he was growing rinderpest, and by the 1960s he had a weakened strain that gave lifelong immunity without side effects. Plowright had made a safe, inexpensive vaccine, and about 100 million doses were delivered throughout Africa from 1962 to 1969. But still the disease returned.

In the 1980s, Nigeria’s new oil wealth created a demand for beef that brought cattle carrying rinderpest from as far as Somalia, and a pandemic soon swept across the continent. Another vaccination campaign followed. The African Union and the United Nations trained health workers and respected villagers, who inoculated livestock, tested animals, and watched for signs of infection—a rigorous education program absent from previous eradication efforts.

By sequencing the virus’s genetic material, scientists discovered that there were several strains, which helped them track the disease to remote areas of East Africa (smallpox’s last refuge, too) and focus their vaccination and surveillance.

The Food and Agricultural Organization says that rinderpest was last spotted in the wild in Kenya in October 2001. Following a decade of testing, the FAO believes that no infected animals remain on Earth. After a seven-decade fight, rinderpest lives on in laboratory freezers—and nowhere else.

Researchers at the University of Maryland, who were funded by the National Institutes of Health/National Institute of Allergy and Infectious Diseases, say the method could be an effective treatment against malaria, especially as mosquitoes increasingly evolve to resist insecticides. Even better, the fungus modification can be targeted to almost any disease-carrying insect, potentially allowing fungus-based prevention for maladies like Lyme disease or dengue fever. The study was reported today in the journal Science.

The Metarhizium anisopliae fungus naturally attacks mosquitoes, and it has already been used to reduce disease transmission — but it only works if the bugs are sprayed with fungus soon after they picked up the malaria-causing Plasmodium falciparum parasite. What’s more, the mosquitoes often die before reproducing, leaving fungus-resistant mosquitoes to take over and render the spray useless. So rather than enhance fungi to better kill mosquitoes, entomology professor Raymond St. Leger and colleagues modified the fungi to block the development of Plasmodium in the mosquito.

They used genes for a human antibody and a scorpion toxin, both of which specifically target Plasmodium, and inserted them into the fungus. They fed some mosquitoes a Plasmodium-infected blood meal, and separated them into three groups. One group got a dose of the transgenic fungus, another got a natural fungus and the third was not sprayed at all. Two weeks after the bugs were exposed to the malaria parasite, the researchers checked for its presence in their salivary glands (this is how it’s transmitted to humans).

Spraying mosquitoes with the transgenic fungus significantly reduced parasite development, the team found.

Malaria is found in 106 countries and there are an estimated 225 million malaria cases every year, including 781,000 deaths, mostly in sub-Saharan Africa. Prevention usually involves spraying bed nets and interior walls with pyrethroid insecticide to kill the mosquitoes, but the bugs are evolving to resist it, and there are no promising prospects for a chemical replacement.

Other teams have genetically altered mosquitoes to resist Plasmodium, and modified other mosquitoes to be sterile in order to reduce their populations. But transgenic mosquitoes could pose some ecological problems. A fungal treatment can be modified to keep up with mosquitoes’ natural adaptations, St. Leger said.

“Mosquitoes have an incredible ability to evolve and adapt, so there may be no permanent fix. However, our current transgenic combination could translate into additional decades of effective use of fungi as an anti-malarial biopesticide,” he said.

Happy V-D!

Gonorrhea is one of very few diseases exclusive to our species, and is one of the oldest recorded diseases in human history. An ancient disease that resembles gonorrhea’s symptoms is even described in the Bible, according to Hank Seifert, senior author of a paper on the gene transfer.

The bacterium apparently picks up a genetic sequence from the host it is infecting, a novel ability that could help the bacteria adapt to its host, according to Seifert, a microbiology and immunology professor at Northwestern University Feinberg School of Medicine. This ability may enable it to develop different strains of itself, he said. The paper is published today in the online journal mBio.

The human genome has plenty of ghost DNA fragments, relics of viruses that entered after some past infection. Lateral gene transfer is pretty common between bacteria and multicellular organisms, according to several studies. But this is the first time that scientists have seen a bacteria pick up the genes, rather than depositing them.

“Whether this particular event has provided an advantage for the gonorrhea bacterium, we don’t know yet,” Seifert said in a NU press release.

Scientists discovered the gene transfer while they were examining the genomic sequences of several gonorrhea strains. Three of them had a piece of DNA wherein the sequence was identical to a sequence found in humans, according to NU. Further examination suggests this evolved relatively recently.

About 700,000 Americans and 50 million people worldwide are infected with gonorrhea every year. It’s curable with an antibiotic, but it developed resistance to several drugs over the past 40 years. Studying the bacteria’s human DNA fragment could conceivably help scientists find better treatments.

“The next step is to figure out what this piece of DNA is doing,” Seifert said.