Antibiotics resistance could kill 10 million a year by 2050


A British government-commissioned review has found that resistance to antibiotics could account for 10 million deaths a year and hit global gross domestic product by 2.0 to 3.5 percent by 2050

A British government-commissioned review has found that resistance to antibiotics could account for 10 million deaths a year and hit global gross domestic product by 2.0 to 3.5 percent by 2050

London (AFP) – A British government-commissioned review has found that resistance to antibiotics could account for 10 million deaths a year and hit global gross domestic product by 2.0 to 3.5 percent by 2050.

The Review on Antimicrobial Resistance said surgeries that have become widespread and low-risk thanks to antibiotics, such as caesarean sections, could become more dangerous without urgent action.

The review announced by British Prime Minister David Cameron was led by Jim O’Neill, former chief economist at US investment bank Goldman Sachs, and included British senior public health experts.

It found the region with the highest number of deaths attributable to antimicrobial resistance would be Asia with 4.7 million, followed by Africa with 4.1 million, while there would be 390,000 in Europe and 317,000 in the United States.

For comparison, the review estimated that the second-biggest killer, cancer, would account for 8.2 million deaths a year by 2050.

“The damaging effects of antimicrobial resistance are already manifesting themselves across the world,” the report said.

“Antimicrobial-resistant infections currently claim at least 50,000 lives each year across Europe and the US alone,” it added.

The calculations were based on existing studies by the think tank Rand Europe and the consultancy KPMG.

It warned drug resistance was not “a distant and abstract risk” and called for “a major intervention to avert what threatens to be a devastating burden on the world’s healthcare systems”.

The review emphasised the economic advantage of investment in tackling the problem early.

It said that three types of bacteria — the Klebsiella pneumonia, Escherichia coli (E. coli) and Staphylococcus aureus — were already showing signs of resistance to medicine.

Treatment of HIV, malaria and tuberculosis were broader public health issues in which resistance “is a concern”, the report said.

In the United States, antibiotic-resistant infections are associated with 23,000 deaths and two million illnesses each year.

The economic costs annually are as high as $20 billion (16 billion euros) in excess direct health care costs and $35 billion (28 billion euros) in lost productivity.

Fast-spreading genetic mutations pose ecological risk


US science academies advise caution in experimenting with gene drives.

Gene drives could be used to combat mosquito-borne diseases such as malaria.

A technique that allows particular genes to spread rapidly through populations is not ready to be set loose in the wild, warns a committee convened by the US National Academies of Sciences, Engineering, and Medicine.

In a report released on 8 June, the committee argued that such ‘gene drives’ pose complex ecological risks that are not yet fully understood. “It is not ready — and we are not ready — for any kind of release,” says Elizabeth Heitman, co-chair of the committee and a research integrity educator at Vanderbilt University School of Medicine in Nashville, Tennessee. “There is a lot of work that needs to be done.”

Even so, Heitman and other members of the committee felt that the potential of gene drives, for example to combat insect-borne diseases, is compelling enough to warrant additional laboratory and field studies.Gene drives have been studied for more than half a century, and have long been postulated as a way to eradicate mosquito-borne diseases such as malaria. But the field was hampered by technical challenges until the recent advent of sophisticated — and easy-to-use — tools for engineering genomes. In the past two years, researchers have used a popular gene-editing technique called CRISPR–Cas9 to develop gene drives that spread a given gene through a population almost exponentially faster than normal in yeast, fruit flies and two species of mosquitoes.

But as molecular biology research on gene drives has surged forward, it has outpaced our understanding of their ecological consequences, says Heitman. Even a small, accidental release from a laboratory holds the potential to spread around the globe: “After release into the environment, a gene drive knows no political boundaries,” the committee wrote.

As a result, oversight of gene drive projects should be coordinated across countries, the committee argued, and best practices should be openly shared among laboratories. The committee also detailed multiple phases of testing that should be used to assess the effects of a gene drive, and stressed the need to involve researchers’ home institutions, regulators and even the public in decision-making.

It is a good overall strategy, says Todd Kuiken, who studies science policy at the Wilson International Center for Scholars, a think tank in Washington DC. But the committee missed an opportunity to set out the infrastructure and safety measures that would be needed to conduct field trials of gene drives, he adds. “They don’t talk about how you would actually do this and where the money is going to come from.”

A gene drive could have unintended effects on the environment if it is unleashed in wild populations: removing one species of insect, for example, could endanger the animals that feed on it. Given this risk, the report also stressed the importance of layering multiple methods of containment to prevent accidental release of engineered species, and of consulting with the public even before gene drive experiments are undertaken in the laboratory. It’s a message that evolutionary engineer Kevin Esvelt worries may not come through strongly enough to individual researchers.

“If you were to accept that there is a risk that building it in the laboratory could lead to its release, then that demands that you tell the world what you’re doing before you do the experiments,” says Esvelt, who works at the Massachusetts Institute of Technology in Cambridge.

Heitman notes that researchers lack tried and tested ways of soliciting input from the public at large about their work. For Esvelt, the bigger barrier is a scientific culture that often discourages researchers from sharing their experiments before they are published, for fear of being beaten to the finishing line by another group. “No one would rationally design the current scientific enterprise,” he says. “And right now it’s easier to engineer biology than culture.”

Malaria first spread from birds.


A new study published by researchers at the Cornell University in New York revealed that mosquito-borne disease Malaria first spread from birds to bats and then on to other mammals. For the study, researchers tested malarial DNA discovered in birds, bats and other small mammals from East African countries. Notably, the disease affected around 214 million people worldwide in 2015.

Extensive testing of malarial DNA revealed that malaria spread from birds to bats and on to other mammals

A file photo of a mosquito through a microscope. Malaria is caused by parasites that are transmitted to people through the bites of infected female mosquitoes. Photo: AP

A file photo of a mosquito through a microscope. Malaria is caused by parasites that are transmitted to people through the bites of infected female mosquitoes.

 The origins of malaria have been under scrutiny for years as researchers tried to find the roots of the disease. A new study now throws light on the evolution of malaria and found that the disease has its roots in birds.

Extensive testing of malarial DNA found in birds, bats and other small mammals from five East African countries revealed that malaria spread from birds to bats and on to other mammals, said the study published this week in the journalMolecular Phylogenetics and Evolution.

“We can’t begin to understand how malaria spread to humans until we understand its evolutionary history,” said lead author Holly Lutz, a doctoral candidate in the fields of ecology and evolutionary biology and population medicine and diagnostic sciences at Cornell University.

“In learning about its past, we may be better able to understand the effects it has on us,” said Lutz.

After drawing blood samples from hundreds of East African birds, bats, and other small mammals, researchers screened the blood for the malarial parasites. When they found malaria in the blood samples, they took samples of the parasites’ DNA and sequenced it to identify mutations in the genetic code. After that, the researchers assessed how different malaria species are related, based on differences in their genetic code.

“Trying to determine the evolutionary history of malaria from just a few specimens would be like trying to reconstruct the bird family tree when you only know about eagles and canaries,” explained Lutz.

Malaria, which affected 214 million people worldwide in 2015, is caused by parasites that are transmitted to people through the bites of infected female mosquitoes. The most deadly malarial parasite, P. falciparum, is most prevalent in Africa, where malaria cases and deaths are heavily concentrated.

“Malaria is notoriously adaptive to treatment, and its DNA holds a host of secrets about how it’s able to change and evolve. Having a better understanding of its evolutionary history could help scientists anticipate its future,” said co-author and Field Museum curator of mammals Bruce Patterson.

‘Gene Drive’ Mosquitoes Engineered to Fight Malaria


Mutant mozzies could rapidly spread through wild populations

An Anopheles stephensi mosquito obtains a blood meal from a human host through its pointed proboscis.


Mutant mosquitoes engineered to resist the parasite that causes malaria could wipe out the disease in some regions—for good.

Humans contract malaria from mosquitoes that are infected by parasites from the genus Plasmodium. Previous work had shown that mosquitoes could be engineered to rebuff the parasite P. falciparum, but researchers lacked a way to ensure that the resistance genes would spread rapidly through a wild population.

In work published on November 23 in the Proceedings of the National Academy of Sciences, researchers used a controversial method called ‘gene drive’ to ensure that an engineered mosquito would pass on its new resistance genes to nearly all of its offspring—not just half, as would normally be the case.

The result: a gene that could spread through a wild population like wildfire.

“This work suggests that we’re a hop, skip and jump away from actual gene-drive candidates for eventual release,” says Kevin Esvelt, an evolutionary engineer at Harvard University in Cambridge, Massachusetts, who studies gene drive in yeast and nematodes.

For Anthony James, a molecular biologist at the University of California, Irvine, and an author of the paper, such a release would spell the end of a 30-year quest to use mozzie genetics to squash malaria.

James and his laboratory have painstakingly built up the molecular tools to reach this goal. They have worked out techniques for creating transgenic mosquitoes—a notoriously challenging endeavour—and isolated genes that could confer resistance to P. falciparum. But James lacked a way to ensure that those genes would take hold in a wild population.

Fast forward
The concept of engineering a gene drive has been around for about a decade, and James’s laboratory had tried to produce them in the past. The process was agonizingly slow.

Then, in January, developmental biologists Ethan Bier and Valentino Gantz at the University of California, San Diego, contacted James with a stunning finding: they had engineered a gene drive in fruit flies, and wondered whether the same system might work in mosquitoes. James jumped at the opportunity to find out.

Bier and Gantz had used a gene-editing system called CRISPR–Cas9 to engineer a gene drive. They inserted genes encoding the components of the system that were designed to insert a specific mutation in their fruit flies. The CRISPR–Cas9 system then copied that mutation from one chromosome to the other. James used that system in mosquitoes to introduce two genes that his past work showed would cause resistance to the malaria pathogen.

The resulting mosquitoes passed on the modified genes to more than 99% of their offspring. Although the researchers stopped short of confirming that all the insects were resistant to the parasite, they did show that the offspring expressed the genes.

“It’s a very significant development,” says Kenneth Oye, a political scientist who studies emerging technologies at the Massachusetts Institute of Technology in Cambridge. “Things are moving rapidly in this field.”

Other teams are developing gene drives that could control malaria. A team at Imperial College London has developed a CRISPR-based gene drive in Anopheles gambiae, the mosquito species that transmits malaria in sub-Saharan Africa. The group’s gene drive inactivates genes involved in egg production in female mosquitoes, which could be used to reduce mosquito populations, according to team member Austin Burt, an evolutionary geneticist. Their results will be published in Nature Biotechnology next month, Burt says.

Oye notes that such technological advances are outpacing the regulatory and policy discussionsthat surround the use of gene drive to engineer wild populations. Gene drives are controversial because of the potential that they hold for altering entire ecosystems.

Before testing gene drive in the field, Oye hopes that researchers will study the long-term consequences of the changes, such as their stability and potential to spread to other species, as well as methods to control them. “I’m less worried about malevolence than getting something wrong,” he says.

Esvelt says that the US-based researchers made a wise decision in selecting a non-native mosquito species for their experiments. (The team worked with Anopheles stephensi, which is native to the Indian subcontinent.) “Even if they escaped the lab, there’d be no one to mate with and spread the drive,” Esvelt says.

James predicts that it will take his team less than a year to prepare mosquitoes that would be suitable for field tests, but he is in no rush to release them. “It’s not going to go anywhere until the social science advances to the point where we can handle it,” he says. “We’re not about to do anything foolish.”

African dams linked to over one million malaria cases annually: New study urges future dam projects to consider better disease control measures.


For the first time, research correlates the location of large dams with the incidence of malaria and quantifies the impacts across sub-Saharan Africa. The study looked at over 1,200 dams and found that the population at risk for malaria around dams is at least four times greater than previously estimated.

Mosquito sucking blood (stock image). The new research has major implications for new dam projects and how health impacts should be assessed prior to construction.

Over one million people in sub-Saharan Africa will contract malaria this year because they live near a large dam, according to a new study which, for the first time, has correlated the location of large dams with the incidence of malaria and quantified impacts across the region. The study finds that construction of an expected 78 major new dams in sub-Saharan Africa over the next few years will lead to an additional 56,000 malaria cases annually.

The research, published in this month’s Malaria Journal, has major implications for new dam projects and how health impacts should be assessed prior to construction. Encouraged by the increased volume of international aid for water resource development, sub-Saharan Africa has, in recent years, experienced a new era of large dam construction.

“Dams are at the center of much development planning in Africa. While dams clearly bring many benefits–contributing to economic growth, poverty alleviation and food security–adverse malaria impacts need to be addressed or they will undermine the sustainability of Africa’s drive for development,” said biologist Solomon Kibret of the University of New England in Australia, the paper’s lead author.

Undertaken as part of the CGIAR Research Program on Water, Land and Ecosystems, the study looked at 1,268 dams in sub-Saharan Africa. Of these, just under two-thirds, or 723, are in malarious areas. The researchers compared detailed maps of malaria incidence with the dam sites. The number of annual malaria cases associated with the dams was estimated by comparing the difference in the number of cases for communities less than five kilometers from the dam reservoir with those for communities further away. The researchers found that a total of 15 million people live within five kilometers of dam reservoirs and are at risk, and at least 1.1 million malaria cases annually are linked to the presence of the dams.

“Our study showed that the population at risk of malaria around dams is at least four times greater than previously estimated,” said Kibret, noting that the authors were conservative in all their analyses.

The risk is particularly high in areas of sub-Saharan Africa with “unstable” malaria transmission, where malaria is seasonal. The study indicated that the impact of dams on malaria in unstable areas could either lead to intensified malaria transmission or change the nature of transmission from seasonal to perennial.

Previous research has identified increased malarial incidence near major sub-Saharan dams such as the Akosombo Dam in Ghana, the Koka Dam in Ethiopia and the Kamburu Dam in Kenya. But until now, no attempt has been made to assess the cumulative effect of large dam building on malaria.

Malaria is transmitted by the Anopheles mosquito, which needs slow-moving or stagnant water in which to breed. Dam reservoirs, particularly shallow puddles that often form along shorelines, provide a perfect environment for the insects to multiply. Thus dam construction can intensify transmission and shift patterns of malaria infection. Many other water bodies, including small dams, ponds and natural lakes and wetlands, provide breeding habitat for mosquitoes. In total, there are an estimated 174 million cases of malaria in sub-Saharan Africa per year.

Many African countries are planning new dams to help drive economic growth and increase water security. Improved water storage for growing populations, irrigation and hydropower generation are indeed badly needed for a fast developing continent. But the researchers warn that building new dams has potential costs as well as benefits.

“Dams are an important option for governments anxious to develop,” said Matthew McCartney of the International Water Management Institute (IWMI) and a co-author of the paper. “But it is unethical that people living close to them pay the price of that development through increased suffering and, possibly in extreme cases, loss of life due to disease.”

The study notes that despite growing evidence of the impact of dams on malaria, there is scant evidence of their negative impacts being fully offset.

The authors make recommendations about how the increased malaria risk can be managed. Dam reservoirs could be more effectively designed and managed to reduce mosquito breeding. For instance, one option is to adopt operating schedules that, at critical times, dry out shoreline areas where mosquitoes tend to breed. Dam developers should also consider increasing investment in integrated malaria intervention programs that include measures such as bed net distribution. Other environmental controls, such as introducing fish that eat mosquito larva in dam reservoirs, could also help reduce malaria cases in some instances.

“The bottom line is that adverse malaria impacts of dams routinely receive recognition in Environmental Impact Assessments, and areas around dams are frequently earmarked for intensive control efforts. The findings of our work hammer home the reality that this recognition and effort–well-intentioned though it may be–is simply not sufficient,” said co-author Jonathan Lautze, a researcher at the International Water Management Institute’s office in Pretoria, South Africa. “Given the need for water resources development in Africa, malaria control around dams requires interdisciplinary cooperation, particularly between water and health communities. Malaria must be addressed while planning, designing and operating African dams.”

New drug has the potential to ward off malaria with a single dose .


And it’ll cost less than $1 per dose.

Lab tests have highlighted the potential of a new drug to treat malaria in affected patients, prevent it from spreading, and ward off future infections with a single dose. Developed by chemists at Dundee University in Scotland and the not-for-profit group Medicines for Malaria Venture, the drug acts against each of the life stages of the malaria parasite, making it a promising option for those already infected and as a vaccination.

“There are other compounds being developed for malaria, but relatively few of [these] have reached the stage we’re at,” lead researcher Ian Gilbert said in a press release. “What’s most exciting is the number of potential attributes, such as the ability to give it in a single dose which will mean that medics can make sure a patient completes the treatment.”

Named DDD107498, the drug has been in development since 2009, and was made using one of almost 4,700 compounds tested for effectiveness against malaria at the Drug Discovery Unit (DDU) facilities in the UK.

In tests with mice and other lab animals, the researchers report that the drug identified and attacked the protein involved in the production of various vital enzymes and proteins in the malaria parasite’s cells throughout all stages of its lifecycle, which prevented the spread and development of the disease. The parasite was successfully cleared from both the blood and livers of the affected animals.

“The compound we have discovered works in a different way to all other antimalarial medicines on the market or in clinical development, which mean that it has great potential to work against current drug-resistant parasites,” one of the team, Kevin Read, said in the release. “It targets part of the machinery that makes proteins within the parasite that causes malaria.”

The results have been published in Nature.

According to Steve Connor at The Guardian, the first phase of clinical trials will begin in the coming months, and if the drug makes it to the market, will likely be sold for less than $1 a dose, “which is considered the maximum price that the poorest affected countries can afford”, he says.

As David Reddit, CEO of Medicines for Malaria Venture, pointed out to BBC News, malaria threatens half the world’s population – the half that can least afford treatment and vaccination against it, so a cheap, one-off medication could be the most promising option in development. “DDD107498 is an exciting compound since it holds the promise to not only treat but also protect these vulnerable populations,” he said.

Watch the video. URL: https://youtu.be/I2qHc4YTDSg

Viagra Could Stop Malaria


Since it first came on the market in 1998, Viagra has been found to address more conditions than just erectile dysfunction—it treats hypertension, altitude sickness, and prostate cancer. Now a team of European researchers has found that everyone’s favorite little blue pill can prevent malaria because of the way an enzyme affects red blood cells, according to a study published in PLOS Pathogens.

Malaria is caused by a parasite that lives in blood and is transmitted between people through mosquito bites. The sexual form of the parasite, Plasmodium falciparum, goes through some stages of its development in mosquitoes, but spends one very important stage in human red blood cells found in bone marrow. Once in the blood, these cells give the impression of being healthy because they are squishy, which allowed them to slip by the spleen, which normally looks for abnormal or dead blood cells, which are firmer, and filters them out.

The researchers figured that a good way to engage the spleen’s cleansing power would be to harden the red blood cells. Viagra, which works for its intended purpose by relaxing certain muscles to increase blood flow, allows the infected cells to remain stiff by inhibiting an enzyme that would keep them squishy. In this study, the researchers tested Viagra on the blood in an artificial spleen and found that the spleen easily weeded out the hardened red blood cells. The researchers see their work as the first step towards new types of antimalarials.

A Chilly Fever


A 30-year-old graduate student presented with fevers associated with shaking chills and severe headaches. He had been well until 1 week before presentation, when he began to have daily fevers, with temperatures as high as 39.4°C. Any fever in a patient who has had possible exposure to malaria should prompt consideration of this diagnosis.

Clinical Pearls

What is the annual incidence of malaria in the United States?

In the United States, the annual incidence of malaria is approximately 1500 cases. In 2010, a total of 1691 cases were reported to the Centers for Disease Control and Prevention (CDC), the largest number reported since 1980; P. falciparum, P. vivax, P. malariae, and P. ovale were identified in 58%, 19%, 2%, and 2% of cases, respectively.

How do malaria and babesiosis differ in appearance on a peripheral blood smear?

Intraerythrocytic parasites are seen in both malaria and babesiosis. Plasmodia metabolize heme to form an intracellular crystallized pigment, hemozoin. Although hemozoin is not invariably identified in cases of malaria, its presence reliably distinguishes malaria infection from babesia infection. Malaria parasites can be distinguished from B. [Babesia] microti by the presence of recognizable gametocytes (characteristically banana-shaped in Plasmodium falciparum and round, with a granular appearance, in nonfalciparum species). In addition, intracellular vacuoles and extracellular merozoites are unusual in malaria but common in babesiosis, and the classic “Maltese cross” (a tetrad of parasites budding at right angles) is unique to babesia species.  Morning Report Questions

Q: Which malaria species can remain dormant in the liver?

A: In the case of P. vivax and P. ovale, some sporozoites (immature malaria parasites) do not replicate immediately when they invade hepatocytes but remain dormant (as hypnozoites) for prolonged periods. The average time to relapse is approximately 9 months, but it can range from weeks to years. The interval to relapse depends on the strain (earlier with tropical strains and later with temperate strains), the initial inoculum, and host factors (e.g., febrile illnesses can trigger relapse associated with P. vivax). None of the commonly used prophylactic agents (chloroquine, mefloquine, doxycycline, or atovaquone-proguanil) eliminate hypnozoites. Primaquine, the only effective drug against dormant hypnozoites, has not been approved by the Food and Drug Administration for primary prophylaxis, but the CDC endorses its use for prophylaxis in Latin American countries where P. vivax predominates, because the drug can prevent both primary attacks and relapses caused by all species that are a source of malarial infection.

Q: How is acute or recurrent P. vivax infection treated?

A: In patients with acute or recurrent malaria infection, treatment depends on the species and the resistance status in the area where the infection was acquired. P. falciparum is resistant to chloroquine in most regions in which it is endemic and resistant to mefloquine in parts of Southeast Asia. In contrast, nonfalciparum malaria parasites do not have substantial resistance to mefloquine, and the distribution of chloroquine-resistant P. vivax malaria is limited, occurring primarily in Indonesia and Papua New Guinea. After treatment is initiated, peripheral-blood smears should be obtained daily for 4 days (parasitemia is typically eliminated by day 4), on days 7 and 28 to confirm eradication, and at any time symptoms recur, suggesting treatment failure. In areas other than those with known chloroquine resistance, chloroquine, followed by a 14-day course of primaquine to prevent subsequent relapses, remains the standard treatment for P. vivax parasitemia. Given the risk of hemolysis in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency who receive treatment with primaquine, potential recipients should be tested for G6PD deficiency. Among patients with a contraindication to primaquine therapy, treatment with chloroquine alone carries a 20% risk of relapse; extended chloroquine prophylaxis can be offered to patients who have frequent relapses.

Vaccine alternative protects mice against malaria.


A study led by Johns Hopkins Bloomberg School of Public Health researchers found that injecting a vaccine-like compound into mice was effective in protecting them from malaria. The findings suggest a potential new path toward the elusive goal of malaria immunization.

Lab mice

Mice, injected with a virus genetically altered to help the rodents create an antibody designed to fight the parasite, produced high levels of the anti-malaria antibody. The approach, known as Vector immunoprophylaxis, or VIP, has shown promise in HIV studies but has never been tested with malaria, for which no licensed vaccine exists.

A report on the research appears online Aug. 11 in the Proceedings of the National Academy of Sciences (PNAS).

Malaria is one of the world’s deadliestinfectious diseases, killing as many as 1 million people per year, the majority of them children in Africa. Malaria patients get the disease from infected mosquitoes. Of the four types of malaria that affect humans, the parasite Plasmodium falciparum is the most lethal, responsible for the majority of malaria cases. Antimalarial treatments and mosquito habitat modification have contributed to a decline in malaria mortality. But the number of cases remains high, and stemming them is a top global health priority.

In their study, researchers used a virus containing genes that were encoded to produce an antibody targeted to inhibit P. falciparum infection. Up to 70 percent of the mice injected with the VIP were protected from malaria-infected mosquito bites. In a subset of mice that produced higher levels of serum , the protection was 100 percent. The mice were tested a year after receiving a single injection of the virus and were shown to still produce high levels of the protective antibody.

“We need better ways to fight malaria and our research suggests this could be a promising approach,” notes study leader Gary Ketner, PhD, a professor in the Department of Microbiology and Immunology at the Johns Hopkins Bloomberg School of Public Health.

There is a fine line between a vaccine and a VIP injection. One key difference: a VIP injection is formulated to produce a specific antibody. VIP technology bypasses the requirement of the host to make its own immune response against malaria, which is what occurs with a vaccine. Instead VIP provides the protective antibody gene, giving the host the tools to target the . “The body is actually producing a malaria-neutralizing antibody,” says Ketner. “Instead of playing defense, the host is playing offense.”

“Our idea was to find a way for each individual to create a long-lasting response against malaria,” says Cailin Deal, PhD, who helped lead the research while completing her doctorate at the School.

One advantage of this targeted approach over a traditional vaccine, the researchers note, is that the body might be able to continue to produce the antibody. With a vaccine, the natural immune response wanes over time, sometimes losing the ability to continue to resist infection, which would require follow-up booster shots. This can be challenging for people living in remote and or rural areas where malaria is prevalent buthealth care access limited. Any immunization protocol that involved one injection would be preferable.

“It’s dose dependent,” adds Deal. “Of course we don’t know what the human dosage would be, but it’s conceivable that the right dosage could completely protect against malaria.”

“Vectored antibody gene delivery protects against Plasmodium falciparum sporozoite challenge in mice” was written by Cailin Deal, Alejandro B. Balazs, Diego A. Espinosa, Fidel Zavala, David Baltimore and Gary Ketner.

Malaria Growing Resistant to Drugs Used to Fight It.


The parasite that causes malaria is growing increasingly resistant to the drugs commonly used to fight it, according to new surveillance reports. But several new drugs are in development, and at least one in early clinical trials may offer new hope against this global killer.

“Although there has been considerable progress in malaria control in the past decade, the battle against malaria is far from won, and there is still much more to do,” said Dr. Brian Greenwood, professor of tropical medicine at London School of Hygiene and Tropical Medicine, who wrote a commentary accompanying the new research.

Especially worrisome is the growing power of malaria parasites to survive the drugs that are designed to kill them, Greenwood said. One study reported widespread resistance to the drug artemisinin across mainland Southeast Asia. A second study found resistance to a drug combination — dihydroartemisinin-piperaquine — in Cambodia. Resistance to this drug is particularly concerning because this combination is often used in the most difficult-to-treat malaria infections.

Fortunately, even those who show resistance may get well when given longer courses of medication. “Many of these patients will get better eventually if they are treated for many days or treated with an additional effective drug,” Greenwood said.

All of the new research, along with Greenwood’s editorial, appears in the July 31 issue of The New England Journal of Medicine.

Malaria is an infection caused by the parasite plasmodium, according to the World Health Organization (WHO). It is transmitted through the bites of infected mosquitoes.

It’s estimated that more than 200 million cases of malaria occur every year, according to the WHO. The annual death toll from malaria around the world has fallen from 1 million 20 years ago to about 650,000, mostly children in Africa, according to Greenwood.

The decline, he said, is due to better funding for treatment and prevention from international donors and national governments in malaria-stricken areas.

Greenwood said researchers are still trying to figure out if the same type of resistance seen in Southeast Asia is happening in India and Africa. The surveillance study on artemisinin resistance did include several sites in India and Africa, but Greenwood pointed out in his editorial that there just wasn’t enough sampling from those areas to definitively say whether or not resistance is developing.

“There is a major concern that artemisinin-resistant parasites will spread to or emerge in sub-Saharan Africa, where the main burden of malaria is found,” he said. “This would be a major catastrophe, but this could be curtailed if alternative drugs can be found.”

One potential alternative medication is known as KAE609, from a class of drugs known as spiroindolones. In another new report, this one funded by the drug company Novartis, scientists report that they successfully treated malaria in 21 patients from Thailand with the medication.

The drug “appears to rapidly clear the blood of the two most common species of the malaria parasite,” said study co-author Thierry Diagana, head of the Novartis Institute for Tropical Diseases in Singapore. It may also prevent transmission of malaria, Diagana said.

However, it’s still too early to know if the drug is a success. The study represents the second phase of three stages of research required of new drugs.

The study was too small to determine if there are any significant side effects, according to Diagana. It’s also too early to know the potential cost of the drug. More studies are needed in the second phase of research for the new drug, Diagana noted.

Greenwood said that the focus must remain on controlling the spread of malaria, treating those who are sick with existing medications, and developing new drugs to control the disease.

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