Curing disease is really a matter of outfoxing evolution. When we assault bacteria or viruses or cancer cells with drugs, they evolve ways of resisting those drugs. We attack, they counter-attack. Take malaria: the Plasmodium parasites that cause the disease have repeatedly evolved to resist our best anti-malarial drugs. The mosquitoes that carry the parasites have evolved to resist the insecticides we poison them with. And now, Victoria Barclay from Pennsylvania State University has found that some malaria vaccines could drive Plasmodium to become even deadlier than it is now.
Several malaria vaccines are in development, but none have been licensed yet. Barclay vaccinated mice with a protein that’s found in several of these vaccines, and then exposed them to Plasmodium. After a few generations, the parasite became more ‘virulent’ – that is, it caused more severe disease. And it did so via an evolutionary escape route that is rarely considered.
A malarial mosquito is a flying factory for Plasmodium – a parasite that fills its guts, and storms the blood of every person it bites. By hosting and spreading these parasites, mosquitoes kill 1.2 million people every year.
But Plasmodium isn’t the only thing living inside a mosquito’s guts. Just as our bowels are home to trillions of bacteria, mosquitoes also carry their own microscopic menageries. Now, Sibao Wang from Johns Hopkins Bloomberg School of Public Health has transformed one of these bacterial associates into the latest recruit in our war against malaria. By loading it with genes that destroy malarial parasites, Wang has turned the friend of our enemy into our friend.
Many groups of scientists have tried to beat malaria by genetically modifying the species of mosquito that carries it – Anopheles gambiae. Marcelo Jacobs-Lorena, who led Wang’s new study, has been at the forefront of these efforts. In 2002, his team loaded mosquitoes with a modified gene so that their guts produce a substance that kills off Plasmodium.
Your skin is teeming with bacteria. There are billions of them, living on the dry parched landscapes of your forearms, and the wet, humid forests of your nose. On your feet alone, every square centimetre has around half a million bacteria. These microbes are more than just passengers, hitching a ride on your bodies. They also affect how you smell.
Skin bacteria are our own natural perfumers. They convert chemicals on our skin into those that can easily rise into the air, and different species produce different scents. Without these microbes, we wouldn’t be able to smell each other’s sweat at all. But we’re not the only ones who can sniff these bacterial chemicals. Mosquitoes can too. Niels Verhulst from Wageningen University and Research Centre has just found that the bacteria on our skin can affect our odds of being bitten by a malarial mosquito.
Every time you exhale, you send out a beacon to hungry mosquitoes. These vampires follow their noses. They’re exquisitely sensitive to carbon dioxide in the air, and can follow faint traces over long distances. Constant streams of the gas won’t do – the mosquitoes are waiting for the rhythmic pulses of carbon dioxide, such as those given off by a breathing human. Once they find such a plume, they fly headlong into it, tracking it back to its blood-filled source.
This tracking ability makes it hard to avoid the attention of mosquitoes, or the diseases that they transmit with their bites. You could simply hold your breath to avoid giving off any telltale gases and because you would quickly die, malaria and dengue fever would not be a problem.
But there is a better way. Stephanie Lynn Turner and Nan Li from the University of California, Riverside, have found a cocktail of chemicals that can turn a mosquito’s senses against it. The chemicals target the very neuron that mosquitoes use to detect carbon dioxide, causing them to go berserk. They fire so wildly that they become useless. By disabling a mosquito’s guidance system, Turner and Li have found a way of making these human-seeking missiles go careening off course.
Meet our newest potential weapon against malaria – a fungus loaded with a chemical found in scorpion venom. Metarhizium anisopliae is a parasitic fungus that infects a wide variety of insects, including the mosquitoes that spread malaria. Their spores germinate upon contact and the fungus invades the insect’s body, slowly killing it. Now, Weiguo Fang from the University of Maryland has modified the fungus to target the malaria parasites lurking inside the mosquitoes.
Fang loaded the fungus with two chemicals that attack the malaria parasite Plasmodium falciparum. The first is a protein called SM1 that prevents the parasites from attaching to the mosquito’s salivary glands. By blocking Plasmodium‘s path, SM1 stops the parasite from travelling down the mosquito’s mouthparts into the people it bites. The second chemical is scorpine – a toxic protein wielded by the emperor scorpion, which kills both bacteria and Plasmodium. This double whammy of biological weapons slashed the number of parasites in mosquito saliva by 98%.
Several million years ago, Plasmodium falciparum – the parasite that causes most cases of human malaria – jumped into humans from other apes. We’ve known as much for decades but for all this time, we’ve pinned the blame on the wrong species. A new study reveals that malaria is not, as previously thought, a disease that came from chimpanzees; instead it’s an unwanted gift from gorillas.
We’ve all heard about “beer goggles”, the mythical, invisible eyewear that makes everyone else seem incredibly attractive after a few pints too many. If only beer had the reverse effect, making the drinker seem irresistibly attractive. Well, the good news is that beer does actually do this. The bad news is that the ones who are attracted are malarial mosquitoes.
Anopheles gambiae (the mosquito that transmits malaria) tracks its victims by their smells. By wafting the aromas of humans over thousands of mosquitoes, Thierry Lefevre found that they find the body odour of beer drinkers to be quite tantalising. The smell of tee-total water drinkers just can’t compare. The somewhat quirky conclusion from the study, albeit one with public health implications, is that drinking beer could increase the risk of contracting malaria.
Lefevre recruited 43 men from Burkina Faso and sent them individually into one of two sealed, outdoors tents. One tent was kept unoccupied. In the second, the volunteer had to drink either a litre of water (just shy of two pints) or a litre of dolo (a local 3% beer and the country’s most popular alcoholic drink). A fan pumped air from the tents, body odour and all, into the two forks of a Y-shaped apparatus. Both branches met in a third arm, which ended in a cup full of mosquitoes. The insects had to decide which branch of the Y to fly down and two pieces of gauze trapped them in their chosen path (and saved the volunteers from an infectious bite).
Lefevre showed that the smell of a beer drinker, 15 minutes after chugging his litre, increased the proportion of mosquitoes inclined to fly into the tubes, and the proportion (65%) who headed down the beer-scented fork. The smell of water-drinkers had no effect, nor did the smell of the occupied tent before its inhabitant started drinking.
This is an updated version of the first post I wrote this year. The scientists in question were looking at ways of recruiting bacteria in the fight against mosquito-borne diseases, such as dengue fever. They’ve just published new results that expand on their earlier experiments.
Mosquitoes are incredibly successful parasites and cause millions of human deaths every year through the infections they spread. But they are no match for the most successful parasite of all – a bacterium called Wolbachia. It infects around 60% of the world’s insect species and it could be our newest recruit in the fight against malaria, dengue fever and other mosquito-borne infections.
Wolbachia doesn’t usually infect mosquitoes but Scott O’Neill from the University of Queensland is leading a team of researchers who are trying to enlist it. Earlier this year, they published the story of their first success. They had developed a strain that not only infects mozzies, but halves the lifespans of infected females. Now, as the year comes to an end, they’re back with another piece of good news – their life-shortening bacteria also guard the mosquitoes from other infections.
It protects them against a species of Plasmodium, related to the parasite that causes malaria in humans, as well as the viruses responsible for dengue fever and Chikungunya. Infected insects are less likely to carry parasites that cause human disease, and those that do won’t live long enough to spread them. It’s a significant double-whammy that could have a lot of potential in controlling mosquito-borne diseases.
Fighting malaria with mosquitoes seems like an bizarrely ironic strategy but it’s exactly what many scientists are trying to do. Malaria kills one to three million people every year, most of whom are children. Many strategies for controlling it naturally focus on ways of killing the mosquitoes that spread it, stopping them from biting humans, or getting rid of their breeding grounds.
But the mosquitoes themselves are not the real problem. They are merely carriers for the true cause of malaria – a parasite called Plasmodium. It suits neither mosquitoes nor humans to be infected with Plasmodium, and by helping them resist it, we may inadvertently help ourselves. With the power of modern genetics and molecular biology, scientists have produced strains of genetically engineered mosquitoes that cannot transmit the malarial parasite.
These ‘GM-mosquitoes’ carry a modified gene – a transgene – that produces chemicals which interfere with Plasmodium‘s development. Rather than being suitable carriers, the bodies of the modified mosquitoes spell death for any invading Plasmodium.
But scientists can’t very well change the genes of every mosquito in the tropics. To actually reduce the burden of malaria, the genetic changes that induce malaria resistance need to be spread throughout the mosquito population. The easiest way to do this is, of course, to let the insects do it themselves. And Mauro Marrelli and colleagues from the Johns Hopkins University have found that they are more than up to the task.
Last year, I blogged about an ironic public health strategy – controlling malaria with mosquitoes. The mozzies in question are genetically engineered to be resistant to the malaria parasite, Plasmodium. The idea is that these GM-mosquitoes would mate with wild ones and spread their resistance genes through the natural population.
The approach seems promising but it relies crucially on the ability of the resistant males to successfully compete for the attentions of females in wild populations. The 1960s and 1970s witnessed several failed attempts to control malaria by swamping natural populations with sterile males released en masse. And while these letdowns had been blamed on ignorance about mosquito mating, this area of research has gone untouched until now.
A new study, which I’ve reported on in New Scientist, shows that size does indeed matter for mosquitoes, but it’s the average Joes that get the girls. Kija Ng’habi, a young Tanzanian MSc student, reared males of different size by controlling their diet as larvae, and pitted them against each other for the attentions of females in a cage.
He found that the average-sized males had twice as much sex as the smaller males. But amazingly, they also secured six times as many matings as the biggest ones, despite having smaller wingspans, lower energy reserves and shorter lifespans. In the long run, the longer lives of the big mozzies are unlikely to make up for their comparative failure to mate with females.