The enemy of my enemy

Strains of antibiotic resistant tuberculosis are becoming more common and it is expected that nearly half of all cases of the disease will survive exposure to traditional front line drugs by 2050. This is driving an intense search for drugs that can bypass the resistances that are commonly seen arising in tuberculosis. Now a team is revealing that they have found a compound produced by another species of bacterium that regularly infects human lungs that looks like it has tremendous potential to control tuberculosis infections.

The compound in question is produced by the species Burkholderia gladioli. While exceptionally rare in most people, B gladioli thrives in the lungs of those suffering from cystic fibrosis. The reason the team behind the new research was attracted to this species is because, once it establishes itself in the lungs, it does an astounding job of making sure that no other bacteria encroach on its turf. This suggested that the species was producing compounds that had the potential to inhibit the growth of competition and this is precisely what the team discovered when they took a closer look. You can read more in The Economist article that I wrote on this here.

Street smart birds

Perfect pest-proofing material.

Image courtesy of SillyPuttyEnemies.

Six years ago a team revealed that the nests of birds that had cigarettes woven into them were less likely to contain blood sucking parasites than the nests of birds that did not have cigarettes in them. Further testing revealed that the nicotine content in the butts played a key part in keeping the parasites away. I wrote that up in Nature at the time and pointed out that the team behind the research did not really know if city birds were doing this by accident or had actually worked out that cigarettes were a valuable tool for use when parasites came to their nests. Now that same team is revealing evidence that the birds know perfectly well what they are doing.

Precisely why birds bring cigarettes to their nests is a matter of debate. Some argue that they collect discarded butts simply because they resemble natural materials like twigs while others argue that they know the butts repel parasites. To test out this latter idea, the team monitored house finch behaviour as they added either dead or living parasites to their nests. When live parasite numbers increased, female finches collected more butts for their nests than females that had dead parasites added. You can read more in The Economist article that I wrote on this here. Alternatively, if you would like to hear me describe the research on The Economist's science podcast, you can do so here.

Simulating the smell of death

Cells sometimes intentionally kill themselves off even if they are not diseased are harmed. This often occurs during normal development (like the forming of fingers in embryos from an initially fin-like appendage). When cells die in this way, bits of them circulate and tell the immune system that their death has been an intentional and somewhat peaceful affair. This is staggeringly different from when cells die during infection. Under those circumstances, their dead fragments usually trigger a powerful immune response that creates intense inflammation. While initially useful, inflammation impairs healing if it lasts for too long. This has led to a lot of research into how inflammation can be better controlled with drugs. Now a team is revealing that they have found a way to do this by releasing compounds into the body that look an awful lot like the fragments of cells that intentionally killed themselves in a peaceful manner.  You can read more in The Economist article that I wrote on this here.

Many snake venom antidotes do not work

Saw-scaled vipers are difficult to spot as they tend to be active at night, have venom that drives people to suffer catastrophic internal haemorrhages and live in places where medical care is limited. As such, it is not surprising that they kill an awful lot of people. Antivenoms are widespread and available where these snakes are found but a team of researchers studying survival data noticed that people were still often dying even if they got the antivenom in time. Concerned and confused, the researchers ran an analysis of antivenom performance against venom milked from a number of the vipers and discovered that many of the antivenoms on the market simply do not work in regions where advertising says they should.

Are we sure we have the right antidote on hand?

Image courtesy of Shantanu Kuveskar

The key issue at hand here is the fact that antivenoms are produced using venom and venom varies from snake to snake, sometimes even within the same species. So, if an antivenom is produced using a species of saw-scaled viper found in both India and Pakistan but only snakes from Pakistan have their venom collected for the creation of the drug, there is chance that the antivenom will not work very well (or at all) when used to treat snake bites in India. This is precisely what appears to have happened and the harm to people in Asia and Africa looks like it is quite significant.

Some of the antivenom companies that I spoke with were remarkably receptive to these findings. One clearly stated that they are going to re-label their bottles immediately so their drugs are only delivered to places where they do actually work. Another stated that they are going to start milking vipers from more regions to build better antivenoms. However, not all is rosy. One company flatly denied that they manufacture a very poorly performing antivenom that is advertised on their own website and another argued that the findings of the researchers were flawed.  You can read more in The Economist article that I wrote on this here.

Not born with bad teeth

Cavities are one of the most problematic chronic oral diseases suffered by children and, for decades, the assumption has been that those who develop severe cavities largely have bad luck by inheriting genes that make their teeth vulnerable to the condition. Now a new study is revealing that this notion is nonsense.

The researchers behind the new work examined the role of genetics, environment, and disease on the composition of the bacteria and fungi that live in the mouth in a whopping 485 pairs of twins. They found that while there are several species of bacteria that are heritable (or prone to grow in mouths due to heritable conditions), these species play little or no part in the formation of cavities.  

These findings prove that chronic cavities have to be almost entirely the result of bad eating behaviours and not down to inherited "bad" oral microbiology. On the larger scale, we are seeing loads of cardiovascular, immunological and respiratory diseases (including several cancers) that have strong connections to the composition of the bacterial bugs living in the gut. Some recent papers show that oral microbiota are important here too and, if that is so, then diet looks very important for preventing or controlling these diseases too while genetics look largely unimportant. You can read more in The Economist article that I wrote on this here.