How concerned should we be about H7N9 flu?

thinkstockphotos-87711730The past few weeks have seen an increasing amount of coverage about an ongoing outbreak of the H7N9 strain of avian influenza in China (often called ‘bird flu’).

Reports suggest that in January almost 200 people were confirmed as being infected with the virus, of whom 79 died. The WHO indicates that many of the people infected were likely to have been exposed to poultry or have been to environments where live birds are kept. This is in keeping with how the vast majority of human infections have occurred since the strain first emerged in 2013.

Does this year’s H7N9 outbreak represent something of wider concern? What are the chances that the virus will evolve and gain the ability to be transmitted between people, rather than from poultry to people? We asked Microbiology Society member Wendy Barclay, Professor of Influenza Virology at Imperial College London.

“I’ve got no inside knowledge other than what’s been reported, but I think that what we’re seeing is the annual trend in H7N9. Around this time of year, we nearly always see a burst of cases, likely because the climate in Southern China is perfect for flu transmission – it’s cold and dry, and quite good for the virus surviving in the environment.”

Earlier this week, evidence from China has shown that one of the surface proteins on the virus has mutated, allowing it to spread to any organ within a chicken, rather than just their intestines and respiratory tracts. This is clearly bad news for the birds, and the increased viral load might in turn result in an increased number of human cases. On the other hand – as was seen for H5N1, the other highly pathogenic bird flu – a virus that kills birds should be easier to spot and control than one that does not. But what is the current risk of H7N9 turning into even more of a public health risk?

“I don’t think that there is any reason to believe that the H7N9 that’s out there now is currently any more likely to cause a pandemic than the one that emerged in 2013,” Wendy explains. “We know that this virus can pass from chickens into humans, but we also know that it doesn’t appear to have the mutations required for person-to-person transmission.

“Genetic barriers still exist – H7N9 doesn’t have the mutations on its external proteins that would allow it to be transmitted through the air, or allow it to be stable enough to survive in the human respiratory tract.”

While the WHO say that at the current time there is “no evidence of sustained human-to-human transmission”, Wendy recommends that H7N9 requires close attention.

“Pandemic flu is rightly one of the top worldwide threats of most concern to researchers and public health officials, but while this current virus is the one that currently causes us the most worry, there are others out there in chickens, pigs and ducks that are also possible pandemic precursors. We continue to try to understand how better to predict which viruses will actually make it across the species barrier and how best to deal with them when they do.”

Benjamin Thompson

Professor Barclay is an Editorial Board Member of the Microbiology Society’s Journal of General Virology (JGV) and a winner of our Peter Wildy Prize. You can find out more about her work here.

You can read JGV’s collection of papers on avian viruses here.

Image credit: Hemera Technologies/Thinkstock
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Bacterial freeloaders: An unexpected mechanism of resistance

Bacteria are very good at evolving resistance to our drugs. Once all-powerful wonder-cures, antibiotics are steadily becoming less effective. If antibiotic resistance continues to spread, reports suggest that by 2050, 10 million people could die every year from infections we won’t be able to treat.

This is a serious problem. To solve it, we need to have a better understanding of the mechanisms that allow bacteria to evade drug treatment. And the science of how they do that is pretty incredible.

For example, bacteria can evolve pumps to bail antibiotic molecules out of their insides. Or they can produce molecules to neutralise antibiotics directly. And sometimes, they even mutate the structure of their own molecules, so that the antibiotics can’t bind to their targets.

But it doesn’t really make sense to think of bacteria as individual, lone survivors. Bacteria are always part of a community – one that’s dynamic, and constantly changing. For one thing, bacteria can share resistance genes between each other. For another, many bacteria live stuck together in communities called biofilms, often with a tough slime coating that protects the inner cells from the reach of antibiotics.

If you want to understand the mechanisms of resistance, you have to understand the interactions between different bacteria. And perhaps one of the most striking examples of this is ‘passive resistance’ – where cells with no resistance to antibiotics can indirectly reap the rewards from others that do.

This can happen when resistant bacteria secrete a neutralising molecule into the surrounding environment, clearing it of antibiotics and allowing susceptible strains to grow. But new research shows it can also happen when bacteria neutralise the antibiotics inside their own cells, acting like tiny decontamination factories for susceptible strains.

The findings, published in PLOS Biology, also describe something totally unexpected about this mechanism. In some cases, bacterial ‘freeloaders’ can actually outcompete their resistant neighbours – even though they have no special abilities themselves.

The researchers looked at Streptococcus pneumoniae, an opportunistic pathogen of humans that lives in the nose and throat. They treated the cells with the antibiotic chloramphenicol and found that, at a certain ‘sweet spot’ of bacterial densities, susceptible bacteria could coexist with resistant species, and sometimes even do better then them.

“It very much depends on how many resistant bacteria you have,” explains Dr Robin Sorg, lead author on the paper. “It’s all about the timing between nutrient consumption and antibiotic deactivation.”

At low cell densities, there simply aren’t enough resistant bacteria present to make a dent in the antibiotic levels, so the susceptible cells die. At very high cell densities, the resistant strains rapidly use up the available nutrients – so the susceptible cells don’t even get going.

But, at the sweet spot, there are enough resistant bacteria to clear the environment of the antibiotic, and the susceptible cells have enough time and resources to start growing. And because it takes extra energy for the resistant bacteria to neutralise the antibiotic, any cells that don’t carry this burden may have a slight advantage.

You can see this in the time-lapse video below, where the phenomenon is demonstrated in between two different pathogenic species: resistant Staphylococcus aureus and susceptible Streptococcus pneumoniae. At first, only the resistant cells grow (the bright green cells). But eventually, they pave the way for susceptible cells, which quickly explode in numbers.

Using mathematical modelling, the researchers also showed that in some situations, the susceptible cells do so well that they actually drive the resistant cells to extinction, by outcompeting them and using up all the nutrients. And without the resistant cells there to detoxify the environment, they ultimately become extinct themselves. Talk about biting the hand that feeds you.

The team then wanted to know whether this could happen in the real world – is the effect medically relevant? To find out, they ran an experiment on mice, infecting them with both resistant and susceptible strains of S. pneumoniae, and then treating them with the antibiotic chloramphenicol.

When they looked at the levels of bacteria in the mice afterwards, they found the same effect – treating with the antibiotic gave the susceptible cells an advantage, and in some cases they outcompeted the resistant cells.

It’s worth pointing out that this was a small study, but although far from conclusive, papers like this raise important questions about how resistance spreads in the real world.

“This might be one mechanism that adds to the dynamics of resistance development,” explains Robin. “Even if there is a small passive resistance effect, it means there is increased survival of susceptible cells – and increased opportunities for them to gain resistance.

“Additionally, you have the resistance genes encoded in the neighbouring cells. So if a couple of them burst, you have the perfect setting for gene transfer. [Passive resistance] could be one big factor that increases spreading of resistance genes.”

Anand Jagatia

Image credit: Nathan Reading on Flickr under CC BY-NC ND 2.0
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You can’t stop an outbreak without breaking a few eggs

Last year, a paper from Microbial Genomics described how scientists used molecular detective work to get to the bottom of an outbreak across Europe.

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In June 2014, there was an outbreak of Salmonella at a hospital in Birmingham. Thirty-two people were affected, and one patient sadly died as a result of infection. Over the following weeks, more outbreaks began popping up in other parts of the UK. Several of these cases were linked to Chinese restaurants across England, and some were traced back to a kebab shop. In total, 247 cases of salmonellosis, caused by the bacterium Salmonella enteritidis, were reported by Public Health England (PHE).

The most likely explanation was that contaminated eggs or chicken were being served to customers who then got sick. But it was more than just a few random incidents – these events were part of a much larger outbreak across Europe, and hundreds of cases were also reported at the same time in Germany, France, Austria and Luxembourg.

So what was going on? Continue reading

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What is Herd Immunity?


When you think of a herd, you probably think of cows, wildebeest or buffalo. In the animal world, there is safety in numbers – more pairs of eyes to look out for predators, for example.

As humans, we don’t generally have to worry about predators, but we can gain the protection of the herd in other ways. “Herd immunity” is the idea that, as long as enough people in a population are immune to a disease (usually through vaccination), they can indirectly protect people who aren’t immune from getting infected.

Dr Adam Kucharski is an Assistant Professor of Epidemiology at the London School of Hygiene and Tropical Medicine, where he works on mathematical models of the spread and control of disease.

Read more about halting epidemics in the latest issue of Microbiology Today.

The numbers that Adam uses for vaccine threshold and herd immunity come from this formula:virus-logo-01

(Ro – 1) / Ro

Where the proportion of people you need to vaccinate is related to how transmissible the disease is (Ro).

The more easily the disease spreads, the greater the proportion of the population you need to vaccinate to get herd immunity. 

Anand Jagatia

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Streptomyces: bacterial explorers

Streptomyces bacteria are some of the most studied microbes on the planet. This genus of soil-dwelling organisms is best known for being prolific producers of many of the antibiotics that we use clinically. However, despite 70 years of study, they still have secrets left to discover.streptomyces

Researchers from McMaster University in Canada have identified a new kind of growth that occurs in some species of Streptomyces, which enables colonies to quickly explore new areas and climb over tiny rocks, a feat proportional to a human climbing Everest. The group published their findings last month in the journal eLife. Continue reading

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Podcast: Microbes in the Deep Dark Ocean

What’s it like to travel right down to the bottom of the ocean?

6982437095_076f9f2b61_kDeep sea microbiologist Julie Huber should know. Her group, at the Marine Biological Laboratory in Massachusetts, USA, is trying to uncover more about the microbes living in the deepest darkest depths of the ocean. But that’s not all – there are even microbes living thousands of metres beneath the ocean floor itself, within the rocks and sediment.

This is an environment that couldn’t be more different to our world on land – no light, huge pressures, underwater volcanoes and hardly any nutrients. So what kind of microbes do we see living there, and how do they manage to make a living?

Anand Jagatia

Image credit: NOAA Submarine Ring of Fire 2006
Music: Sacred Motion by staRpauSe
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On the Horizon: What is Oropouche virus?

Sloth in the Jungle

In this edition of our On the Horizon series, we take a look at an obscure virus that may cause an important emerging disease in 2017, or may remain in obscurity for much of the world.

That is, except for South America, where the virus is estimated to have caused over 500,000 infections since its discovery in 1955. Its name? Oropouche, named after an area of Trinidad, where it was first isolated from a 24-year-old forest worker. Continue reading

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