ONE-THIRD of the world’s population is infected with the same disease: tuberculosis. It seems almost inconceivable to us here in the UK, where the notion of TB conjures up images of long-dead writers or Victorian poverty.

But it’s true. In the 21st century, over 2 two billion people worldwide are currently infected with a form of TB. The disease is relatively treatable, yet around 1.5 million TB-related deaths occurred in 2015, making it the second biggest infectious killer after HIV.

So why is a disease that hit its UK peak in the 19th century still wreaking global havoc in 2017? Well, TB wasn’t always the global health crisis it is today.

A vaccination developed in the early 20th century, along with the 1943 discovery of streptomycin, the first antibiotic effective against TB, helped us to fight back against the disease. More antibiotic treatments followed in the latter half of the 20thtwentieth century, and by the 1970’s there was great hope amongst scientists that we might eliminate tuberculosis entirely.

But in the 1980s, things took a turn for the worse. We began to see strains of tuberculosis emerging which had evolved resistance to antibiotics. In recent years, we’ve had half a million new cases of ‘multi-drug resistant’ TB every year: strains that are resistant to more than one type of antibiotic.

And this is a growing problem. Cases recently reported in India, Italy and Iran appear to be resistant to every antibiotic available. It’s clear that we need to act quickly if we’re to combat this global health emergency.

Unfortunately, TB is immensely difficult to treat. Patients must take a course of several antibiotics over a 6six-month period, but this is really hard to enforce. People often see signs of recovery and so stop taking their medicine, and this gives the bacteria a chance to evolve new defence mechanisms against the drugs.

Like a small amount of virus in the form of a flu jab helps us to develop immunity against the infection, a small amount of exposure to antibiotics allows pathogens like tuberculosis to develop resistance.

Along with concerted public health campaigns and consideration of the wider social factors at play in the spread of TB, it’s important that we learn more about the bacteria itself and how it manages to sidestep our antibiotics.

And there is real progress in this area. Thanks to improved scientific technology, we’re now able to study the various building blocks inside TB better than ever before. These building blocks, known as proteins, are what keep TB alive and well, even in the face of antibiotic attack.

In Oxfordshire, early-stage research into TB proteins could ultimately support moves towards new drugs against the disease. Using advanced techniques, scientists have been able to visualise the structure of an enzyme involved in the formation of the protective wall that surrounds TB cells.

This waxy wall makes it harder for antibiotics to penetrate and destroy TB cells. So knowing the basic structure of one of these wall-forming proteins could be an early step towards developing drugs that switch this process off, leaving the TB cells vulnerable to attack.

Experts are also using our science infrastructure to study the microscopic mechanisms by which existing TB drugs work on the molecular level. The sort of knowledge could help us to enhance the therapeutic effect of existing medicines.

Fighting back against tuberculosis is no easy feat. In fact, it’s one of the greatest challenges the global community faces. But that’s not to say it can’t be done. With a combination of approaches – including education, policy-work and in-depth scientific research – we can and must turn the tide on TB.