Thirteen people on a cruise ship have been struck down by a mystery illness causing severe flu-like symptoms. Two have died, others are in a critical condition, and everyone else on the ship is terrified. Is help on its way? Will they be allowed off? What’s infecting everyone? IS THIS THE NEXT PANDEMIC??

When the recent hantavirus news broke, Dr Charlotte Hammer, Assistant Professor in Health Security and Infectious Diseases, stepped up to help international media cover the story. But how could she speak so authoritatively about dealing with a rare virus she’s not a specialist in?

“The great thing about field epidemiology training is that rather than becoming a specialist in a pathogen, we learn the skills to respond to outbreaks whatever they are - even if the pathogen has never been encountered before,” says Hammer.

“Many of the media questions I answered about the hantavirus outbreak had relatively little to do with the specific virus - like figuring out how it was spreading and what to do with the infected people, and how different nations would coordinate a response given there were people from various countries on board the ship."

"The advice is adapted, based on what we learn about the virus’s transmissibility, but a lot of it is very fundamental."

Based at Cambridge’s Centre for the Study of Existential Risk and Downing College, Hammer has worked at the German National Public Health Institute, the UK Health Security Agency, the Finnish Institute for Health and Welfare, and the World Health Organisation. Now she studies emerging risks likely to lead to disease epidemics and pandemics - including what she calls ‘cascading risks’, where multiple risks interact to create one giant, pulsating super-risk.

Surprisingly, she’s discovered that the Arctic is a potential hotspot of risks for disease emergence.

“In terms of risk interactions, the Arctic is a real problem area, and we’ve already seen one significant human anthrax outbreak there,” says Hammer.

For example, thawing permafrost is exposing the carcasses of reindeer that have died of anthrax. It also makes mining the Arctic’s rich mineral, oil and gas reserves more feasible – a cause of rising geopolitical tensions. And climate-driven ice melt means that the Northwest and Northeast Passages - two important Arctic shipping routes - are becoming more accessible for more of the year.

“Imagine a person caught anthrax by standing unknowingly near a thawing reindeer carcass in the Arctic, flew home to New York, and then fell ill and went to their doctor. If they receive antibiotic treatment early enough it’s usually fine. But the doctor must suspect anthrax to actually treat it – and by the time they figure it out, it might be too late.”

Anthrax doesn’t spread from person to person. But what if a more transmissible pathogen emerged under similar conditions?

“Whereas in the past you might have had a handful of infections in people who stay local, with the increasing activity in the Arctic you potentially have people going off all over the world carrying the infection with them.”

“Depending on how long it takes to identify a pathogen, it can be difficult to find out where it has come from and how far it has spread,” says Hammer. “If we then think through some of the things we saw on a very small scale with hantavirus on the cruise ship - like contact follow-up - it becomes a significantly bigger logistical challenge.”

International relations are vital in helping to contain outbreaks that spread across countries, and when governments don’t cooperate, outbreaks can’t be contained as efficiently as hantavirus was.

“If countries don’t announce there’s a problem, share information on disease cases, or ask for support, then we don’t contain outbreaks as well as we could,” says Hammer. “But if the response when countries act openly is to impose travel bans or trade bans on them, what is the incentive for them to share again next time? It’s a vicious circle.”

Hammer has identified conflict zones as another surprising risk hotspot for potential disease outbreaks, with the war in Ukraine proving real-time information.

“In some areas of Ukraine there’s basically been a return to trench warfare. A lot of the injuries are particularly susceptible to infection, but with supply chain issues the antimicrobial drugs aren’t getting through."

"People who are injured on the front lines receive emergency treatment in Ukraine, and some of them are then evacuated for definitive treatment elsewhere in Europe. We’re seeing considerable potential for antimicrobial resistance to emerge in this context, with risks of spread to other countries,” she says.

For the last century, antibiotics have been vital in healthcare: they’re lifesaving drugs used to treat or prevent bacterial infections. But every time they’re used, antimicrobial resistance - when the bugs acquire genetic variations that make them resistant to treatment - has more chance to develop.

"Antimicrobial resistance is a global health threat, and the pipeline for developing new drugs is failing."

"Not long after a drug is put into use, we see bacteria develop resistance to it and we need to develop a new one," says Professor Kate Baker in the University of Cambridge’s Department of Genetics.

Working closely with public health agencies, Baker uses a powerful technique called genomic surveillance to track how antimicrobial resistance evolves and spreads across the world. During the COVID pandemic, the technique was used to track the spread of coronavirus variants. When Omicron appeared and started spreading quickly, genomic information allowed scientists to see exactly how the virus had mutated – and work out how to respond.

“If you're just taking lateral flow tests, you see something's spreading really quickly but can't understand whether changes in the pathogen are contributing. The beauty of genomics is if you see something new emerge, you can track it as well as look at whether that pathogen has changed,” says Baker.

The genomic surveillance infrastructure developed during COVID has since been regeared towards tracking other pathogens, and Baker has found many examples of bugs becoming newly resistant to antimicrobial drugs. Their spread is being helped by the ever-increasing movement of people around the world.

"Enhanced international transmission of antimicrobial-resistant bugs is a real challenge."

"But because we track the genomics, we're keeping a very close eye on how these bugs are changing. We detect new antimicrobial-resistant lineages all the time,” says Baker.

Her team detected the emergence of a bug called ‘extensively drug resistant Shigella’ – a highly contagious pathogen that causes severe stomach cramps and diarrhoea. They checked genomic data with collaborators in Australia, France, Belgium and the US and found that the bug was already widespread across the world. Realising that the recommended antimicrobial treatments would no longer work, they worked with public health agencies to urge rapid updates to treatment guidelines.

In that scenario, an alternative antimicrobial drug was available. But in future we could run out of treatment options.

“It’s partly because of this antimicrobial resistance crisis that there have been renewed efforts into developing vaccines, the idea being that if we can’t treat infections, then we have to prevent them in the first place,” Baker says.

If we are to win in the battle against the bugs, it’s no longer good enough to rely on traditional approaches. The world is complex and changing fast in unpredictable ways. Hammer and Baker are among a whole network of scientists at Cambridge working to stay one step ahead of infectious diseases - and prevent outbreaks developing into pandemics.

This year, Hammer received Springboard funding from the Academy of Medical Sciences to investigate why dangerous infectious disease outbreaks are more likely to emerge and escalate in regions affected by conflict, environmental degradation or humanitarian crises.

By identifying critical ‘tipping points’ where early action could help prevent wider epidemics or pandemics, Hammer aims to help health systems to better target surveillance and early-warning efforts.

She says that the latest Ebola outbreak in the Democratic Republic of Congo reflects a broader pattern in how infectious disease risk is evolving. Events like this emerge from interacting environmental, social, and political pressures that make outbreaks harder to anticipate in straightforward ways.

Ebola and hantavirus are distinct pathogens with different transmission contexts, but both originate at the human-animal interface and are shaped by changing environmental and social conditions. What matters is not only the pathogen, but the system in which it appears.

"We won’t necessarily prevent outbreaks, but with early containment we can prevent them becoming a massive global issue."

Hammer adds: “We can’t afford to put disease surveillance everywhere, so it needs to be focused on particular places where large outbreaks are most likely. I want to better anticipate where, how and when infectious diseases will emerge, so we can put field epidemiologists and health workers there."

Baker’s MRC-funded work takes a similar approach to the growing threat of antimicrobial resistance: instead of waiting until a superbug has already spread, she’s trying to understand the earliest signs that one is about to emerge.

Focusing on Shigella, a highly contagious cause of diarrhoeal disease that’s becoming increasingly resistant to treatment, her team is using genomic surveillance data to track how resistance genes move through bacterial populations.

“Some antimicrobial resistance spreads because resistant bacteria themselves spread from person to person. But resistance can also move between bacteria, and we still don’t fully understand which of these routes is most likely to take off,” says Baker, adding:

“If we can identify the genetic features and epidemiological patterns that act as early warning signs, we can start to predict which resistant bugs are most likely to become a public health problem - and intervene before they become much harder to control.”