As virologists and public health officials focused anxiously on reports of an Andes virus outbreak aboard a cruise ship — 13 infections and three deaths — another dangerous crisis was unfolding with far less attention. In the Democratic Republic of the Congo, Bundibugyo virus, the cause of the current Ebola outbreak, has been spreading quietly but alarmingly, with more than 1,250 reported cases and at least 362 deaths.

Bundibugyo virus is a severe and often deadly pathogen. Illness can begin abruptly, bringing headaches, diarrhoea, kidney and liver dysfunction, and, in some cases, internal and external bleeding — the reason these infections are often described as “haemorrhagic disease”. One of the most distressing features is that the virus can remain contagious after death, putting relatives and loved ones at risk when they wash and dress the body before burial.

For now, the urgent task is clear: resources must be directed toward containing the outbreak. With no widely established, proven vaccine available for Bundibugyo virus, health workers are left to rely on the demanding basics of outbreak control — isolating patients, identifying contacts and monitoring anyone who may have been exposed.

Once the immediate danger is brought under control, however, two questions will become impossible to avoid: why did this outbreak occur, and where did the virus come from? Understanding those answers is essential if future outbreaks are to be prevented, or at least contained more quickly.

Bundibugyo virus belongs to the same broader family as the better-known Zaire Ebola virus, which has caused sporadic outbreaks of Ebola virus disease in remote African rainforest regions since the 1970s. Zaire Ebola later became infamous during the devastating west African epidemic from 2014 to 2016.

Despite Ebola viruses ranking high on lists of potential bioterror agents, surprisingly little is known about how they behave in the wild. Marburg virus, a more distant relative that also causes haemorrhagic fever, is known to persist in large fruit bats. That discovery has encouraged a plausible but still unproven assumption: that bats may also serve as reservoir hosts for other members of the Ebola virus family.

Fruit bats are common, widespread, large and easy to notice, which makes them convenient suspects whenever an Ebola outbreak occurs. But hard evidence that bats can maintain and transmit Zaire Ebola virus in nature has remained frustratingly difficult to find. For now, blaming bats for Bundibugyo virus is still speculation. Having a distant cousin who wears a kilt does not make you Scottish.

Historically, the first known human cases in Ebola virus outbreaks have often been associated with contact with other mammals, including forest antelopes, gorillas and chimpanzees. Studies have also shown that experimentally infected pigs can shed infectious Ebola viruses and pass them to primates. Taken together, the evidence suggests Ebola viruses may use a range of animal hosts. It is also possible that the virus can persist silently in a host for years before re-emerging, which could help explain why Ebola viruses sometimes seem to disappear for long stretches, only to return without warning.

How then would you go about determining Bundibugyo virus transmission patterns in tropical forest? How do you convince a group of wary canopy-dwelling monkeys to provide samples? Capture them? Shoot them? Analyse their faeces? Or should you target herds of bush pigs? Or giant fruit bats? Or all of the above? And if this disease is rare, and outbreaks in humans occur after the disease has spilled from wildlife, then how on earth do you capture the virus red-handed?

These issues make muddy waters for understanding how diseases emerge; just look at the controversies surrounding the origins of Covid-19. And now imagine attempting this kind of scientific research in an area of political unrest, and in the face of ruthless cost-cutting of research and health funds by the US and UK and the consequent evaporation of infrastructure.

Yet these questions need to be answered. Before 2010, the largest Ebola virus outbreaks rarely exceeded 300 cases, but since then there have been three outbreaks where cases are counted in the thousands. The trend is indubitably one of larger epidemics.

If we knew how Ebola viruses worked, we could mitigate against them by reducing human exposure, whether it be using wildland buffers or discouraging consumption of wild animals. Or we could adopt integrated surveillance programmes that look for signs of disease spread among wildlife, livestock and humans.

The problem is, if we don’t know the source, not only do humans remain at risk but local wildlife can also suffer needlessly via retaliations against perceived wildlife culprits, like the bat-killing sprees in the aftermath of Covid-19: in Cuba, people set fire to roosts; in Rwanda, government workers aimed water cannon at bats; and in many other countries bat roosts were attacked and destroyed.

This kind of action will achieve nothing for human health if the species is unrelated to the pathogen’s transmission, and disturbing or culling wildlife populations can unintentionally exacerbate disease spread, whether it’s Marburg virus, rabies or bovine tuberculosis. And if habitat destruction is the driver of recurrent Ebola virus outbreaks, Bundibugyo or otherwise, we ought to get smarter at answering these questions.

These links between humans, wildlife and environment are cruxes of the so-called “one health” approach, explicitly recognising the connections and how that might affect the health of all three components.

The interwoven implication is that optimising health for one element can simultaneously boost health in another. It’s not a concept that is limited to Bundibugyo. It can be locally applied anywhere: chicken farms and wild swimming in the Wye or bovine tuberculosis in badgers and cows. The burning question is whether this outbreak might provide the incentive to act to try to prevent future epidemics.

Dan Salkeld is a disease ecologist and the author of Emerging Zoonotic and Wildlife Pathogens