How Many Tasmanian Devils Are Left in the World?

Roughly 16,900 Tasmanian devils remain in the wild, down from a peak of about 53,000 in the mid-1990s. That collapse, driven almost entirely by a contagious facial cancer, has made the species one of the most closely monitored conservation cases on Earth. Adding to the wild count, an insurance population of over 700 captive and semi-wild devils exists as a genetic safety net, but the wild population is the one that matters most for the species’ long-term survival.

The Scale of the Decline

The numbers are stark. A 2022 analysis using 25 years of trapping and survey data estimated that the wild devil population peaked at around 53,000 in 1996, which was itself less than half of earlier guesses. By 2020, a contagious cancer called devil facial tumour disease (DFTD) had spread across more than 90 percent of the species’ range and caused local population crashes averaging 82 percent. The total wild population had fallen to roughly 16,900.¹

The disease was first noticed in the mid-1990s in northeastern Tasmania. Within a decade it had been confirmed at dozens of sites covering over half of mainland Tasmania, and at some trapping locations more than 80 percent of trapped adults showed facial tumours. Spotlighting surveys in the region where DFTD first appeared recorded an 80 percent drop in sightings between the early 1990s and the early 2000s.² The disease spread fastest through areas where devils were densely packed, then slowed as it reached lower-density regions in the west and southwest of the island.¹

A Cancer You Can Catch

DFTD is not a virus or a bacterium. It is a transmissible cancer, one of only a handful known in the natural world. The tumour cells themselves are the infectious agent: living cancer cells pass from one devil to another when they bite each other, which happens frequently during mating season and fights over food.³ Once transferred, the foreign cells grow into large, disfiguring masses around the face and mouth. These tumours eventually make it impossible for the animal to eat, and most infected devils die within six to twelve months of the tumours becoming visible.

The original cancer lineage, now called DFT1, traces back to a single female devil. Every DFT1 tumour in every infected devil is a clone of that one animal’s Schwann cells, the type of cell that normally insulates nerves. In 2015, researchers discovered something alarming: a second, independently arisen transmissible cancer, DFT2, in five devils in southern Tasmania. DFT2 causes facial tumours that look almost identical to DFT1 but are genetically distinct and carry a Y chromosome, meaning they originated from a male devil.⁴ The fact that a single species spawned two separate transmissible cancer lineages was unprecedented and raised concerns that something about devil biology makes them unusually prone to this phenomenon.

Part of the answer lies in how DFT2 evades the immune system. Unlike DFT1, which shuts down the surface markers that would normally flag a cell as foreign, DFT2 cells actually display those markers. The catch is that the particular versions of these molecules expressed by DFT2 happen to be very common among Tasmanian devils, so the host’s immune system does not recognize the tumour cells as foreign.⁵ It is a different trick from DFT1’s approach, but the result is the same: the cancer slips past immune defenses.

Why Devils Are So Genetically Vulnerable

Tasmanian devils have strikingly low genetic diversity, and that vulnerability is not a recent development. Analysis of museum specimens dating back to the mid-1800s and even older subfossil material shows that the immune system genes most critical for recognizing foreign tissue were already remarkably uniform well before European settlement. Researchers concluded that this low diversity has been a feature of devil populations since at least the mid-Holocene, thousands of years ago, and may explain why the species has weathered repeated population crashes throughout its history.⁶

When a population’s immune genes are very similar across individuals, transplanted tissue is less likely to trigger a rejection response. That is precisely the problem with DFTD: the cancer cells can graft onto a new host because, immunologically speaking, devils are too alike. The only other well-studied naturally occurring transmissible cancer, a venereal tumour in dogs, has persisted for thousands of years using similar immune-evasion strategies, though it and DFTD evolved completely independently.⁷

Signs That Devils Are Fighting Back

For years the prognosis looked grim: DFTD appeared to be universally fatal, with essentially no immune response detected in infected animals. But over the past decade, researchers have found encouraging evidence that both individual devils and populations as a whole are beginning to push back against the disease.

Some wild devils have been documented with tumours that spontaneously shrank and disappeared, a phenomenon called tumour regression. Whole-genome analysis of these animals identified several genomic regions associated with immune response and cancer resistance that were consistently different in the devils whose tumours regressed compared to those whose tumours grew unchecked. The variation appears to be regulatory rather than structural, meaning the same genes are present in most devils but are expressed differently in the ones that fight off the cancer.⁸

Beyond these individual cases, broader evidence suggests that natural selection is reshaping devil populations in response to DFTD. Epidemiological modeling combined with genomic data points toward rapid evolutionary changes, and researchers have proposed that DFTD may gradually shift from being a catastrophic epidemic to something more like an endemic disease, still present but no longer causing the same scale of devastation. Both immunized devils in laboratory settings and some wild devils have demonstrated measurable immune responses to DFTD cells, something that was barely detectable in earlier years of the epidemic.⁹

The Insurance Population

Recognizing that wild populations could collapse entirely, the Tasmanian government and its partners established an insurance metapopulation in 2006. The program collected 120 founding individuals, predominantly from western Tasmania where DFTD had not yet arrived, and housed them across a network of zoos, wildlife parks, fenced reserves, and an island sanctuary. The population has since grown to over 700 devils representing at least 180 founders across this range of management settings.¹⁰

A major concern with any captive breeding program is whether the captive animals drift genetically from their wild counterparts, potentially losing adaptations they would need if released back into the wild. Genome-wide analysis comparing the insurance population to wild devils found that the captive devils retained representative levels of diversity, including at functionally important immune and reproductive genes and at the specific genetic regions thought to be associated with DFTD resistance. In other words, fears that captive-bred devils would be genetically “naive” compared to their wild relatives turned out to be unfounded.¹¹

Despite significant variation in how closely related individual captive devils were to each other, the population showed no detectable signs of inbreeding depression, the loss of fitness that sometimes plagues small captive populations.¹² This is good news for the program’s long-term viability and for any future release efforts.

Progress and Limits of Vaccination

If wild devils could be vaccinated before they encounter DFTD, the disease’s spread might slow enough for populations to stabilize. Two immunization trials tested this idea on cohorts of devils bound for wild release, using modified DFTD cells as the vaccine antigen. About 95 percent of the vaccinated devils developed antibodies against the tumour.¹³ That sounds like a success, but the reality in the field turned out to be more complicated.

In 2016, 33 vaccinated devils were released at a site in northern Tasmania where DFTD was already present. Over the following two and a half years, researchers managed to re-trap eight of those animals. Six of the eight had developed DFTD. The vaccine clearly had not prevented infection. But there were intriguing differences between the vaccinated and unvaccinated animals: antibodies persisted for up to two years after vaccination, and tumour biopsies from vaccinated devils showed infiltration by immune cells, something almost never seen in unvaccinated animals whose tumours are typically “immune deserts.” The vaccinated devils’ tumours also showed molecular markers associated with active anti-tumour immune responses.¹⁴

The current thinking is that vaccination can prime the devil immune system to recognize DFTD cells, but that priming alone is not enough. Additional immune manipulation, perhaps booster doses or immunotherapy after tumour development, may be needed to tip the balance toward tumour regression. Lab experiments in captive devils have shown that a combination of vaccination followed by immunotherapy after tumour growth can trigger complete regression, so the pathway exists. But scaling that approach to wild animals spread across Tasmania’s rugged landscape is a formidable challenge. Researchers also observed that under immune pressure, DFT1 cells can shift their identity, adopting different molecular profiles that may help them evade the immune response.¹⁵ The cancer, in other words, is a moving target.

Ecological Consequences of Losing Devils

Devils are the largest surviving marsupial carnivore, and their decline has rippled through Tasmania’s ecosystems in measurable ways. As devil numbers fell in DFTD-affected areas, feral cat populations increased. Research found that cat occurrence was significantly and negatively associated with devil presence: where devils vanished, cats moved in. At the same time, the eastern quoll, a much smaller marsupial predator, declined rapidly after DFTD arrived in its habitat, apparently because it had lost the indirect protection that devils had provided by keeping larger predators in check.¹⁶

The relationship is not entirely straightforward. Some researchers have cautioned that the evidence for direct competitive suppression between devils, cats, and quolls is still limited and somewhat mixed.¹⁷ But the overall pattern, bigger predator declines and smaller predator increases, fits what ecologists predict when a top predator is removed from a system. The practical result is that saving devils is not just about saving one species. Their presence shapes the behavior and abundance of other animals across Tasmania.

The Trade-offs of Translocating Devils

One strategy for protecting devils has been to establish populations on DFTD-free islands and in fenced reserves. Maria Island, off Tasmania’s east coast, received a founding group of devils as part of this effort. The results were a conservation lesson in unintended consequences. Devil activity on the island did suppress feral cats and brush-tail possums, which was welcome. But the devils themselves turned out to be even harder on nesting short-tailed shearwaters than the predators they displaced. Being larger and able to dig, devils raided shearwater burrows so effectively that colony occupancy at monitored sites dropped to zero within four years of the devil introduction.¹⁸

Maria Island illustrates a tension that runs through devil conservation. The animals need safe refuges free from DFTD, but placing a powerful predator into a small, closed ecosystem can devastate species that never evolved alongside it at such high densities. Every translocation site requires careful assessment of what else lives there and how a new apex predator will reshape the food web.

Why Devils Disappeared from Mainland Australia

Tasmanian devils once lived across the Australian mainland, but they vanished there around 3,000 years ago, long before European contact. The question of what caused this extinction has been debated for decades. Climate change was an obvious candidate, but modeling work has found that environmental conditions on the mainland did not become unsuitable for devils during the mid-Holocene. Instead, the most likely explanations involve changes in the human population, including the intensification of Aboriginal land management, or competition from the dingo, which arrived in Australia around 3,500 years ago and never reached Tasmania.¹⁹

Tasmania’s isolation from the mainland may have both saved and doomed the modern devil. It saved the species by keeping dingoes out, allowing devils to persist as the island’s top marsupial predator. But island life also meant a smaller gene pool, the very factor that left devils unable to reject a foreign cancer. Their low immune diversity, documented in specimens spanning centuries, appears to be a deep feature of their biology rather than something DFTD itself caused.⁶ The species has survived bottlenecks before, and some researchers view DFTD as the latest in a long series of crises that this genetically constrained population has weathered. Whether it can weather this one depends largely on the interplay between evolving host resistance, conservation management, and whether the disease continues to burn through the remaining pockets of uninfected devils faster than natural selection can catch up.