"It's a bit frightening," says Dr Daniel O'Brien, an infectious diseases specialist at Barwon Health in Geelong who has treated perhaps 700 Buruli victims. "Each year has been getting worse, and there's no reason to think this year won't be worse again. I'd be flabbergasted if it's not." McLachlan's ulcer was the size of a saucer. Credit:Courtesy of David McLachlan The insidious little invader is seemingly on the move, too. At the turn of the millennium, cases were confined mostly to the Bellarine Peninsula (the western side of the bay below Melbourne). But more recently they have died down there and leapt – no one knows exactly how or why – across Port Phillip Heads to the Mornington Peninsula on the eastern side. McLachlan was almost certainly exposed to the bacteria there, at his beach house in Blairgowrie, the centre of an "endemic region" that is – alarmingly – expanding. Cases have begun popping up in nearby Rosebud, Rye and Frankston, and seem to be creeping – no, marching – toward the inner suburbs of bayside Melbourne. The bug rarely moves far inland and, aside from one ulcer that turned up in Eden on its south coast, hasn't yet threatened NSW. But if it takes hold in a densely populated area like Victoria's capital, a localised outbreak could become a public health calamity. There was once a question of attribution: did Melburnians simply get it on holiday in Tootgarook? However, that no longer explains the epidemiology, says Professor Tim Stinear, a microbiologist and leading Buruli expert. Too many cases are clustering by postcode, or even by street, for them to be down to chance anymore.

"That's definitely happening in Beaumaris. Definitely happening in Black Rock. And definitely happening in Sandringham," says Stinear. "We're hitting a threshold." The ulcer does not end in death (except in rare, untreated cases) but does cause suffering and disfigurement. McLachlan's benign blemish from July 2018, for instance, soon became a degraded lesion the size of a saucer, eating through the skin down to his Achilles tendon. He found himself in hospital for surgical debridements – removal of manky flesh on the rim of the wound – and then skin grafts, surrendering healthy strips of thigh meat to patch the problem. He wore a vacuum dressing – a drainage device carried in a bag the size of a football – which "sucks out all the goobies". Heavy painkillers led to disturbing ketamine nightmares. He took powerful antibiotics, which affect mood and sense of taste, and make your sweat turn yellow and your tears turn orange. He asked, naturally, how the infection is caught and spread, but there are few definitive answers. Once, in desperation, he asked a more plaintive question: "Can I get my foot amputated?" McLachlan was advised against it, but others have had no choice but to shed infected limbs. "I really thought they would need to cut off the leg below the knee," he says now, sighing. "It's reduced me to tears a couple of times. I had a couple of breakdowns. That's what it does." Microbiologist Tim Stinear (at left) and Buruli bug PhD student Andrew Buultjens collecting possum poo. Credit:Simon Schluter

I meet Tim Stinear at the Peter Doherty Institute for Infection and Immunity, a facility in Melbourne where bespectacled lab coat wearers carry eskies filled with you-don't-wanna-know what. Stinear takes me through his laboratory, pointing out the high contamination room where they keep "the nastiest of the nasties". He explains how the ulcer works, in a story punctuated by phrases such as "We don't know why" and "We really don't know the answer". "Some of this is a guesstimate," he begins. Essentially, the bacteria is inoculated beneath the skin (we'll discuss how later), and a few cells reside there, under the surface. Our bodies are challenged with bacteria all the time, and usually the immune system is good at hunting them out, but this bacteria is coated in a lipid – a compound called mycolactone – which acts as a kind of invisibility cloak. Sitting snug, keeping shtum, the micro-organism feasts on our delicious subcutaneous tissue, quietly making more of its immunosuppressive toxin. Oh, the toxin has analgesic qualities, too, completely numbing what should be an incredibly painful, festering wound. In the lexicon of science, it's a sneaky little bastard. By the time the skin surface breaks down in the centre, collapsing to reveal itself as an ulcer – between two to nine months after inoculation – you've already got extensive necrosis (death) of the fat cells, and curling skin at the sides of the crater, forming what's called an undermined edge. An organised immune response kicks in – too little, too late – and people go see a specialist, often someone like Buruli guru Dr Paul Johnson of Austin Health in Melbourne. David McLachlan. Credit:Simon Schluter I listen to Johnson at the Alfred Hospital on a busy Friday morning, as he gives what's called a "grand round": a medical presentation to staff, this one titled, "The Flesh Eating Bug on the Mornington Peninsula". "It's a geographically restricted infection," Johnson tells the audience of 40-odd doctors and nurses, "which means – to paraphrase Bob Marley – 'No visit, no cry'. You cannot get it sitting here. You cannot get it person-to-person. But if you move a few kilometres into an area where it's prevalent, you can get it very quickly." He shows a confronting photo of a volcanic sore. The room gasps. "This is the elbow of a guy who went to Ocean Grove on Mother's Day, with his girlfriend, under sufferance – so he knows exactly when he was there." The room giggles. "He was in an endemic area for four hours, and presented seven months later with this."

Johnson believes the most common and likely mode of transmission is the mosquito. But the animal that concerns him more is the humble ringtail possum. This is based on a discovery made shortly after an outbreak in Point Lonsdale on the Bellarine Peninsula around 2002. While sampling bark and leaves, soil and bugs, Johnson tested a pellet of possum poo for the bacteria. "And we got a signal that was 10,000 times stronger than anything we'd ever detected in the environment before." They went spotlighting next, and began seeing possums with ulcers on their face, tails and feet, surrounded by clouds of mosquitoes. Professionals trapped 42 possums, luring them into cages with apples coated in peanut butter, before taking them to a nearby house for testing. A quarter had the disease. "Then they were returned to the trees to tell their relatives they'd been abducted by aliens and anally probed," Johnson tells his tittering audience. "I told that joke at a meeting in the US, and it didn't go so well." This brings him to his "grand unifying theory" of what's happening in Victoria. It's called a "zoonosis" – an infection in animals that spreads to humans. Basically, the possum acts as a reservoir for the bacteria. Possums are caecotrophs, meaning they feed faecal matter to their young, thereby spreading it from generation to generation. They also drop huge volumes of excreta, contaminating the environment. The bacteria can end up in humans when mosquitoes – the "vector" – feed from open possum ulcers (or perhaps spawn in water tainted with possum scat), then bite us. Which is why I find myself a few mornings later on a bicycle alongside Stinear and Johnson in the bayside suburb of Sandringham, scanning sunny parkland for possum shit. "It's funny," Johnson says, peering at the base of a tree, "but once you know what you're looking for, you begin seeing possum poo everywhere. It's like speaking another language – you can't say a word at first and then suddenly you're fluent." He's right. After 30 seconds of looking – ignoring an empty Coke can and a used condom – I spy a few pellets of poop, help "bag and tag" the sample, then we pedal to another site according to a strict GPS grid they've used to create what I'm calling their crap map. The crew has already taken and tested 1076 samples from the Mornington Peninsula, and found Mycobacterium ulcerans in about 20 per cent. "We are trying to build this picture: here's where the possums are carrying the bacteria and here's where people are getting the disease, and asking, 'Do those things overlap?' " says Stinear, the lead investigator. "And data to date shows that they do."

Possums would be an ideal way to spread the disease. They're everywhere, for starters. They're territorial, but offspring colonise new areas. People relocate them, too. It's rumoured the disease jumped peninsulas when someone smuggled possums across the heads on the Queenscliff-Sorrento ferry, in a car boot. It's not so far-fetched. One of McLachlan's neighbours in Blairgowrie had an ulcer, and told him he had "dealt with the problem". The neighbour had trapped around 30 possums over a matter of months – even though it's illegal to kill or move the native marsupial – and dropped them off elsewhere. (Note to Red Hill residents: avoid your local wildlife.) It's a compelling story – but not everyone buys the narrative. The most notable sceptic is Barwon Health's Daniel O'Brien, who suspects there is much more going on than a neat triangle between mosquitoes, possums and people. Stinear describes the schism: "Dan's quick to say we don't know anything, which is infuriating because it's not true, and a bit alarmist. But even though we disagree with Dan, we publish together. He's like a rogue family member." I've had families where more than one kid has got the disease, who moved out of the area. Or families who won't let their grandkids come down here to see nanna. O'Brien makes time for me on the 7am ferry to Sorrento, where he's headed to conduct a one-day Buruli clinic. It's dark and rainy outside, making our voyage into an infectious disease hotspot more foreboding. "I want to be able to look you in the eye and say, 'When you come over here today to Sorrento, you're not going to catch the disease,' " he tells me. "But I can't do that, because we don't know." O'Brien started treating people in Sorrento perhaps five years ago, because a GP friend began seeing more and more cases.

"As a specialist in my field, prior to this outbreak if you saw five cases in your lifetime it would be amazing. And I'm seeing 150 cases in a year. Probably more than anyone in the world." The global epidemiology is shrinking. Cases in Africa are often gruesome (because health services are under-resourced; because patients rely on traditional healers; because they hide ulcers through stigma and shame), yet their case numbers have dropped by half in five years. In Buruli County, Uganda, it disappeared decades ago – people can't even remember the ulcer. Meanwhile in Victoria, cases leap by about 40 per cent every year. "We're going in opposite directions," O'Brien says. "And nobody knows why." Another unknown: why does one victim end up with a sore the size of a five-cent piece, which heals after eight weeks of medication, and another suffers a veritable mutilation requiring 15 surgeries over two years? The proportion of severe local cases seems to have doubled in the past few years, too, leaving elderly sufferers unable to walk, and teenagers stigmatised and isolated. The disease can't pass between people but "contagion fear" remains rife anyway. "There's real trauma here, and worry," O'Brien says. "I've had families where more than one kid has got the disease, who moved out of the area. Or families who won't let their grandkids come down here to see nanna. And fair enough." The mosquito and possum story is our best guess at what's happening, he says, but it doesn't explain everything. Toddlers are always getting bitten by mosquitoes, for example, yet very few get ulcers. And a disproportionate number of people who work with soil – gardeners, tradies, landscapers – end up with the bug.

"Let me just show you something," O'Brien says, pointing out the ferry window as we pass by the clifftop mansions and beach boxes of Portsea, one of the wealthiest postcodes in Australia. "Have a look at this beautiful coastal area. We don't get cases here. And yet by the time we get to the [Sorrento] pier," he says, pointing barely a kilometre away, "we get a multitude of cases. So what's the difference?" He thinks it's something to do with soil type (some research suggests the microorganism might enjoy the pH and salinity of a sandy gravel mix), but it could also be vegetation, topography, water tables, birds, urban development, insects and population density. It's a complex situation, a classic "one-health" scenario. (That's a scientific buzzword for thinking about human, animal and environmental health as inextricably linked.) "My gut feeling would be that it's in the soil in many parts of the world, but you need something to bring it out and amplify it," O'Brien says. "And then it gets out of control. But it's pure theory." Infectious diseases expert Daniel O’Brien. Credit:Simon Schluter Some history here. Before it was called the Buruli ulcer it was actually the "Bairnsdale ulcer", named for the small town in eastern Victoria where it first turned up, in about 1940. "Patient Zero" was believed to be a 15-year-old girl, a domestic helper who was working for a local solicitor and developed a lesion after scratching her leg during a fall down the office stairs. Her ulcer was cut out and sent to the Alfred Hospital, where it became Mycobacterium ulcerans – recognised and cultivated by the legendary oncologist Peter MacCallum, and others, who published a seminal 1948 paper, A New Mycobacterial Infection in Man.

Dr John Hayman, 85, was at the time an awed trainee there, before being sent to work as a pathologist in Bairnsdale in 1965. "And blow me down, there were still these ulcers occurring. I remember looking at it under a microscope and thinking, 'Whoopee!' " he says, tucking into a hot-cross bun at his home in Kew. "Pathologists are queer people. If we find something unusual, we get really excited." Hayman eventually devoted his career to the pathogen. He interviewed almost every victim from the region, learning how they developed their ulcer after being cut in the cattle yards, or hit on the shin with a hockey stick, or scratched on a barbed-wire farm fence. The only patient he didn't meet was a two-year-old boy, who died after being transferred to hospital in Melbourne in 1940, an ulcer consuming two-thirds of his little leg. Hayman did his doctoral thesis on the ulcer, travelled the world tracking outbreaks, and spoke at medical conventions in Geneva (as Stinear, Johnson and O'Brien have all done). He owns what he believes is the world's largest collection of glass slide samples of the lesion. He points out that it's also been known as the Daintree ulcer, because of a case cluster near the Mossman post shop in far north Queensland (there have also been outbreaks in Rockhampton, Beerwah and the Tiwi Islands). It's been found in Sumatra, Malaysia, Cameroon, Mexico, Bolivia, Brazil and French Guiana. Says Hayman: "I had this wonderful theory – now proved wrong – that it was of Gondwanan origin, from 150 million years ago, and that was the reason it was in Africa and Australia. I actually got a paper in The Lancet out of that, but I was wrong." (Stinear proved it originated from other mycobacteria about 60,000 years ago.) "My current theory – which is totally evidence-free – is that it's spread by migrating birds." Possums, he agrees, may well play a role. Koalas have been infected before, as well as a potoroo, and a bandicoot found in far north Queensland. In colonial-era Belgian Congo, bats were the suspected carrier. Perhaps more importantly, the ulcer often goes hand-in-hand with significant environmental disturbances. In Buruli the disease appeared after flooding of the Nile River. In Papua New Guinea it turned up after Mount Lamington erupted, and was also known as "Sik-Beloya-Sepik" – an infection along the overflowing Sepik River. In Bairnsdale, it arrived after the Mitchell River burst its banks – a major event that killed livestock and washed bodies from the cemetery, carrying coffins out to sea. A 1990s outbreak in Langwarrin happened downstream from an illegal sand mining operation. In Phillip Island, it occurred near a golf course using treated effluent water. But what about the Mornington and Bellarine peninsulas? Hayman laughs – no disturbances there. I've seen this same perverse smile in every Buruli expert. They seem to derive pleasure from watching new people meet the same deductive dead-ends they've been running down their entire career. He believes the bacteria lurks in soil, until stagnant water with a high nutrition value helps it proliferate. Within that water, decaying vegetable matter gives rise to microscopic droplets that reach the surface and become a micro-aerosol, which is blown on the wind, and into our lives. "But," he adds, grinning, "it's just a theory."

One reason there are so many unproven theories is that the disease hasn't been adequately studied – until now. It's classified by the World Health Organisation as a "neglected disease", not thoroughly examined because it usually doesn't threaten life, and outbreaks are often contained, or confined to Third World countries. But an epidemic in a Western nation – specifically well-heeled holiday villages and middle-class metro suburbs – has turned heads. It simply wouldn't do for the bacteria to pick up a new moniker (although I do think "Sorrento sore" or "Beaumaris bursa" would be pretty catchy), and so there is a huge joint research program under way, with about $3 million of funding from the federal National Health and Medical Research Council and the state Department of Health and Human Services (DHHS), in conjunction with the Doherty Institute, Barwon Health, the Austin Hospital and the CSIRO. The crap map project is one part. Another is a surveillance study capturing mosquitoes and testing them through the AgriBio facility at La Trobe University. (Early results suggest 2 per cent of mozzies on the Mornington Peninsula are carrying the bacteria. Says Stinear: "In vector ecology terms, 2 per cent is very high.") There's an intervention program coming, too. In October, the Mornington Peninsula will be divided into blocks, and half will be subject to "fogging" with a synthetic pyrethroid (industrial Mortein, misted from the back of a truck), plus residual spraying (which settles on vegetation and can kill mozzies for weeks), and also larviciding (dropping methoprene blocks into waterways to prevent breeding). The question the intervention poses is a public health one: can an intensive mosquito control program reduce human disease? Johnson accepts the idea that contaminated dirt could get into a cut, or that possum pee might splash a rose thorn that then pricks the skin. "But if you think there's 500 different ways of getting it, there's not much you can do. However, if there's one main way of getting it, then there is something you can do." O'Brien is happy, too, because there's also a larger backstop "case-control" study. That's explained to me by a scientist named Kim Blasdell, in a concrete bunker at the Australian Animal Health Laboratory of the CSIRO in Geelong, the kind of workplace where loudspeakers scream warnings about lockdowns for liquid nitrogen refilling. That study, Blasdell says, looks at all the risk factors in play, by contacting people in endemic areas who have the ulcer, plus control households, to ask questions and visit homes. They look at what people wear, their work, hobbies, vaccination history, whether they use insect repellent or gardening gloves, and whether they've had any major earthworks done. During the field visit, they gather samples of dirt, leaves, prickles, plus stagnant water in gutters or birdbaths. They pick up scat pellets and catch bugs with sticky traps. "It's kind of a needle-haystack situation," Blasdell says. "We're recording a lot of data." Epidemiologists mightn't be able to synthesise all the information for a few years yet, but Dr Brett Sutton, Victoria's Chief Health Officer, takes a beaker-half-full perspective. "We've got a golden opportunity to take a closer look, and we've got to take it. We owe it to the global community."

With the ulcer being a "notifiable disease" (like measles, mumps, Ebola and HIV), GPs and laboratories that come across the bacteria must immediately notify DHHS, which can communicate the risk. They've rolled out a "beat the bite" campaign with a list of helpful hints: 1. Cover up by wearing long sleeves, long pants and gloves when gardening.

2. Avoid insect bites – especially mosquitoes or March flies – and clean and cover any cuts or wounds immediately.

3. Any suspicious blemish, lump or lesion should be checked out by a doctor – and always ask, "Could this be a Buruli ulcer?" There's also a learning module to help doctors diagnose and manage the infection. "Our stance is, 'If you see an ulcer, think Buruli ulcer,' " Sutton says. "Clearly you don't get 100 per cent coverage, but I think we're doing well in places where it's common." Not well enough, however, for David Jones, a 47-year-old plumber from Rye. Taking a break for a coffee in Sorrento, he shows me his elbow, where an ulcer the size of a 50-cent piece is almost healed, 12 months after he first saw it. "As soon as I looked in the mirror, I've gone, 'That's Buruli – that's the ulcer', because my partner had one four years ago." Jones saw a doctor immediately, and said he thought it was Buruli, but the doctor said it wasn't, and gave him a course of mild antibiotics, without swabbing the wound to check. A week passed and it got worse, so the doctor gave him another antibiotic and a steroid. It got bigger, and angrier, so Jones went to another doctor, and was referred to hospital. They prescribed medication, which took three weeks to arrive, in the wrong dose. It was six weeks before he was being properly treated. "People just don't know enough about it," he says, shaking his head. His dismay is fair. If a doctor in a place like Rye, one of the world's biggest Buruli hotspots, can't identify the ulcer or at least suspect enough to do a biopsy, what chance does anyone else have? "I was dirty as – bloody filthy. It was a f…ing joke."