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https://www.theatlantic.com/health/archive/2020/07/flesh-eating-bacteria-are-spreading/613762/
Australia Has a Flesh-Eating-Bacteria Problem

In the beach towns south of Melbourne, everyone, it seems, knows someone
who’s been attacked.
[image: Illustration]
Melanie Lambrick
- Story by Brendan Borrell
<https://www.theatlantic.com/author/brendan-borrell/>
- July 3, 2020
-
Health <https://www.theatlantic.com/health/>
-
About a week after Steven Mikac began taking antibiotics for the strange
spot on his leg, the flesh around his ankle started to tighten and swell.
The moist orifice of a wound opened up and took the form of a small bullet
hole. A plug of tissue had gone missing—dissolved into pus and slime.
Walking was excruciating. Working, unbearable. In early October of last
year, Mikac showed his ankle to a colleague at the hospital where he works
in Melbourne, in the Australian state of Victoria. She suggested that it
might be Buruli ulcer—a disease caused by a strain of flesh-eating bacteria.

Though Mikac had seen local television reports about an outbreak of this
tropical disease in Victoria, it sounded so freakish, so unlikely, that he
hardly considered it a possibility. But like hundreds of Australians before
him, he was about to become all too familiar with Buruli, a slow-moving
horror show that has proved, in many ways, even more baffling to
infectious-disease researchers than the novel coronavirus. After decades of
research, scientists still aren’t certain who, or what, is spreading this
strange malady around the world.

In late October, Mikac met me inside the infectious-disease ward at the
hospital where he works and is now a patient. He is a soft-spoken man of 54
with the body of an aging rugby player. He was dressed in shorts and
flip-flops. A bandage had been slapped on his left ankle. “It was just a
little spot, but I felt there was something different about it,” he said.

We were soon called into an exam room where Mikac’s white-haired,
bespectacled doctor, Paul Johnson
<https://www.austin.org.au/infectious_diseases/staff/pjohnson>, greeted us.
Johnson has been studying Buruli cases in Australia for decades, and he
sees every new case as a chance to crack the disease’s enigma. A few weeks
earlier, Mikac had divulged to Johnson one telling clue. His parents own a
beach house in the town of Rye, on the Mornington Peninsula south of
Melbourne. He had recently helped them out by doing brushwork on the
property, and had likely returned to the city with the usual scratches and
mosquito bites.

Johnson’s ears had perked up at that. Mikac had been inside a Buruli hot
spot, a place where caseloads were far higher than in surrounding areas,
and Mikac had been doing the kinds of outdoor activities that notch up a
person’s risk. Johnson confirmed Mikac’s diagnosis with a DNA test. The
process is more traumatic than one might expect: He had to plunge a cotton
swab into the maw of Mikac’s open wound and scrape out the gunk inside as
Mikac cringed in pain. Johnson put Mikac on two powerful antibiotics,
clarithromycin and rifampicin, which turned Mikac’s urine the color of
orange Fanta.

Two weeks into the eight-week course of antibiotics, Johnson was now
checking on Mikac, his fourth Buruli case of the day. Mikac lay on his side
on the exam table as a nurse removed the bandage. “Do you feel like it’s
getting worse, better, or the same?” Johnson asked him.

“Worse,” Mikac groaned.

“What you’ve got—the infection is that big,” Johnson said as he sketched a
circle around the wound, like the flanks of a small volcano. “But it’s
going to get bigger.” He warned Mikac that the antibiotics had shut down
Buruli’s defenses, and now the body would launch an attack on the infected
tissue. The pus was building up under the skin, and it was about to blow.
“Once it breaks through,” he said, “it will feel a lot better.”

Buruli gets its name from a former county in Uganda on the western bank of
the Victoria Nile, which emerges from Lake Victoria and flows north toward
Sudan. Apart from their shared British imperial history, the two Victorias
have little in common. Uganda is steamy and tropical, sitting squarely on
the equator; the temperate state of Victoria, in southern Australia, lies
1,000 miles south of the Tropic of Capricorn. Buruli is said to be a
disease of poverty
<https://www.tandfonline.com/doi/abs/10.1080/00291950802335855?journalCode=sgeo20>,
springing from swamps and river basins, but southern Victoria is Pinot Noir
country, perched on the precipice of drought.

Since Buruli’s formal description in the mid-20th century, medicine has
paid relatively little attention to a condition that, however cruel,
primarily afflicts Africa’s poorest residents. Untreated, the pathogen
slowly worms its way under the flesh before breaking through the surface,
maiming and disfiguring its victims. Their necrotic limbs reek of rot.
Although they rarely die of the disease, they are sometimes ostracized in
their villages, left jobless and destitute.

Read: America’s never-ending battle against flesh-eating worms
<https://www.theatlantic.com/science/archive/2020/05/flesh-eating-worms-disease-containment-america-panama/611026/>

Australia has had occasional Buruli cases dating back to the 1930s, but
health authorities noticed an uptick in 2017, when more than 100 people
contracted the disease <https://wwwnc.cdc.gov/eid/article/24/11/17-1593-f3>.
The following year, 340 Australians were diagnosed with Buruli, and one of
them was a 13-year-old girl named Ella Crofts. After three major operations
on her knee, she posted a petition
<https://www.change.org/p/greg-hunt-mp-fight-tropical-third-world-disease-that-s-rampant-on-mornington-peninsula>
demanding that the government fight the “tropical third-world disease
that’s rampant” on the Mornington Peninsula. “If we, a wealthy country,
could research this disease we might save countless people from
disfigurement and disability,” she wrote alongside photos of her weeping
wounds. Her petition gathered more than 16,000 signatures and the
government listened, devoting $1.1 million to prevention and research over
two years.

Late last year, I booked a couple of nights in an Airbnb on the Mornington
Peninsula and drove south from Melbourne to the workaday town of Rye and on
through the exclusive communities of Blairgowrie, Sorrento, and Portsea,
places where the seaside estates have names such as Cliff Crest and
Westbank. Wherever I went, everyone, regardless of their social standing,
seemed to know someone who’d had an ulcer. No one was immune from the
disease, and everyone had an opinion on it—whether it was something they’d
read in the newspaper or a rumor they’d heard from a friend or just an idea
they’d come up with over a pint of Victoria Bitter.

When I stopped into a pub in Sorrento, a bartender named Hannah Smeeton
served me a beer and showed me the circular scar on her ankle. She then
introduced me to her boss, who also happened to have one. They both knew a
plumber in a nearby town who had nearly lost an arm. Smeeton has cut back
on her gardening and is wary of mosquitoes, which are both considered risk
factors
<https://www2.health.vic.gov.au/public-health/infectious-diseases/beating-buruli>.
“But you have got to live your life,” she said.

When I interviewed David Gill, then the mayor of Mornington Shire, he asked
his executive assistant to tell me about her partner’s ulcer, but he played
down the disease’s impact on the community. “Nothing will stop the tourists
from coming to Mornington,” he insisted with the kind of nonchalance we’ve
gotten used to hearing amid the coronavirus  pandemic: Things will keep
going the way they have been, because having it any other way is too
disruptive.

In a normal year, nearly 2 million visitors pack the shores of the
Mornington Peninsula during the four months of spring and summer. It’s
during this period, scientists say, that most Buruli infections in
Australia are contracted. The infections take anywhere from four weeks to
eight months to reveal themselves, meaning that cases peak during the
Australian winter
<https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0006757>
.

Around Victoria, Buruli ulcer is sometimes referred to as Bairnsdale ulcer,
after the farming community where the disease was first identified. It’s on
the coast a few hours east of the Mornington Peninsula, in the region that
was hit hard by wildfires late last year
<https://www.cbsnews.com/pictures/australia-fires-deadly-wildfire-photos-2019-2020/7/>.
Back in February 1940, according to medical records, a
two-and-a-half-year-old boy was brought to a local hospital, his leg
swollen from the knee to the ankle. The doctor, David George Alsop, made an
incision in an attempt to drain any infection under the skin. Over the next
five months, an ulcer gnawed away at the boy’s flesh, exposing the red
muscle of his leg. Alsop sent a sample off for microscopic analysis and
continued trying to treat the ulcer with antibiotics.

“The report came [back] to me in a manila envelope heavily endorsed in red
‘Personal—Strictly Confidential’ or words to that effect,” he later wrote.
Under a microscope, the samples were teeming with rod-shaped bacteria, but
the colored dyes used to make them stand out wouldn’t stick to the bacteria
using ordinary techniques. When the slides had been washed with an acid,
however, the bacteria appeared bright red against the blue background stain.

Read: How long will Australia be livable?
<https://www.theatlantic.com/science/archive/2020/01/only-way-confront-australias-wildfires/604546/>

This was significant: It meant that these bacteria were producing
specialized chemicals, known as mycolic acids, which make them hard to kill
and keep them from drying out in an environment. The bacteria that can do
this are known as mycobacteria*—*the culprits behind tuberculosis and
leprosy.

The boy was transferred to a hospital in Melbourne and ended up dying
suddenly from an undiagnosed abdominal condition, possibly a complication
from the ulcer. As more of the strange ulcers turned up on patients in
Bairnsdale, researchers at the University of Melbourne tried to grow
colonies of the bacteria on glass petri dishes inside incubators kept at
the temperature of the human body. When their first attempts failed, they
added different vitamins and human cells to the dishes, but nothing worked.
For years, the only consistent way they could keep this still-unnamed type
of mycobacteria alive was by injecting it into the body cavity of a rat and
then transferring it to another rat when that one died.

In one set of Petri dishes, however, the bacteria did grow for some odd
reason. The scientists eventually discovered that the incubator’s heater
wasn’t working properly. It all suddenly made sense: These bacteria,
christened *Mycobacterium ulcerans*, grew best at lower temperatures—just
over 91 degrees Fahrenheit, the temperature of our skin. Buruli is so
sensitive to temperature that it can be killed by wrapping heating pads
around a victim for several weeks.

Our skin is our armor: a millimeter-thick layer of cells that divides the
outside world from our insides. It is something we don’t think about—until
the moment it fails us. Until there is a tear. A gash. A puncture. A
conduit through which the microbial world without can enter the microbial
world within.

Kingsley Asiedu first encountered Buruli ulcer in the early 1990s, when he
was working at a Catholic hospital in a remote rural district of Ghana. “I
had never learned about it in medical school,” he says. Asiedu was
horrified to discover that approximately 20 percent of the people in the
district—Amansie West—had ulcers, the highest prevalence of the disease
anywhere. Seventy percent of the cases he encountered were in children.
Because many parents believed the disease was a result of witchcraft, they
would often take their children to traditional healers first, bringing them
to the hospital only when their cases became severe. By that point, Asiedu
says, “You don’t even know where to start the surgery and where to end.
There was very little we could do.” Infections often recurred, and
amputation was often the only solution.

Buruli is not a common disease: Just 25,919 cases have been recorded in 17
countries since 2010, according to the World Health Organization, but
experts say those numbers underestimate its toll in places such as Nigeria
and Papua New Guinea, where formal censuses have never been properly
conducted. Global funding for Buruli research is typically less than $3
million
<https://s3-ap-southeast-2.amazonaws.com/policy-cures-website-assets/app/uploads/2020/01/30100951/G-Finder-2019-report.pdf>
a year, about one-tenth of a percent
<https://www.ncbi.nlm.nih.gov/books/NBK62528/> of the total devoted to
combatting all neglected tropical diseases.

The British doctor Sir Albert Cook, whose handwritten records from Uganda,
dating back to 1897, likely contain the earliest known medical descriptions
of the ulcers, found that they often occurred after some minor trauma, such
as a scratch from a sharp stick. Later studies suggested that Africans were
mostly acquiring Buruli when they bathed or swam in lakes and rivers.
Researchers associated the outbreaks with dams, deforestation, and other
environmental changes.
[image: image.png]
Melanie Lambrick

Unlike tuberculosis or leprosy, Buruli ulcer doesn’t spread easily from
person to person. *Mycobacterium ulcerans* seems to be more like tetanus
bacteria—hardy microorganisms that can survive in the environment for long
periods of time until they find that passageway through the skin. This
makes sense because the bacteria evolved from an aquatic pathogen that
forms ulcers on fish and frogs (and occasionally on the fingers of pet-shop
owners <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3401166/>). But while
tetanus can be cultured from the environment, researchers in Africa were
unable to isolate *Mycobacterium ulcerans* directly from the soil, water,
or plants in areas where people were getting the disease.

In the mid-’90s, the number of Buruli-ulcer cases in Australia began to
climb. Paul Johnson, the doctor, heard that a couple of his neighbors on
Phillip Island, which is six miles east of the Mornington Peninsula and
connected to mainland Victoria by a 2,000-foot bridge, had developed the
condition. Johnson was intrigued. “I was a young infectious-disease doctor
looking for a project,” he told me. One of the things he noticed was that
all the cases seemed to occur near a golf course irrigated with recycled
water stored in an open reservoir.

Read: The bacteria lurking in American showerheads
<https://www.theatlantic.com/science/archive/2018/11/never-home-alone-mycobacteria-lurk-american-showers/576292/>

Johnson reached out to a microbiologist named Tim Stinear
<https://www.doherty.edu.au/people/associate-professor-tim-stinear>, who
was working for the state water-testing laboratory, developing techniques
to amplify and detect the DNA of pathogens such as giardia and
cryptosporidium. These pathogens are so rare in the environment that
collecting a sample of water and finding them under a microscope is
extremely unlikely. Nor is growing them in the lab easy. But if you know
the gene sequence of the pathogen you’re looking for, you can use an enzyme
to amplify that sequence if it is present in the sample. This process
produces millions of copies of the sequence, which scientists can then
detect.

Johnson wondered whether that technique could be used with *Mycobacteria
ulcerans*. Stinear honed in on a previously identified sequence of
DNA—IS2404—that occurred 213 times in the bacteria’s genome. Its frequency
made it easier to detect in environmental samples. The water supply at the
golf course tested positive. The dam was drained and the irrigation system
was reconfigured to prevent contamination. The epidemic seemed to vanish,
but questions remained.

“We don’t know what precisely led to the disappearance of the disease,”
Stinear says. A few years later, cases of the ulcer suddenly appeared 30
miles to the west at Point Lonsdale on the Bellarine Peninsula, just across
the bay from the Mornington Peninsula. There were a couple of golf courses
in the area, but their water supplies didn’t have the same obvious
problems. “At that point, we started thinking about something else,”
Johnson said.

One Tuesday afternoon, I pulled up to a neighborhood park in Rye, the town
where Mikac likely got infected, to meet Stinear, now with the University
of Melbourne. He was accompanied by a team of volunteers, including his
yoga-instructor daughter and her boyfriend, who were slopping on sunscreen
and donning Day-Glo vests that identified them as members of the Beating
Buruli in Victoria effort. Stinear wheeled two motor scooters out of the
back of a trailer. Each had a box on the back filled with empty ziplock
bags. As Stinear strapped on his helmet, he recalled the time a passerby
handed him a letter.

“I’m not a postie,” he said, using the Australian term for a mail carrier.

“Well, what are you, then?”

“I’m collecting possum poop—it’s a job, I suppose.”

Possum poop. This is where the Buruli puzzle takes a sharp turn: In the
early 2000s, when Stinear and Johnson were working at Point Lonsdale,
trying to hone in on the environmental source of the disease, they happened
to open a drain that was filled with dry bark, leaves, and copious amounts
of droppings. When they tested the droppings for *Mycobacterium ulcerans*,
the results came back positive. In 2008 and ’09, their colleague Janet Fyfe
at the Victorian Infectious Diseases Reference Laboratory trapped 42
ringtail possums in the area. Eleven of them had lesions eating away at
their feet, ears, tails, or faces. Five more were asymptomatic but had
*Mycobacteria
ulcerans* DNA in their feces. All told, nearly 40 percent of the population
was infected.

Koalas with ulcers had been seen near Bairnsdale, but ringtails have much
greater potential for contact with humans. As backyard denizens, they are
both beloved (for their giant eyes and gentle demeanor) and reviled (for
their tendency to nest in roof cavities and feast on rosebuds and dog
food). In northern Queensland—Australia’s rain-forest region—Buruli DNA has
turned up in the feces of bandicoots, rabbit-like marsupials. This ugly
disease is apparently being spread by the world’s most adorable mammals.
And because Australia’s native wildlife is strictly protected, culls are
out of the question.

Read: President Taft ate a lot of possums
<https://www.theatlantic.com/notes/2015/11/president-taft-ate-a-lot-of-possums/417873/>

We were working in a Buruli hot spot, and the plan was to collect the
pill-size droppings at 25-meter intervals. In the lab, the samples would be
crushed, liquefied, and analyzed for genetic traces of the disease, giving
the team a block-by-block map of the prevalence of the bacteria in the
environment. Once I knew what I was looking for, I started to see the
droppings everywhere, piled up at the bases of trees and telephone poles.

A poop map could one day function as an early-warning system for health
officials and residents, helping predict where and when Buruli ulcer might
break out. But that effort is hampered by questions about whether, and how,
the bacteria is spreading from possums to people. People might pick it up
while gardening in soil contaminated by droppings; they might scratch
themselves on a thorn coated with bacteria. Stinear and Johnson, however,
believe that mosquitoes are the main pathway, transferring Buruli from
possums to people. Approximately 1 percent of mosquitoes in hot spots
around Victoria test positive for the bacteria, and people who regularly
wear mosquito repellent are about half as likely to end up with ulcers as
those who don’t. The ulcers, when they do appear, seem to turn up on the
extremities, where people are likely to get mosquito bites: ankles, calves,
backs of elbows.

Stinear doesn’t think the bacteria are surviving and multiplying *inside*
mosquitoes, like the parasites that cause malaria do. Instead, he thinks
the mosquitoes are simply acting as dirty needles, picking up a few
bacteria cells from a possum and injecting them under humans’ skin, in a
process called mechanical transmission. Tularemia, or rabbit fever, is also
thought to be spread this way. In an experiment published in 2017 in *PLOS
Neglected Tropical Diseases*
<https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0005553>,
Stinear and Johnson collaborated with the American entomologist John Wallace
<https://www.millersville.edu/biology/faculty/j-wallace.php> to test that
theory. The researchers coated a mouse’s tail with *Mycobacterium ulcerans*
and allowed a mosquito to bite it. One-third of the time, an ulcer
developed.

With the latest Buruli outbreak, Stinear saw a chance to finally test this
link in the field by running an experimental mosquito-control program on
the Mornington Peninsula. “You’ve got the disease on your back
doorstep—that’s bad—but it’s also the opportunity to get strong evidence
about how we should act,” he says. Some areas would get sprayed, others
wouldn’t. He’d measure whether the number of Buruli infections went down.

When the government agreed to fund Stinear’s study, the pitchforks came
out. A bee-loving environmental activist, Simon Mulvaney, called it the
“Mornington Peninsula Insect Massacre.” He stood up at council meetings and
warned of cancer clusters, toxic agricultural produce, and economic
catastrophe. Mornington Peninsula’s “reputation will be tarnished as a
tourist destination,” he wrote in a petition
<https://www.change.org/p/greg-hunt-mornington-peninsula-insect-massacre?use_react=false>
that gathered more than 22,000 signatures. Maybe the tourists really would
stop coming. “We got a public response that wasn’t quite what we
anticipated,” Stinear told me diplomatically. The spraying program was
shelved.

As we’re so often seeing with COVID-19, science took a back seat to the
soapbox. Stinear’s team shifted strategies. They would count mosquitoes in
different areas to see whether there was a link between their numbers and
caseloads. They’d also try house-by-house interventions, telling some
people to dump out standing water where mosquitoes breed, but that would be
costly, and its effectiveness uncertain. For the most part, they’d be
looking for correlations, not testing causations. Whatever result they came
up with would have a whiff of scientific uncertainty about it.

After all these years, all these data, and all the people who had suffered,
Buruli was going to remain a mystery, but not for lack of trying. “We
always felt we had a chance to stop it,” Stinear said.

Lack of knowledge will always be the greatest obstacle to fighting
infectious disease. If you don’t have a robust testing program, who can say
for sure whether you caught that nasty cough at your choir practice or the
voting booth? If you don’t run an experiment, who can say for sure whether
spraying could have put an end to Buruli? Amid an outbreak, such scientific
uncertainty can erode trust of the public, opening the door to conspiracy
theories and to those actors who may seek to exploit it for their own ends.

With Buruli, the bottom line is that a single ulcer has never been
definitively tied to a mosquito bite. Who remembers a mosquito bite five
months later? Before we headed into the neighborhood to collect possum
poop, I asked Stinear whether I should put on insect repellent, but he
gestured at the blue sky and said it was too hot for mosquitoes. A few
minutes later, I felt an itch on my right wrist, and watched as a bite
began to swell on my skin. Stinear grinned. “Let me know if you develop an
ulcer there when you get back home,” he said.

Buruli’s most mysterious feature is that it doesn’t seem to have a single
mode of transmission. On the heels of Australia’s mosquito research, more
than 4,000 mosquitoes were screened
<https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0003941>
in the West African country of Benin. Not a single one tested positive for
the bacteria. No African mammals have been proven to carry the bacteria
either <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073983/>.

What has consistently tested positive in Africa? Giant water bugs. Up to
three inches long, these nightmarish insects are variously known as
toe-biters and alligator ticks. They are primarily predators of small
vertebrates and other insects, but if you happen to step on one of them,
they’ll jab you with their pointed rostrum, delivering an unforgettably
painful bite. It’s such a memorable—and uncommon—event that if giant water
bugs were the primary vector, locals would certainly know it.

When I first learned about the Buruli outbreak, what grabbed me about the
story was the idea that a disease of tropical Africa had spread to one of
the whitest, wealthiest parts of southern Australia. But Buruli ulcer, like
syphilis and smallpox, is probably a disease of colonization. The
Australian and African strains of the disease share a common origin in
Papua New Guinea, dating back at least 1,000 years. By sequencing samples
collected from Australian patients over the past 70 years, Stinear has
found that Buruli ulcer first arrived in Victoria around the time of the
first European settlement in 1803. In Africa, Buruli ulcer was likewise
relatively limited in its reach until European powers arrived. Amid the
violence and upheaval of that period, local people began to move more
widely, possibly spreading the disease from one river basin to another.

Read: A new way to keep mosquitos from biting
<https://www.theatlantic.com/science/archive/2019/02/how-to-stop-mosquito-bites/582190/>

If COVID-19 has shown us anything, it’s how quickly international travelers
can carry a disease from one side of the world to the other. Potential
treatments can travel quickly too, but that journey takes concerted action.
When I spoke with Asiedu, who now works at the WHO’s Department of Control
of Neglected Tropical Diseases, he told me that the new research in
Australia could be beneficial to Africans, even if they were not its
original focus. Thanks in part to Australian doctors’ experience with
antibiotic treatment regimes, and following a successful clinical trial in
Africa, the WHO will soon be recommending oral—rather than
injectable—antibiotics, reducing the need for hospital stays in both
Australia and Africa. Researchers at Australia’s Commonwealth Scientific
and Industrial Research Organization are also developing a new
environmental test for Buruli ulcer that is based on RNA, which breaks down
more rapidly in the environment than DNA. This makes it better suited for
identifying places where the bacteria is alive and being actively
transmitted.

The latest news from Australia is that just 30 cases of Buruli have been
reported in 2020, compared with reports of 50 or so by this time in recent
years. That could be good news, or it could just be a consequence of people
staying away from doctors’ offices because of  COVID-19. Stinear had to
temporarily halt his on-the-ground surveys in March because of the
coronavirus, adding Buruli to the list of diseases, such as tuberculosis
and polio, that may gain ground as a result of the pandemic
<https://www.latimes.com/world-nation/story/2020-04-15/coronavirus-could-erode-global-fight-against-other-diseases>.
With coronavirus cases on the rise again, Australia’s tourism minister has
recently announced that the country may shut its borders until 2021.

But cooped-up locals will still need an escape. Nothing, after all, can
keep the tourists away. And maybe they’re not entirely wrong to take that
risk: They’ll probably end up all right. Others aren’t so lucky. That’s
because this disease—like COVID-19, like so much else—will be tamed in
Australia long before the suffering ends in Africa. And the reason for that
is no mystery at all.
Brendan Borrell <https://www.theatlantic.com/author/brendan-borrell/> is a
Los Angeles–based writer. He is currently working on a book about the
coronavirus-vaccine race.