more_vert
A STEEP increase in Buruli ulcer cases in parts of Victoria has prompted experts to call for urgent funding for research to inform prevention measures.
Writing in the MJA, Associate Professor Daniel O’Brien, Deputy Director of Barwon Health’s Department of Infectious Diseases, and co-authors said that national governments needed to urgently commit to funding the research needed to stop Buruli ulcer, which is caused by Mycobacterium ulcerans.
“As a community, we are facing a rapidly worsening epidemic of a severe disease without knowing how to prevent it,” the authors wrote. “We therefore need an urgent response based on robust scientific knowledge acquired by a thorough and exhaustive examination of the environment, local fauna, human behaviour and characteristics, and the interactions between them.”
The authors wrote that in 2016, 182 new cases of Buruli ulcer were reported in Victoria, a higher number than ever previously reported by 72%. Case reports had continued to increase in 2017, with 236 reports to November, a 51% increase compared with the same period in 2016 (236 v 156 cases). Worldwide, around 2000 cases are reported per year.
This “worsening epidemic” of Buruli ulcer – also known in Australia as Bairnsdale or Daintree ulcer – is focused in Victoria’s Mornington and Bellarine peninsulas.
Buruli ulcer cases have also been frequently reported in a small area in Far North Queensland between Mossman and the Daintree River. Less frequently, cases have been reported on Queensland’s Capricorn Coast, in the Northern Territory, New South Wales and Western Australia.
Professor Paul Johnson, Director of Research at Austin Health, said that there was an “incredible paradox” in the epidemiology of this neglected tropical disease.
“Buruli is increasing rapidly in a [high income country] setting in a temperate area; while in West Africa, although it is more common in terms of absolute numbers, it seems to be declining,” he said. “It’s very interesting, and alarming for individual people who are exposed.”
Professor Johnson supported the position taken in the MJA article.
“We have quite a lot of new information and new leads to follow up, but still we don’t have answers to the fundamental questions of: why does it suddenly appear? why is it getting worse? and how do we stop it?” he said.
Professor Johnson said that research conducted by his group had shed light on the possible source and transmission of M. ulcerans.
“Our hypothesis, based on our published research cited in the MJA article, is that it’s an epidemic in possums, with humans as a spill-over host,” Professor Johnson said. “So, it’s moving through the possum population, which contaminates the environment, and humans are getting indirectly or directly infected, via mosquitoes or other biting insects.”
Professor Johnson said that while the reservoir and mode of transmission were not yet completely understood, people living in or visiting endemic areas could take practical prevention measures to avoid insect bites, and clean and cover cuts and abrasions sustained while working or playing outside.
Professor Tim Stinear, Scientific Director of Applied Microbial Genomics at the Doherty Institute, agreed that a more concerted research effort was needed.
“We actually know quite a lot about environmental reservoirs and good leads on transmission that have led to the public health measures currently recommended by the Victorian Health Department,” he said.
“We just need more clarity. We know that the infectious dose is quite low. The bacteria can be introduced by small lesions, whether they be delivered by a biting insect or perhaps by a gardening mishap.”
Question marks remained on how the disease was spread, the role of biting insects in transmission, and the range of insects that might be spreading the disease, he said.
“The bigger question is: why are we seeing this big increase in and around Melbourne at the moment? It may be a stochastic event where over time more and more possums have become infected and perhaps the bacteria have changed subtly. The possums may now be more susceptible to infections. Or, these issues could have coalesced, but we need more of a research effort to find answers.”
Professor Johnson said that the good news about Buruli was that an effective, rapid diagnostic test was available, and ulcer treatment had improved enormously in recent years.
While surgery was once the mainstay of treatment, for some years Australian doctors have been using a combination of antibiotics – such as rifampicin and clarithromycin – with success, although, the MJA authors noted, these drugs are not listed on the Pharmaceutical Benefits Scheme for use in this condition.
“It’s changed from a surgical disease to a medical disease, but it’s still not completely straightforward to treat. The side effects from the drugs can be considerable, particularly in the elderly, and you can often get marked inflammatory reactions during treatment where the condition paradoxically worsens before it gets better,” Professor Johnson said.
There is also still a role for surgery, particularly in severe cases, he said, but more research was needed to work out how best to combine treatment modalities.
A case report, also published in the MJA, detailed the case of a 68-year-old man from Queensland who developed M. ulcerans osteomyelitis in his ankle 10 months after treatment for an M. ulcerans nodule on his forearm. The involvement of M. ulcerans in the osteomyelitis was not detected for several months, and the patient went on to require a below-knee amputation.
Professor Johnson, a co-author of the case report, emphasised that such a severe secondary infection was “very rare”.
He said that the initial presentation of M. ulcerans was correctly treated. “It then relapsed in a way that no-one expected, and that I haven’t seen before,” Professor Johnson said.
The message to doctors, he said, was to keep in mind a past history of M. ulcerans when dealing with an unusual presentation of a bone or joint infection, because the infection could recur at different sites on the body with unusual presentations.
To find a doctor, or a job, to use GP Desktop and Doctors Health, book and track your CPD, and buy textbooks and guidelines, visit doctorportal.
Have you ever tried to give vitamin D to burili ulcer patients? Vitamin D seems to be very important in the immune responses against mycobacterium, and some people have a big deficit of it, special people with black skin. You should try to do that, even as a preventive method.
A useful question to ask each of the diagnosed with ulcerans is “where on your body did it first start”.
Is there any differences to West Africa where they tend to occur on exposed flesh -esp below knee.
If like in the comment above it seems to have been higher (spread to thigh and torso, was the initial ulcer above knee?). Also common is the areas of arms not often seen by the patient (elbow).
Another question I have is what is the serum Vit.D status of those infected. As in M.tuberculosis? Does Vit D help or does having Vit D deficiency increase risk of initial infection?
I understand that the suggestion of a cull of possums was met with threats of violence from animal activists.
And despite the alarming epidemiological trend, the threat to tourism means that councils are ‘hastening slowly’ and the issue has been allocated a low profile.
My husband suddenly developed an ulcer a single one initially, which just ate into his skin, it then spread to his abdomen and thighs, weeping and bleeding and just eating into the dermis.He visited his GP who was unable to diagnose it,I was of the opinion it was a flesh eating bacteria having worked in a Tropical Sri Lanka for a few years.HE was soon referred to the hospital for an inpatient admission due the severity of spread of the ulceration.The ulcers were just weeping,bleedind and excavating the skin and finally causing a scarring.A team of Specialists did over fifty various tests at the Austin Hospital in Melbourne which is a teaching hospital and they were unable to to come to a DIAGNOSIS!! They commence giving him high doses of prednisone orally and this gave him other side effects at the age of 62. They also gave him a topical application for the ulcers.They did not give him antibiotics.They did suspect that he could have been infected by a potting mix he had meddled with since he loves gardening however they never suspected that it could be the Bairnsdale Ulcer! We live in Melbourne and had a big garden at the back with fruit trees etc and birds and other animals visiting the garden in the night.The ulcers have improved over the periods of 2 years however they are recurrent and keep presenting even recently.He is now 64 years old and a Dentist in Melbourne .My own opinion is as a Medical officer is that he has the Bairnsdale Ulcer that the Dermatologist ,Immune specialist did not diagnose accurately and told him that his Immune system was suppressed and hence the Ulceration was due to that.