“We had this global idea of how HIV infects this tissue [of the genital tract]; but following something live is completely different,” Morgane Bomsel, a molecular biologist at the Institut Cochin in Paris and a senior author of the study, said in a statement. “The precise sequence of events can be defined.”
For the video, the researchers created a model of genital tissue in a lab dish, which included the cells that line the genital mucous membranes, known as epithelial cells. The virus, which infects cells of the immune system, is labeled with a green fluorescent protein.
In the video, a type of immune cell called a T cell is infected with HIV, and this cell comes into contact with epithelial cells. Once these cells are in contact, a pocket called a virological synapse forms, allowing viral particles to travel from the infected cell to the uninfected cell.
In what looks like a shooting ray gun from a sci-fi movie, the HIV spurts from the T cell into the epithelial cell. The HIV doesn’t actually infect the epithelial cell, but instead travels across the cell and is later gobbled up bymacrophages, another type of immune cell that HIV targets.
After about 20 days, HIV enters a latent or “dormant” stage, but it’s still inside the macrophages, which makes the virus harder to target with drugs. A goal for new HIV prevention strategies would be “to act extremely early upon infection to avoid this reservoir formation” in the macrophages, Bomsel said. By shedding light on the early steps of HIV transmission, the new study may help researchers take steps toward this goal. One idea would be to make a vaccine that’s active at the genital mucous membranes, “because you can’t wait” to stop the spread of HIV, Bomsel said.
The findings were described in a study published today (May 8) in the journal Cell Reports.
How Did This Soldier ‘Grow’ an Ear on Her Forearm?
By Brandon Specktor, Senior Writer |
Army Pvt. Shamika Burrage’s left ear is unlike other ears, though you might not realize it at first. Like her right ear, it is made from Burrage’s own cells, and connected to her head by her own blood vessels. She can hear perfectly well out of it, and feel perfectly well when you touch it. And yet, until a few days ago, Burrage’s left ear was not on her head — it was on her arm.
Burrage lost her left ear during a single-car crash in Odessa, Texas, in 2016. Now, she is the latest recipient of a cosmetic reconstruction procedure called prelaminated forearm free flap surgery — a sci-fi-sounding operation that involves “growing” new tissue by implanting a patient’s cartilage under their forearm skin. While many civilians around the world have successfully undergone the procedure, Burrage is the first American soldier to receive the novel reconstruction process, according to astatement from the U.S. Army. [The 27 Oddest Medical Cases]
“The whole goal is, by the time she’s done with all this, it looks good, it’s sensate and in five years if somebody doesn’t know her they won’t notice,” Lt. Col. Owen Johnson III, chief of plastic and reconstructive surgery at William Beaumont Army Medical Center in El Paso, Texas, said in the statement. “As a young active-duty soldier, they deserve the best reconstruction they can get.”
To lend an ear
So how does prelaminated forearm free flap surgery work? First, surgeons create a mold of the new prosthetic ear by harvesting some of the patient’s cartilage — usually from the patient’s ribs. The cartilage is shaped, sometimes with the help of a 3D-printed mold, and then inserted under a flap of skin cut open on the patient’s forearm. (In another variant of the surgery, patients have had cartilage implanted under their forehead skin to grow new noses.)
Because the molded cartilage comes from the same cells as the patient’s arm tissues, the skin will begin to grow around the mold. New blood vessels begin to form inside the transplanted tissue and, after several months of healing, the newly formed ear can be safely transplanted to the head. In Burrage’s case, extra skin from her forearm was also used to cover scar tissue around her jawline.
“[The ear] will have fresh arteries, fresh veins and even a fresh nerve so she’ll be able to feel it,” Johnson said. In addition, Burrage will even be able to hear out of it, because surgeons were able to reopen her ear canal following the trauma of her accident.
“I didn’t lose any hearing and [Johnson] opened the canal back up,” Burrage said in the statement. “It’s been a long process for everything, but I’m back.”
A growing field
While this sort of transplant may be a first for the Army, similar operations have been performed successfully on civilians around the world. In 2017, a team of Chinese plastic surgeons led by Dr. Guo Shuzhong completed a similar surgery on a man who lost his ear during a traffic accident. (The forearm-ear transplant took about 7 hours to complete.) Guo told the Daily Mail that he and his team perform similar procedures on about 500 children each year.
Famously, not all recipients of the surgery have been human. In 1995, perhaps the first patient to “grow” a human ear using transplanted cartilage was a laboratory mouse at the University of Massachusetts Medical School. The mouse — nicknamed the “earmouse” or the “Vacanti mouse,” after lead researcher Charles Vacanti — carried the ear on its back and spurred a wave of controversy about genetic engineering.
In fact, the Vacanti mouse was not genetically engineered at all: He was a regular (albeit hairless) mouse who had simply received what is fast becoming a standard — and life-changing — plastic surgery procedure.
Melanoma is a type of skin cancer that begins in the skin’s pigment-producing cells, called melanocytes. These cells make melanin, which is responsible for the color in skin, eyes and hair.
The National Cancer Institutesaid that only 2 percent of all skin cancers are melanoma, so it is very rare. It is also very dangerous. Of all types of skin cancer, melanoma is the deadliest. In 2017, the National Institute of Health (NIH) estimates that there will be 87,110 new cases of melanoma and 9,730 deaths.
While men are usually diagnosed in their 60s, women can get the disease at any age, with risk increasing based on family history and amount of sun exposure. Melanoma is one of the highest cancer killers of women in their mid-20s to mid-30s, said Doris Day, a dermatologist in New York City and an attending physician at Lenox Hill Hospital, also in New York.
“Melanoma is the least common, but most serious of all the skin cancers,” Day told Live Science. Basal cell and squamous cell skin cancers occur more often than melanoma, according to the Skin Cancer Foundation.
Causes & risk factors
Exposure to ultraviolet (UV) rays from sunlight is a leading cause behind melanoma. When sunlight hits melanocytes, they make more of the pigment melanin, darkening the skin. This can result in a tan, freckles or moles — the vast majority of which are benign.
Researchers think that enough UV radiation exposure can damage the DNA in melanocytes, causing them to grow out of control into a tumor. Blistering sunburns in childhood, use of tanning beds and any excessive exposure to UV radiation increases the risk for melanoma, according to the Mayo Clinic.
A melanoma tumor often originates in an existing mole or starts as its own lesion that looks like a mole. People with more than 50 ordinary moles are more likely to develop melanoma, according to the National Cancer Institute.
Melanoma also strikes fair-skinned people more often. Having less pigment in your skin means you have less protection from UV radiation. Caucasians are 30 times more likely to develop invasive melanoma than people of African descent, according to the National Cancer Society.
Melanoma tumors most often occur in areas of the body that are exposed to direct sunlight such as the arms, legs, head and face, according to the Mayo Clinic. Yet, melanoma can form anywhere on the body where there is melanin, including the eyes and the small intestines, according to the National Cancer Institute.
“I had somebody who had it in the bellybutton, and that’s not somewhere that gets a lot of sun exposure,” Day said. “It can occur anywhere in your body.”
One type of melanoma, called acral lentiginous melanoma, may appear as a black or brown discoloration on the soles of the feet, under the nails or on the palms of the hand.
Since melanoma can occur in areas of the body with little to no sun exposure, doctors believe a combination of genetic and environmental factors — including UV exposure — may lead to melanoma, according to the Mayo Clinic.
People with a family history of melanoma are more likely to develop the cancer. One in 10 people diagnosed with melanoma have a family member who was also diagnosed with the disease, according to the National Cancer Institute.
Symptoms & diagnosis
The first signs of melanoma appear as an unusual mole or as changes to an existing mole.
A mole that is asymmetric in shape, has a ragged border, has uneven coloration, is larger than the diameter of a pencil eraser and has changed in appearance may be a sign of melanoma.
An easy way to remember what changes to look for in moles is to refer to your ABCs: A is for asymmetry, B is for border, C is for color, D is for diameter and E is for evolving, Day said.
A mole that bleeds or itches is also a warning sign for melanoma.
Trained dermatologists can perform head-to-toe screenings to find any irregular moles. However, the only way to diagnose melanoma is with a biopsy, according to the Mayo Clinic.
A MelaFind scanner, a technology developed in conjunction with NASA, can also help doctors examine suspect moles. The researchers who developed MelaFind scanned and biopsied more than 10,000 brown marks, and developed an algorithm that gives information about the lesion, Day said.
The scan, which costs about $175 out of pocket for an examination of several spots, can look 0.08 inches (2 millimeters) down into the skin, and doesn’t require cutting, Day said.
If the scan finds the spot may be cancerous, doctors will biopsy the area and send it to a lab, where researchers “look at the pattern of cells and how quickly they’re dividing, and then they give us a report,” Day said.
Melanoma often has good prognosis when the cancer is caught early. If the lesion has not spread beyond the surface of the skin, simple surgery may be enough to cure cancer.
“If it’s less than 1 millimeter [0.04 inches], then we just cut it out with a good margin,” Day said.
The National Cancer Institute estimates people diagnosed with localized melanoma have a five-year survival rate of 91.7 percent. Luckily, 84 percent of melanoma cases are diagnosed at this stage.
However, if melanoma spreads to other parts of the body, it can be difficult to treat, according to the NIH.
If the spot is more than 1 millimeter in depth, doctors may do a sentinel node biopsy, which uses a dye to see if the tumor has spread to the lymph node system. Then, doctors will remove the spot, as well as the dyed lymph nodes, which are then checked for cancer. If the sentinel nodes are cancer-free, then the cancer probably hasn’t spread, and doctors won’t have to remove more lymph nodes, Day said.
If a person has melanoma, doctors will also check the person’s head and chest.
“Every cancer has its place it likes to go,” Day said. “Melanoma likes to go to the brain and the lungs, so we get chest X-ray and a brain scan.”
If melanoma has spread under the skin to nearby lymph nodes, the five-year survival rate is 62 percent. If it has spread to distant parts of the body, the five-year survival rate is 16 percent.
People whose melanoma has spread beyond their skin may require chemotherapy, radiation or biological therapy to treat the cancer. Traditional chemotherapy doesn’t work well for melanoma, but many patients use interferon, a protein that helps the immune system.
“[But] interferon unfortunately was not an ideal treatment because it extends life for 11 months or so in advanced cases, but it was a miserable 11 months,” Day said.
Now, doctors can map each person’s melanoma to see whether it has a genetic pattern that can be treated with chemotherapy. “And if it does, there are some specific chemo agents that work better, and have a much greater chance of remission and long-term survival with [fewer] side effects,” Day said.
Metastatic, or spreading, melanoma used to be a death sentence, but now it’s “basically a chronic illness,” she said.
Preventing melanoma can be a lifelong task, but it only takes a few simple precautions to reduce the risk.
Avoiding tanning beds is an easy step, as is wearing sunscreen year-round. Choose a sunscreen that has a high SPF rating for the best protection. “Use a sunscreen of at least 30 SPF, even on overcast days,” said Dr. Dheeraj Taranath, a regional medical director with MedExpress in Reading, Pennsylvania. Here is some important information on sunscreen. Wearing hats, visors and tightly woven clothing is also a great way to block UV rays.
Finally, staying out of the midday sun — between 10 a.m. and 4 p.m. — will protect skin from the sun’s radiation when it is strongest.
“Stay out of the sun and get regular skin cancer screenings so that if you find it, you find it early,” Day said.
Additional reporting by Alina Bradford, Live Science Contributor.
Mysterious Eye Cancer Cases Pop Up in 2 States, and Doctors Can’t Explain It
By Rachael Rettner, Senior Writer |
Dozens of people in Alabama and North Carolina have developed a rare eye cancer — and doctors don’t know what’s behind the apparent spike in cases in these areas, according to news reports.
So far, 18 people with this eye cancer, known as ocular melanoma, have been identified in Huntersville, North Carolina; and another group of more than 30 people in Auburn, Alabama, also say they’ve been diagnosed with the condition, according to CBS News. The condition typically affects just six out of every 1 million people per year, CBS reported.
What’s more, three of the Alabama cases are friends who attended Auburn University at the same time.
“Most people don’t know anyone with this disease,” Dr. Marlana Orloff, an oncologist treating some of the patients at Thomas Jefferson University’s Sidney Kimmel Cancer Center (SKCC) in Philadelphia, told CBS News. “We said, ‘OK, these girls were in this location, they were all definitively diagnosed with this very rare cancer — what’s going on?'” [10 Do’s and Don’ts to Reduce Your Risk of Cancer]
Right now, doctors don’t know the answer to the question, but they say something in the environment could be a factor, CBS reported.
Ocular melanoma is a cancer that develops in cells in the eye that produce the pigment melanin, according to the American Academy of Ophthalmology (AAO). The cancer usually begins in the middle layer of the eye called the uvea. The exact cause of ocular melanoma is unknown, but according to AAO, risk factors for the condition include: exposure to sunlight or tanning beds over long periods; light eye color; older age; and certain inherited skin conditions or having a mole in the eye.
Ocular melanoma can cause vision loss, and the cancer may also spread to other parts of the body, including the liver, lungs and bones, according to the Mayo Clinic. About 3 out of 4 people (75 percent) diagnosed with ocular melanoma survive at least five years after their diagnosis, according to the American Cancer Society.
In Huntsville, researchers who studied the group of cases there recently announced that they did not find anything that could be directly attributed to the cause of the cancer cases, according to local news outlet WCNC.
One of the Auburn patients has set up a Facebook page to raise awareness, and so far, 36 people have responded saying they also attended Auburn University and were diagnosed with ocular melanoma.
“We’ve got to have it so that we can start linking all of them together to try to find a cause,” Lori Lee, an Auburn University graduate with the cancer, told CBS News.
Biofilms are a collective of one or more types of microorganisms that can grow on many different surfaces. Microorganisms that form biofilms include bacteria, fungi and protists.
One common example of a biofilm dental plaque, a slimy buildup of bacteria that forms on the surfaces of teeth. Pond scum is another example. Biofilms have been found growing on minerals and metals. They have been found underwater, underground and above the ground. They can grow on plant tissues and animal tissues, and on implanted medical devices such as catheters and pacemakers.
Each of these distinct surfaces has a common defining feature: they are wet. These environments are “periodically or continuously suffused with water,” according to a 2007 article published in Microbe Magazine. Biofilms thrive upon moist or wet surfaces.
Biofilms have established themselves in such environments for a very long time. Fossil evidence of biofilms dates to about 3.25 billion years ago, according to a 2004 article published in the journal Nature Reviews Microbiology. For example, biofilms have been found in the 3.2 billion-year-old deep-sea hydrothermal rocks of the Pilbara Craton in Australia. Similar biofilms are found in hydrothermal environments such as hot springs and deep-sea vents.
Biofilm formation begins when free-floating microorganisms such as bacteria come in contact with an appropriate surface and begin to put down roots, so to speak. This first step of attachment occurs when the microorganisms produce a gooey substance known as an extracellular polymeric substance (EPS), according to the Center for Biofilm Engineering at Montana State University. An EPS is a network of sugars, proteins and nucleic acids (such as DNA). It enables the microorganisms in a biofilm to stick together.
Attachment is followed by a period of growth. Further layers of microorganisms and EPS build upon the first layers. Ultimately, they create a bulbous and complex 3D structure, according to the Center for Biofilm Engineering. Water channels crisscross biofilms and allow for the exchange of nutrients and waste products, according to the article in Microbe.
Multiple environmental conditions help determine the extent to which a biofilm grows. These factors also determine whether it is made of only a few layers of cells or significantly more. “It really depends on the biofilm,” said Robin Gerlach, a professor in the department of chemical and biological engineering at Montana State University-Bozeman. For instance, microorganisms that produce a large amount of EPS can grow into fairly thick biofilms even if they do not have access to a lot of nutrients, he said. On the other hand, for microorganisms that depend on oxygen, the amount available can limit how much they can grow. Another environmental factor is the concept of “shear stress.” “If you have a very high flow [of water] across a biofilm, like in a creek, the biofilm is usually fairly thin. If you have a biofilm in slow flowing water, like in a pond, it can become very thick,” Gerlach explained.
Finally, the cells within a biofilm can leave the fold and establish themselves on a new surface. Either a clump of cells breaks away, or individual cells burst out of the biofilm and seek out a new home. This latter process is known as “seeding dispersal,” according to the Center for Biofilm Engineering.
Why form a biofilm?
For microorganisms, living as a part of a biofilm comes with certain advantages. “Communities of microbes are usually more resilient to stress,” Gerlach told Live Science. Potential stressors include the lack of water, high or low pH, or the presence of substances toxic to microorganisms such as antibiotics, antimicrobials or heavy metals.
There are many possible explanations for the hardiness of biofilms. For example, the slimy EPS covering can act as a protective barrier. It can help prevent dehydration or act as a shield against ultraviolet (UV) light. Also, harmful substances such as antimicrobials, bleach or metals are either bound or neutralized when they come into contact with the EPS. Thus, they are diluted to concentrations that aren’t lethal well before they can reach various cells deep in the biofilm, according to a 2004 article in Nature Reviews Microbiology.
Still, it is possible for certain antibiotics to penetrate the EPS and make their way through a biofilm’s layers. Here, another protective mechanism can come into play: the presence of bacteria that are physiologically dormant. In order to work well, all antibiotics require some level of cellular activity. So, if bacteria are physiologically dormant to begin with, there is not much for an antibiotic to disrupt.
Another mode of protection against antibiotics is the presence of special bacterial cells known as “persisters.” Such bacteria do not divide and are resistant to many antibiotics. According to a 2010 article published in the journal Cold Spring Harbor Perspectives in Biology, “persisters” function by producing substances that block the targets of the antibiotics.
In general, microorganisms living together as a biofilm benefit from the presence of their various community members. Gerlach cited the example of autotrophic and heterotrophic microorganisms that live together in biofilms. Autotrophs, such as photosynthetic bacteria or algae, are able to produce their own food in the form of organic (carbon containing) material, while heterotrophs cannot produce their own food and require outside sources of carbon. “In these multi-organismal communities, they often cross feed,” he said.
Biofilms and us
Given the vast range of environments in which we encounter biofilms, it is no surprise that they affect many aspects of human life. Below are a few examples.
Health and disease
As research has progressed over the years, biofilms — bacterial and fungal — have been implicated in a variety of health conditions. In a 2002 call forgrant applications, the National Institutes of Health (NIH) noted that biofilms accounted “for over 80 percent of microbial infections in the body.”
Biofilms can grow on implanted medical devices such as prosthetic heart valves, joint prosthetics, catheters and pacemakers. This in turn leads to infections. The phenomenon was first noted in the 1980s when bacterial biofilms were found on intravenous catheters and pacemakers. Bacterial biofilms have also been known to cause infective endocarditis andpneumonia in those with cystic fibrosis, according to the 2004 article in Nature Reviews Microbiology, among other infections.
“The reason that biofilm formation is a great cause of concern is that, within a biofilm, bacteria are more resistant to antibiotics and other major disinfectants that you could use to control them,” said A.C. Matin, a professor of microbiology and immunology at Stanford University. In fact, when compared to free-floating bacteria, those growing as a biofilm can be up to 1,500 times more resistant to antibiotics and other biological and chemical agents, according to the article in Microbe. Matin described biofilm resistance combined with the general increase in antibiotic resistance among bacteria as a “double whammy” and a major challenge to treating infections.
Fungal biofilms can also cause infections by growing on implanted devices.Yeast species such as the members of the genus Candida grow on breast implants, pacemakers and prosthetic cardiac valves according to a 2014 article published in the journal Cold Spring Harbor Perspectives in Medicine. Candida species also grow on human body tissues, leading to diseases such as vaginitis (inflammation of the vagina) and oropharyngeal candidiasis (a yeast infection that develops in the mouth or throat). However, the authors note that drug resistance was not shown in these instances.
Sometimes, biofilms are useful. “Bioremediation, in general, is the use of living organisms, or their products — for example, enzymes — to treat or degrade harmful compounds,” Gerlach said. He noted that biofilms are used in treating wastewater, heavy metal contaminants such as chromate, explosives such as TNT and radioactive substances such as uranium. “Microbes can either degrade them, or change their mobility or their toxic state and therefore make them less harmful to the environment and to humans,” he said.
Nitrification using biofilms is one form of wastewater treatment. During nitrification, ammonia is converted to nitrites and nitrates throughoxidation. This can be done by autotrophic bacteria, which grow as biofilms on plastic surfaces, according to a 2013 article published in the journal Water Research. These plastic surfaces are just a few centimeters in size and distributed all through the water.
The explosive TNT (2,4,6-Trinitrotoluene) is considered a soil, surface water and groundwater pollutant. The chemical structure of TNT consists of benzene (a hexagonal aromatic ring made of six carbon atoms) attached to three nitro groups (NO2) and one methyl group (CH3). Microorganisms degrade TNT by reduction, according to a 2007 article published in the journal Applied and Environmental Microbiology. Most microorganisms reduce the three nitro groups, while some attack the aromatic ring. The researchers — Ayrat Ziganshin, Robin Gerlach and colleagues — found that the yeast strain Yarrowia lipolytica was able to degrade TNT by both methods, though primarily by attacking the aromatic ring.
Microbial fuel cells
Microbial fuel cells use bacteria to convert organic waste into electricity. The microbes live on the surface of an electrode and transfer electrons onto it, ultimately creating a current, Gerlach said. A 2011 article published in Illumin, an online magazine of the University of Southern California, notes that bacteria powering microbial fuel cells break down food and bodily wastes. This provides a low-cost source of power and clean sustainable energy.
Our world is teeming with biofilms. In fact, by the mid-20th century, more bacteria were found on the inside surfaces of containers holding bacterial cultures, than floating freely in the liquid culture itself, according to the 2004 article in Nature Reviews Microbiology. Understanding these complex microbial structures is an active area of research.
“Biofilms are amazing communities. Some people have compared them to multicellular organisms because there is a lot of interaction between single cells,” Gerlach said. “We are continuing to learn about them, and we are continuing to learn about how to control them better; both for reduced detriment, as in the field of medicine, or for increased benefit as in bioremediation. We are not going to run out of interesting questions in that area.”
Deadly Fungus Cells Talk Amongst Themselves to Infect You Better
By Rachael Rettner, Senior Writer |
The idea of microbes joining forces inside your body to wreak havoc and cause disease sounds frightening — and it should. Now, scientists have found that a particular type of fungus does just that, and the fungal cells use a surprising method to team up and communicate with each other.
What’s more, the findings may explain why this fungus can infect healthy people, a characteristic that’s unusual for fungal infections, which more typically strike people with weakened immune systems.
The study focused on a fungus called Cryptococcus gattii, which lives in soil and is found mostly in tropical and subtropical regions. However, in 1999, a strain of this fungus popped up in British Columbia, Canada, and later, in Oregon and Washington state, mostly causing infections in otherwise-healthy people.
The infection, which people catch by inhaling fungal spores, can be life-threatening, causing a pneumonia-like illness in the lungs, as well as serious infections of the brain and tissues surrounding the brain and spinal cord. From 2004 to 2010, there were 60 reported causes ofCryptococcus gattii in the U.S., and among the 45 cases with known outcomes, nine (20 percent) died from their infections, according to a 2010 study from researchers at the Centers for Disease Control and Prevention.
Previously, researchers found that Cryptococcus gattii was so virulent because it had the “remarkable ability to grow rapidly within human white blood cells,” study author Ewa Bielska, a postdoctoral research fellow at the University of Birmingham in the United Kingdom, said in a statement. In 2014, Bielska’s colleagues found that this rapid growth resulted from a “division of labor,” meaning that the fungal cells worked together to coordinate their behavior and drive rapid growth. [10 Bizarre Diseases You Can Get Outdoors]
In the new study, Bielska and colleagues figured out exactly how the fungal cells are joining forces: The microbes use microscopic, fluid-filled sacs called extracellular vesicles to communicate.
“These vesicles act like ‘carrier pigeons,’ transferring messages between the fungi and helping them to coordinate their attack on the host cell,” said study senior author Robin May, director of the University of Birmingham’s Institute of Microbiology and Infection.
This is the first time that scientists have found a connection between extracellular vesicles and fungal virulence, the researchers said.
The scientists also found that, surprisingly, the fungal cells could use extracellular vesicles to communicate across relatively long distances between cells.
“Our initial expectation was that the fungus would only be able to communicate within a single host cell, but in fact we discovered that it can communicate over very large — in microbiology terms — distances and across multiple host cell barriers,” May said.
The findings “provides us with a potential opportunity to develop new drugs that work by interrupting this communication route during an infection,” he said.
The study was published April 19 in the journal Nature Communications.
This Mysterious ‘Flesh-Eating’ Disease Is Spreading in Australia
By Rachael Rettner, Senior Writer |
It sounds like a movie plot: A mysterious “flesh-eating” disease is spreading, and no one knows how to stop it. But that’s the situation health officials in Australia are facing now as they try to tackle a growing “epidemic” of a condition called Buruli ulcer.
In recent years, Australia has seen a rapid rise in cases of Buruli ulcer, an infection that causes ulcers on the skin that can destroy skin and soft tissue. In 2016, there were 186 reported cases of the infection in Australia, up from 74 cases in 2013 — an increase of 150 percent, according to the World Health Organization. Cases increased even further in 2017, with a projected 286 cases for that year, according to a new report from researchers in Victoria, Australia.
“As a community, we are facing a rapidly worsening epidemic of a severe disease without knowing how to prevent it,” the researchers wrote in the report, published on yeserday (April 16) in the Medical Journal of Australia. “We therefore need an urgent response” to tackle the disease, they said.
Buruli ulcer is not unique to Australia; the infection has been reported in 33 countries in Africa, South America and Western Pacific, according to the WHO. In 2016, there were 2,206 cases worldwide, with Australia and Nigeria reporting the most cases. And although cases have been reported in Australia as far back as 1948, the country has seen a spike in cases since 2013.
The situation is particularly concerning in Victoria, where cases appear to be “becoming more severe in nature, and occurring in new geographic areas,” the report said.
Buruli ulcer is caused by bacteria called Mycobacterium ulcerans, which belong to the same family of microbes that cause tuberculosis andleprosy. The bacteria produce a toxin that destroys tissue, leading to large ulcers, often on the arms or legs, the WHO says. Without early treatment, patients may develop long-term disabilities, such as limited joint movement, or require plastic surgery.
Although it’s unclear exactly how the disease is spread, researchers have some theories — for example, the disease may pass to humans from insects found in water, according to the U.S. Centers for Disease Control and Prevention. Specifically, mosquitoes have been suggested as carries of the disease; the insects have been found to test positive for M. ulcerans, and the use of insect repellent has been linked with a reduced risk of infection, according to the new report.
Animals in Australia, including possums, dogs, cats and koalas, have also been found to develop Buruli ulcer, but it’s still uncertain whether they play a role in spreading the disease, the report said. Recent evidence suggests that the infection does not spread from person-to-person.
The researchers call for a “thorough and exhaustive examination of the environment, local fauna, human behavior and characteristics, and the interactions between them” to better understand the disease and its risk factors. “It is only when we are armed with this critical knowledge that we can hope to halt the devastating impact of this disease through the design and implementation of effective public health interventions,” the researchers concluded.