The pathogenic fungus Aspergillus fumigatus is an environmentally common mold found throughout the world. However, for people with a weakened immune system, this can be a serious threat. The fungus avoids elimination from superficial human lung cells by binding to human protein. A current scientific work highlights the concern about a very possible pandemic from the fungus Aspergillus fumigatus.
A certain individual superorganism lives within us and on us, even more individual than our own genetic uniqueness of DNA, consisting of a community of microorganisms constantly interacting with each other and with our body. Without symbiosis with this superorganism, the biological existence of a person is simply impossible. The number of participants in this superorganism exceeds the number of our own cells from 10 to 100 times, according to various sources. The diversity is simply incalculable.
As the author of a new study rightly noted: “Unlike viruses such as COVID-19, fungi do not need a host to spread. They can travel on people, through trade, and even in strong winds.”
In this regard, we think it is wise to take a few minutes to read this article and perhaps this information will help you in a critical situation.
McMaster’s new study has shown that a disease-causing fungus harvested from one of the world’s most remote regions is resistant to common antifungal drugs used to treat infections.
A study published in mSphere found that seven percent of Aspergillus fumigatus specimens collected from the Three Parallel Rivers area in Yunnan Province, China, were found to be drug-resistant.
Located 6,000 meters above sea level and guarded by the stunning glacial peaks of the Eastern Himalayas, this region is sparsely populated and undeveloped, making the presence of antimicrobial resistant strains of A. fumigatus all the more striking to Jianping Xu, who led the study with colleagues in China.
“Seven percent may not seem like much, but these drug-resistant strains are able to multiply very quickly and take over local and regional populations of this species,” explains Xu, a professor of biology at McMaster University and a member of the Michael J. DeGroot Institute for Infectious Disease Research. “Surveillance for drug resistance in the environment needs to be strengthened in different geographic regions.”
This study is the third in a trio of related studies by Xu and colleagues. The first study found that approximately 80 percent of A. fumigatus specimens from Yunnan’s greenhouses were resistant to commonly used antifungal drugs, and the second study found that approximately 15 percent of specimens from Yunnan’s agricultural fields, lake sediments, and forests were also resistant.
Xu, whose research is also supported by the Global Nexus School of Pandemic Prevention and Response, says that although there is increasing evidence that resistance naturally develops in the environment, the external gradation of resistance in greenhouses indicates that these resistant Himalayan strains of A. fumigatus probably originated from spores of other fungi that were found in greenhouses, which in turn were overexposed to agricultural fungicides in other conditions.
The fact that these drug-resistant spores have the potential to travel to and multiply in such remote areas raises concerns about the global spread, Xu said.
“This fungus is very ubiquitous – it’s all around us all the time,” he explains. “It is estimated that we all inhale hundreds of spores of this species every day. Although it does not always cause noticeable health problems, three to four million people experience symptoms of A. fumigatus every year. This can be very dangerous – it can lead to the removal of a lung or even death – and now, increasingly, many of these infections will be subject to drug resistance.”
Already doing other research, Xu has studied identical resistance mechanisms in fungal strains found in the Northwest Territories and India—about 10,000 kilometers apart.
“Unlike viruses like COVID-19, fungi don’t need a host to spread,” Xu explains. “They can travel on people, through trade, and even in high winds.”
With the latter in mind, Xu will soon return to China’s mountainous regions to take air samples for fungal spores, which he hopes will add clarity to how these resistant strains reach and grow in such remote regions.
Strain of fungus can also be used as a bioweapon
There is a belief this pathogen can also be used as a bioweapon, very successfully disguised as a natural spread of a strain of fungus resistant to existing antimycotics.
Researchers at the Leibniz Institute for Natural Products Research and Biology of Infection (Leibniz-HKI) report that they have discovered a possible new target against fungal infection.
The results are published in the journal Cell Host & Microbe in an article titled “Aspergillus fumigatus hijacks human p11 to redirect fungal-containing phagosomes to non-degradative pathway.”
“Deciding whether endosomes enter a degradative or recirculating pathway in mammalian cells is fundamental to pathogen eradication, and its malfunctioning has pathological consequences,” the researchers write. “We found that human p11 is a critical factor for this decision.”
The Leibniz-HKI team has now discovered that fungal spores can suppress the defense response of lung surface cells. “These epithelial cells in our lungs are an important barrier against fungal spores and other potential pathogens in the air,” explained Axel Brahage, director of the Leibniz-HKI and professor at the Friedrich Schiller University in Jena.
Unlike immune cells, lung epithelial cells are not specialized to kill pathogens, but they are capable of doing so. Cells surround foreign bodies, forming a membrane-bound compartment known as the phagosome.
The researchers found that the human p11 protein appears to be linked to a fungal protein. “When we disable the fungal protein that binds to p11, we find fungal spores in ‘mature’ phagosomes, which means they are killed. Similarly, if we knock out the human p11,” Jia said. “However, if the fungal protein and p11 are intact, the phagosomes remain “immature.” Lung epithelial cells contain fungal spores but do not kill them. The researchers were also able to observe this under a microscope.
These results reveal the role of p11 in mediating evasion from fungal invasion.
“Patients with a specific mutation in the p11 gene were less likely to develop invasive aspergillosis. This result helps to understand why patients who are at higher risk should be especially closely monitored,” Jia said. Both the fungal protein that binds to p11 and the human protein itself are possible targets for the treatment of fungal infection.