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Although bacteria are single-celled and microscopically small, they still need energy to survive, just like us. One of the most effective ways to generate energy for bacteria is through sweet, soluble carbohydrates: sugar.
In fact, the fatal ability of the deadly bacteria Streptococcus pneumoniae using the plant-derived sugar refinosis can explain how it spreads through the human body.
S. pneumoniae is a bacterium that can rapidly develop antibiotic resistance. Each year, it causes millions of infections and about a million deaths. Its “ecological niche”
But from there, S. pneumoniae can spread in the lungs, blood and brain or more locally in the ear to cause diseases such as pneumonia, bacteremia, meningitis and otitis media (middle ear inflammation).
Unfortunately, S. pneumoniae is a genetically diverse pathogen, meaning it has many different strains. This complicates research efforts to identify how the bacteria spread to specific sites in the body.
New research published today in Nature Communications Biology by my colleagues and I bypassed these genetic diversity issues by studying closely related strains of S. pneumoniae. We discovered a difference in a gene between two bacterial strains that regulated their use of raffinose, and this resulted in one being more likely to spread and cause disease.
Sick sweet, sugar and bacterial disease
In our previous research, two closely related strains of S. pneumoniae was isolated, one from the blood of a patient and the other from the ear. Their sequenced genomes were adjusted to select differences that may affect how they spread to different parts of the body, and thus how they cause disease.
We found a difference in the regulatory gene rafR which is responsible for the uptake of raffinose. This difference allowed the bacteria in the blood sample to use raffinose more efficiently than in the ear sample.
When infected mice lungs with S. pneumoniae Through their noses, we found that the blood test remained in the lungs causing invasive disease. However, the ear sample was removed from the lungs and was unable to cause disease.
Remarkable to swap rafR gene between the strains changed their ability to use raffinose, and the way the disease progressed in both cases also reversed. This confirmed rafR the gene actually played a major role in causing disease.
In our recent work, we wanted to find out how this sugar-regulating gene so profoundly affected the course of the disease.
Using an advanced sequencing technique during live mouse infections, we discovered the difference in rafR the gene altered how both mice and bacteria responded to infection. Strains containing rafR from the ear sample resulted in several neutrophils, an important immune cell, at the site of infection.
In experiments where neutrophils were discharged into the lungs, the ear sample was not removed and the risk of disease was more. This study highlights how this single difference in the gene increased neutrophil levels during infection and prevented S. pneumoniae from causing invasive disease.
Potential research effects
Raffinose is found mainly in vegetables, grains and legumes. It is not known if the human body ever has high enough levels of it to dramatically affect the likelihood of disease. It may be a carbohydrate similar to raffinose activating the raffinose regulator rafR instead.
Nevertheless, our research provides insights into how S. pneumoniae causing illness. Once we understand what allows this deadly bacterium to spread through the body, several pathways are opened to stop it.
If this refinement phenomenon turns out to be widespread everywhere S. pneumoniae strains that block their ability to use raffinose can prevent them from surviving in and thus invading the lungs.
Treatments that prevent S. pneumoniae Spreading around the body may be better at preventing illness compared to simply inhibiting or killing the bacteria, as is the current practice.
S. pneumoniae can stay in our noses and throats where it does not cause illness. It plays an import role in this ecosystem. When this bacterium is killed, other deadly bacteria can take place and spread to places like the lungs to cause disease.
The risk of not finding new treatments
S. pneumoniae’s the ability to rapidly develop antibiotic resistance has led the World Health Organization and the US Centers for Disease Control and Prevention to list it as a priority pathogen.
Although vaccines are available, they are far from perfect and do not cover all the different strains S. pneumoniae. If new treatments and vaccines are not soon established, the already deadly effect of this bacterium can be increased.
Despite the known dangers, research into the discovery of new antibiotics has been slow. Many treatments in the pipeline do not provide much benefit over existing antibiotics. Effective new treatments are usually not widely implemented and are instead used as a backup if all else fails. This greatly reduces their profitability, which in turn reduces the incentives to do so.
At worst, antibiotic-resistant bacteria can kill up to ten million people each year by 2050. To avoid such a disaster, more research is needed on how bacteria cause disease. And with this knowledge, we may be able to reduce the likelihood of future pandemics.
Vikrant Minhas, PhD candidate, University of Adelaide
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Image: Wikimedia Commons
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