Drug-resistant infections have been a growing concern across the medical and pharmaceutical industries. In the United States alone, approximately 23,000 people die each year from infections that are resistant to antibiotics. Now, researchers may know why this happens.
New findings from researchers at Imperial College London show that these bacterial infections are able to reject antibiotics by “closing tiny doors in their cell walls.”
By understanding how these cells are able to shut the doors, the researchers said this could provide new understandings for drugmakers to develop treatments that will “pick the locks” of the closed doors. The result of the research was published today in Nature Communications In the study, the Imperial College researchers, who are focused on antibiotic resistance, looked at the bacterium Klebsiella pneumoniae, which causes infections in the lungs, blood and wounds of people in hospitals. Patients that have compromised immune systems are especially vulnerable to this bacterium. The researchers said K. pneumoniae is becoming increasingly resistant to antibiotics, particularly a family of drugs called Carbapenems, which are used in hospitals when others have failed or are ineffective. Because of this resistance to the powerful antibiotics, the World Health Organization listed Carbapenem-resistant K. pneumoniae as a critical problem.
The researchers found that K. pneumoniae is able to resist Carbapenems by shutting down it surface pores, which is how the antibiotics typically attack the bacteria. The team compared the structures of K. pneumoniae bacteria that were resistant to Carbapenems to those that weren’t and found the resistant bacteria had modified or absent versions of a protein that creates pores in the cell wall. Resistant bacteria have much smaller pores, blocking the drug from entering, the researchers said in a statement. Joshua Wong, from the Department of Life Sciences at Imperial and first author of the study, said with the growing threat of antibiotic-resistant bugs like K. pneumoniae, it’s important to understand how it happened in order to provide “vital insights that could allow new strategies and drugs to be designed.”
There is some good news though from this finding. The researchers said that the bacteria grow at a much slower rate when its doors are closed due to its inability to absorb nutrients while being attacked by the antibiotics.
Those closed doors will present a challenge to drug developers. Gad Frankel, head of the study team, said the ability of the bacteria to shut its doors to the antibiotics will also provide a mechanism to counteract many other drugs. He said that ability will be difficult to get around.
“However, we hope that it will be possible to design drugs that can pick the lock of the door, and our data provide information to help scientists and pharmaceutical companies make these new agents a reality,” Frankel said in a statement.
Over the past few years, there have been multiple stories about the rise of drug-resistant pathogens. Recently, a dangerous fungal infection known as Candida auris reared its head in a New York hospital. The facility had to tear out part of the room a patient was housed in due to the spread of the fungal infection, which can be fatal. With growing concerns about the rise of drug-resistant bacteria, multiple companies are developing new forms of antimicrobials to take on serious health concerns, such as carbapenem-resistant enterobacteriaceae, Clostridium difficile, better known as C. diff, or Staphylococcus infections
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