AI Summary
The article discusses how monoclonal antibodies could offer a solution to antimicrobial resistance. A team at the University of Cambridge has developed a monoclonal antibody drug using genetically engineered mice to combat infections caused by the bacteria Acinetobacter baumannii, which is increasingly resistant to antibiotics and commonly found in hospitals, particularly in Asia. This research is crucial as current antibiotics are becoming less effective against this bacteria, making them difficult to treat.
Monoclonal antibodies – treatments developed by cloning a cell that makes an antibody – could help provide an answer to the growing problem of antimicrobial resistance, say scientists.
A team lead by researchers at the University of Cambridge has developed a monoclonal antibody drug, using a technique involving genetically engineered mice, that may help prevent infection from Acinetobacter baumannii, a bacteria associated with hospital-acquired infections, which is particularly common in Asia.
A. baumannii bacteria can cause life-threatening respiratory illness and sepsis in vulnerable individuals, particularly in newborn babies whose immune systems have not fully developed. It is usually spread through contaminated surfaces, medical equipment and via contact with others. In recent years infections with strains of this bacteria that are resistant to almost every antibiotic available have become common.
A. baumannii is good at sticking to medical equipment, and if people are vulnerable or don’t have a particularly well-developed immune system, they can succumb to this infection and get aggressive pneumonia requiring ventilation – and in many cases, the patients can acquire the infection from the ventilation itself.
The bacteria are naturally resistant to many antimicrobials, but as they’re now found in hospitals, they’ve acquired resistance to almost everything we can use. In some hospitals in Asia, where the infections are most common, there isn’t a single antibiotic that will work against them. They’ve become impossible to treat.”
Professor Stephen Baker, Cambridge Institute of Therapeutic Immunology and Infectious Disease, University of Cambridge
In a study published today