The face of the University's 'Old Joe' clock tower will be lit blue to mark the awareness week, which is led by the World Health Organization and aims to encourage people to seek advice from a qualified healthcare professional before taking antibiotics.
The face of Old Joe clock tower is being lit blue to mark World Antibiotic Awareness Week
Scientists from the University of Birmingham are uniting to support World Antibiotic Awareness Week (WAAW) from November 13th to 19th.
The face of the University’s ‘Old Joe’ clock tower will be lit blue to mark the awareness week, which is led by the World Health Organization and aims to encourage people to seek advice from a qualified healthcare professional before taking antibiotics.
Antimicrobial resistance is becoming an increasingly serious threat. If not addressed, by 2050 it could kill millions of people - more than from cancer or road traffic accidents.
The University of Birmingham has one of the biggest teams of microbiologists in the European Union, devoted to tackling this global issue by carrying out pioneering research to better understand how bacteria cause infection, how antibiotics work, the causes of resistance, prevention of spread of resistant bacteria and finding new ways to treat infections.
Professor Laura Piddock, of the University of Birmingham’s Institute of Microbiology and Infection, said: “Antimicrobial resistance (AMR) threatens the effective prevention and treatment of an ever-increasing range of infections caused by bacteria, parasites, viruses and fungi.
“New resistance mechanisms are emerging and spreading globally, threatening our ability to treat common infectious diseases, resulting in prolonged illness, disability, and death.
“Without effective antimicrobials for prevention and treatment of infections, medical procedures such as organ transplantation, cancer chemotherapy, diabetes management and major surgery become very high risk.
“Antimicrobial resistance occurs naturally over time, usually through genetic changes. However, the misuse and overuse of antimicrobials is providing the pressure to select drug resistant microbes.
“The University of Birmingham is leading the way in carrying out vital new research to tackle this global threat.”
The University of Birmingham’s Institute of Microbiology & Infection is tackling antibiotic resistance in three ways:
For more information or to arrange interviews contact Emma McKinney, Communications Manager (Health Science), University of Birmingham: +44 (0)121 414 6681.
Tuberculosis (TB) is an ancient infectious disease caused by an intracellular bacterium called Mycobacterium tuberculosis. According to current WHO estimates, TB continues to affect one third of the world’s population and in 2016, 1.3 million people died from TB infection. M. tuberculosis is an extremely successful pathogen and one of the reasons is due to its unique cell wall. Acting like a ‘molecular fortress’, the cell wall protects the bacterial cell from host defence mechanisms and attack from commonly used antibiotics.
Building a molecular fortress involves complex metabolic pathways and requires exquisite coordination between multi-enzyme factories that produce the molecular components before being exported outside the cell and finally joined together. In this regard, our laboratory at the University of Birmingham is interested in the precise molecular events that govern these processes. Having a better understanding how these molecules are ‘stitched’ together opens new possibilities for therapeutic intervention and the development of new drugs.
Using a combination of molecular, genetic and biochemical experiments, we identified a specific protein in mycobacteria called Lcp1, which is responsible for joining together two crucial cell wall components called peptidoglycan and arabinogalactan. We demonstrated that deletion of the Lcp1 gene in mycobacteria causes a massive loss of cell wall integrity and rapid cell lysis. This novel discovery confirmed that Lcp1 is essential in mycobacteria, thereby validating Lcp1 as a drug target with potential for further chemotherapeutic development.
Trillions of bacteria colonise the human body. Collectively, these bacteria are called the human microbiome. Most bacteria of our microbiome are harmless or even beneficial to our health. However, bacteria that can cause infections are also part of the microbiome. In healthy individuals the immune system keeps these bacteria at bay, but patients in hospitals frequently develop infections with bacteria from their own microbiome. These infections are often difficult to treat as antibiotic resistance is particularly widespread among this group of bacteria.
In a recent study, Professor Van Schaik, with collaborators in the Netherlands and Finland, performed a study on the microbiome of patients in Intensive Care Units (ITUs). The gut microbiome of ITU patients was found to change rapidly after admittance to the ITU, presumably due to the patients’ critical illness and the use of antibiotics. Genes conferring antibiotic resistance were abundant in the patients’ microbiome, but, due to a novel therapy aimed at reducing infections in ITU patients, levels of the ‘hospital bug’ Escherichia coli remained low. The results of this study are used for the development of interventions that minimise or prevent the presence of antibiotic-resistant bacteria in the gut microbiome of critically ill patients, which, in turn, will reduce the number of hospital-acquired infections in these patients.
Recent research by Dr Alan McNally and his team showed that not all strains of E. coli are alike when it comes to antimicrobial resistance. By using cutting edge analysis of the genomes of hundreds of E. coli the team showed that only some strains of the bacterium are capable of becoming multi-drug resistant ‘superbugs’. These danger strains are unique in that they can pick up very large pieces of DNA from their environment. Very commonly such pieces of DNA contain the genes that make E. coli drug resistant, and when the danger strains pick up the resistance-encoding DNA they can then keep these foreign DNA chunks without any detrimental effect on the cell. Only certain strains of E. coli can do this, which means we now can target only those strains with the potential to become the most dangerous superbugs, and potentially target their ability to take up and keep these pieces of foreign DNA that encode the resistance problem.
