Antimicrobial resistance
Our research addresses the complexity of antimicrobial resistance (AMR) by targeting multiple facets of the problem. Using microbial molecular genetics our researchers investigate the evolution, spread, and the molecular basis of AMR in bacterial pathogens. Our work focuses on unravelling the success of AMR pathogens and how antibiotic resistance influences disease and colonisation. Recognising that AMR is not just a problem of pathogens and disease, we work in an interdisciplinary way integrating clinical, scientific, and behavioural data to study the burden and drivers of AMR. We are also addressing the problem of decreasing effective antibiotic treatment options due to rising AMR, by conducting research that is developing novel therapeutics approaches, and also research looking to repurpose existing antibiotics and drugs through combination therapies. combinations.
Principal Investigators
Projects of Interest
The HATUA study (Holistic Approach to Unravel Antibacterial Resistance in East Africa) established an East African AMR Surveillance Network across three countries: Uganda, Tanzania and Kenya. The project characterised the ABR bacteria that cause disease in these locations, mapped the use of ABs and captured the behaviour and attitudes of AB use in humans.
The interdisciplinary CARE study (COVID-19 and Antimicrobial Resistance in East Africa – impact and response) investigated the extent to which COVID-19 changed health-seeking behaviour for common bacterial illnesses and the availability and usage of antibiotics in both Tanzania and Uganda.
Antibiotics are a precious resource but are not always treated as such. Indiscriminate use of antibiotics in the past 80 years has lead to an alarming rise in antimicrobial resistance (AMR). Combining antibiotics into single therapies can not only drastically reduce the chance of resistance occurring in the bacterial pathogen but also lower the concentrations of the antibiotics such that toxicity to the patient is significantly reduced.
Tuberculosis is caused by the bacillus Mycobacterium tuberculosis (Mtb). Mtb can enter a so-called dormant state after infecting the lung of a patient. Once the bacterium has become dormant the patient enters a new phase of infection- latent TB. Latent TB can become active TB again- this process is known as relapse. Dormant Mtb are typified by a lowered metabolism and containing lipid inclusion vesicles (LBs). This lowered metabolism makes Mtb less susceptible to the typical antibiotics we use to treat TB. The LBs make the dormant bacteria identifiable by microscopy. We can identify and quantify the LB-Mtb from infected patients and estimate their risk of drug resistance and chance of developing latent TB and identify if a patient with active TB was a case of relapse or a novel infection.