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ORIGINS' Dental Screening project has completed its feasibility study, showing that the tested smartphone app, enabling remote screening of children's teeth by dental professionals, has the potential to help remote families access dental care, among other benefits.

Find out how you can get involved with our work at Phage WA.

Here are some of the most common questions about phage, phage therapy and antimicrobial resistance (AMR).

The Wal-yan Respiratory Research Centre is seeking expressions of interest from Western Australians to join an Antimicrobial Resistance (AMR) Community Reference Group, to provide vital community perspectives on the research activities into this global health concern. 

Researchers from the Wal-yan Respiratory Research Centre are aiming to combine artificial intelligence with natural, infection-fighting viruses to help save lives from an increasingly common medical emergency found in hospitals.

Patients battling antibiotic-resistant superbugs will soon have access to life-saving WA-made therapies that could help treat lung, skin and ear infections as well as bacterial infections like Golden Staph. Western Australia's inaugural phage manufacturing facility – spearheaded by a team at the

Dr Daniel Laucirica is a translational researcher focused on developing bacteriophage therapies for drug-resistant infections.

Burkholderia cepacia complex causes life-threatening respiratory infections. Here, a bacteriophage with activity against B. cenocepacia was isolated from wastewater. It has a genome size of 70,144 bp and has the taxonomic classification Irusalimvirus. It has no genes associated with lysogeny, bacterial resistance, or virulence. 

Burkholderia cepacia complex is a cause of serious lung infections in people with cystic fibrosis, exhibiting extremely high levels of antimicrobial resistance. These infections are difficult to treat and are associated with high morbidity and mortality. 

A population of neutrophils recruited into cystic fibrosis (CF) airways is associated with proteolytic lung damage, exhibiting high expression of primary granule exocytosis marker CD63 and reduced phagocytic receptor CD16. Causative factors for this population are unknown, limiting intervention. Here we present a laboratory model to characterize responses of differentiated airway epithelium and neutrophils following respiratory infection.