This module will explore how bacteria of clinical and public health importance interact with their human host, cause disease, and how they can be treated and prevented.

We will introduce general concepts and provide insights into the strategies that bacteria use to colonise distinct host niches; hijack host molecular functions and transmit to other hosts. We will explore how in addition to direct tissue toxicity, life-threatening disease is caused by the host immune/ inflammatory response to bacterial invasion. We will also introduce new molecular and cellular techniques that are being used to probe interactions between bacteria and their hosts. We will explore the impact of antimicrobial resistance on bacteria and their hosts. Finally, we will show how new knowledge of cellular bacteriology, and bacterial and human genomes is being used to develop novel anti-bacterial treatments and vaccines.

This module will consist of a series of state-of-the-art lectures given by leaders in their fields followed by a journal club focused on a high impact paper relevant to the previous lecture led by post-doctoral scientists. The purpose of these scientist-led journal clubs together with student presentations is to develop your communication, presentation, critical appraisal and data interpretation skills.

Learning outcomes

By the end of the module, students will be able to:

Explain the host and pathogen contribution to colonisation, disease and transmission, illustrating key concepts with examples.
	Outline the virulence factors and strategies used by pathogens to undermine host defences, including the role of the microbiome.
	Discuss the relationship between antimicrobial resistance (AMR) and bacterial pathogenesis, and new approaches to overcoming the threat of AMR, including vaccination.
	Comprehend the cellular, molecular and genomic approaches to investigating microbial pathogenesis.
	Interpret, communicate and critically discuss scientific research experimental data and approaches to the study of bacterial pathogenesis.