Advanced Topics in Microbiology 2025 – 2026

Advanced Topics in Microbiology 2025-2026

LESSONS FROM YEAST: CHROMATIN, EPIGENETICS AND DISEASE

The yeast Saccharomyces cerevisiae has long been used as a model system for the study of eukaryotic cells. Recent developments have seen this model system used as a powerful experimental tool to understand complex biological processes, particularly those associated with human diseases. The first part of this course will explore the experimental approaches offered by yeast as a model biological system. With this background information, you will review how many of the fundamental chromatin-mediated cellular processes were first identified in yeast and were then found to exist in human cells. Finally, we will discuss how using yeast as a model organism has offered insight into when chromatin-mediated processes become aberrant and the relevance of this failure of function to cellular aging and cancer.

Topics discussed in first 7 lectures:

1:  Yeast as a Model Organism

2:  The Yeast Deletion Library: Looking for Phenotypes

3:  A brief history of chromatin research: from obscurity to the cutting edge

4 & 5: Early studies in yeast which first demonstrated chromatin regulates transcription

6:  Chromatin and aging

7:  Chromatin and cancer

Sessions 8, 9 and 10 will involve class discussion of topical papers (to be selected).

In-course assessment: 5% Presentation of a recent scientific paper relevant to the topic.

SMALL RNA-MEDIATED GENE REGULATION IN GRAM-NEGATIVE BACTERIA

To respond to environmental changes, the gene expression programs in bacteria must be tightly controlled. In addition to gene regulation by transcription factors or DNA topology, small, non-coding RNA molecules have been established as a class of regulatory elements in the bacterial cell. Throughout the course of this class, we will discuss current knowledge such as the identification, mechanism of action and biological functions of selected small RNAs and their RNA-binding proteins in Gram-negative bacteria. Guided by selected research articles, we will follow the cellular path of a regulatory sRNA from expression to target interaction and subsequent degradation. The course involves in-depth reading of primary literature as a group and discussions on experimental design and interpretation.

In-course assessment: 5% MCQ.

THE PANDEMIC POTENTIAL OF HIGHLY PATHOGENIC H5N1 INFLUENZA A VIRUSES

At irregular intervals Influenza A virus causes pandemics of varying severity. The 2009 “swine ‘flu” pandemic had a mortality rate similar to seasonal influenza A viruses, whilst the pandemic in 1918 is thought to have infected a third of the world’s population with 50-100 million deaths. It is impossible to predict which influenza A virus will cause the next pandemic, however since its first emergence in 1996, highly pathogenic avian influenza (HPAI) H5N1 virus has been considered a virus with pandemic potential. This concern has significantly increased with the spread of HPAI H5N1 into cattle in the USA in 2024.

In this course we will explore the emergence of HPAI H5N1, the outbreaks it has caused amongst people, and its evolution to become a panzootic virus that is currently causing global infection amongst a wide variety of wild and domesticated animals. Using primary research papers and reviews, we will investigate the viral mutations that have allowed this virus to broaden its host tropism, as well as mutations of concern that may allow HPAI H5N1 to cause a pandemic in humans. We will discuss routes of transmission and methods for controlling HPAI outbreaks.

The course will be divided into five 2-hour classes. Recommended multi-media resources will be available before each class. Each class will be comprised of a mixture of lecture material, followed by a class discussion. All students are expected to engage with the material provided before the classes and to participate in the class discussions.  

In-course assessment: 5% Question-led summaries of the class material that will form the foundation for revision for the exam.

“THE SILENT PANDEMIC OF ANTIBIOTIC RESISTANCE IN ESKAPE PATHOGENS – FROM NEW DRUGS TO NOVEL THERAPEUTICS”

The rapid emergence of multidrug resistance in bacteria occurring worldwide is jeopardizing the efficacy of available antibiotics, which for decades have saved millions of lives. In addition, the development of new drugs continues to decline with pharmaceutical companies curtailing their anti-infective research programs. The “silent pandemic” of antimicrobial resistance (AMR) is a neglected global crisis that requires urgent attention and action. Appropriate prescription and optimised use of antimicrobials guide the principles of antimicrobial stewardship activities, together with quality diagnosis and treatment. However, there are several threats that can affect antimicrobial stewardship activities and continue to drive antimicrobial resistance. Furthermore, hospital admissions increase the risk of health-care-associated infections and the transmission of multidrug-resistant organisms, which in turn leads to increased antimicrobial use. Due to this concerning situation, in 2017, the WHO published a list of pathogens for which new antimicrobial development is urgently needed. Within this list, ESKAPE (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species) pathogens were designated “priority status”. This highlights the urgency in the development and discovery of new drugs or the repurpose of existing ones. This course will discuss the lack of new antimicrobial compounds to treat multidrug resistant infections caused by ESKAPE pathogens, as well as the (still) problematic (mis)use of antibiotics. We will focus on the process of discovery and development of new drugs and the reason why thousands of new molecules never reach the market. We will also discuss the use of potential alternative therapeutics that are focused on shifting the current drug discovery paradigm from “finding new drugs” to “combining existing agents”. Some examples of the approaches to be discussed will include host-directed therapeutics; bacteriophage-based therapies; anti-virulence strategies; development of biofilm inhibitors/disruptors; among others. Using this background information, we will review cutting-edge papers where these approaches are discussed, opening the way to the discovery of new drugs or to the repurpose of existing ones. The students will have the opportunity to read and discuss fundamental papers in this area as well as to work with their peers in critically presenting their view about antimicrobial resistance. Group work will be focused on potential solutions to tackle this public health issue and discover/design a new antimicrobial. The students will also be challenged to be the next Antimicrobial Resistance Ambassadors for public engagement and to develop new ideas and solutions to engage with the public to raise awareness of this Global Public Health Issue.

In course assessment: 5% Presentation of a scientific paper on novel drugs/treatments to treat MDR ESKAPE pathogens and preparation of Flash cards with summary information on AMR to be distributed during AMR awareness week (18-24 November 2025).

BACTERIAL STRESS RESPONSES

Learning Aims

Students will develop an understanding of the molecular mechanisms underlying bacterial stress responses, and how these mechanisms contribute to bacterial pathogenicity, survival, and evolution.

Module Content

This module will consist of 10 lectures dedicated to exploring the diverse strategies bacteria use to sense and respond to stress. While humans face exams, deadlines, and bills, bacteria experience very different stresses in their environments, from nutrient limitation and oxidative stress to host immune defenses and antibiotic pressure.

  • In this course, we will systematically examine:
  • The molecular mechanisms of stress sensing and regulation.
  • Specific examples of stress responses in clinically and environmentally relevant bacteria.
  • The role of stress responses in pathogenicity and antibiotic resistance.
  • The importance of population heterogeneity as a survival strategy under stress.

As part of the module, students will take part in a mini-conference on recent discoveries in bacterial stress responses. Active participation will form part of the in-course assessment, giving students the chance to critically evaluate primary research and share their findings in a supportive, conference-style setting.

This course will be particularly valuable for students interested in bacterial regulation, antibiotic resistance, and microbial evolution.

Learning Outcomes

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

  • Describe the diversity of bacterial stress response mechanisms.
  • Explain the genetic and molecular regulation of bacterial stress responses.
  • Discuss the connections between stress responses, pathogenicity, and bacterial evolution.

In course assessment: 5% Presentation and discussion in a conference-style setting

METABOLISM MEETS VIRULENCE

An individual’s appearance, behaviours and lifestyles are shaped by the foods they eat. The same is true in many respects for bacteria. Bacterial virulence mechanisms are often metabolically costly to produce, and their expression must be controlled precisely to ensure activity in the appropriate infection niche. A plethora of signals from the environment, the host, the diet, and endogenous sources therefore converge on virulence factor-encoding genes and their regulators to facilitate niche-specific virulence control.

This course will focus on clinically relevant bacterial pathogens, aiming to build an understanding of how diverse virulence factors are regulated in response to the sensing and breakdown of metabolites during infection. You will learn about how host-associated environments vary in their metabolite profiles and the strategies employed by pathogens to exploit these variations to optimise infection. The experimental methodologies used to analyse alterations in metabolism and dissect how this affects specific virulence factors will also be discussed. A problem-based learning activity focussed on response to an emerging pandemic threat will be conducted alongside the course. Students will be tasked with analysing relevant literature and preparing a group presentation to inspire discussion.

In-course assessment: 5% Problem-based learning activity assessed by group presentation.

AN INTRODUCTION TO EVOLUTIONARY MICROBIOLOGY

Microbes show a remarkable ability to rapidly adapt to harsh and changing environments. Such rapid evolution can have direct consequences for our health and wellbeing. Antimicrobial resistance, vaccine escape and the switch from acute to chronic infection are all driven by the evolution and spread of adapted strains.

This course introduces the principles of microbial evolution through discussion of cutting-edge literature and real-time experimental evolution studies. These “living fossil records” allow us to trace evolutionary dynamics, identify novel genomic changes, and quantify the fitness advantages that underpin microbial adaptation. We will examine the factors that influence the rate and likelihood of evolutionary change, and explore strategies for leveraging—or redirecting—evolution to reduce the impact of pathogens on their hosts. A central case study will be Lenski’s long-term E. coli experiment, which has tracked over 50,000 bacterial generations and provided unprecedented insight into evolutionary processes. Expect fitness conflicts, trade-offs, bacterial warfare and invasions.

  • Lecture 1: Introduction to Evolutionary Biology
  • Lecture 2: Experimental Evolution 1
  • Lecture 3: Experimental Evolution 2: Criticisms and Caveats
  • Lecture 4: Evolution of Microbial Cooperation
  • Lecture 5: Mobile Genetic Elements in Evolution
  • Lecture 6: Guest speaker, Dr Kaitlin Schall, University of Liverpool (double period)
  • Lecture 7: Clinical Evolutionary Microbiology
  • Lecture 8: Group Presentations (double period)

In course assessment: 5% Oral presentations

ENTERIC DISEASE GENOMICS AND EPIDEMIOLOGY  

Bacterial pathogens cause a range of enteric and diarrhoeal disease across the globe, with particularly high mortality and morbidity in low-middle income countries and amongst the immunocompromised and children under the age of five. The advent of relatively inexpensive whole-genome sequencing (WGS) has expanded our understanding of how these pathogens evolve, cause disease, and transmit worldwide. This advanced course will examine the population biology and genome dynamics of several bacterial aetiological agents of enteric and diarrhoeal disease. Using case studies, we will build on basic biological and molecular pathogenesis concepts introduced earlier in the moderatorship, and explore how these relate directly to modern disease control strategies. We will focus on real-world examples of how WGS has informed, evolved, and accelerated public health microbiology and surveillance. The course is dynamic and highly applied, and will involve active discussion of real genomic, epidemiological, and phylogenetic data, applying theoretical concepts to real-life disease outbreak scenarios, and understanding how population-level surveillance genomics can complement and reinforce bacteriology, functional molecular biology, and genomic data. Guidance will be provided to support students’ independent learning through selected articles, discussion, and the structured in-course assessment design.  

In-course assessment (5%): Students will be provided with data describing a fictional disease outbreak, and through guided independent learning time, will produce a two-page summary of the scenario. Assessment will consist of the two-page document submitted, and a 5-10 minute verbal discussion of the document with the lecturer, held after the final session (dates TBC).