Medicine and war have long been entwined, with massive social disruptions and new weapons engendering the spread of disease and producing unprecedented injury, in turn driving medical innovation and practice whose impacts last long beyond the conflict in which they originated. So began penicillin in the Second World War: antibiotics arose in war.  Today, in the context of long-running military conflicts, we see harbingers of the end of antibiotics.  Our subject is multidrug resistant Acinetobacter baumannii, which emerged as a major health threat in 2003 with the US invasion of Iraq and has been increasing in both virulence and resistance at an alarming rate, leading it to be assessed as the number one priority pathogen for research and development by the WHO. We focus specifically on the social and physical factors that have driven the rapid genetic evolution of this formerly little-known and non-pathogenic organism, including historical legacies of sanctions affecting antibiotic availability, wounding, munitions, refugee movement, and destruction of the built environment.

This 3-day workshop will explore the interlinked hypotheses that heavy metals, particularly in the context of the contemporary Middle Eastern conflicts, are driving global antibiotic resistance (ABR), and that Acinetobacter baumannii is a key mediator by acting both as a reservoir for ABR and as an epidemiological pump for disseminating ABR genes into bacterial populations. War can drive ABR by heavy metal (HM) contamination of the environment. This can occur as a direct result of conflict (via heavy metal contamination of wounds by shrapnel and weapon fragments, or environmental contamination by ordinance and leakage from destroyed infrastructure) or indirectly (via war-related impacts on antibiotic stewardship, agricultural practices, etc.). Multidrug resistance Acinetobacter baumannii (MDRAb) appears to be a key mediator in this pathway.

This pathway and its broader relevance is suggested by evidence that: 1) conflicts have led to HM contamination in the Middle East; 2) HM can generate ABR in bacteria; 3) MDRAb has emerged as a major public health concern in the wake of the conflict 4) MDRAb appears geographically correlated to the conflict and tracks along troop and population movements; 5) Acinterobacter baumannii appears ideally suited to acquire, maintain and transmit ABR genes present in the environment; and 6) a currently widespread MDR gene (blaNDM) of major clinical concern originated in Acinterobacter baumannii.

The workshop will be organized to allow participants to present and discuss in detail their research findings. Four panels (each for a ½ day) will consider:

 

1. Panel 1- Heavy metals and ABR: How do heavy metals induce antibiotic resistance? Is it plausible to assume an epidemiological effect?

 

2. Panel 2- Acinetobacter baumannii and ABR: Acinetobacter baumannii: what is the evidence for its role in driving antibiotic resistance?

 

3. Panel 3- War wounds and ABR: How does conflict expose populations to heavy metals? To what extent could this explain emergence of ABR in this setting?

 

4. Panel 4- War and ABR across history: What might history (notably other conflicts) teach us about the relationship between war and antibiotic resistance?

 

A final panel will be dedicated to critical discussion, particularly in light of the findings presented, of a paper exploring the ‘war-HM-ABR-A.baumannii’ pathway in greater detail. A draft is in preparation and will be circulated for discussion.