Antimicrobial Resistance — a Major Global Health Threat of the 21st Century and Search for Novel Therapeutic Agents

Abstract
Increasing antimicrobial resistance (AMR) threatens the global capacity for responding to infectious diseases. Drug-resistant microbes will kill about 10 million people worldwide, becoming the leading cause of mortality by 2050 and costing around $100 trillion in lost output. Although antibiotics naturally select for resistant strains, widespread and unregulated use in animal husbandry, agriculture, and integrated fish farming to improve production has accelerated the development of drug resistance. In developing countries, additional socio-economic factors such as poverty, poor sanitation, and inadequate health care and surveillance systems enhance the spread of resistant strains. There is an urgent need to develop new strategies to identify antimicrobials or extend the life of those currently in use. Even with novel therapeutics, resistance will continue to increase without education, research, and infrastructure improvement. The talk will focus on Pseudomonas aeruginosa as a case study and educational efforts underway in Asia for community education.
Collaborating with the Innate Immune System to Treat Multidrug-Resistant Superbugs

Abstract
Antibiotic resistance presents an ever-increasing challenge to the public health with a dearth of new drugs in the development pipeline. A single-minded focus on direct antimicrobial activities overlooks the fact that significant infections are really a disease of the host-pathogen interaction. Indeed, before the patient has even seen a doctor, their infection is already being treated by multiple antimicrobials – namely the cellular and molecular components of the innate immune system. We see value in exploring potential novel therapeutic approaches for drug-resistant bacteria that aim to tip the host-pathogen interaction back in favor of the host. This talk will illustrate novel therapeutics that re-sensitize the pathogen to innate immune killing or directly boost the antibacterial killing capacity of host cells.