ABSTRACT
Tuberculosis (TB) is a lung disease caused by the bacterium Mycobacterium tuberculosis, which kills around 1.5 million people each year and remains a serious challenge for global public health. This chapter investigates the rates of drug resistance acquisition in a natural population using molecular epidemiological data from Bolivia. It explains the rate of direct acquisition of double resistance from the double sensitive state within patients and compares it to the rates of evolution to single resistance. The chapter addresses whether or not double resistance can evolve directly from a double sensitive state within a given host. It disregards latent infections for simplicity and focuses on active infections which are the larger source of new infections. The chapter estimates epidemiological parameters describing the acquisition of multi-drug resistance in M. tuberculosis from molecular epidemiological data using approximate Bayesian computation. It concludes that the evidence favours the drugs being acquired at different rates, specifically, isoniazid resistance evolves faster than rifampicin resistance.
