Before the advent of antibiotics, an infected paper cut could be deadly. Now we can use antibiotics to treat bacterial meningitis, strep throat and even tuberculosis. However, unlike most antibiotic prescriptions, tuberculosis treatment requires a regime of three different antibiotics and takes between six months and a year. This type of prolonged exposure to antibiotics drives the development of antibiotic resistance.

Scientists do not completely understand why such an extended course is needed to treat tuberculosis. They do know, however, that antibiotics must enter all of the bacterially-infected cells in order to be effective. Therefore, if scientists could develop antibiotics that enter the host cells as efficiently as the bacteria does, this could shorten the course of treatment required - reducing the risk of antibiotic resistance developing.

Researchers at the Francis Crick Institute in the UK and the University of Western Australia tackled this problem by developing an imaging technique to see which infected lung cells the antibiotics could enter. The team infected mice with Mycobacterium tuberculosis and treated them with the antibiotic bedaquiline. They used a new microscopy method, called CLEIMiT (correlative light, electron, and ion microscopy in tissue), to identify the specific cells that the antibiotic was taken up by.

They found that bedaquiline was unable to enter all of the infected lung cells, meaning while some bacteria were being killed, others managed to evade the treatment. This could explain why such a long treatment regime for tuberculosis is required. CLEIMiT offers the possibility of characterizing current antibiotics that we use to assess their cell-specific uptake, as well as aiding the development of more efficient antibiotics. This will ultimately reduce the risk of the development of antibiotic resistance.