Prof. Wilbert Bitter

Head of research section Bacteriology Research at Amsterdam University Medical Center

I was born in 1965 in a small village in the center of the Netherlands. I chose biology as the topic of my studies because I wanted to better understand the beauty of nature and how living organisms work. During my studies, I realised that this could be studied best in microorganisms, where it is possible to link molecular effects to ecological relationships.

At the same time, I also wanted to make a positive contribution to society and specialised in pathogenic bacteria and the discovery of new antimicrobials. My main interest is in tuberculosis, but with the success of our zebrafish embryo model we are now broadening our scope and also including Gram-negative pathogens.

In 2010 I was appointed professor of Molecular Microbiology at the Vrije Universiteit and Professor of Medical Microbiology at the Amsterdam UMC.

I live in the old city of Utrecht, close to Amsterdam, and have a passion for history, art, and nature.

When Wilbert Bitter started his own research group on tuberculosis in the Amsterdam UMC he decided to focus on the mycobacterial cell envelope that was crucial to be understand the pathogen in question and to ultimately control this disease. However, to be able to do this not only biochemistry and genetics of pathogenic mycobacteria had to be mastered, but also an amenable and reliable infection model. For this the zebrafish was introduced and more specifically the zebrafish embryo infection model using Mycobacterium marinum as a host. Wilbert’s group was the first to describe the function of the ESX-5 secretion system in pathogenic mycobacteria and he also coined the term type VII secretion for these systems. Subsequently his group uncovered the composition and structure of type VII secretion systems, the secretion signal for substrates and the structure of the type VII secretion membrane complex (CM Bunduc et al., Nature 2021).

Wilbert’s group was also the first to use zebrafish embryos as an infection model for mycobacterial infections. This model turned out to be highly suited for antimicrobial drug testing, including antimycobacterial drugs. This model has been used in different IMI projects for antibiotic development. In recent years, Wilbert Bitter’s lab has continued to unravel the host-pathogen interactions of mycobacteria and identified a new hypervirulence factor in clinical isolates of M. tuberculosis (LS Ates et al., Nature Microbiology 2018), but also started to work on the identification of new compounds that affect cell wall functioning in M. tuberculosis (Patent Application No.: EP19193612, Title: IINHOBITION OF MYCOBACTERIAL TYPE VII SECRETION). After the lab successfully established the zebrafish screening platform for antimycobacterial compounds we have used it to identify a new inhibitor of Aspartyl tRNA synthetase and a highly synergistic compound for M. tuberculosis.

Wilbert Bitter is editor of FEMS Microbiology Reviews and chair of the Dutch microbiology science committee to organise the yearly spring meeting. Four of the PhD students that Wilbert Bitter has supervised have won the Westerdijk award for best microbiology thesis in the Netherlands.

  • An anti-tuberculosis compound screen using a zebrafish infection model identifies an aspartyl-tRNA synthetase inhibitor. Habjan E et al. (2021) Dis Model Mech. 2021 14:dmm049145.


  • Structure and dynamics of a mycobacterial type VII secretion system. Bunduc CM, Fahrenkamp D, Wald J, Ummels R, Bitter W, Houben ENG, Marlovits TC. (2021) Nature. 593:445-448.


  • Heterologous expression of ethA and katG in Mycobacterium marinum enables the rapid identification of new prodrugs active against Mycobacterium tuberculosis. Ho VQT et al. (2021) Antimicrob Agents Chemother. 65:e01445-20.


  • Zebrafish Embryo Model for Assessment of Drug Efficacy on Mycobacterial Persisters. Commandeur S, Iakobachvili N, Sparrius M, Nur MM, Mukamolova GV, Bitter W. (2020) Antimicrob Agents Chemother. 64:e00801-20.


  • Mycobacteria employ two different mechanisms to cross the blood-brain barrier. van Leeuwen LM et al. , (2018) Cell Microbiol. 20:e12858.


  • Mutations in ppe38 block PE_PGRS secretion and increase virulence of Mycobacterium tuberculosis. Ates LS et al. (2018) Nat Microbiol. 3:181-188.