Pasteurella multocida is an upper respiratory tract commensal in most mammals and birds that can cause several distinct animal diseases, as well as zoonotic diseases in humans. Despite the large economic impact P. multocida animal diseases have on agricultural industries, little is known about how P. multocida virulence factors are regulated. Capsule is an important P. multocida virulence factor, and P. multocida strains that lack capsule are unable to cause disease. We adapted transposon-directed insertion site sequencing (TraDIS) for use in P. multocida and used TraDISort methodology to investigate capsule production in P. multocida strain VP161. We produced a VP161 Himar1 mutant library with over 81,000 unique insertion sites, giving a unique insertion every 28 bp. We then used percoll gradients to separate mutants with a high cell density phenotype, corresponding with reduced capsule production, from those with a low cell density phenotype, corresponding to wild-type levels of capsule production. TraDISort comparison of the high cell density (acapsular) and low cell density (capsulated) VP161 Himar1 mutants identified 69 genes important for capsule production, including all previously characterised capsule biosynthesis genes, and regulators of capsule production. Several novel genes identified by the TraDISort analysis were involved in regulation or activation of the stringent response. Two of the identified genes associated with the stringent response, relA and spoT, encode proteins that control the concentration of the guanosine alarmone molecules that are responsible for mediating stringent response activation. Disruption of the 3’ end of spoT, which encodes C-terminal regulatory domains, resulted in loss of capsule production and reduced expression of capsule biosynthesis genes. Overall, this study has comprehensively characterised capsule production in P. multocida and identified the stringent response as a negative regulator of capsule production.