Yersinia pestis, the plague bacillus, infects wild rodent populations in many parts of the world and is transmitted primarily by fleas. Y. pestis undergoes a characteristic development in the flea gut that leads to transmission. After being taken up by a flea in a blood meal, the bacteria multiply in the midgut to form dense aggregates that are surrounded by an extracellular matrix. The aggregates can adhere to the cuticle-covered spines in the proventriculus, a valve that connects the midgut to the esophagus. The bacterial biofilm interferes with the valvular action of the proventriculus and eventually blocks the flow of blood into the midgut. Transmission occurs when bacteria released from the biofilm are regurgitated into the bite site when a blocked flea attempts to feed. The ability to form a proventricular biofilm depends on the Y. pestis hms genes, which are homologous to genes in other biofilm-forming bacteria that are responsible for the synthesis of the extracellular polysaccharide matrix of the biofilm. Biochemical evidence indicates that the Y. pestis synthesizes an Hms-dependent extracellular polymer of N-acetyl glucosamine that is required to produce a proventricular biofilm. This extracellular matrix is produced only at temperatures below 28°C in the flea, and appears to contain lipid derived from the flea blood meal as well as the Hms-dependent polysaccharide. It is in this flea-specific context that Y. pestis is transmitted to a mammal.