November 21, 2013
Introduction Yersinia pestis is a gram negative, rod-shaped, facultative anaerobic bacterium, known for causing the plague. The reason why Y. pestis is so successful is because of their elusiveness to the host’s immune system and their ability to suppress it. Traces of the plague go as far back as to ancient times and specifically 5th century BC Athens and Sparta.
Pathophysiology
“Y. pestis produces two anti-phagocytic antigens, F1 antigen and VW antigen. These antigens are both required for virulence and are only produced when the organism grows at 37 degrees C temperatures, which explains why fleas, whose body temperatures are lower than that, can act as a vector. Y. pestis can also resist phagocytosis by injecting macrophages and immune cells with YOPS (Yersinia Outer Proteins). The YOPS are able to create pours in the cell, allowing more YOPS to get into the cytoplasm and limit phagocytosis.”(Dramcourt, M., 2013)
“Yersinia Pestis is primarily a rodent pathogen, with humans being an accidental host when bitten by an infected rat flea.”(Schoenstadt, A., 2013) “Yersinia pestis infections occur more frequently during spring and summer months, especially in males and people under the age of 20. There are two cycles to the plague: Sylvatic
Cycle and Urban Cycle. The Sylvatic Cycle is pre-human infection. Y. pestis, during this cycle, starts out in wild rodents which are then bit by fleas. The fleas will transfer the plague between the wild rodents until that population is dead. This cycle continues on in this fashion until either all the rodents are dead, or the fleas find a new food source, usually domestic rats. Once a domestic rat gets bitten, or another domestic animal, the Urban Cycle starts. The start of this cycle is similar to the Sylvatic cycle, where the fleas will bite one domestic animal and then spread it to the