The bacterium Yersinia pestis causes plague, a disease known for devastating pandemics like the Black Death. The pathogen’s movement between hosts and throughout an infected body is not self-propulsion but a series of sophisticated interactions with its carriers and the host’s defenses. This multi-stage strategy involves hitching a ride in insects and manipulating the cells of its mammalian host.
The Flea: Yersinia pestis’ Primary Mode of Travel
Yersinia pestis uses fleas as its primary vehicle for moving between mammalian hosts. The journey begins when a flea ingests blood from an infected animal. Inside the flea’s digestive tract, the bacteria multiply rapidly, especially in the proventriculus, a valve in the foregut. Here, the bacteria form a dense, sticky biofilm that can grow large enough to physically block the flea’s digestive tract.
Unable to get nourishment, the starved flea bites more frequently. During these feeding attempts, the biofilm prevents blood from passing through, causing the flea to regurgitate blood mixed with Y. pestis bacteria into the bite wound of a new host. This regurgitation is the bacterium’s primary method for moving from its insect vector to a mammal.
Breaching Defenses: Entering the Mammalian Host
Once in the skin of a mammal, Yersinia pestis invades the host’s tissues. The bacteria are deposited in the dermis and must contend with the immune system. To aid its spread, Y. pestis uses a protein called the plasminogen activator (Pla). This enzyme degrades the extracellular matrix and breaks down fibrin clots that the body forms to wall off infections, allowing the bacteria to move freely.
From the dermis, the bacteria invade the lymphatic system, traveling through lymphatic channels to the nearest lymph nodes. Inside the lymph nodes, Y. pestis replicates to enormous numbers. This multiplication causes the lymph nodes to become severely swollen and painful, forming the lesions known as buboes, the classic sign of bubonic plague.
Journey Through the Body: Systemic Spread
The movement of Yersinia pestis does not stop in the lymph nodes. As the bacteria multiply, the lymph node’s structure breaks down, allowing pathogens to escape into the bloodstream. The presence of large numbers of bacteria in the blood is known as septicemic plague. With access to the circulatory system, Y. pestis travels rapidly throughout the body, seeding infections in organs like the spleen, liver, and lungs, which causes severe damage and inflammation.
If the bacteria establish a population in the lungs, the infection can progress to pneumonic plague. This form opens a new route of movement between hosts. Infected individuals can transmit Y. pestis directly to others through respiratory droplets when coughing. This person-to-person aerosol transmission makes pneumonic plague particularly dangerous and contagious.
Microscopic Tactics: Cellular Movement and Evasion
At the microscopic level, Yersinia pestis uses sophisticated tactics to survive within the host. At the temperature of a mammalian body, the bacterium does not produce flagella, the whip-like tails used for propulsion, rendering it non-motile. Instead of moving itself, it manipulates the host’s cells and can survive and replicate within immune cells called macrophages, which may transport them deeper into tissues.
A primary tool is the Type III Secretion System (T3SS). This acts like a microscopic syringe, allowing the bacterium to inject proteins called Yersinia outer proteins (Yops) directly into host immune cells.
The Yops proteins disrupt the host cell’s internal communication, preventing it from mounting an effective defense. They can paralyze the ability of phagocytic cells to engulf the bacteria, trigger programmed cell death (apoptosis) in immune cells, and suppress the overall inflammatory response. By dismantling the immune response at a cellular level, Y. pestis facilitates its unhindered spread throughout the body.