16.8
Plague is a zoonotic disease caused by Yersinia pestis, a Gram-negative, rod-shaped bacterium.
Wild rodents usually carry these bacteria. Fleas that bite infected rodents can pass the bacteria to humans.
Once inside the host, macrophages engulf Y. pestis.
The bacteria activate stress-response pathways that inhibit phagosome maturation and acidification, allowing bacterial survival and proliferation.
These infected macrophages then migrate to the nearby lymph nodes.
Eventually, the bacteria trigger the apoptosis of infected macrophages, allowing them to escape into the extracellular space.
As the infection progresses, the bacteria utilize a type III secretion system to inject Yersinia outer proteins (Yops) into surrounding immune cells, inhibiting phagocytosis and inducing apoptosis.
At this stage, the bacteria express the F1 antigen, forming an antiphagocytic capsule.
This progression of infection leads to severe inflammation and swelling of the lymph node, characteristic of bubonic plague.
Plague is a highly virulent zoonotic disease caused by Yersinia pestis, a Gram-negative, facultatively anaerobic coccobacillus. This pathogen primarily circulates among rodent populations and is transmitted to humans through the bite of infected fleas. Additional transmission routes include direct contact with infected animal tissue or inhalation of respiratory droplets from individuals with pneumonic plague. These multiple transmission pathways highlight the bacterium’s potential for rapid spread and severe outbreaks.
Virulence Factors: Y. pestis evades host defenses using several virulence mechanisms. In the flea, it forms biofilms in the foregut that partially or completely block the flea’s digestive tract, interfering with normal blood-feeding. Blocked fleas repeatedly attempt to feed, and the blockage causes them to regurgitate infected material into the bite wound, which is the principal mechanism of transmitting Y. pestis to mammals.
In the mammalian host, its type III secretion system injects Yersinia outer proteins (Yops) into immune cells, disrupting signaling, inhibiting phagocytosis, and inducing apoptosis. The F1 antigen forms an antiphagocytic capsule, while virulence factors such as LcrV modulate host immune responses. Adhesins such as Pla, Ail, and Psa promote host cell invasion. Additionally, endotoxins—specifically lipopolysaccharides—trigger systemic inflammation and can contribute to septic shock.
Types of Plague: Plague presents in three forms. Bubonic plague, the most common, typically results from flea bites and causes painful, swollen lymph nodes (buboes). Septicemic plague occurs when bacteria enter the bloodstream, leading to hemorrhage, tissue necrosis, and multi-organ failure. Pneumonic plague, acquired via inhalation or secondary spread from another form, causes severe pneumonia and is highly fatal if left untreated.
Symptoms and Treatment: Bubonic plague symptoms include fever, chills, and lymphadenopathy. Septicemic cases may present with hypotension, bleeding, and skin necrosis. Pneumonic plague is characterized by cough, hemoptysis, and respiratory distress. Prompt treatment with antibiotics—such as streptomycin, gentamicin, doxycycline, or ciprofloxacin—significantly reduces mortality. Without early intervention, pneumonic and septicemic forms have extremely high mortality rates.
Plague is a zoonotic disease caused by Yersinia pestis, a Gram-negative, rod-shaped bacterium.
Wild rodents usually carry these bacteria. Fleas that bite infected rodents can pass the bacteria to humans.
Once inside the host, macrophages engulf Y. pestis.
The bacteria activate stress-response pathways that inhibit phagosome maturation and acidification, allowing bacterial survival and proliferation.
These infected macrophages then migrate to the nearby lymph nodes.
Eventually, the bacteria trigger the apoptosis of infected macrophages, allowing them to escape into the extracellular space.
As the infection progresses, the bacteria utilize a type III secretion system to inject Yersinia outer proteins (Yops) into surrounding immune cells, inhibiting phagocytosis and inducing apoptosis.
At this stage, the bacteria express the F1 antigen, forming an antiphagocytic capsule.
This progression of infection leads to severe inflammation and swelling of the lymph node, characteristic of bubonic plague.
From Chapter 16:
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