Plague

Plague is primarily transmitted through infected flea bites. When fleas feed on infected rodents, they become blocked with bacteria in their foregut. These blocked fleas repeatedly attempt to feed and regurgitate infected material into bite wounds, transmitting Yersinia pestis to humans. Direct contact with infected animal tissue or inhalation of respiratory droplets from pneumonic plague cases also transmit the disease.

Yersinia pestis employs multiple evasion strategies. Its type III secretion system injects Yersinia outer proteins (Yops) into immune cells, disrupting signaling and inhibiting phagocytosis. The F1 antigen forms an antiphagocytic capsule protecting the bacterium. Additionally, virulence factors like LcrV modulate host immune responses, while adhesins promote host cell invasion and endotoxins trigger systemic inflammation.

Once macrophages engulf Yersinia pestis, the bacteria activate stress-response pathways that inhibit phagosome maturation and acidification, allowing bacterial survival and proliferation. These infected macrophages migrate to nearby lymph nodes. Eventually, bacteria trigger apoptosis of infected macrophages, allowing them to escape into the extracellular space and continue spreading the infection.

Bubonic plague, the most common form, results from flea bites and causes painful, swollen lymph nodes called buboes. Septicemic plague occurs when bacteria enter the bloodstream, causing hemorrhage, tissue necrosis, and multi-organ failure. Pneumonic plague, acquired through inhalation or secondary spread, causes severe pneumonia and is highly fatal if untreated.

Bubonic plague presents with fever, chills, and lymphadenopathy, particularly swollen lymph nodes in the groin, armpit, or neck regions. Septicemic cases may additionally present with hypotension, bleeding, and skin necrosis. Pneumonic plague is characterized by cough, hemoptysis, and respiratory distress, making it the most severe and rapidly fatal form.

Prompt antibiotic treatment significantly reduces plague mortality. Effective antibiotics include streptomycin, gentamicin, doxycycline, and ciprofloxacin. Early intervention is critical because without treatment, pneumonic and septicemic forms have extremely high mortality rates. Bubonic plague also requires rapid antibiotic therapy to prevent progression to systemic disease.

As Yersinia pestis infection progresses, bacteria express the F1 antigen and utilize virulence factors to evade immune defenses while triggering intense host inflammatory responses. Endotoxins, specifically lipopolysaccharides, trigger systemic inflammation. This combination of bacterial proliferation and immune activation causes severe inflammation and characteristic swelling of lymph nodes, defining bubonic plague's clinical presentation.