Pathogenesis of plague

Initial period and generalization

Upon entering the body, the plague bacillus typically encounters lymphatic barriers. However, in rare cases, the pathogen bypasses them and immediately penetrates the mononuclear phagocyte system. Settling directly in the liver, lungs, and spleen, it forms the primary septic or primary pulmonary forms of the disease.

The clinical presentation begins with turbulent bacteremia and toxinemia. The main culprit behind the intoxication is lipopolysaccharide (LPS). It acts not so much directly, but indirectly by forcing the body's own cells (activated leukocytes, endothelial cells, and platelets) to produce massive amounts of inflammatory mediators.

Peak: microcirculatory disorders and dissemination

At the site of entry, a focus of hemorrhagic infiltration and necrosis forms, where the bacterial multiplication rate sharply increases. Severe circulatory disorders develop, driven by two causes:

1. Direct cytotoxic action of the bacteria themselves.
2. Attack by the body's own sensitized macrophages, neutrophils, and lymphocytes.

These morphological changes lay the foundation for three life-threatening conditions: severe intoxication syndrome, DIC syndrome, and acute respiratory distress syndrome (ARDS), which manifests clinically as hemorrhagic pulmonary edema with frothy bloody sputum.

Next, the pathogen spreads via two pathways:

• Lymphogenous: formation of primary secondary-order buboes.
• Hematogenous: formation of secondary buboes in distant lymph nodes, as well as foci in the nervous system, gastrointestinal tract, and parenchymal organs.

Mechanisms of shock

Total vascular damage, increased permeability, sludge syndrome, and thrombosis trigger an irreversible pathological cascade. Tissue hypoxia exacerbates tissue necrobiosis, leading to multiple organ dysfunction syndrome and septic shock—the leading cause of death in plague.

Infectious-toxic shock (ITS) here has unique features:

• The bacterial murine toxin acts as a $\beta$-blocker. This disrupts the natural compensatory responses of the cardiovascular system (manifesting as a drop in blood pressure and absolute tachycardia up to 150 bpm).
• Shock is accompanied by prominent hemorrhagic syndrome. In addition to consumption coagulopathy, powerful primary fibrinolysis occurs because the bacterium secretes its own plasminogen activator (fibrinolysin).

Pathomorphology of inflammation

The inflammatory process in tissues always follows a strict dynamic: from serous-hemorrhagic to hemorrhagic-necrotic. Purulent inflammation occurs only later as a reaction to established necrosis.

Characteristic changes in organs:

• Skin: potential appearance of a phlyctenule—a specific vesicle containing bloody fluid and a massive number of pathogens.
• Lymph nodes (buboes): a conglomerate with periadenitis, the tissue is soaked in blood and visually resembles clots. Outcome: melting, gangrene, or sclerosis.
• Lungs: pseudolobar bronchopneumonia develops with turbid, viscous exudate. An important distinction from lobar pneumonia is the complete absence of fibrin in the alveolar exudate (unless the patient received antibiotics).
• Spleen: becomes "septic"—flabby, enlarged by 1.5–2 times, with dark red pulp yielding abundant scrape.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Clinical manifestations of intoxication and the formation of facies pestica
• Evolution of the local lesion in cutaneous plague (stages of phlyctenule development)
• Neuropsychiatric disorders: development of infectious delirium and CNS involvement
• Classification of clinical forms of plague according to G.P. Rudnev and ICD-10
• Features of the disease course at the beginning and peak of an epidemic (ambulatory and fulminant forms)

Other topics in the section "Zoonotic infections — 2024 study guide"

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