Cutaneous form and plague carbuncle
The primary lesion at the site of pathogen entry (most commonly insect bite marks on the ankles and dorsum of the feet) can develop in two scenarios. In an abortive course, the lesion quickly dries up, becomes covered with a crust, and the inflammation disappears without a trace. However, a progressive course is much more common, in which the primary phlyctenule transforms into a plague carbuncle involving the subcutaneous adipose tissue.
The evolution of a plague carbuncle goes through several stages:
- The vesicle with hemorrhagic contents increases in size, and inflammation builds up around it.
- A "crimson rim" is formed — a protruding border of intense crimson color. The border with healthy skin remains blurred.
- Due to pronounced edema and the formation of an underlying bubo, the initially mobile carbuncle loses its mobility.
- The contents of the vesicle turn black, and the roof bursts. In its place, an ulcer forms with a hard, yellowish base, which eventually turns into a black scab surrounded by a crimson rim.
Differential diagnosis: visually, a plague carbuncle strongly resembles an anthrax lesion. The key difference lies in the sharp tenderness of the plague focus — at the slightest pressure, the pain becomes excruciating. Such ulcers heal slowly by secondary intention with scar formation.
Bubonic and cutaneous-bubonic forms
The initial period of the bubonic form lasts 1–2 days. It is characterized by severe general toxic syndrome and the onset of increasing local pain in the area of the future bubo. Due to this pain, the patient adopts a forced posture of the limb.
Dynamics of bubo development:
- Adenitis (first hours): the skin over the node is shiny and taut. Lymph nodes are palpated as sharply painful bean-sized formations.
- Periadenitis: tissue edema and crimson-cyanotic skin hyperemia join in. The lesion acquires a cartilage-like consistency, losing clear contours and mobility.
- Growth and maturation: the bubo can grow for up to 8–10 days, reaching the size of a fist. Pain changes from localized to diffuse and becomes slightly duller due to inflammatory damage to nerve endings. The skin thins, and fluctuation appears.
- Resolution: the bubo ruptures spontaneously, discharging thick chocolate-colored fluid or bloody pus. After the rejection of necrotic masses, a deep ulcer forms.
Most commonly, buboes are localized in the femoropupertal (inguinal-femoral) region, less often in the axillary and cervical regions. If infection occurred via the oral route, the lymphoid tissue of the oropharynx is affected, resulting in pharyngeal plague (plague tonsillitis).
In the cutaneous-bubonic form signs of skin and lymph node damage appear almost simultaneously. A specific marker of this form is the complete absence of ascending lymphangitis.
Primary pneumonic form: from euphoria to shock
This is the most severe and fulminant form of plague. Transmission occurs via aerosol, contact, or alimentary routes. The initial period is shortened to 8–12 hours. Temperature rapidly spikes to 38–39°C. Patients often demonstrate "ostentatious vigor": they are euphoric, agitated, and refuse hospitalization. Objectively, tremor (of the body and tongue), dilated pupils, and eyes of a "sleep-deprived person" are detected. At the same time, significant pathology from the heart and lungs is not yet present.
During the peak period the picture changes dramatically:
- Euphoria is replaced by apathy and adynamia. Infectious-toxic delirium with delusions and an unsteady gait is possible.
- Temperature reaches 42°C.
- Clinical-auscultatory dissociation develops: despite the extremely severe general condition (hypotension, tachycardia, stupor), only scanty rales are auscultated in the lungs.
- Later, dyspnea (up to 50–60 respiratory movements per minute) and cough increase. Sputum appears late; it can be transparent-mucous with blood, "rusty", or abundantly bloody. In the variant of "dry plague pneumonia" sputum is completely absent.
The terminal period is characterized by progression into sopor and coma. The patient's appearance is specific: facial features become sharp, the skin acquires a grayish-earthy hue. Dark cyanotic spots appear on the cheekbones and nose. Before death, the temperature drops sharply, a cold sweat breaks out on the face ("pestis dew"), and a hemorrhagic rash appears on the trunk — "spots of death". Decompensated septic shock becomes the direct cause of death.
Briefly: answers to topical questions
Which pathogens cause plague?
The causative agent of plague is Yersinia pestis.
In the presented sources, it is listed as the causative agent of plague; the materials also indicate that it is a Gram-negative facultatively anaerobic rod.
What laboratory diagnostic methods are used for plague?
A set of specific laboratory methods is used to confirm the diagnosis of plague.
- Bacterioscopic method — detection of ovoid microbial cells in smears (includes fluorescent serological microscopy).
- Bacteriological method — isolation of Yersinia pestis culture from bubo aspirate, sputum, or blood on solid nutrient media.
- Biological method — infection of laboratory animals (guinea pigs) with the test biomaterial followed by examination of parenchymatous organs.
- Serological method — detection of antibodies to the capsular antigen of the pathogen using ELISA and IHA.
- Immunological method — detection of the FI antigen of the plague microbe.
- Molecular biological method — application of PCR and hybridization methods to detect single pathogen cells.
What antibiotics are used to treat plague?
Antibiotics in maximum therapeutic doses and in a prolonged course are used to treat plague.
- Streptomycin — the drug of choice, administered intravenously and intramuscularly.
- Tetracycline — an alternative drug for oral administration.
- Doxycycline — an alternative drug for oral or intravenous administration.
- Chloramphenicol — an alternative drug for oral or intravenous administration.
- Rifampicin — an alternative drug for oral or intravenous administration.
- Bactrim — can be used for the cutaneous form of plague.
In disseminated forms, alternative drugs are used in combination therapy with streptomycin, which allows reducing the dose of streptomycin and its toxicity.
For the differential diagnosis of carbuncles, use the mnemonic: Plague is Painfully agonizing. Unlike the anthrax eschar (which is painless), a plague carbuncle causes excruciating pain upon any palpation.
Class and exam questions
What is the essence of "clinico-auscultatory dissociation" in pneumonic plague?
This is a phenomenon where the extreme severity of the patient's condition (delirium, hemodynamic disorders, fever up to 42°C) completely contrasts with the sparse physical findings detected upon percussion and auscultation of the lungs in the early stages.
Which symptom allows differentiating the cutaneobubonic form from other lymphadenitis?
A specific sign is the total absence of ascending lymphangitis between the entry portal of the infection on the skin and the inflamed regional lymph node.
What are "plague dew" and "spots of death"?
These are prognostically unfavorable signs of the terminal stage of pneumonic plague. "Dew" is the appearance of profuse sweating on the face against the background of a sharp drop in temperature, and "spots of death" are a hemorrhagic rash about 1 cm in size on the trunk and limbs.
What else to study on this topic
- Mechanisms of formation of secondary buboes along the lymphatic drainage pathway.
- Features of the course of pharyngeal plague (pestis angina).
- Pathogenesis of infectious-toxic shock development and causes of mortality.
- Criteria for the transition of local forms to secondary disseminated forms and the development of sepsis.
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