Clinical presentation and history taking
The disease begins extremely acutely with a severe intoxication syndrome: shaking chills, high fever, severe headache, muscle, joint, and bone pain (myalgia, arthralgia, ossalgia).
An important sign is early encephalopathy. The patient's consciousness rapidly deteriorates: disorientation, shivering tremor, inadequate behavior, delirium, or conversely, stupor and depression may be observed. Because of this, medical history taking must be as prompt and thorough as possible, as the patient may soon become unresponsive.
Cardiovascular function progressively worsens: tachycardia increases, blood pressure drops, pulse pressure decreases, arrhythmias and muffled heart sounds appear. Dyspnea and hemorrhagic tissue infiltration are also characteristic.
Laboratory diagnostics
Complete blood count reveals nonspecific signs of severe infection: neutrophilic leukocytosis with a left shift (down to myelocytes and promyelocytes), toxic granularity of neutrophils, Türk cells. There is also a tendency toward decreased red blood cells, the appearance of binuclear monocytes and lymphocytes, polychromasia, and normoblasts.
Specific diagnostics include:
- Bacterioscopy: detection of ovoid bipolar-stained cells.
- Bacteriological method: inoculation of material onto nutrient media (e.g., Hottinger agar).
- Biological assay: infection of laboratory animals (death on day 5 with isolation of the pathogen).
- Serology and immunology: ELISA, indirect hemagglutination assay (IHA) to detect antibodies and the FI antigen.
- Molecular biological methods: PCR.
Treatment: antibiotics and pathogenetic therapy
Treatment is initiated before laboratory test results are available. Hospitalization is mandatory and urgent.
Antibacterial therapy: The drug of choice is Streptomycin (intravenously and intramuscularly, 1.0 g twice daily). Alternative drugs (tetracycline, doxycycline, chloramphenicol, rifampicin) are used for disseminated forms in combination with streptomycin to reduce its dosage and toxicity, or as monotherapy in case of intolerance. The duration of the course for disseminated forms is at least 10 days.
Pathogenetic therapy is aimed at combating sepsis and shock:
- Hemodynamic support (crystalloids, colloids, vasopressors).
- Respiratory support (oxygen therapy, mechanical ventilation).
- Corticosteroids (in case of adrenal insufficiency).
- Hemostasis correction, extracorporeal detoxification, and nutritional support.
Discharge criteria
A patient can be discharged only if two conditions are met:
- Complete clinical recovery. For disseminated forms, a stable normalization of body temperature for at least 30 days is required, as well as complete resolution of pneumonia or other septic foci.
- Bacteriological clearance. Two negative bacteriological test results are required with an interval of 5–6 days (strictly after completion of antimicrobial therapy).
Convalescents undergo dispensary follow-up for 3 months.
Briefly: answers to topical questions
How does primary septicemic plague differ from secondary septicemic plague?
The main difference is that primary septicemic plague is characterized by the absence of an identifiable visible port of entry for the infection, whereas secondary septicemic plague develops in patients with cutaneous, bubonic, or pneumonic forms of plague.
| Sign | Primary septicemic plague | Secondary septicemic plague |
|---|---|---|
| Pathogenesis | No visible port of entry for the infection can be identified. | Develops in patients with cutaneous, bubonic, or pneumonic forms. |
| Manifestations | Septic forms are characterized by an extremely pronounced hemorrhagic syndrome. | Sharp intensification of the intoxication syndrome; appearance of secondary phlyctenae, carbuncles, bullous, pustular, and hemorrhagic rashes; formation of secondary buboes; possible development of disseminated intravascular coagulation (DIC) syndrome and multiple organ dysfunction syndrome. |
What postmortem changes are detected in internal organs in septicemic plague?
Postmortem changes in septic forms are accompanied by an extremely pronounced hemorrhagic syndrome and massive hemorrhages into internal organs.
The following changes are detected:
- Parenchymatous organs — signs of granular and fatty degeneration, hemorrhages, foci of necrosis.
- Spleen — enlarged 1.5–2 times, flaccid consistency (dark red pulp on cross-section).
- Lungs — macroscopic picture of hemorrhagic edema.
- Central nervous system — edema, hyperemia, hemorrhages in the brain and meninges.
- Serous cavities — presence of serosanguineous exudate.
Class and exam questions
By interviewing the patient themselves as quickly as possible, since they may soon lose consciousness due to escalating encephalopathy. It is important to find out the exact time of disease onset (first chills) and epidemiological history (contact with rodents, stay in endemic zones).
First, an epidemiological history should be taken (contact with rodents, stay in endemic foci) and the exact time of onset of the first symptoms should be determined. The interview must be prompt due to the risk of impending disturbance of the patient's consciousness.
Which antibiotic is the drug of choice?
The drug of choice is Streptomycin. It is administered intravenously and intramuscularly at a dose of 1.0 g twice a day.
What conditions are necessary for discharge after the disseminated form?
Stable normalization of temperature for at least 30 days, clinical resolution of all foci, and two negative bacteriological culture results taken with an interval of 5–6 days after the end of antibiotic therapy.
What else to study on this topic
- Features of the development and clinical presentation of the bubonic form of plague
- Management tactics for the cutaneous form of plague and the use of Bactrim
- Specifics of discharging patients after the pneumonic form of plague
- Factors prolonging the incubation period of plague
- Immunosubstitutive therapy (pentaglobin) in pathogenetic treatment
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