Plague

Plague– an acute illness of a group of quarantine infections, occurring with severe intoxication, fever, damage to the lymph nodes, septicemia and pneumonia. Etiology. The causative agent is the immobile gram-negative bacterium Yersinia pestis of the Enterobacteriaceae family. Epidemiology. The main natural reservoir is all kinds of rodents (rats, squirrels, prairie dogs, marmots, etc.), cats play a certain role in the transmission of the pathogen. In the transmission of plague to humans, the leading role is played by adult individuals of rat fleas (Xenopsylla cheopsis), which retain the pathogen for life. It has been shown that a person becomes infected not so much with a bite, but after rubbing flea feces or masses regurgitated during feeding into the skin. Pathogenesis. The causative agent is introduced into the body at the site of a flea bite; in turn, fleas become infected with bacteria, feeding on the blood of rodents during the period of bacteremia preceding the death of animals (there is no transovarial transmission of the pathogen in fleas, the bacteria die when they enter the intestines of the larvae). At a flea body temperature of 28 °C, the pathogen does not form products that are toxic to humans. In the human body, cells absorbed by neutrophils partially die, but the surviving bacteria begin to synthesize toxic substances. The pathogenesis of the disease is not fully understood. None of the antigens or toxin produced by the pathogen alone can cause disease. The mechanism of development of the disease includes 3 stages. At a flea body temperature of 28 °C, the pathogen does not form products that are toxic to humans. In the human body, cells absorbed by neutrophils partially die, but the surviving bacteria begin to synthesize toxic substances. The pathogenesis of the disease is not fully understood. None of the antigens or toxin produced by the pathogen alone can cause disease. The mechanism of development of the disease includes 3 stages. At a flea body temperature of 28 °C, the pathogen does not form products that are toxic to humans. In the human body, cells absorbed by neutrophils partially die, but the surviving bacteria begin to synthesize toxic substances. The pathogenesis of the disease is not fully understood. None of the antigens or toxin produced by the pathogen alone can cause disease. The mechanism of development of the disease includes 3 stages.

• • Lymphogenic transport from the site of penetration to the lymphatic barriers.
  • Spread of bacteria from the lymph nodes into the bloodstream (bacteremia).
  • Spread of viruses to barrier cell systems (generalized septicemia).
  • Note. Penetrated pathogens actively absorb mononuclear and polymorphonuclear phagocytes, however, phagocytic reactions are incomplete and contribute to the further spread of the pathogen. Of particular importance are the rapid reproduction of the pathogen, its localization within the capillaries and blood vessels, causing rapid penetration into the bloodstream. At the same time, the plague bacillus spreads lymphogenously, causing multiple polyadenitis.

clinical picture. The incubation period is 3-6 days (with epidemics or septic forms it is reduced to 1-2 days). The disease begins with a sudden rise in body temperature with a headache and a feeling of weakness; characteristic plaque on the tongue (rubbed with chalk), its edema, as a result of which speech becomes slurred; in severe cases, psychosis develops. Against the backdrop of the overall picture, other signs join. Most often, the pathogen is introduced through the skin, but only 3-4% of patients have a local reaction in the form of highly contagious pustules and carbuncles (skin plague). More often, the plague bacillus does not cause inflammatory changes in the skin and migrates to the nearest lymph node. Within 2-6 days, serous-hemorrhagic inflammation develops in the lymph nodes, and a sharply painful bubo is formed. It is not uncommon to observe the attachment of a regional bubo to skin plague, which is manifested by the skin-bubonic form of plague. Pathogenetically distinguish between primary (always associated with the site of the entrance gate of infection) and secondary buboes (appear hematogenously). According to clinical manifestations, mainly local forms (cutaneous, cutaneous-bubonic and bubonic), generalized or internally septic forms (primary and secondary septic) and externally disseminated forms (primary and secondary pulmonary, intestinal) are distinguished.

• • Bubonic plague. The cardinal sign is a bubo (usually axillary or inguinal), an early sign is a feeling of severe pain at the site of the future development of the bubo (often the patient is forced to take unnatural postures). Increasing to 1-10 cm in diameter, it softens, can fester and drain spontaneously. In the case of the development of hemorrhagic necrosis of the lymph node and the loss of the barrier function, a large number of bacteria enter the bloodstream, which leads to secondary plague pneumonia and / or generalized plague sepsis. As a complication, secondary pulmonary plague accounts for 5-10% of bubonic lesions and sharply aggravates the patient’s condition; sometimes recorded (due to generalization) secondary plague meningitis, as a rule, ends in the death of the sick person. The mortality rate for untreated bubonic plague is 75%.
  • Primary pneumonic plague is a fulminant and extremely contagious form; spreads by airborne droplets and is epidemically the most dangerous. The patient excretes a large number of pathogens with sputum, while the volume of sputum can reach huge amounts. The mortality rate in untreated cases is close to 100%. Death begins in 2-6 days after the primary aerogenic contact with the infection.
  • Intestinal plague is manifested by profuse diarrhea with copious secretions of blood and mucus, severe pain in the epigastric region and a feeling of general malaise are possible, traditionally ending in the death of the sick person.
  • Primary septic plague is characterized by numerous hemorrhages on the skin and mucous membranes; severe cases are characterized by massive bleeding from the kidneys, intestines and blood in the vomit. The generalization of the process occurs without previous phenomena of a local order; exceptionally rapid dissemination of the pathogen in the body, massive intoxication and bacteremia are typical. The disease quickly ends with the death of the sick person.
  • Secondary septic plague – the outcome (complication) of other forms of the disease, is also extremely difficult, clinically manifested by the occurrence of secondary foci of infection, buboes and signs of hemorrhagic septicemia.
  • The secondary pulmonary form is a complication of bubonic plague, clinically similar to the primary one.

Research methods

• • Examination of discharged bubo (in the bubonic form), the contents of an ulcer or other skin lesions (cutaneous form), sputum and mucus from the throat (pulmonary form), blood (all forms), feces and CSF (with lesions of the intestines or meninges). The material should be obtained before starting antibiotic therapy.
  • It is possible to carry out accelerated diagnosis of plague using bacteriophage Yersinia pestis
  • Fluorescein-labeled ATs are also used for rapid detection (allows detection of Yersinia pestis during the first 2 hours of the study), AT neutralization reaction, precipitation reaction in standard agar plates and the method of accelerated growth of Yersinia pestis on enrichment media
  • The probability of isolating the pathogen increases the biological test on laboratory animals. Methods have been developed that speed up the biological test, for example, the administration of glucocorticoids or chicken yolk to infected animals, which speeds up the diagnosis of plague in cases of reduced virulence or when using a low infectious dose.

Differential diagnosis is carried out with other conditions accompanied by bacteremia, with pneumococcal pneumonia and lymphangitis of various etiologies.

Treatment:

• • Streptomycin 30 mg/kg/day IM in 4 doses every 6 hours for 7-10 days. Presumably equally effective gentamicin. With a septic or pulmonary form, treatment should begin on the first day of the disease.
  • An alternative product is tetracycline 25–50 mg/kg b. 4 doses within 10 days.
  • In plague meningitis – chloramphenicol (levomycetin) at an initial dose of 25 mg / kg IV, then 10-15 mg / kg IV or orally 4 r / day for 10 days.
  • Precautions
  • In renal failure, streptomycin is prescribed at 20 mg / kg / day every day or 8 mg / kg / day after 3 days
  • Pregnant women and with hearing impairment, streptomycin is prescribed only for 3 days after the cessation of fever.

Complications

• • Progression of the bubonic form to septic and pulmonary forms
  • Bubo necrosis
  • Pericarditis
  • Adult Respiratory Distress Syndrome
  • Meningitis. ICD. A20 Plague

Literature

• 129:286-288
• Plague. Domaradsky IV. M.: Medicine, 1998