Characteristic features of the bubo during the plague. Plague as a biological weapon. Currently, the incidence of human plague is relatively low. Active enzootic foci remain in Southeast Asia, Africa and America

Plague– an acute zoonotic natural focal infectious disease with a predominantly transmissible mechanism of transmission of the pathogen, characterized by damage to the lymph nodes, skin and lungs, severe intoxication and often the development of sepsis. Refers to particularly dangerous infections.

Etiology: Yersinia pestis - Gr-bacillus, pathogenicity factors - endo- and exotoxins, a number of enzymes (coagulase, hemolysin, etc.)

Epidemiology: the main sources (reservoir) are various rodents and lagomorphs (among people, epidemics are caused by the migration of rats); transmission mechanisms - transmissible (during a bite, a flea infected by blood-sucking rodents regurgitates the contents of the stomach with a large number of plague bacilli into the blood of the new host), aerosol (especially from patients with plague pneumonia), contact (through damaged skin when caring for a patient, etc. ), nutritional (when eating meat from sick animals)

Pathogenesis: introduction of MB into the body through the skin, mucous membranes of the respiratory and digestive tracts --> migration through the lymphatic vessels without lymphangitis to regional lymph nodes. --> intensive reproduction in l.u. with the development of lymphadenitis with a sharp increase in lymph nodes, their fusion and the formation of conglomerates ( bubonic plague) --> hemorrhagic necrosis of the l.u. --> breakthrough of a large number of MB into the blood --> bacteremia ( septic form of plague) --> formation of secondary foci in various organs (rapidly progressing plague pneumonia with hemorrhagic necrosis is especially dangerous), massive intoxication due to the breakdown of MB and the release of endotoxin

Clinical picture of plague:

The incubation period is on average 3-5 days (from several hours to 10 days)

Acute onset with a rapid increase in temperature to 39 ° C or higher, severe chills, intense headache, pain in the spine, muscles and joints, muscle weakness, sometimes vomiting with blood or the color of coffee grounds or liquid stool mixed with mucus and blood

The patient is initially excited, frightened, delirious, often jumps out of bed, trying to run away somewhere, uncoordinated movements, staggering gait (“drunk”), slurred speech

The characteristic appearance of the patient: the face is hyperemic, puffy, amicable, the conjunctiva and sclera are injected, sometimes with pinpoint hemorrhages, the skin is hot, dry; in a serious condition, the facial features sharpen, the face becomes cyanotic, and an expression of fear and suffering appears (“plague mask”)

The mucous membranes of the oropharynx and soft palate are hyperemic, with pinpoint hemorrhages, the tonsils are enlarged, swollen, the tongue is thickened, covered with a characteristic white coating (“rubbed with chalk”)

Blood circulation and breathing are sharply impaired, characterized by tachycardia, muffled heart sounds, thready pulse, progressive hypotension, tachypnea

The abdomen is swollen, the liver and spleen are enlarged, in severe conditions the urge to defecate becomes more frequent (up to 6-12 times a day), stool becomes unformed and contains an admixture of blood and mucus

Diuresis sharply decreases, protein is detected in the urine

Other manifestations depend on the clinical form of the plague:

1) predominantly local forms:

a) cutaneous form– rarely observed, a spot appears at the site of the flea bite, then a papule, vesicle and pustule; the pustule is surrounded by a zone of hyperemia, located on a hard base, filled with serous-hemorrhagic contents, and is characterized by significant pain, sharply increasing with pressure; when the pustule bursts, an ulcer forms, the bottom of which is covered with a dark scab; it slowly heals with the formation of a scar.

b) bubonic form– occurs most often, buboes develop in those places where the skin is usually exposed to flea bites (inguinal, less often axillary and cervical areas)

The first sign of a developing bubo is severe pain, which makes it difficult to move the limbs and neck, forcing patients to take forced positions (bent leg, neck, arm pulled to the side)

Initially, individual painful nodes are identified by palpation, then the inflammatory process quickly increases, the nodes are soldered together, forming a conglomerate, the surrounding tissues (periadenitis) and the skin are involved in the inflammatory process - a cutaneous bubo is formed; the skin over the bubo is hot to the touch, purple-bluish

At first, the bubo has a cartilaginous consistency, then a fluctuation appears and on the 6-8th day the bubo opens with the release of thick greenish-yellow pus, which may contain a pathogen; Extensive ulcerations may form in place of the opened buboes

After opening the bubo, the general condition begins to improve, the buboes are slowly healing

The formation of secondary buboes is possible as a result of hematogenous introduction of the pathogen, but in these cases the process usually does not reach suppuration

The most dangerous are axillary (as secondary pneumonic plague often develops) and cervical buboes (as they are accompanied by swelling of the mucous membranes of the pharynx and larynx)

c) cutaneous bubonic form– a combination of the two previous forms

2) generalized forms:

a) septic form(primary septic - develops primarily and secondary septic - against the background of buboes) - a fatal form of the disease, the incubation period is from several hours to 1-2 days, begins suddenly, acutely, against the background of severe toxicosis, extensive, confluent, purplish hemorrhages appear on the skin blue color (“black plague”, “black death”), hemorrhages on the mucous membranes, nosebleeds and other bleeding, infectious-toxic shock quickly develops with the subsequent death of the patient; bacteremia is so pronounced that the pathogen is easily detected by Gram staining of the light layer of the blood clot

b) pulmonary form, or plague pneumonia(primary pulmonary - with an aerosol mechanism of infection and secondary pulmonary - develops against the background of buboes) - the most severe form of the disease:

Begins hyperacutely with severe chills, rapid rise in body temperature, severe headache, dizziness, repeated vomiting, aches in muscles and joints

After a few hours, chest pain appears when breathing, a dry cough, shortness of breath, then the cough becomes productive; sputum is initially viscous, mucous, then it becomes liquid, foamy, bloody, and contains a huge amount of plague bacilli

Physically, slight shortening of the pulmonary sound over the affected lobe, auscultation of mild fine bubbling rales

The condition of patients progressively worsens, neurotoxicosis increases, death occurs from cardiovascular and respiratory failure

Diagnosis of plague:

1) epidemiological history (stay in endemic areas, living in places where animal deaths are observed or cases of the disease have already been registered) and a typical clinic

2) bacterioscopic (detection of Gr-bipolarly colored rods is possible within 1 hour) and bacteriological (culture identification is possible within 3-5 days) examination of punctate or discharge of opened buboes, contents of skin elements, sputum, blood, vomit, feces, urine

3) biological test on animals

4) serological diagnostic methods (RNGA, RSK, indirect immunofluorescence reaction, etc.)

Differential diagnosis of bubonic plague is carried out with:

a) with the bubonic form of tularemia– unlike the plague, the formation of a bubo in tularemia is not accompanied by a sharp pain syndrome, l.u. do not form a conglomerate, suppuration occurs in the late stages of the disease

b) with infectious mononucleosis– unlike the plague, generalized lymphadenopathy is characteristic, detected from the first days of the disease by palpation of the lymph nodes. elastic consistency, sensitive or painful, moderately enlarged, formation of buboes and suppuration of l.u. does not occur, hepatosplenomegaly, tonsillitis and specific changes in peripheral blood (appearance of mononuclear cells) are characteristic, Paul-Bunnel and Hoff-Bauer reactions are positive

c) with HIV– unlike the plague, generalized lymphadenopathy and enlarged lymph nodes are characteristic. moderate density, sensitive or painful on palpation, not fused with each other and with surrounding tissues, their contours are smooth, characterized by progressive weakness, decreased performance, loss of body weight, and subsequently numerous infectious complications

Doctor’s tactics for suspected quarantine infection:

When identifying a patient suspected of having a quarantine infection, all primary anti-epidemic measures are carried out when preliminary diagnosis based on clinical and epidemiological data and include the following steps:

1. identification of the patient and information about the identified patient - the primary alarm about the identification of a patient with a particularly dangerous infection (EDI) is carried out to three main authorities: 1) the chief physician of the health care facility; 2) ambulance stations; 3) the chief physician of the territorial Center for Hygiene and Epidemiology. The chief doctor of the Center for Hygiene and Epidemiology puts into effect the plan of anti-epidemic measures, informs the relevant institutions and organizations about the case of the disease

2. clarification of the diagnosis, isolation of the patient followed by hospitalization and treatment

3. observational, quarantine and other restrictive measures - carried out taking into account the incubation period of the infectious disease (for plague - 6 days, for cholera - 5 days, Lassa fever, Ebola - 21 days)

4. identification, isolation, emergency prophylaxis for persons in contact with the patient - when identifying cholera patients, only those persons who interacted with them during the period of clinical manifestations of the disease are considered contacts; medical workers who have been in contact with patients with plague or hemorrhagic fevers are subject to isolation until a final diagnosis is made or for a period equal to the incubation period

5. provisional hospitalization of patients with suspected acute respiratory infections

6. identification of those who died from unknown causes, pathological autopsy of the corpse with collection of material for laboratory research, proper transportation and burial of corpses

7. disinfection measures

8. emergency prevention of the population with subsequent monitoring of it

9. sanitary control of the external environment (laboratory research of possible factors of infection transmission, monitoring the number of rodents and their fleas, conducting an epizootological examination, etc.)

10. health education

Activities are carried out by local authorities and health care institutions together with anti-plague and other institutions that provide methodological guidance, advisory and practical assistance.

Therapeutic measures for plague:

1. If plague is suspected, patients are hospitalized on special transport to special guarded hospitals.

2. Etiotropic therapy begins immediately, without waiting for laboratory confirmation of the diagnosis: aminoglycosides (streptomycin 3-5 g/day, gentamicin up to 240 mg/day), tetracycline 4-6 g/day, chloramphenicol up to 6 g/day parenterally for 7-10 days ; simultaneously with ABT, intensive detoxification is carried out, because rapid bacteriolysis can lead to infectious-toxic shock.

3. Pathogenetic therapy: detoxification agents (colloids and crystalloids IV + furosemide / lasix - formed diuresis) and, if indicated, anti-shock therapy, correction of respiratory failure, in the presence of hemorrhages - relief of DIC syndrome (fresh frozen plasma, heparin), plasmapheresis, etc.

4. Local treatment of buboes is not indicated until fluctuation appears or spontaneous drainage of the bubo occurs: the introduction of antistaphylococcal antibiotics (oxacillin, methicillin) into the buboes.

Plague- a vector-borne infection that has a natural focal nature and, due to its danger, is included in the list of infections that are subject to the International Health Regulations.

The name of the disease comes from the Arabic word “jumma”, which means “bean”, since in the plague the lymph nodes take on a bean-shaped shape. The disease was known even before our era; earlier, the plague often took the form of a pandemic, claiming hundreds of thousands of human lives. There have been three plague pandemics in history. The first lasted from 527 to 580 - known in historical documents as the “Justinian” plague. Starting in Egypt, the dangerous infection spread to port cities in the Mediterranean, the Middle East and reached Europe. During the entire pandemic, more than 100 million people died. The second pandemic, during which the plague was nicknamed the “Black Death,” began in 1334 and lasted more than thirty years. Foci of the plague first appeared in China, then the population of India, Africa and Europe became infected. In 1364, the plague reached Asia and entered Russia. Only in 1368 were the first attempts to introduce anti-plague quarantine measures made in Venice. During the entire pandemic, about 50 million people died. The third plague pandemic, which began in 1894, spread from Canton and Hong Kong, covering all continents of the globe. This led to the death of 87 million people. During the period of the third pandemic, some scientific discoveries were made, which subsequently served as an impetus for the development of anti-plague measures. Thus, in 1984, A. Yersin discovered the causative agents of plague in the corpses of dead people and rats. The mechanism of transmission of the disease from sick rodents to healthy ones and from infected rats to humans was also discovered: through fleas. Soviet scientist D.K. Zabolotny in 1912 proved the natural focal nature of the plague. All this gradually led to a significant decrease in cases of plague infection, but isolated cases are still found in natural foci.

Etiology of plague

The causative agent of plague is Yersinia pestis, most often having the shape of a stick. However, Yersinia has also been described in the form of threads and grains. Yersinia pestis has a capsule, but does not form spores, and is gram-negative. It has a peculiarity: when stained with aniline dyes, it acquires a bipolar color. Yersinia pestis is a facultative anaerobe and grows well on meat-peptone media. The causative agent of plague produces exo- and endotoxins and has about 20 antigens.

Boiling leads to the death of Yersinia pestis within a few seconds; low temperatures contribute to the long-term preservation of the bacterium. The plague pathogen can remain on food products for up to 3 months. Soil and rodent burrows can harbor Yersinia pestis for months. The bacterium lives in fleas and ticks for about a year. Conventional disinfectants and antibiotics are destructive for Yersinia pestis: streptomycin, tetracycline, chloramphenicol.

Epidemiology of the plague

Plague is a naturally occurring, vector-borne zoonosis.. There are primary and secondary foci of plague. The former are also called natural, the latter - anthropourgic. In natural foci - in steppes, deserts and semi-deserts - the circulation of the disease is maintained thanks to natural reservoirs - rodents and infection carriers - fleas. The existence of such foci does not depend on human activity.

Active reproduction of Yersinia pestis occurs in the proventriculus of the flea. This leads to the formation of a gelatinous substance in it, blocking the lumen of the stomach. After sucking blood, the flea “burps” bacteria into the wound.

Human infection with plague occurs in various ways. The vector-borne route of infection is described above. Contact-household infection can occur when skinning infected commercial rodents or when cutting up a camel carcass. Eating foods contaminated with Yersinia is a food route of infection. Airborne transmission of the disease occurs through contact with patients with pneumonic plague.

Humans are very susceptible to plague. In areas with a temperate climate, a large number of cases of the disease are registered in the summer-autumn period, in areas of hot climates - mainly in winter.

Pathogenesis of plague

Penetration of Yersinia pestis into the human body occurs more often through a wound, less often through the mucous membrane of the stomach and respiratory tract. More often than not, no traces remain at the site of pathogen penetration. Sometimes it is possible to form a primary affect, which manifests itself as inflammation and ulceration. Next, the pathogen travels with the lymph flow to the nearest regional lymph nodes. This is where Yersinia pestis reproduces and accumulates. Bacteria are captured by macrophages, but phagocytosis remains incomplete, which leads to the formation of an intracellular form of bacteria. The presence of Yersinia pestis in the lymph nodes leads to the occurrence of serous-hemorrhagic inflammation, occurring against the background of necrosis of lymphoid tissue. Lymph nodes increase in size, and the surrounding tissues become inflamed. As a result, a conglomerate of lymph nodes is formed - a bubo. The breakthrough of the pathogen into the bloodstream leads to bacteremia, intoxication and spread of Yersinia pestis to other organs with the formation of secondary foci of infection. Dissemination of bacteria leads to the development of sepsis and secondary septic forms of the disease (secondary pulmonary form). Sometimes the plague immediately takes the form of sepsis, occurring without pronounced reactions from the regional lymph nodes.

Endotoxins trigger a number of processes that underlie infectious-toxic shock. Damage to blood vessels and the hemostatic system is of great importance in the pathogenesis of plague, which leads to the development of disseminated intravascular coagulation syndrome.

After surviving the disease, strong immunity remains.

Clinical picture of plague

Currently they use the classification of plague proposed by G.P. Rudnev.

1. Local forms:
   • cutaneous;
   • bubonic;
   • cutaneous bubonic;
2. Generalized forms:
   1. internally disseminated:
      • primary septic;
      • secondary septic;
   2. externally disseminated:
      • primary pulmonary;
      • secondary pulmonary.

Incubation period of plague lasts from three to six days. The disease begins acutely, often without a prodromal period. A sick person's temperature rises to 39-40 ° C and chills appear. Intoxication syndrome is expressed in excruciating headaches and muscle pain, nausea and vomiting often develop. The face becomes puffy, hyperemic, later acquires a bluish tint, and circles appear under the eyes. Dry lips are noticeable. The tongue is trembling, dry, covered with a white coating.

One of the first manifestations of the plague- damage to the cardiovascular system: tachycardia, weak pulse filling, arrhythmia. Heart sounds become muffled, blood pressure drops.

Symptoms of damage to the nervous system can vary. Some patients develop insomnia, stupor, and lethargy, while others develop agitation, delirium, and hallucinations. Due to the appearance of slurred speech, staggering gait and lack of coordination, such patients are often mistaken for drunken people.

From the gastrointestinal tract, abdominal bloating, pain, enlargement of the liver and spleen can be noted. In severe cases of the plague, vomiting like coffee grounds and diarrhea with blood and mucus may occur.

Bubonic plague

Bubonic plague is the most common (80-90% of all cases of the disease). Bubo - enlarged, painful lymph nodes; more often they are located near the site of introduction of the pathogen. A sharply painful formation with a diameter of 1 to 10 cm forces patients to take a forced position. The lymph nodes are immobile, fused to the surrounding subcutaneous tissue. The skin over the bubo is tense and hyperemic. After a week, the bubo becomes softer, the skin over it acquires a bluish-purple color. On days 8-12, the bubo opens. In this case, serous-purulent contents mixed with blood are released. Bubo secretions contain large amounts of Yersinia pestis. With a favorable course of the disease, the bubo resolves within a week or its sclerosis occurs.

In most cases, the buboes are located in the groin and thigh, less often in the axillary, cervical, and parotid areas. Most often one bubo is formed, but there may be several.

Cutaneous plague

Cutaneous plague rarely occurs in isolation and more often develops into a cutaneous-bubonic form. At the site of pathogen penetration, a spot is formed, which gradually passes through the stages of papules, vesicles, and pustules. The surrounding tissues form the so-called crimson shaft - an infiltrated and raised area of ​​skin. Next, ulceration of the pustule occurs. The bottom of the ulcer is infiltrated and yellow. Plague ulcers take a long time and heal poorly, leaving a scar after healing.

Cutaneous bubonic plague

Cutaneous bubonic plague combines signs of cutaneous and bubonic forms of the disease.

Primary septic form of plague

Primary septic form develops in the absence of previous changes in the skin and lymph nodes. This form of the disease is rare. The primary septic form of plague proceeds rapidly - after a short incubation period, symptoms of intoxication, damage to the cardiovascular and nervous system, and hemorrhagic syndrome come to the fore.

Patients complain of the sudden onset of headache, muscle pain, fever, chills. Damage to the nervous system is manifested by delusions, hallucinations, and the possible development of meningoencephalitis. The development of hemorrhagic syndrome is indicated by the appearance of nasal, gastrointestinal, and pulmonary bleeding. The liver and spleen increase in size, nausea, vomiting, and loose stools appear. Plague in this form often ends fatally 1-3 days after its onset.

Secondary septic form of plague

Secondary septic form often accompanies the bubonic form of the disease. It occurs with severe intoxication and the appearance of secondary foci of infection.

Primary pneumonic form of plague

During the most dangerous form of plague in epidemiological terms, three periods are distinguished - the beginning, the height and the terminal.

• The initial period of the primary pneumonic form of plague begins with the sudden onset of chills and fever. The patient becomes restless, complains of headaches and muscle pain, nausea, and vomiting. A day later, cutting pain in the chest, shortness of breath, and tachycardia appear. Cough in the pulmonary form of plague may be accompanied by sputum production (“wet” form of plague pneumonia), but it may be absent (“dry” form of plague pneumonia). At first, the sputum is net-shaped and transparent, then it takes on a bloody appearance and gradually becomes bloody. A characteristic feature of sputum during plague pneumonia is its liquid consistency. The sputum of a patient with pneumonic plague contains a large amount of the pathogen.
• IN peak period, which lasts from several hours to two days, the patient’s face becomes hyperemic, his eyes are bloodshot, shortness of breath and tachycardia worsen. Blood pressure decreases.
• Terminal period- the patient's condition is serious. Chest pain becomes unbearable, stupor develops. Blood pressure drops sharply, the pulse becomes thready. Death occurs due to hemodynamic disturbances and pulmonary edema.

Secondary pneumonic form of plague

Secondary pneumonic form of plague can be a complication of any other form of the disease and proceeds in the same way as the primary pulmonary form of plague.

Complications

Localized complications- secondary septic and secondary pulmonary forms, as well as plague meningitis. Nonspecific complications - secondary infection, suppuration of buboes. Generalized forms of plague often lead to infectious-toxic shock, coma, pulmonary edema, and massive bleeding.

Forecast

Disease prognosis always serious. The lack of adequate treatment for the bubonic form of plague leads to death in 40-90% of cases, and with generalized infection - in 90% of cases.

Diagnosis of plague

Recognizing the disease during an epidemic outbreak is not difficult. Sporadic cases of plague are often difficult to diagnose.

Epidemiological history (stay in an endemic or epizootic focus of plague), high fever, pneumonia, inflammation of the lymph nodes is important when making a diagnosis.

In a general blood test, there are typical signs of an inflammatory process: neutrophilic leukocytosis with a shift in the leukocyte formula to the left. Protein, granular, hyaline casts, and red blood cells can be detected in the urine.

Bacteriological examination plays an undeniable role in the diagnosis of plague. Material for research is obtained by puncturing the bubo and collecting sputum. You can also take mucus from the throat and blood for bacteriological examination.

Express diagnostics is Gram staining of smears.

The biological research method involves infecting laboratory animals - guinea pigs or white mice. When the disease occurs, the animal dies within 3-9 days.

Serological tests (ELISA, RPGA, RNGa) are also widely used in the diagnosis of plague and for retrospective analysis.

Treatment of plague

Patients with plague or even any suspicion of this disease should be urgently hospitalized and isolated. Early prescription of antibiotics - streptomycin, amikacin, tetracycline, levomethicin - is important. Generalized forms of plague require the simultaneous administration of several antibiotics. The course of antibiotic treatment is 7-10 days.

Simultaneously with antibiotic therapy, measures aimed at detoxification are carried out. Symptomatic therapy includes correction of disorders of the cardiovascular, respiratory, and nervous systems.

Prevention of plague

All plague patients are subject to strict isolation. Those who have been in contact with sick people or corpses should be monitored in a hospital for 6 days for emergency prophylaxis. In the outbreaks of the disease, vaccination is carried out for high-risk groups - shepherds, hunters, geologists, etc. Vaccination is carried out with a live dry plague vaccine. Immunity after a single injection lasts for a year.

It is advisable to supplement emergency prevention with the prescription of antibiotics - doxycycline or streptomycin. The plague outbreak is subject to ongoing and final disinfection.

Important preventive measures aimed at combating the plague are disinsection and deratization.

Plague is an acute natural focal infectious disease, characterized by severe intoxication, fever, damage to the skin, lymph nodes, lungs, and the ability to take a septic course. Refers to particularly dangerous infections.

Etiology: Yersinia pestis - Gr-MB.

Epidemiology: reservoir - various rodents and lagomorphs, predators; Among people, epidemics are caused by the migration of rats, the carrier is a flea. Infection occurs when bitten by a flea, which regurgitates the contents of the stomach with a large number of plague bacilli, or from a person by airborne droplets in the pulmonary form.

Pathogenesis: the pathogen migrates through the lymphatic vessels of the skin without lymphangitis to regional lymph nodes, where it is captured by mononuclear cells, multiplies in them with the development of an inflammatory reaction in the lymph nodes, which leads to a sharp increase in lymph nodes, fusion and formation of conglomerates (bubonic form ). Then hemorrhagic necrosis of the lymph node develops, in which a huge number of microbes are able to break into the bloodstream and penetrate into the internal organs. As a result of the breakdown of the microbe, endotoxins are released, causing intoxication. The pathogen enters the blood and spreads throughout the body (septic form). Particularly dangerous from an epidemic point of view are the “screenings” of infection into the lung tissue with the development of a secondary pulmonary form of the disease (airborne spread), in which rapidly progressing widespread pneumonia with hemorrhagic necrosis develops.

Some patients experience severe signs of sepsis without a detectable bubo (primarily septic).

With airborne infection, a primary pulmonary form of the disease develops; serous-hemorrhagic inflammation with a pronounced necrotic component develops in the lung tissue.

Clinical picture: incubation period 3-5 days. It starts suddenly. Body temperature with severe chills quickly rises to 39°C and above. Intoxication appears early and quickly increases - severe headache, dizziness, feeling of severe weakness, muscle pain, sometimes vomiting. In some cases, an admixture of blood appears in the vomit in the form of bloody or coffee grounds. Some patients experience increased anxiety, unusual fussiness, and excessive mobility. Consciousness is impaired and delirium may occur. The patient is initially excited and frightened. In delirium, patients are restless, often jumping out of bed, trying to run away somewhere. Coordination of movements is impaired, speech becomes unclear, and the gait becomes unsteady. The appearance of patients changes: the face is initially puffy, and later haggard with a cyanotic tint, dark circles under the eyes and a pained expression. Sometimes it expresses fear or indifference to the environment.

When examining the patient, the skin is hot and dry, the face and conjunctiva are hyperemic, often with a cyanotic tint, hemorrhagic elements (petechiae or ecchymosis, quickly taking on a dark purple hue). The mucous membrane of the oropharynx and soft palate is hyperemic, with pinpoint hemorrhages. The tonsils are often enlarged, swollen, sometimes with a purulent coating. The tongue is covered with a characteristic white coating (“rubbed with chalk”) and is thickened. Blood circulation is severely disrupted. The pulse is frequent (120-140 beats/min and more often), weakly filled, dicrotic, sometimes thread-like. Heart sounds are muffled. Blood pressure is reduced and falls progressively. Breathing is rapid. The abdomen is distended, the liver and spleen are enlarged. Diuresis decreases sharply. Some patients with severe forms develop diarrhea. The urge to defecate becomes more frequent (up to 6-12 times a day), stool becomes unformed and contains an admixture of blood and mucus.

Clinical forms:

A) cutaneous form - a spot first appears on the skin, then a papule, vesicle, pustule and, finally, an ulcer. The pustule, surrounded by a zone of redness, is filled with dark bloody contents, is located on a hard base of a red-purple color and is characterized by significant pain, sharply increasing with pressure. When the pustule bursts, an ulcer forms, the bottom of which is covered with a dark scab. Plague ulcers on the skin have a long course, heal slowly, forming a scar.

B) bubonic form - characterized by the appearance of lymphadenitis (plague bubo). In the place where the bubo should develop, the patient feels severe pain, which makes it difficult to move the leg, arm, and neck. Later, patients may take forced positions due to pain (bent leg, neck, arm pulled to the side). A bubo is a painful, enlarged lymph node or a conglomerate of several nodes fused to the subcutaneous tissue, has a diameter of 1 to 10 cm and is localized in the groin area in 60-70% of patients. In addition, buboes can develop in the area of ​​the axillary (15-20%) or cervical (5%) lymph nodes or affect the lymph nodes of several locations simultaneously. The process usually involves the tissue surrounding the lymph nodes, which gives the bubo its characteristic features: a tumor-like formation of dense consistency with unclear contours, sharply painful. The skin over the bubo, hot to the touch, is initially unchanged, then becomes purplish-red, bluish, and shiny. Secondary blisters with hemorrhagic contents (plague conflicts) may appear nearby. At the same time, other groups of lymph nodes—secondary buboes—enlarge. The lymph nodes of the primary focus undergo softening; upon puncture, purulent or hemorrhagic contents are obtained, microscopic analysis of which reveals a large number of gram-negative rods with bipolar staining. In the absence of antibacterial therapy, the festering lymph nodes are opened. Then gradual healing of the fistula occurs. Fever and chills are important symptoms of the disease, sometimes they precede the appearance of buboes by 1-3 days. More than half of the patients experience abdominal pain, often emanating from the inguinal bubo and accompanied by anorexia, nausea, vomiting and diarrhea, sometimes with blood. Skin petechiae and hemorrhages occur in 5-50% of patients, and in later stages of the disease they can be extensive. Disseminated intravascular coagulation in a subclinical form is observed in 86% of cases. In 5-10% of them, this syndrome is accompanied by pronounced clinical manifestations in the form of gangrene of the skin, fingers, and feet.

In cases of a sharp decrease in the nonspecific resistance of the macroorganism, pathogens are able to overcome the barriers of the skin and lymph nodes, enter the general bloodstream through the bloodstream and lymph flow, and cause the generalization of the infectious process with the formation of secondary foci of infection in the liver, spleen and other internal organs (septic form of plague). In some cases, it develops from the very beginning of clinical manifestations of plague (primary), in others - after damage to the skin and lymph nodes (secondary).

C) primary septic form - begins suddenly, acutely, after incubation lasting from several hours to 1-2 days. Against the background of complete health, chills suddenly appear, accompanied by myalgia and arthralgia, general weakness, severe headache, nausea, vomiting, appetite disappears and body temperature rises to 39°C or higher. After a few hours, mental disturbances appear - agitation, lethargy, and in some cases a delirious state. Speech becomes slurred. Frequent vomiting is observed, and blood may appear in the vomit. Body temperature quickly reaches 40°C or more. The face becomes puffy, with a cyanotic tint and sunken eyes. There is pronounced tachycardia - the pulse is very frequent - 120-130 beats/min, dicrotic. Heart sounds are weakened and muffled. Blood pressure is reduced. Breathing is frequent. The liver and spleen enlarge. In most patients, after 12-40 hours from the moment of illness, signs of cardiovascular failure begin to progress (tachycardia and arterial hypotension intensify), oliguria, and soon anuria, as well as hemorrhagic syndrome, manifested by nosebleeds, blood in the vomit masses, hemorrhages in various areas of the skin, in some cases - hematuria and the appearance of blood in the stool. The noted changes are caused by infectious-toxic shock with characteristic hemorrhagic manifestations, reflecting disseminated intravascular coagulation with the development of consumption coagulopathy. In the absence of adequate medical care, patients, as a rule, die within 48 hours. With such fulminant sepsis, bacteremia is so pronounced that the pathogen is easily detected by Gram staining of the light layer of the blood clot. The number of leukocytes in this form of plague is extremely high and reaches 40-60 thousand per 1 ml3.

D) secondary septic form - the condition of patients very quickly becomes extremely severe. Symptoms of intoxication increase by the hour. The temperature after severe chills rises to high febrile levels. All signs of sepsis are noted: muscle pain, severe weakness, headache, dizziness, congestion of consciousness, up to its loss, sometimes agitation (the patient rushes about in bed), insomnia. Minor hemorrhages appear on the skin, bleeding from the gastrointestinal tract (vomiting of bloody masses, melena), severe tachycardia, and a rapid drop in blood pressure are possible.

D) primary pulmonary form - the disease has a hyperacute onset. Against the background of complete health, severe chills (sometimes sharp, repeated), a rapid increase in body temperature, a very severe headache, dizziness, and often repeated vomiting suddenly appear. Sleep is disturbed, aches and pains appear in the muscles and joints. When examined in the first hours, there is tachycardia and increasing shortness of breath. In the following hours, the patients' condition progressively worsens, weakness increases, and body temperature rises. Characterized by hyperemia of the skin, conjunctiva, and injection of scleral vessels. Rapid breathing becomes shallow. The act of breathing involves auxiliary muscles and the wings of the nose. Breathing takes on a harsh tone; in some patients, crepitating or fine bubbling rales, local dullness of percussion sound, and sometimes a painless cough with viscous glassy transparent sputum are detected. At the height of pneumonic plague, signs of toxic damage to the central nervous system come to the fore. Mental status is impaired. Patients become agitated or inhibited. Their speech is slurred. Coordination of movements is impaired, tremors appear, and articulation becomes difficult. Abdominal and knee reflexes increase, sensitivity to light, cold, lack of fresh air, etc. increases. Damage to the central nervous system by toxins of the plague bacillus leads to the development of infectious-toxic encephalopathy and cerebral hypertension, impaired consciousness according to the type of its depression, which manifests itself first as somnolence, then stupor and coma. From the 2-3rd day, body temperature often exceeds 40°C. Tachycardia corresponds to the severity of fever. There may be a short-term loss of pulse or arrhythmia. Blood pressure decreases to 95/65-85/50 mm Hg. Art. Acute renal failure and hemorrhagic syndrome develop. Increasing cyanosis and acrocyanosis indicate a disorder of microcirculation. Disorders of the respiratory system are more pronounced than in the initial period, but during a clinical examination, attention is drawn to the paucity of detected data from the lungs and their inconsistency with the extremely serious condition of the patient, which is typical for plague. Signs indicating the development of lobar, often right-sided, lower lobe pneumonia are determined. Cutting pain in the chest when inhaling and coughing intensify. As the disease progresses, the amount of sputum produced increases. An admixture of scarlet blood is found in the sputum; it does not coagulate and always has a liquid consistency. If pulmonary edema occurs, the sputum becomes foamy and pink. Interstitial and alveolar pulmonary edema develops, which is based on toxic damage to the pulmonary microvessels with a sharp increase in their permeability. The duration of the peak period usually does not exceed 1.5-2 days. Sputum microscopy is of diagnostic importance during this period, which allows one to detect a huge number of bipolar-stained rods. Polymorphonuclear leukocytosis of 15-20-30-109/l is detected in the blood, as well as toxic changes in white blood cells.

E) secondary pulmonary form - has the same clinical manifestations as the primary pulmonary form. On the 2-3rd day of the disease, against the background of minimal ifiltrative changes in the lungs, cough, fever, and tachypnea appear. These symptoms quickly grow and intensify, severe shortness of breath develops, bloody sputum appears, and signs of respiratory failure appear. The sputum is replete with plague bacillus and is highly contagious when airborne aerosols formed during coughing are disseminated.

Diagnosis: epidemiological history (stay in endemic areas), clinic, bacterioscopic, bacteriological and serological (RPGA, RN, indirect immunofluorescence reactions) studies (examination of the punctate of suppurating l.u., sputum, patient’s blood, discharge from fistulas and ulcers, pieces of corpse organs, air samples and swabs from objects in the room where the patient was).

Treatment:

1) if plague is suspected, etiotropic treatment should be started immediately, without waiting for laboratory confirmation of the diagnosis

2) use antibiotics (streptomycin, tetracyclines, levomycin, ampicillin, gentamicin), which are administered parenterally in doses depending on the clinical form of plague. Simultaneously with AB, saline solutions, hemodez and corticosteroids are administered, because parenteral administration of AB can lead to rapid bacteriolysis and a sharp drop in blood pressure.

3) pathogenetic therapy: detoxification agents (colloids and crystalloids intravenously in combination with forced diuresis, glucocorticosteroids), antishock therapy, in the presence of hemorrhages - relief of DIC syndrome (fresh frozen plasma), plasmapheresis.

4) local treatment of buboes is not indicated until fluctuation appears or spontaneous drainage of the bubo occurs. In these cases, antibiotics that are effective against staphylococci (oxacillin, methicillin and others) are prescribed, which are injected into the buboes.

The plague has deep historical roots. Humanity first encountered the disease in the 14th century. The epidemic, which was dubbed the “Black Death,” claimed more than 50 million human lives, which was equal to a quarter of the population of medieval Europe. The mortality rate was about 99%.

Facts about the disease:

• The plague affects the lymph nodes, lungs, and other internal organs. As a result of infection, sepsis develops. The general condition of the body is extremely difficult. The body is subjected to constant attacks of fever.
• The period of development of plague after infection is on average about three days, depending on the general condition of the body.
• At the moment, the mortality rate from this disease is no more than 10% of all identified cases.
• There are about 2 thousand cases of the disease per year. According to WHO, in 2013, 783 cases of infection were officially registered, of which 126 cases resulted in death.
• Outbreaks of the disease mainly affect African countries and a number of countries in South America. Endemic countries are the Democratic Republic of Congo, the island of Madagascar and Peru.

In the Russian Federation, the last known case of plague was documented in 1979. Every year, more than 20 thousand people are at risk, being in the zone of natural foci of infection with a total area of ​​more than 250 thousand km2.

CAUSES

The main cause of plague is flea bites. This factor is due to the specific structure of the digestive system of these insects. After a flea bites an infected rodent, the plague bacterium settles in its crop and blocks the passage of blood to the stomach. As a result, the insect experiences a constant feeling of hunger and, before its death, manages to bite, thereby infecting up to 10 hosts, regurgitating the blood it drinks along with plague bacteria into the bite.

After a bite, the bacteria enters the nearest lymph node, where it actively multiplies and, without antibacterial treatment, affects the entire body.

Causes of infection:

• bites of small rodents;
• contact with infected domestic animals, stray dogs;
• direct contact with an infected person;
• cutting up carcasses of animals affected by disease;
• treatment of the skin of killed animals that carry the disease;
• contact of bacteria with the human mucosa during autopsy of corpses of those who died from the plague;
• eating meat from infected animals;
• entry of particles of saliva of an infected person into the oral cavity of a healthy person by airborne droplets;
• military conflicts and terrorist attacks using bacteriological weapons.

The plague bacterium is highly resistant to low temperatures, multiplies vigorously in a humid environment, but does not tolerate high temperatures (above 60 degrees), and dies almost instantly in boiling water.

CLASSIFICATION

Varieties of plague are divided into two main types.

• Localized type- the disease develops after plague microbes get under the skin:
  • Skin plague. There is no primary protective reaction, only in 3% of cases redness of the affected areas of the skin with induration occurs. Without visible external signs, the disease progresses, eventually forming a carbuncle, then an ulcer, which scars as it heals.
  • Bubonic plague . The most common form of the disease. It affects the lymph nodes, forming “buboes”. Characterized by painful inflammatory processes in them. Affects the groin area and armpits. Accompanied by severe fever and general intoxication of the body.
  • Bubonic skin plague. Plague bacteria travel along with the lymph, end up in the lymph nodes, causing an inflammatory process that affects neighboring tissues. The “buboes” mature, and the rate of development of the pathology decreases.
• Generalized type- the pathogen enters the body by airborne droplets, as well as through the membranes of the mucous surfaces of the body:
  • Septicemic plague. The pathogen penetrates through the mucous membranes. The high virulence of the microbe and a weakened body are the reasons for its easy entry into the patient’s blood, bypassing all his defense mechanisms. A fatal outcome with this form of the disease can occur in less than 24 hours, the so-called. "lightning plague"
  • Pneumonic plague. Entry into the body occurs through airborne droplets, infection through dirty hands and objects, as well as through the conjunctiva of the eyes. This form is primary pneumonia, and also has a high epidemic threshold due to the abundant secretion of sputum containing pathogenic bacteria during coughing.

SYMPTOMS

The incubation period of the plague ranges from 72 to 150 hours. Most often it appears on the third day. The disease is characterized sudden manifestation without primary symptoms.

Clinical history of plague:

• a sharp jump in body temperature up to 40 degrees;
• acute headaches;
• nausea;
• reddish tint to the face and eyeballs;
• muscle discomfort;
• white coating on the tongue;
• enlarged nostrils;
• dry skin of lips;
• manifestations of a rash on the body;
• feeling of thirst;
• insomnia;
• causeless excitement;
• difficulties in coordinating movements;
• delusions (often of an erotic nature);
• impaired digestion;
• difficulty urinating;
• high fever;
• cough with sputum containing blood clots;
• bleeding from the gastrointestinal tract;
• tachycardia;
• low blood pressure.

Hidden primary symptoms lead to outbreaks of disease epidemics. Thus, a potential carrier of plague can travel long distances, feeling absolutely healthy, while infecting everyone who comes into contact with the plague bacteria.

DIAGNOSTICS

Returning from travel to areas endemic for the spread of plague, with the slightest signs of the disease - urgent reason to isolate the patient. Based on the medical history, all persons who have had any contact with the potentially affected person are identified.

Diagnostics is carried out in the following ways:

• bacterial culture from blood, sputum and lymph node tissue samples;
• immunological diagnostics;
• polymerase chain reaction;
• passage on laboratory animals;
• serological technique;
• isolation of pure culture with subsequent identification;
• laboratory diagnostics based on fluorescent antiserum.

In today's medical environment, direct transmission from the patient to the attending physician and hospital staff is virtually impossible. However, everything laboratory tests are carried out in specialized premises for working with particularly dangerous infectious diseases.

TREATMENT

Since 1947 plague treatable with antibiotics group of aminoglycosides with a broad spectrum of action.

Inpatient treatment is used in isolated wards of infectious diseases departments in compliance with all safety rules when working with plague patients.

Course of therapy:

• The use of antibacterial drugs based on sulfamethoxazole and trimethoprim.
• Intravenous administration of chloramphenicol simultaneously with streptomycin.
• Detoxification procedures.
• Improving microcirculation and repair. Achieved by entering .
• Taking cardiac glycosides.
• Use of respiratory analeptics.
• Use of antipyretics.

Treatment is most effective and does not cause any consequences in the initial stages of plague.

COMPLICATIONS

Because the disease is included in the group of fatal, the main complications in case of an incorrect diagnosis or lack of proper treatment may be the transformation of the plague from a mild form to more severe ones. Thus, cutaneous plague can develop into septicemic plague, and bubonic plague into pneumonic plague.

Complications from plague also affect:

• Cardiovascular system (pericarditis develops).
• Central nervous system (purulent meningoencephalitis).

Although a patient who has recovered from the plague receives immunity, he is not completely immune from new cases of infection, especially if preventive measures are taken carelessly.

PREVENTION

At the state level, a whole range of directive preventive measures for the plague has been developed.

The following decrees and rules are in effect on the territory of the Russian Federation:

• “Instructional and methodological guidelines for the diagnosis, treatment and prevention of plague”, approved by the USSR Ministry of Health on September 14, 1976.
• Sanitary and epidemiological rules SP 3.1.7.1380-03 dated 06.06.2003, approved by the Resolution of the Chief State Sanitary Doctor in the part “Prevention of plague”.

Set of measures:

• epidemiological surveillance of natural foci of disease;
• disinsection, reducing the number of potential disease carriers;
• a set of quarantine measures;
• training and preparing the population to respond to outbreaks of plague;
• careful handling of animal corpses;
• vaccination of medical staff;
• use of anti-plague suits.

PROGNOSIS FOR RECOVERY

The mortality rate from plague at the present stage of therapy is about 10%. If treatment is started at a later stage or is absent altogether, the risks increase to 30-40%.

With the right choice of treatment methods the body recovers in a short time, performance is fully restored.

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Plague (pestis) is an acute infectious disease characterized by severe intoxication, fever, damage to the lymphatic system, lungs and other organs. Plague belongs to the group of especially dangerous quarantine infections.

The relevance of the plague.

It is determined by the importance of this pathology for humanity as a whole - a particularly dangerous, quarantine infection, with high mortality and multiple organ damage.

Characteristics of the plague causative agent.

The causative agent of plague (Yersinia pestis) belongs to the family Enterobacteriaceae, genus Yersinia, has the appearance of a polymorphic rod 1-3 microns long and 0.3-0.7 microns wide; its ends are rounded, and the middle is somewhat swollen, as a result of which it has a barrel-shaped (ovoid) shape. The rod is easily stained with conventional aniline dyes, is gram-negative, is characterized by bipolar coloring, when the middle part is stained paler than the ends, does not form spores, is enclosed in a mucous capsule, and is immobile. The causative agent of plague is a facultative anaerobe; it grows well, but slowly, on ordinary nutrient media at a pH of 6.9-7.2 and an optimal temperature of 38°C. There are heat-stable somatic antigen and heat-labile capsular antigen.

The resistance of the plague microbe to external influences is low. High temperature, direct sunlight, drying, and competition of putrefactive microbes are especially harmful to it; It tolerates low temperatures well. Heating kills the stick at 60°C within 40-60 minutes, at 70°C in 6-10 minutes and at 100°C the stick dies in a few seconds. Conventional disinfectants (sublimate dilution 1:1000, 3-5% Lysol solution, 5% carbolic acid solution, 10% lime milk solution) cause the death of the pathogen within 2-5-10 minutes.

The main manifestations of the epidemic process of plague.

There are 2 types of plague foci: anthropourgic (“rat” or “urban”), the youngest foci, the existence of which is associated with human activity, and natural “wild” foci, foci where the infection has been maintained since ancient times in wild rodents. ground squirrels, tarbagans (marmots), gerbils, myppi and some other rodents. Among rodents, rats are of greatest epidemiological importance. Rodents usually become ill with an acute form of plague and die; in temperate climates, rodents hibernate in winter and their plague disease becomes protracted and becomes a dormant infection. The pathogen thus preserved causes the appearance of an epizootic in the spring.

Fleas are carriers of infection from rodent to rodent and from rodent to humans. It is believed that the infection is transmitted to humans by a flea bite. A flea is capable of transmitting plague infection 5-7 days after it has fed on infected blood. Such fleas try to suck blood again, but the resulting “plague block” prevents the blood from moving into the stomach, as a result of which regurgitated masses containing the pathogen end up in the wound at the site of the flea bite.

A person sick with bubonic plague does not pose a danger to others before opening the bubo, and even after opening the festering bubo, this danger is small, since the excreted pus contains very few plague microbes or the latter are completely absent. When bubonic plague passes into the septic or pneumonic form, the patient, excreting the pathogen with sputum, urine, and feces, becomes a source of plague infection. During this period, a person can become infected from another person through contaminated household items or through airborne droplets. The nutritional route of infection is also known - by eating camel meat.

When pneumonic forms of plague occur, the main, and perhaps the only source, is a sick person. The disease pneumonic plague, as a rule, occurs upon contact with patients with the bubonic form who have developed secondary plague pneumonia. Inflammation of the lungs caused by the plague pathogen is usually accompanied by a severe cough with copious discharge of foamy sputum mixed with blood containing a huge amount of the pathogen. Epidemics of pneumonic plague usually arise and develop in the autumn-winter season.

Human susceptibility to plague infection is very high. The transferred disease leaves a fairly strong immunity, although repeated cases of plague are possible.

Pathomorphogenesis of plague.

The causative agent of plague can be introduced into the human body in various ways: through the skin, mucous membranes, respiratory tract, and digestive tract. The location of the entrance gate influences the clinical manifestations of plague.

The most common site of infection is the skin, and infection can occur without visible violations of its integrity. In these cases, a spot appears on the skin, turning successively into a papule, vesicle, pustule with bloody-purulent contents. The pustule ulcerates and an ulcer forms with red edges raised in the form of a roller. Sometimes the primary skin lesion appears as a dense, immobile carbuncle. An ulcer forms at the site of the carbuncle. Pustules and carbuncles contain a large number of plague microbes.

Much more often, the plague bacillus, having got on human skin and without causing inflammatory changes, penetrates further and is carried with the lymph flow into the nearest regional lymph node. Pathogenetically, primary and secondary buboes are distinguished. Arising lymphogenously, primary buboes always have a territorial connection with the site of entry to the infection. Secondary buboes always arise hematogenously, most often this occurs at a later date, and a variety of lymph nodes, both peripheral and deep, can be affected. Secondary buboes are often multiple. Primary buboes, depending on the progress of the infection, are usually divided into buboes of the first, second, etc. order. Most often, primary buboes are single, less often there are two or more. From primary buboes, microbes spread by lymphogenous and hematogenous routes. Secondary buboes are characterized by smaller sizes and the absence of periadenitis.

The cutaneous form of plague, as a rule, is subsequently combined with an adjoining regional bubo (cutaneous bubonic form).

In the primary septic form of plague (1-10%), the pathogen penetrates due to a number of conditions (massive dose of the infectant, insufficiency of the body's protective factors, weakness of the lymphatic barrier, etc.) through the skin and mucous membranes, into the lymph nodes and into the general system. blood flow, which quickly causes generalization of the process. Bacteremia is observed with the introduction of the pathogen into internal organs and tissues. Characterized by small and large hemorrhages, hemolysis of red blood cells, saturation of the endocardium and vascular walls with hemoglobin. Dystrophic changes are noted in the internal organs. The spleen is enlarged, congested, with hemorrhages in the capsule. At autopsy the characteristic picture is hemorrhagic septicemia.

The so-called intestinal form of plague is a secondary manifestation of septicemia and cannot be considered as an independent primary form.

In primary pneumonic plague, pneumonia first has a serous-hemorrhagic character, and subsequently becomes necrotic. The pleura is often involved in the pathological process with the development of fibrinous or fibrinous-hemorrhagic pleurisy.

Pathomorphologically, three variants of manifestations of primary pneumonic plague are distinguished:

lobular bronchopneumonia;

confluent lobular (pseudolobar) bronchopneumonia;

lobar pneumonia.

Plague clinic. Classification.

The incubation period ranges from several hours to 6 days, most often it lasts 3-6 days. In persons who received preventive vaccinations or antibiotics for prophylactic purposes, the incubation period can be extended to 8-10 days. With primary pneumonic and septic forms of plague, the incubation period is usually shorter (1-2 days and even several hours).

Regardless of the clinical form, the disease usually begins suddenly, without a prodromal period. A picture of severe intoxication quickly develops. With sudden, often repeated chills, the temperature rises to 38-39°C and higher. Characterized by severe headache, increasing feeling of weakness, muscle pain, and sometimes vomiting. The temperature continues to remain at high levels, and in more severe patients it rises even higher. Some patients experience increased anxiety, unusual fussiness, and excessive mobility. Headache and feeling of exhaustion increase, fever is combined with facial flushing and especially conjunctivitis. The tongue becomes covered with a characteristic white coating (“rubbed with chalk”) and swells, which, together with dry mouth, makes speech slurred. In more severe cases, delusions of a hallucinatory nature develop; in delirium, patients are especially restless, often jumping out of bed, trying to run away somewhere. A staggering gait, flushing of the face and conjunctiva, as well as slurred speech resemble the behavior of those who are intoxicated. Later, in especially severe cases, cyanosis, sharpening of facial features, and sometimes the appearance of a pained expression on it, sometimes horror, are noted.

On the part of the cardiovascular system, there are obvious and sharp disturbances in the pulse, its filling, rhythm, frequency (up to 120-160 or more per minute), dull tones and a significant decrease in blood pressure. The pulse in plague is a very accurate and sensitive indicator of the severity of the disease process. In seriously ill patients, a frequent, often dicrotic, sometimes thread-like pulse is detected. Blood pressure has almost the same value. Plague patients die with increasing weakness of cardiac activity.

The picture of peripheral blood is characterized by neutrophilic leukocytosis with a shift to the left and an increase in ESR.

Depending on the development of a particular clinical form of plague, in addition to the general symptoms described, others are added. According to the classification of Rudnev G.P. (1970) distinguish the following clinical forms of plague:

Predominantly local forms (usually peripheral with relatively scant external dissemination): cutaneous; bubonic, cutaneous bubonic.

Internally disseminated, or generalized, forms: primary septic; secondary septic, I Externally disseminated forms (central, often with abundant external dissemination): primary pulmonary, secondary pulmonary, intestinal.

In the cutaneous form, which is observed relatively rarely and, as a rule, turns into cutaneous-bubonic, changes in the skin occur in the following order: spot, papule, vesicle, pustule, ulcer. However, the presence of all these stages is not necessary. The pustule, surrounded by a zone of redness, with a purple tint closer to the center, is filled with dark bloody, sometimes blackish contents. The red zone clearly protrudes above the level of adjacent healthy skin (purple shaft), from which it is not sharply demarcated. Such a plague carbuncle is characterized by significant pain, sharply increasing with pressure, which is important for diagnosis. When the pustule bursts, an ulcer with a yellowish infiltrated hard bottom is formed, which is then covered with a dark scab. Plague ulcers on the skin are characterized by an extreme duration of course, heal slowly, forming scars.

For the bubonic form of plague, the bubo is a cardinal symptom. For early detection it is necessary to carry out a thorough objective examination. Early signs are the following: in the place where the bubo should develop, the patient feels severe pain, which makes it difficult to move the arm, leg, etc. Later, the patient may take an unnatural, forced position due to pain (bent leg, protruding arm, bent neck, etc.), but these phenomena are not always observed. Primary buboes of the first order usually develop in the very first days of the disease. Secondary buboes (generally optional in every case of bubonic plague) usually appear later, at different times after the onset of the disease. Lymphangitis, as a rule, is not observed.

Most often (about 55%) buboes appear on the lower extremities, less often in the axillary region, on the neck, in the parotid region. In prognostic terms, cervical and axillary buboes are the most dangerous, since they most often lead to complications in the form of secondary pneumonic plague.

Clinically, the bubo is characterized by the following signs: the skin over the emerging or already formed bubo is not changed in the first period, then, as the bubo enlarges, it turns red, stretches, and sometimes becomes somewhat shiny and glossy. In the first days of the disease, the bubo itself can be palpated as a separate small lump, attracting the patient’s attention with its sharp pain. Subsequently, the lymph node enlarges, sometimes the surrounding tissue becomes somewhat swollen, and the skin above it acquires a cyanotic tint, mainly in the center. The pain may decrease somewhat during this time. The process usually involves the entire group of lymph nodes and surrounding tissues (periadenitis), a single conglomerate is formed, only occasionally retaining the character of tuberous lobulation. The absence of clear contours of the bubo should be considered as a very important and characteristic diagnostic sign of the plague bubo. The further outcome of the bubo may be as follows: complete resorption; purulent softening with self-ulceration; persistent hardening (a long-term condition as if preserved by the bubo), or the so-called sclerosis of the bubo (often observed).

Patients with bubonic plague may develop secondary septic plague, which is observed more often in seriously ill patients and significantly increases the epidemiological danger of such patients. Secondary plague meningitis, which occurs occasionally, is usually fatal.

Primary pneumonic plague is the most epidemiologically dangerous and extremely severe clinical form of the disease. According to G.P. Rudnev, three main periods of the disease are distinguished: the period of initial febrile excitation, the period of the height of the disease and stuporous (terminal). Usually there is a sudden onset, chills, a rapid rise in temperature, a very severe headache, often repeated vomiting, later cutting pain in the chest, palpitations, excessive heart rate, severe shortness of breath, often delirium, even later prostration and, finally, coma leading to death .

The primary septic form of plague is characterized by numerous hemorrhages into the skin and mucous membranes. Severe septicemia is combined with bleeding from the kidneys, intestines and hematemesis. It is important that the generalization of the process arises and develops without previous local phenomena. In the clinical picture of the septic form of plague, in addition to the noted characteristic multiple hemorrhages, against the background of high fever, the phenomena of general intoxication and especially depression of the central nervous system predominate. Severe shortness of breath, cyanosis, and threadlike pulse are evident. The septic form of the disease usually quickly leads to death.

Treatment of plague.

Plague patients are subject to mandatory hospitalization to a special plague hospital. Treatment of patients should be comprehensive, including etiotropic and pathogenetic agents, in compliance with a strict individual approach in each individual case.

Antibacterial therapy is prescribed until laboratory confirmation of the diagnosis. The following are considered effective for all forms of plague: doxycycline 100 mg IV 2 times a day or chloramphenicol (in case of intolerance to tegracyclines) at a dose of 500 mg 4 times a day. or streptomycin (in case of intolerance to the above antibiotics) at a dose of 1 g every 12 hours intramuscularly or intravenously, or gentamicin 80 mg 3 times a day intramuscularly. The duration of therapy is at least 10 days.

In addition to ethnotropic therapy, an important principle is the fight against intoxication and hemodynamic disorders. Among detoxifying agents, intravenous drip administration of Ringer-Locke solutions "Trisol", "Quartasol" is used. 5% glucose solution, rheopolyglucin. These solutions are administered as a stream until pulse and blood pressure are restored, and after acute vascular insufficiency has been eliminated - by drip. If the introduction of medicinal solutions into a vein fails to eliminate vascular disorders, catecholamines (adrenaline, norepinephrine, mesatone) are added to the perfusion fluid in normal doses. 2-3 ml of cordiamine, glucocorticosteroids (100-150 mg of prednisolone or equivalent doses of other drugs). The mixture is infused at a rate of 40-60 drops per minute until the complete and permanent elimination of acute vascular disorders.

Local therapeutic measures are carried out for bubonic and cutaneous bubonic forms of plague, in the form of ointment dressings. In the presence of persistent fluctuation or the development of necrotic processes, an incision is indicated. Convalescents of the bubonic form of plague are discharged from the hospital no earlier than 4 weeks from the day of clinical recovery after a double (5-6 days later) control puncture of the bubo with a negative result during bacteriological examination of the punctate.

For pneumonic plague The convalescent person is discharged after the disappearance of all clinical manifestations, provided that a normal radiograph of the lungs and the presence of normal body temperature for 6 weeks, as well as after a three-time negative bacteriological examination of sputum and mucus from the throat, carried out every two weeks.

Prevention of plague.

Plague is a conventional disease, the control and prevention measures of which are regulated by international rules and regulations. It seems possible to distinguish two groups of measures carried out to prevent the plague: preventive and anti-epidemic measures.

Preventive measures include protecting the territory of the country from the introduction of infection; prevention of disease in natural foci - consistent improvement of natural foci.

In cases where the disease appears in a person, a system of anti-epidemic measures is deployed, which provides for: isolating a plague patient in a special hospital and treating him; active identification of patients through door-to-door visits; isolation of patients with suspected plague (febrile) in a provisional hospital: isolation of persons who communicated with a plague patient (for 6 days); disinfection in the outbreak; deratization and disinfestation measures; restrictive (quarantine) measures that exclude the possibility of spreading the infection beyond the affected area; If necessary, vaccination of the population can be carried out

Vaccination against plague carried out according to epidemiological indications using a live vaccine intradermally. The duration of immunity is up to 5 months, therefore, if indicated, revaccination is carried out after six months.

Persons exposed to the plague are given emergency prophylaxis with broad-spectrum antibiotics.. In order to prevent infection, medical personnel in hospitals for plague patients work in protective (anti-plague) suits.