Orders for ooi mz rf. Anti-epidemic measures for especially dangerous infections

"Center medical prevention the city of Stary Oskol»

Restriction of entry and exit, export of property, etc.,

Export of property only after disinfection and permission of the epidemiologist,

Strengthening control over food and water supply,

Normalization of communication between separate groups of people,

Disinfection, deratization and disinfestation.

Prevention of especially dangerous infections

1. Specific prevention of especially dangerous infections is carried out by a vaccine. The purpose of vaccination is to induce immunity to the disease. Vaccination can prevent infection or significantly reduce its negative consequences. Vaccination is divided into planned and epidemic indications. It is carried out with anthrax, plague, cholera and tularemia.

2. Emergency prophylaxis for persons who are at risk of contracting a particularly dangerous infection is carried out with antibacterial drugs (anthrax).

3. For prevention and in cases of illness, immunoglobulins (anthrax) are used.

Anthrax Prevention

Vaccine use

Used to prevent anthrax live vaccine. Vaccinations are subject to workers associated with animal husbandry, workers in meat processing plants and tanneries. Revaccination is carried out in a year.

The use of anthrax immunoglobulin

Anthrax immunoglobulin is used to prevent and treat anthrax. It is administered only after an intradermal test. When using the drug with therapeutic purpose anthrax immunoglobulin is given as soon as the diagnosis is made. In emergency prophylaxis, anthrax immunoglobulin is administered once. The drug contains antibodies against the pathogen and has an antitoxic effect. For seriously ill patients, immunoglobulin is administered for therapeutic purposes for health reasons under the cover of prednisone.

Use of antibiotics

Antibiotics are used as a prophylactic measure when necessary for emergency indications. All persons who have contact with sick and infected material are subject to antibiotic therapy.

Anti-epidemic measures

Identification and strict accounting of disadvantaged settlements, livestock farms and pastures.

Establishing the time of the incident and confirming the diagnosis.

Identification of a contingent with a high degree of risk of disease and the establishment of control over the conduct of emergency prevention.

Medical and sanitary measures for plague

Plague patients and patients with suspected disease are immediately transported to a specially organized hospital. Patients with pulmonary form plagues are placed one at a time in separate chambers, the bubonic form of plague - several in one chamber.

After discharge, patients are subject to a 3-month follow-up.

Contact persons are observed for 6 days. In case of contact with patients with pneumonic plague, prophylaxis with antibiotics is carried out for contact persons.

Plague Prevention(vaccination)

Preventive immunization of the population is carried out when a mass spread of plague among animals is detected and a particularly dangerous infection is imported by a sick person.

Scheduled vaccinations are carried out in regions where there are natural endemic foci of the disease. A dry vaccine is used, which is administered once intradermally. It is possible to re-administer the vaccine after a year. After vaccination with the anti-plague vaccine, immunity persists for a year.

Vaccination is universal and selective - only to the threatened contingent: livestock breeders, agronomists, hunters, purveyors, geologists, etc.

Re-vaccinate after 6 months. persons at risk of re-infection: shepherds, hunters, agricultural workers and employees of anti-plague institutions.

Maintenance personnel are given prophylactic antibacterial treatment.

Anti-epidemic measures for plague

The identification of a plague patient is a signal for the immediate implementation of anti-epidemic measures, which include:

Carrying out quarantine measures. The introduction of quarantine and the determination of the quarantine territory is carried out by order of the Extraordinary Anti-Epidemic Commission;

Contact persons from the focus of the plague are subject to observation (isolation) for six days;

Implementation of a set of measures aimed at the destruction of the pathogen (disinfection) and the destruction of carriers of the pathogen (deratization and disinsection).

When a natural focus of plague is detected, measures are taken to exterminate rodents (deratization).

If the number of rodents living near people exceeds the 15% limit of their falling into traps, measures are taken to exterminate them.

Deratization is of 2 types: preventive and destructive. General sanitary measures, as the basis for the fight against rodents, should be carried out by the entire population.

Epidemic threats and economic damage caused by rodents will be minimized if derat control is carried out in a timely manner.

Anti-plague suit

Work in the focus of the plague is carried out in an anti-plague suit. The anti-plague suit is a set of clothing that is used by medical personnel when working in conditions of possible infection with a particularly dangerous infection - plague and smallpox. It protects the respiratory organs, skin and mucous membranes of personnel involved in medical and diagnostic processes. It is used by the sanitary and veterinary services.

Medical and sanitary and anti-epidemic measures for tularemia

epidemic surveillance

Tularemia surveillance is the continuous collection and analysis of episode and vector data.

Prevention of tularemia

A live vaccine is used to prevent tularemia. It is designed to protect humans in tularemia foci. The vaccine is administered once, starting from the age of 7 years.

Anti-epidemic measures for tularemia

Anti-epidemic measures for tularemia are aimed at the implementation of a set of measures, the purpose of which is the destruction of the pathogen (disinfection) and the destruction of the carriers of the pathogen (deratization and disinfestation).

Preventive actions

Anti-epidemic measures carried out on time and in in full, can lead to a rapid cessation of the spread of especially dangerous infections, localize and eliminate the epidemic focus in the shortest possible time. Prevention of especially dangerous infections - plague, cholera, anthrax and tularemia is aimed at protecting the territory of our state from the spread of especially dangerous infections.

Main literature

1. Bogomolov B.P. Differential Diagnosis infectious diseases. 2000

2. Lobzina Yu.V. Selected issues of therapy of infectious patients. 2005

3. Vladimirova A.G. infectious diseases. 1997

In stock
Delivery throughout Russia

It is designed to take material from people for research on especially dangerous infectious diseases.

Laying anti-epidemic UK-5M completed on the basis of MU 3.4.2552-09 dated 1.11.2009. approved by the Head of the Federal Service for Supervision of Consumer Rights Protection and Human Welfare, Chief State sanitary doctor Russian Federation G.G. ONISCHENKO.

Purpose of laying UK-5M:
Universal stacking for collecting material from people is designed for primary anti-epidemic measures:
- taking material from the sick or dead in medical institutions (MPI) and at checkpoints across the state border;
- pathoanatomical autopsy of dead people or animal corpses, carried out in accordance with the established procedure for diseases of unclear etiology, suspected of a particularly dangerous infectious disease;
- sanitary and epidemiological examination of the epidemic focus of especially dangerous infections (DOI);
- identifying and accounting for persons who have been in contact with patients with suspected ASI;
- modern implementation of a complex of sanitary and anti-epidemic (preventive) measures for the localization of the epidemic focus of AIO.

Laying for especially dangerous infections is intended for:
- anti-plague institutions (PCHU),
- specialized anti-epidemic brigades (SPEB),
- medical institutions general profile LPU),
- feldsher-obstetric stations (FAP),
- sanitary-quarantine point (SKP)
- FGUZ
- FP
- PAO
- BSME
Composition of laying at OOI:
1. Test tube (PP) (4 ml) for blood sampling and serum production
2. Test tube (PP) (4 ml) for blood sampling with EDTA or sodium citrate (for PCR diagnostics)
3. Spear scarifier disposable, sterile
4. Pre-injection disinfectant wipe
5. Venous hemostatic tourniquet
6. Sterile medical gauze bandage
7. Sterile medical gauze napkin
8. Band-Aid
9. Syringe with a needle (up to 20 ml) medical disposable, sterile
10. Cotton swab on a wooden stick, size 150x2.5 mm, sterile
11. Cotton swab in a polyethylene test tube, size 150x22
mm, sterile
12. Tweezers (150 mm) disposable, sterile
13. Straight tongue spatula, single use, sterile
14. Female urological catheter for single use, sterile
15. Male urological catheter for single use, sterile
16. Medical hygroscopic cotton wool, sterile
17. Container (100 ml) polypropylene with screw cap, sterile
18. Container (60 ml) polypropylene screw cap with spatula, sterile
19. Container (60 ml) polypropylene with a screw cap for collecting sputum, sterile
20. Microtube (PP) 1.5 ml with disposable cap
21. Sterile cryovial 2.0 ml
22. Self-sealing sterilization bag 14x26 cm
23. 3L autoclaving bag
24. Medical cotton balls are non-sterile
25. Container for dumping waste and sharp instruments
26. Cylindrical bottle with screw cap, ungraded, 100 ml (for alcohol)
27. Anatomical tweezers 250 mm
28. Surgical tweezers 150 mm
29. Scalpel surgical sharp 150 mm
30. Straight scissors with 2 sharp ends 140 mm
31. Automatic pipette up to 200 µl
32. Automatic pipette up to 5000 µl
33. Tip for microdoser up to 200 microns
34. Tip for microdosing up to 5000 µl
35. Stand-box for cryotubes with a transparent lid
36. Stand - box for 1.5 ml test tubes with a transparent lid
37. Glass object
38. Cover glass
39. Spirit lamp
40. Oilcloth lining with PVC coating
41. Protective overalls for a limited period of use made of airtight material
42. Mask-respirator
43. Latex medical gloves
44. Medical shoe covers
45. Canned glasses
46.Polymer container for disinfection and
pre-sterilization treatment of medical devices (1000 ml)
47. Ballpoint pen
48. Black lead pencil
49. Permanent marker
50. Scissors
51. Glue PVA-M
52. Paper clip
53. Scotch
54. Clip folder
55. A4 sheet paper for office equipment
56. Filter paper
57. Carbon paper
58. Scotch "biohazard"
59. Protective tape "Biohazard"
60. Stickers on jars "Biohazard"
61. Instructions for taking material
62. Referral for research (forms)
63. Styling bag

Download MU for laying OOI 3.4.2552-09 dated 1.11.2009. Download file:

The list of especially dangerous infections includes those diseases that are of particular epidemic danger, i.e. able to spread widely among the population. They are also characterized by a severe course, high risk lethality and can form the basis of biological weapons of mass destruction. Consider which infections are included in the list of especially dangerous ones, as well as how you can protect yourself from infection.

Particularly dangerous infections and their pathogens

In world medicine, there are no uniform standards on which infections should be considered especially dangerous. The lists of such infections are different in different regions, may be supplemented by new diseases and, conversely, exclude some infections.

Currently, domestic epidemiologists adhere to a list that includes 5 especially dangerous infections:

• anthrax;
• plague;
• tularemia;
• yellow fever (and related Ebola and Marburg).

anthrax

Zoonotic infection, i.e. transmitted to humans from animals. The causative agent of the disease is a spore-forming bacillus that persists in the soil for decades. The source of infection is sick domestic animals (large and small cattle, pigs, etc.). Infection can occur in one of the following ways:

• contact;
• air-dust;
• alimentary;
• transmissible.

The disease has a short incubation period (up to 3 days). Depending on the clinical picture of anthrax, 3 types of anthrax are distinguished:

• skin;
• gastrointestinal;
• pulmonary.

Cholera

An acute bacterial disease belonging to the group of intestinal infections. The causative agent of this infection is Vibrio cholerae, which is well preserved at low temperatures and in the aquatic environment. Sources of infection are a sick person (including those at the stage of recovery) and a carrier of vibrio. Infection occurs by the fecal-oral route.

The incubation period of the disease is up to 5 days. Especially dangerous is cholera, which occurs in erased or atypical forms.

Plague

An acute infectious disease characterized by extremely high contagiousness and a very high probability of death. The causative agent is the plague bacillus, which is transmitted by sick people, rodents and insects (fleas, etc.). The plague wand is very stable, withstands low temperatures. Transmission routes are different:

• transmissible;
• airborne.

There are several forms of plague, the most common of which are pneumonic and bubonic. The incubation period can be up to 6 days.

Tularemia

Natural focal infection, which is one of the most dangerous, has recently become known to mankind. The causative agent is anaerobic tularemia bacillus. Reservoirs of infection are rodents, some mammals (hares, sheep, etc.), birds. At the same time, sick people are not contagious. There are the following ways of infection:

• transmissible;
• respiratory;
• contact;
• alimentary.

The incubation period, on average, is 3 to 7 days. There are several forms of tularemia:

• intestinal;
• bubonic;
• generalized;
• ulcerative bubonic, etc.

Yellow fever

Algorithm of actions of medical staff in case of detection of a patient suspected of having OOI

If a patient suspected of having an OOI is identified, a doctor will organize work in the outbreak. Nursing staff is required to know the scheme of anti-epidemic measures and carry them out by order of the doctor and administration.

Scheme of conducting primary anti-epidemic measures.

I. Measures to isolate the patient at the place of his detection and work with him.

If a patient is suspected of having ASI, health workers do not leave the room where the patient was identified until the arrival of consultants and perform the following functions:

1. Notification of suspicion of OOI by phone or through the door (by knocking on the door to attract the attention of those outside the outbreak and verbally convey information through the door).
2. Request all packing according to the OOI (laying for the prevention of medical staff, packing for taking material for research, packing with anti-plague suits), disinfectants for yourself.
3. Prior to the receipt of styling for emergency prevention, make a mask from improvised means (gauze, cotton wool, bandages, etc.) and use it.
4. Before the laying arrives, close the windows, transoms, using improvised means (rags, sheets, etc.), close the cracks in the doors.
5. When receiving packing to prevent your own infection, carry out emergency prevention of infection, put on an anti-plague suit (for cholera, a lightweight suit - a dressing gown, an apron, possibly without them).
6. Paste windows, doors, ventilation grilles with adhesive tape (except for the focus of cholera).
7. Provide emergency assistance to the patient.
8. To carry out a sampling of material for research and prepare records and referrals for research to the bacteriological laboratory.
9. Carry out current disinfection in the room.

^ II. Measures to prevent the spread of infection.

Head department, the administrator, when receiving information about the possibility of detecting OOI, performs the following functions:

1. Blocks all the doors of the floor where the patient is identified, puts up posts.
2. At the same time, organizes the delivery to the room with the patient of all necessary packing, disinfectants and containers for them, medicines.
3. The reception and discharge of patients is stopped.
4. Notifies the higher administration of the measures taken and awaits further orders.
5. Lists of contact patients and medical staff are compiled (taking into account close and distant contact).
6. Explanatory work is carried out with contact patients in the outbreak about the reason for their delay.
7. Gives permission for consultants to enter the hearth, provides them with the necessary suits.

Exit from the focus is possible with the permission of the head physician of the hospital in the prescribed manner.

Rabies

Rabies- acute viral disease warm-blooded animals and humans, characterized by progressive damage to the central nervous system (encephalitis), fatal to humans.

^ The causative agent of rabies neurotropic virus of the Rabdoviridae family of the genus Lyssavirus. It has a bullet shape, reaches a size of 80-180 nm. The nucleocapsid of the virus is a single-stranded RNA. Exceptional affinity of the virus rabies to the central nervous system was proved by the work of Pasteur, as well as by microscopic studies of Negri and Babesh, who invariably found peculiar inclusions, the so-called Babesh-Negri bodies, in sections of the brain of people who died from rabies.

Source - domestic or wild animals (dogs, cats, foxes, wolves), birds, bats.

Epidemiology. Human infection rabies occurs as a result of bites by rabid animals or when they salivate the skin and mucous membranes, if these covers have microtraumas (scratches, cracks, abrasions).

The incubation period is from 15 to 55 days, in some cases up to 1 year.

^ clinical picture. Conventionally, there are 3 stages:

1. Harbingers. The disease begins with an increase temperature up to 37.2-37.5 ° C and malaise, irritability, itching at the site of the animal bite.

2. Excitation. The patient is excitable, aggressive, fear of water is pronounced. At the sound of pouring water, and sometimes at its sight, convulsions can occur. Increased salivation.

3. Paralysis. The paralytic stage lasts from 10 to 24 hours. At the same time, paresis or paralysis of the lower extremities develops, paraplegia is more often observed. The patient lies motionless, muttering incoherent words. Death comes from paralysis of the motor center.

Treatment. Wash the wound (bite site) with soap, treat with iodine, apply a sterile bandage. Therapy is symptomatic. Lethality - 100%.

Disinfection. Treatment with a 2% solution of chloramine dishes, linen, care items.

^ Precautionary measures. Since the patient's saliva contains the rabies virus, nurse you must wear a mask and gloves.

Prevention. Timely and complete vaccinations.

^

Yellow fever

Yellow fever is an acute viral natural focal disease with transmissible transmission of the pathogen through a mosquito bite, characterized by a sudden onset, high biphasic fever, hemorrhagic syndrome, jaundice and hepatorenal insufficiency. The disease is common in tropical regions of America and Africa.

Etiology. The causative agent, yellow fever virus (flavivirus febricis), belongs to the genus flavivirus, family Togaviridae.

Epidemiology. There are two epidemiological types of yellow fever foci - natural, or jungle, and anthropourgical, or urban.
The reservoir of viruses in the case of the jungle form are marmoset monkeys, possibly rodents, marsupials, hedgehogs and other animals.
carrier of viruses in natural foci yellow fever mosquitoes are Aedes simpsoni, A. africanus in Africa and Haemagogus sperazzini and others in South America. Human infection in natural foci occurs through the bite of an infected A. simpsoni or Haemagogus mosquito, capable of transmitting the virus 9-12 days after infecting bloodsucking.
The source of infection in urban foci of yellow fever is a sick person in the period of viremia. Virus carriers in urban outbreaks are Aedes aegypti mosquitoes.
Currently, sporadic incidence and local group outbreaks are recorded in the tropical forest zone in Africa (Zaire, Congo, Sudan, Somalia, Kenya, etc.), South and Central America.

Pathogenesis. The inoculated yellow fever virus hematogenously reaches the cells of the macrophage system, replicates in them for 3-6, less often 9-10 days, then re-enters the blood, causing viremia and clinical manifestation of the infectious process. Hematogenous dissemination of the virus ensures its introduction into the cells of the liver, kidneys, spleen, bone marrow and other organs where pronounced dystrophic, necrobiotic and inflammatory changes develop. The most characteristic are the occurrence of foci of colliquation and coagulation necrosis in the mesolobular sections of the hepatic lobule, the formation of Councilmen's bodies, the development of fatty and protein degeneration of hepatocytes. As a result of these injuries, cytolysis syndromes develop with an increase in ALT activity and a predominance of AST activity, cholestasis with severe hyperbilirubinemia.
Along with liver damage, yellow fever is characterized by the development of cloudy swelling and fatty degeneration in the epithelium of the tubules of the kidneys, the appearance of areas of necrosis, which cause the progression of acute renal failure.
With a favorable course of the disease, stable immunity is formed.

clinical picture. During the course of the disease, 5 periods are distinguished. The incubation period lasts 3-6 days, rarely extended to 9-10 days.
The initial period (phase of hyperemia) lasts for 3-4 days and is characterized by a sudden increase in body temperature to 39-41 ° C, severe chills, intense headache and diffuse myalgia. As a rule, patients complain of severe pain in the lumbar region, they have nausea and repeated vomiting. From the first days of the disease, most patients experience pronounced hyperemia and puffiness of the face, neck and upper chest. The vessels of the sclera and conjunctiva are brightly hyperemic (“rabbit eyes”), photophobia, lacrimation are noted. Often you can observe prostration, delirium, psychomotor agitation. The pulse is usually rapid, and bradycardia and hypotension develop in the following days. Preservation of tachycardia may indicate an unfavorable course of the disease. In many, the liver is enlarged and painful, and at the end of the initial phase one can notice icterus of the sclera and skin, the presence of petechiae or ecchymosis.
The phase of hyperemia is replaced by a short-term (from several hours to 1-1.5 days) remission with some subjective improvement. In some cases, recovery occurs later, but more often a period of venous stasis follows.
The patient's condition during this period noticeably worsens. The temperature rises again to a higher level, jaundice increases. Skin pale, in severe cases cyanotic. On the skin of the trunk and extremities, a widespread hemorrhagic rash in the form of petechiae, purpura, ecchymosis. There is significant bleeding of the gums, repeated vomiting with blood, melena, nasal and uterine bleeding. In severe cases, shock develops. The pulse is usually rare, weak filling, blood pressure is steadily decreasing; develop oliguria or anuria, accompanied by azotemia. Often there is toxic encephalitis.
The death of patients occurs as a result of shock, liver and kidney failure on the 7-9th day of illness.
The duration of the described periods of infection averages 8-9 days, after which the disease enters the convalescence phase with a slow regression of pathological changes.
Among local residents of endemic areas, yellow fever can occur in a mild or abortive form without jaundice and hemorrhagic syndrome, which makes it difficult to identify patients in a timely manner.

Forecast. Currently, the mortality rate from yellow fever is approaching 5%.
Diagnostics. Recognition of the disease is based on the identification of a characteristic clinical symptom complex in individuals belonging to the high-risk category of infection (unvaccinated people who visited the jungle foci of yellow fever for 1 week before the onset of the disease).

The diagnosis of yellow fever is confirmed by the isolation of the virus from the patient's blood (in the initial period of the disease) or antibodies to it (RSK, NRIF, RTPGA) in the later periods of the disease.

Treatment. Yellow fever patients are hospitalized in mosquito-proof hospitals; prevent parenteral infection.
Therapeutic measures include a complex of anti-shock and detoxification agents, correction of hemostasis. In cases of progression of hepatic-renal failure with severe azotemia, hemodialysis or peritoneal dialysis is performed.

Prevention. Specific prophylaxis in the foci of infection is carried out with a live attenuated vaccine 17 D and less often with the Dakar vaccine. Vaccine 17 D is administered subcutaneously at a dilution of 1:10, 0.5 ml. Immunity develops in 7-10 days and lasts for 6 years. Vaccination is registered in international certificates. Unvaccinated individuals from endemic areas are quarantined for 9 days.

^

Smallpox

Smallpox - acute highly contagious viral disease occurring with severe intoxication and the development of vesicular-pustular rashes on the skin and mucous membranes.

Etiology. Pathogen smallpox– orthopoxvirus variola from the genus orthopoxvirus, family Poxviridae – is represented by two varieties: a) O. variola var. major - the actual causative agent of smallpox; b) O. variola var. minor is the causative agent of alastrim, a benign form of human smallpox in South America and Africa.

The causative agent of smallpox refers to DNA-containing viruses measuring 240-269 x 150 nm, the virus is detected in a light microscope in the form of Paschen bodies. The causative agent of smallpox is resistant to various physical and chemical factors; at room temperature, it does not lose viability even after 17 months.

Epidemiology. Smallpox is a particularly dangerous infection. The reservoir and source of viruses is a sick person who is contagious from the last days of the incubation period until complete recovery and the crusts fall off. The maximum infectivity is noted from the 7-9th day of illness. Infection with smallpox occurs by airborne droplets, airborne dust, household contact, inoculation and transplacental routes. Of greatest importance is airborne route transmission of pathogens. Human susceptibility to natural smallpox is absolute. After the disease, stable immunity is maintained.

Pathogenesis. After entering the human body, the virus replicates in the regional lymph nodes, then spreads by blood to the internal organs (primary viremia), where it replicates in the elements of the mononuclear phagocyte system (within 10 days). In the future, generalization of the infection occurs (secondary viremia), which corresponds to the beginning of the clinical manifestation of the disease.
Possessing a pronounced tropism for tissues of ectodermal origin, the virus causes edema, inflammatory infiltration, ballooning and reticular degeneration in them, which is manifested by rashes on the skin and mucous membranes. In all forms of the disease, parenchymal changes develop in the internal organs.

clinical picture. Distinguish the following forms of the disease: severe - hemorrhagic smallpox (smallpox purpura, pustular-hemorrhagic, or black, smallpox) and confluent smallpox; moderate - disseminated smallpox; lungs - varioloid, smallpox without rash, smallpox without fever.
The clinical course of smallpox can be divided into a number of periods. The incubation period lasts an average of 9-14 days, but can be 5-7 days or 17-22 days. The prodromal period lasts 3-4 days and is characterized by a sudden increase in body temperature, pain in the lumbar region, myalgia, headache, and often vomiting. Within 2-3 days, half of the patients develop a prodromal morbilliform or scarlatiniform rash, localized mainly in the area of ​​Simon's femoral triangle and thoracic triangles. By the end of the prodromal period, the body temperature decreases: at the same time, smallpox rash appears on the skin and mucous membranes.
The period of the rash is characterized by a repeated gradual increase in temperature and a staged spread of smallpox rash: first it occurs on the linden, then on the trunk, on the extremities, affecting the palmar and plantar surfaces, thickening as much as possible on the face and extremities. On one area of ​​the skin, the rash is always monomorphic. The elements of the rash look like pink spots, quickly turning into papules, and after 2-3 days into smallpox vesicles that have multi-chamber structure with umbilical tension in the center of the element and surrounded by a zone of hyperemia.
From the 7-8th day of the disease, suppuration of smallpox elements develops, accompanied by a significant rise in temperature, a sharp deterioration in the patient's condition. Pustules lose their multi-chamber structure, subside at a puncture, and are extremely painful. By the 15th-17th day, the pustules open up, dry out with the formation of crusts, while;) then the pain decreases, unbearable skin itching appears.
During the 4-5th week of the disease, against the background of normal body temperature, intense peeling, falling off of crusts are noted, in place of which deep whitish scars remain, giving the skin a rough (pockmarked) appearance. The duration of the disease with an uncomplicated course is 5-6 weeks. Hemorrhagic forms of smallpox are the most severe, often accompanied by the development of infectious-toxic shock.

Forecast. With an uncomplicated course of the disease, mortality reached 15%, with hemorrhagic forms - 70-100%.

Diagnostics. Based on epidemiological anamnesis data, results clinical examination. Specific diagnostics involves the isolation of the virus from the elements of the rash (electron microscopy), infection of chicken embryos and the detection of antibodies to the smallpox virus (using RNHA, RTGA and the method of fluorescent antibodies).

Treatment. Complex therapy is used, including the use of anti-small immunoglobulin, metisazon, antibiotics a wide range actions and detoxification agents.

Prevention. It is necessary to isolate patients, and also to conduct observation of contact persons with their vaccination within 14 days. Quarantine measures are being implemented in full.

^

anthrax

Anthrax is an acute bacterial zoonotic infection characterized by intoxication, the development of serous-hemorrhagic inflammation of the skin, lymph nodes and internal organs and proceeding in the form of a skin (with the formation of a specific carbuncle in most cases) or septic form.

Etiology. The causative agent of anthrax, bacillus anthracis, belongs to the genus bacillus, family Bacillaceae. It is a large spore-forming gram-positive rod measuring (5-10) x (1-1.5) µm. Anthrax bacilli grow well on meat-peptone media. They contain capsular and somatic antigens, are able to secrete exotoxin, which is a protein complex consisting of a protective and lethal component that causes edema. Vegetative forms of anthrax die quickly when exposed to common disinfectants and boiling. Spores are incomparably more stable. They remain in the soil for decades. When autoclaved (110 °C), they die only after 40 minutes. Activated solutions of chloramine, hot formaldehyde, and hydrogen peroxide also have a sporicidal effect.

Epidemiology. The source of anthrax are sick domestic animals: cattle, horses, donkeys, sheep, goats, deer, camels, pigs, in which the disease occurs in a generalized form. It is most often transmitted by contact, less often by alimentary, airborne and transmissible. In addition to direct contact with sick animals, human infection can occur with the participation of a large number transmission factors. These include secretions and skins of sick animals, their internal organs, meat and other food products, soil, water, air, objects environment contaminated with anthrax spores. In the mechanical inoculative transmission of the pathogen, blood-sucking insects (gadflies, fly zhigalka) are important.
Susceptibility to anthrax is related to the routes of infection and the magnitude of the infectious dose.
There are three types of anthrax foci: professional-agricultural, professional-industrial and domestic. The first type of foci is characterized by summer-autumn seasonality, the rest occur at any time of the year.

Pathogenesis. The entrance gate of anthrax pathogens is usually damaged skin. In rare cases, it is introduced into the body through the mucous membranes of the respiratory tract and gastrointestinal tract. Anthrax carbuncle occurs at the site of the pathogen penetration into the skin (less often - adematous, bullous and erysipeloid forms of skin lesions) in the form of a focus of serous-hemorrhagic inflammation with necrosis, edema of adjacent tissues, and regional lymphadenitis. The development of lymphadenitis is due to the drift of the pathogen by mobile macrophages from the site of introduction to the nearest regional lymph nodes. The local pathological process is caused by the action of exotoxin of anthrax pathogens, some components of which cause pronounced microcirculation disorders, tissue edema and coagulation necrosis. Further generalization of anthrax pathogens with their breakthrough into the blood and the development of a septic form occurs extremely rarely in the cutaneous form.
Anthrax sepsis usually develops when the pathogen enters the human body through the mucous membranes of the respiratory tract or gastrointestinal tract. In these cases, a violation of the barrier function of the tracheobronchial (bronchopulmonary) or mesenteric lymph nodes leads to a generalization of the process.
Bacteremia and toxinemia can cause the development of infectious-toxic shock.

clinical picture. Duration incubation period anthrax ranges from several hours to 14 days, more often 2-3 days. The disease can occur in localized (skin) or generalized (septic) forms. The cutaneous form occurs in 98-99% of all cases of anthrax. Its most common variety is the carbuncle form; less common are edematous, bullous and erysipeloid. Mostly open parts of the body are affected. The disease is especially severe when carbuncles are localized on the head, neck, mucous membranes of the mouth and nose.
Usually there is one carbuncle, but sometimes their number reaches 10-20 or more. A spot, papule, vesicle, ulcer develop sequentially at the site of the entrance gate of infection. A spot with a diameter of 1-3 mm, reddish-bluish in color, painless, resembles insect bite marks. After a few hours, the spot turns into a copper-red papule. Increased local itching and burning sensation. After 12-24 hours, the papule turns into a vesicle 2-3 mm in diameter, filled with serous fluid, which darkens and becomes bloody. When scratched or spontaneously, the vesicle bursts, its walls collapse, an ulcer is formed with a dark brown bottom, raised edges and serous-hemorrhagic discharge. Secondary ("daughter") vesicles appear along the edges of the ulcer. These elements undergo the same stages of development as the primary vesicle and, by merging, increase the size of the skin lesion.
A day later, the ulcer reaches 8-15 mm in diameter. New "daughter" vesicles that appear along the edges of the ulcer cause its eccentric growth. Due to necrosis, the central part of the ulcer, after 1-2 weeks, turns into a black, painless, dense scab, around which a pronounced red inflammatory ridge forms. In appearance, the scab resembles a coal on a red background, which was the reason for the name of this disease (from the Greek anthrax - coal). In general, this lesion is called a carbuncle. The diameter of carbuncles varies from a few millimeters to 10 cm.
The tissue edema arising along the periphery of the carbuncle sometimes captures large areas with loose subcutaneous tissue, for example, on the face. Impacts with a percussion hammer in the area of ​​​​edema often cause gelatinous trembling (Stefansky's symptom).
The localization of the carbuncle on the face (nose, lips, cheeks) is very dangerous, since the edema can spread to the upper respiratory tract and lead to asphyxia and death.
Anthrax carbuncle in the area of ​​necrosis is painless even with needle pricks, which is an important differential diagnostic sign. Lymphadenitis, which develops in the cutaneous form of anthrax, is usually painless and does not tend to suppurate.
The edematous variety of the cutaneous anthrax is characterized by the development of edema without the presence of a visible carbuncle. In more late dates disease, necrosis occurs and a large carbuncle is formed.
With a bullous variety, blisters with hemorrhagic fluid form at the site of the entrance gate of infection. After the opening of the blisters or necrosis of the affected area, extensive ulcerative surfaces are formed, taking the form of a carbuncle.
The peculiarity of the erysipeloid variety of the cutaneous form of anthrax is the development a large number bubbles with clear liquid. After their opening, ulcers remain that undergo transformation into a scab.
The cutaneous form of anthrax in about 80% of patients proceeds in mild and moderate form, in 20% - in severe form.
At easy course disease intoxication syndrome is expressed moderately. Body temperature is normal or subfebrile. By the end of the 2-3rd week, the scab is rejected with the formation (or without it) of a granulating ulcer. After its healing, a dense scar remains. The mild course of the disease ends with recovery.
In moderate and severe course of the disease, malaise, fatigue, headache are noted. By the end of 2 days, the body temperature may rise to 39-40°C, the activity of the cardiovascular system is disrupted. With a favorable outcome of the disease, after 5-6 days the temperature drops critically, there is a reverse development of general and local symptoms, swelling gradually decreases, lymphadenitis disappears, the scab disappears by the end of the 2-4th week, the granulating ulcer heals with the formation of a scar.
The severe course of the cutaneous form can be complicated by the development of anthrax sepsis and have an unfavorable outcome.
The septic form of anthrax is quite rare. The disease begins acutely with a tremendous chill and fever up to 39-40 °C.
Already in the initial period, marked tachycardia, tachypnea, shortness of breath are observed. Often, patients have pain and a feeling of tightness in the chest, cough with the release of foamy bloody sputum. Physically and radiologically, signs of pneumonia and effusion pleurisy (serous-hemorrhagic) are determined. Often, especially with the development of infectious-toxic shock, hemorrhagic pulmonary edema occurs. Sputum secreted by patients coagulates in the form of cherry jelly. A large number of anthrax bacteria are found in blood and sputum.
Some patients develop acute cutting pains in the abdomen. They are joined by nausea, bloody vomiting, loose bloody stools. Subsequently, intestinal paresis develops, peritonitis is possible.
With the development of meningoencephalitis, the consciousness of patients becomes confused, meningeal and focal symptoms appear.
Infectious-toxic shock, edema and swelling of the brain, gastrointestinal bleeding and peritonitis can cause death in the first days of the disease.

Forecast. In the cutaneous form of anthrax, it is usually benign; in the septic form, it is in all cases serious.

Diagnostics. It is carried out on the basis of clinical, epidemiological and laboratory data. Laboratory diagnostics includes bacterioscopic and bacteriological methods. Immunofluorescence is sometimes used for early diagnosis. Allergological diagnostics of anthrax is also used. For this purpose, an intradermal test with anthraxin is carried out, which gives positive results after the 5th day of illness.
The material for laboratory research in the skin form is the contents of vesicles and carbuncles. In the septic form, sputum, vomit, feces, and blood are examined. Studies require compliance with the rules of work, as with especially dangerous infections, and are carried out in special laboratories.

Treatment. Etiotropic therapy of anthrax is carried out by prescribing antibiotics in combination with anthrax immunoglobulin. Apply penicillin at a dose of 6-24 million units per day until the symptoms of the disease stop (but not less than 7-8 days). In the septic form, it is advisable to use cephalosporins 4-6 g per day, levomycetin sodium succinate 3-4 g per day, gentamicin 240-320 mg per day. The choice of dose and combination of drugs is determined by the severity of the disease. Immunoglobulin is administered with a mild form at a dose of 20 ml, with moderate and severe -40-80 ml. The course dose can reach 400 ml.
In the pathogenetic therapy of anthrax, colloid and crystalloid solutions, plasma, and albumin are used. Glucocorticosteroids are prescribed. Treatment of infectious-toxic shock is carried out in accordance with generally accepted methods and means.
Not required for dermal local treatment, surgical interventions can lead to a generalization of the process.

Prevention. Preventive measures are carried out in close contact with veterinary service. Measures for the prevention and elimination of morbidity in farm animals are of primary importance. Identified sick animals should be isolated, and their corpses should be burned, contaminated objects (stalls, feeders, etc.) should be decontaminated.
For disinfection of wool, fur products, the steam-formalin method of chamber disinfection is used.
Persons who have been in contact with sick animals or infectious material are subject to active medical supervision for 2 weeks. If the development of the disease is suspected, antibiotic therapy is performed.
Important is the vaccination of humans and animals, for which a dry live vaccine is used.

Cholera

Cholera is an acute anthroponotic infectious disease caused by vibrio cholerae, with a fecal-oral mechanism of pathogen transmission, occurring with the development of dehydration and demineralization as a result of watery diarrhea and vomiting.

Etiology. The causative agent of cholera, vibrio cholerae, is represented by two biovars, V. cholerae biovar (classic) and V. cholerae biovar El-Tor, similar in morphological and tinctorial properties.

Vibrio cholerae have the form of small, (1.5-3.0) x (0.2-0.6) microns, curved rods with a polarly located flagellum (sometimes with 2 flagella), providing high mobility of pathogens, which is used for their identification, spores and capsules do not form, gram-negative, well stained with aniline dyes. Vibrio cholerae has been found to have toxic substances.

Vibrio cholerae are highly sensitive to drying, ultraviolet irradiation, chlorine-containing preparations. Heating to 56 ° C kills them after 30 minutes, and boiling instantly. They can be stored for a long time at low temperatures and in the organisms of aquatic organisms. Vibrio cholerae are highly sensitive to tetracycline derivatives, to ampicillin, chloramphenicol.

Epidemiology. Cholera is an anthroponotic intestinal infection prone to pandemic spread. The reservoir and source of pathogens is an infected person who excretes cholera vibrios with feces into the external environment. Vibrio excretors are patients with typical and erased forms of cholera, cholera convalescents and clinically healthy vibrio carriers. The most intense source of pathogens are patients with a pronounced clinical picture of cholera, who in the first 4-5 days of illness excrete into the external environment per day up to 10-20 liters of stool containing 106-109 vibrios per 1 ml. Patients with mild and erased forms of cholera excrete a small amount of feces, but remain in the team, which makes them epidemically dangerous.

Vibrio-carrier convalescents secrete pathogens on average within 2-4 weeks, transient carriers - 9-14 days. Chronic carriers of V. cholerae can shed pathogens for a number of months. Possible life-long carriage of vibrios.

The mechanism of infection with cholera is fecal-oral, realized through water, alimentary and contact-household ways of spreading the infection. The leading route of transmission of cholera pathogens, leading to the epidemic spread of the disease, is water. Infection occurs both when drinking infected water, and when using it for household purposes - for washing vegetables, fruits and when bathing. Due to the processes of urbanization and the insufficient level of treatment and disinfection of wastewater, many surface water bodies can become an independent contaminating environment. The facts of re-isolation of El Tor vibrios after exposure to disinfectants from the silt and mucus of the sewer system, in the absence of patients and carriers, have been established. All of the above allowed P.N. Burgasov to come to the conclusion that sewer discharges and infected open water bodies are the habitat, reproduction and accumulation of El Tor vibrios.

Foodborne outbreaks of cholera usually occur among a limited number of people who consume contaminated foods.

It has been established that the inhabitants of various reservoirs (fish, shrimps, crabs, mollusks, frogs and other aquatic organisms) are able to accumulate and retain El Tor vibrios in their bodies for a long time (act as a temporary reservoir of pathogens). The use of hydrobionts for food (oysters, etc.) without careful heat treatment led to the development of the disease. Food epidemics are characterized by an explosive onset with simultaneous outbreaks of disease.

Infection with cholera is also possible through direct contact with a patient or a vibrio carrier: the pathogen can be brought into the mouth with hands contaminated with vibrios, or through objects infected with the secretions of patients (linen, dishes and other household items). Cholera pathogens can be spread by flies, cockroaches and other household insects. Outbreaks of the disease caused by the contact-household route of infection are rare and are characterized by slow spread.

Often there is a combination of different transmission factors that cause mixed outbreaks of cholera.

Cholera, like other intestinal infections, is characterized by seasonality with an increase in the incidence rate in the summer-autumn period of the year due to the activation of pathways and factors for the transmission of pathogens (drinking large amounts of water, an abundance of vegetables and fruits, bathing, "fly factor", etc. .).

Susceptibility to cholera is universal and high. The transferred disease leaves behind a relatively stable species-specific antitoxic immunity. Relapses are rare, although they do occur.

Pathogenesis. Cholera is a cyclic infection that leads to a significant loss of water and electrolytes with intestinal contents due to the predominant damage to enterocyte enzyme systems. Vibrio cholerae that enter through the mouth with water or food partially die in acidic environment gastric contents, partially, bypassing the acid barrier of the stomach, enter the lumen small intestine, where they multiply intensively due to the alkaline reaction of the environment and the high content of peptone. Vibrios are localized in the superficial layers of the mucous membrane of the small intestine or in its lumen. Intensive reproduction and destruction of vibrios is accompanied by the release of a large number of endo- and exotoxic substances. Inflammatory reaction does not develop.

clinical picture. The clinical manifestations of cholera caused by vibrios, including the classic vibrio El Tor, are similar.

The incubation period is from several hours to 5 days, averaging about 48 hours. The disease can develop in typical and atypical forms. In a typical course, mild, moderate and severe forms of the disease are distinguished in accordance with the degree of dehydration. With an atypical course, erased and fulminant forms are distinguished. With El Tor cholera, a subclinical course of the infectious process is often observed in the form of vibrio carrying.

In typical cases, the disease develops acutely, often suddenly: at night or in the morning, patients feel an imperative urge to defecate without tenesmus and abdominal pain. Discomfort, rumbling and transfusion around the navel or in the lower abdomen are often noted. The stool is usually plentiful, the stools are initially fecal in nature with particles of undigested food, then become liquid, watery, yellow in color with floating flakes, later brighten, taking on the form of odorless rice water, with the smell of fish or grated potatoes. In the case of a mild course of the disease, there may be from 3 to 10 bowel movements per day. The patient's appetite decreases, thirst and muscle weakness quickly appear. Body temperature usually remains normal, a number of patients revealed subfebrile condition. On examination, you can detect an increase in heart rate, dryness of the tongue. The abdomen is retracted, painless, rumbling and fluid transfusion along the small intestine is determined. With a favorable course of the disease, diarrhea lasts from several hours to 1-2 days. Fluid loss does not exceed 1-3% of body weight (I degree of dehydration). Physicochemical properties of blood are not violated. The disease ends with recovery. In the case of progression of the disease, there is an increase in the frequency of stools (up to 15-20 times a day), stools are plentiful, watery in the form of rice water. Usually joins repeated profuse vomiting "fountain" without nausea and pain in the epigastrium. The vomit quickly becomes watery with a yellowish discoloration due to the admixture of bile (Greek chole rheo - “bile flow”). Profuse diarrhea and repeated profuse vomiting quickly, within a few hours, lead to severe dehydration (II degree of dehydration) with a loss of fluid amounting to 4-6% of the patient's body weight.

The general condition is deteriorating. Increased muscle weakness, thirst, dry mouth. Some patients experience short-term convulsions calf muscles, feet and hands, diuresis decreases. Body temperature remains normal or subfebrile. The skin of patients is dry, its turgor is reduced, unstable cyanosis is often observed. Mucous membranes are also dry, hoarseness often appears. Characterized by increased heart rate, lowering blood pressure, mainly pulse. Violations of the electrolyte composition of the blood are unstable.

In the absence of rational and timely therapy often within a few hours, fluid loss reaches 7-9% of body weight (III degree of dehydration). The condition of patients progressively worsens, signs of pronounced exsicosis develop: facial features become sharper, eyes sink, dryness of the mucous membranes and skin intensifies, it wrinkles on the hands (“washerwoman’s hands”), the muscular relief of the body also increases, aphonia is pronounced, tonic convulsions of individual muscle groups appear . Sharp arterial hypertension, tachycardia, widespread cyanosis are noted. Oxygen deficiency in tissues exacerbates acidosis and hypokalemia. As a result of hypovolemia, hypoxia and loss of electrolytes, glomerular filtration in the kidneys decreases, oliguria occurs. The body temperature is normal or low.

With a progressive course of the disease in untreated patients, the amount of fluid lost reaches 10% of body weight or more (IV degree of dehydration), decompensated dehydration shock develops. In severe cases of cholera, shock may develop within the first 12 hours of illness. The condition of patients is steadily deteriorating: profuse diarrhea and repeated vomiting, observed at the beginning of the disease, decrease or completely stop in this period. A pronounced diffuse cyanosis is characteristic, often the tip of the nose, auricles, lips, marginal edges of the eyelids acquire a purple or almost black color. Facial features become even more pointed, cyanosis appears around the eyes (a symptom of "dark glasses"), eyeballs deep sunk, turned up (symptom of "setting sun"). Suffering is expressed on the face of the patient, a plea for help - facies chorelica. The voice is silent, consciousness is preserved for a long time. Body temperature drops to 35-34 °C. The skin is cold to the touch, easily gathers into folds and does not straighten out for a long time (sometimes within an hour) - the “cholera fold”. The pulse is arrhythmic, weak filling and tension (filamentous), almost not palpable. Tachycardia is pronounced, heart sounds are almost inaudible, blood pressure is practically not determined. Shortness of breath increases, breathing is arrhythmic, superficial (up to 40-60 breaths per minute), ineffective. Patients breathe rapidly open mouth due to suffocation, muscles are involved in the act of breathing chest. Convulsions of a tonic nature extend to all muscle groups, including the diaphragm, which leads to excruciating hiccups. Abdomen sinks, painful during spasms of its muscles, soft. Anuria usually occurs.

Dry cholera proceeds without diarrhea and vomiting, is characterized by an acute onset, rapid development dehydration shock, sharp drop blood pressure, increased respiration, aphonia, anuria, convulsions of all muscle groups, meningeal and encephalitic symptoms. Death occurs within a few hours. This form of cholera is very rare in debilitated patients.

In the fulminant form of cholera, a sudden onset and rapid development of dehydration shock with severe dehydration of the body are observed.

Forecast. With timely and adequate therapy favorable, mortality is close to zero, but it can be significant with a fulminant form and delayed treatment.

Diagnostics. The diagnosis is based on a combination of anamnestic, epidemiological, clinical and laboratory data.

Treatment. Patients with all forms of cholera are subject to mandatory hospitalization in hospitals (specialized or temporary), where they undergo pathogenetic and etiotropic therapy.

main direction medical measures is the immediate replenishment of the deficit of water and electrolytes - rehydration and remineralization with the help of saline solutions.

Simultaneously with rehydration measures, patients with cholera are given etiotropic treatment - oral tetracycline is prescribed (for adults, 0.3-0.5 g every 6 hours) or levomycetin (for adults, 0.5 g 4 times a day) for 5 days. In severe cases of the disease with the presence of vomiting, the initial dose of antibiotics is administered parenterally. Against the background of taking antibiotics, the severity of diarrheal syndrome becomes less, and therefore the need for rehydration solutions is almost halved.

Patients with cholera do not need a special diet and after the cessation of vomiting should receive normal food in a slightly reduced volume.

Patients are usually discharged from the hospital on the 8-10th day of illness after clinical recovery and three negative results. bacteriological research bowel movements and a single study of bile (portions B and C).

Prevention. The system of measures for the prevention of cholera is aimed at preventing the introduction of this infection into our country from disadvantaged areas, the implementation of epidemiological surveillance and the improvement of the sanitary and communal condition of populated areas.

For the purpose of specific prophylaxis, cholerogen is used - an anatoxin, which in vaccinated people causes in 90-98% of cases not only the production of vibriocidal antibodies, but also antitoxins in high titers. Vaccinations are performed once with a needleless injector at a dose of 0.8 ml of the drug for adults. Revaccination according to epidemiological indications can be carried out no earlier than 3 months after the primary vaccination. A more effective oral vaccine has been developed.

Plague

Plague is an acute natural focal transmissible disease caused by Y. pestis, characterized by fever, severe intoxication, serous hemorrhagic inflammation in the lymph nodes, lungs and other organs, as well as sepsis. It is a particularly dangerous quarantine (conventional) infection, which is subject to the "International Health Regulations". Conducting scientifically based anti-plague measures in the 20th century. allowed to eliminate plague epidemics in the world, however, sporadic cases of the disease are recorded annually in natural foci.

Etiology. plague agent yersinia pestis belongs to the genus yersinia of the family Enterobacteriaceae and is a fixed ovoid short rod 1.5-0.7 microns in size. The stability of the plague pathogen outside the body depends on the nature of the factors affecting it external environment. With a decrease in temperature, the survival time of bacteria increases. At a temperature of –22 °C, bacteria remain viable for 4 months. At 50-70 °C, the microbe dies after 30 minutes, at 100 °C - after 1 minute. Conventional disinfectants in working concentrations (sublimate 1:1000, 3-5% lysol solution, 3% carbolic acid, 10% lime milk solution) and antibiotics (streptomycin, chloramphenicol, tetracyclines) have a detrimental effect on Y. pestis.

Epidemiology. There are natural, primary (“wild plague”) and synanthropic (anthropurgic) foci of plague (“urban”, “port”, “ship”, “rat”). Natural foci of disease developed in ancient times. Their formation was not connected with man and his economic activity. The circulation of pathogens in natural foci of vector-borne diseases occurs between wild animals and blood-sucking arthropods (fleas, ticks). A person, getting into a natural focus, can be exposed to the disease through the bites of blood-sucking arthropods - carriers of the pathogen, in direct contact with the blood of infected game animals. About 300 species and subspecies of rodents carrying the plague microbe have been identified. In rats and mice, plague infection often occurs in a chronic form or as an asymptomatic carrier of the pathogen. The most active carriers of plague pathogens are the rat flea, the flea of ​​human dwellings and the marmot flea. Human infection with plague occurs in several ways: transmissible - through the bites of infected fleas, contact - when removing the skins of infected commercial rodents and cutting the meat of infected camels; alimentary - when eating foods contaminated with bacteria; aerogenic - from patients with pneumonic plague. The most dangerous for others are patients with pneumonic plague. Patients with other forms can pose a threat if there is a sufficient flea population.

The pathogenesis is largely determined by the mechanism of infection transmission. Primary affect at the site of implementation, as a rule, is absent. With the flow of lymph, plague bacteria are carried to the nearest regional lymph nodes, where they multiply. Serous-hemorrhagic inflammation develops in the lymph nodes with the formation of a bubo. The loss of the barrier function by the lymph node leads to a generalization of the process. Bacteria are hematogenously spread to other lymph nodes, internal organs, causing inflammation (secondary buboes and hematogenous foci). The septic form of plague is accompanied by ecchymosis and hemorrhages in the skin, mucous and serous membranes, walls of large and medium-sized vessels. Severe dystrophic changes in the heart, liver, spleen, kidneys and other internal organs are typical.

clinical picture. The incubation period of the plague is 2-6 days. The disease, as a rule, begins acutely, with severe chills and a rapid increase in body temperature to 39-40 ° C. Chills, feeling of heat, myalgia, excruciating headache, dizziness are characteristic initial signs illness. The face and conjunctiva are hyperemic. The lips are dry, the tongue is swollen, dry, trembling, lined with a thick white coating (as if rubbed with chalk), enlarged. Speech is slurred and unintelligible. Typically toxic injury nervous system, expressed in varying degrees. Damage to the cardiovascular system, tachycardia (up to 120-160 beats per 1 minute) is determined early, cyanosis, arrhythmia of the pulse appear, and blood pressure is significantly reduced. Seriously ill patients have bloody or coffee grounds-colored vomiting, loose stools with mucus and blood. An admixture of blood and protein is found in the urine, oliguria develops. The liver and spleen are enlarged.

Clinical forms of plague:

A. Predominantly local forms: skin, bubonic, skin-bubonic.

B. Internally disseminated, or generalized forms: primary septic, secondary septic.

B. Externally disseminated (central, often with abundant external dissemination): primary pulmonary, secondary pulmonary, intestinal.

The intestinal form is not recognized as independent by most authors.

Erased, mild, subclinical forms of plague are described.

skin form. At the site of introduction of the pathogen, changes occur in the form necrotic ulcers, furuncle, carbuncle. Necrotic ulcers are characterized by a rapid, sequential change of stages: spot, vesicle, pustule, ulcer. Plague skin ulcers are characterized long course and slow healing with scar formation. Secondary skin changes in the form of hemorrhagic rashes, bullous formations, secondary hematogenous pustules and carbuncles can be observed in any clinical form of plague.

bubonic form. The most important sign of the bubonic form of plague is bubo - a sharply painful enlargement of the lymph nodes. Bubo, as a rule, there is one, less often there is the development of two or more buboes. The most common localizations of plague buboes are the inguinal, axillary, and cervical regions. early sign the emerging bubo - a sharp soreness, forcing the patient to take unnatural postures. Small buboes are usually more painful than large ones. In the first days, individual lymph nodes can be felt at the site of the developing bubo, later they are soldered to the surrounding tissue. The skin over the bubo is tense, acquires a red color, the skin pattern is smoothed out. Lymphangitis is not observed. At the end of the stage of bubo formation, the phase of its resolution begins, which proceeds in one of three forms: resorption, opening, and sclerosis. With timely antibacterial treatment, complete resorption of the bubo occurs more often within 15-20 days or its sclerosis. According to the severity of the clinical course, cervical buboes take the first place, then axillary and inguinal. The greatest danger is the axillary due to the threat of developing secondary pneumonic plague. In the absence of adequate treatment, mortality in the bubonic form ranges from 40 to 90%. With early antibacterial and pathogenetic treatment death rarely occurs.

Primary septic form. It develops rapidly after a short incubation, ranging from several hours to 1-2 days. The patient feels chills, body temperature rises sharply, severe headache, agitation, delirium appear. Possible signs of meningoencephalitis. A picture of infectious-toxic shock develops, coma quickly sets in. The duration of the disease is from several hours to three days. Recovery cases are extremely rare. Patients die with symptoms of severe intoxication and severe hemorrhagic syndrome, increasing cardiovascular insufficiency.

Secondary septic form. It is a complication of other clinical forms of infection, characterized by an exceptionally severe course, the presence of secondary foci, buboes, pronounced manifestations of hemorrhagic syndrome. Lifetime diagnosis of this form is difficult.

Primary pulmonary form. The most severe and epidemiologically the most dangerous form. There are three main periods of the disease: the initial, peak period and soporous (terminal) period. The initial period is characterized by a sudden rise in temperature, accompanied by a sharp chill, vomiting, severe headache. At the end of the first day of illness, cutting pains in the chest, tachycardia, shortness of breath, delirium appear. The cough is accompanied by sputum production, the amount of which varies greatly (from a few "spitting" in "dry" plague pneumonia to a huge mass in the "copious wet" form). At first, the sputum is clear, glassy, ​​viscous, then it becomes frothy, bloody, and finally bloody. Liquid sputum is a typical symptom of pneumonic plague. Excreted with mucus great amount plague bacteria. Physical data are very scarce and do not correspond to the general severe condition of the patients. The peak period of the disease lasts from several hours to 2-3 days. Body temperature remains high. Attention is drawn to hyperemia of the face, red, "bloodshot" eyes, severe shortness of breath and tachypnea (up to 50-60 breaths per minute). Heart sounds are deaf, the pulse is frequent, arrhythmic, blood pressure is reduced. As intoxication increases, the depressed state of patients is replaced by general excitement, delirium appears. The terminal period of the disease is characterized by an extremely severe course. Patients develop a soporous condition. Shortness of breath increases, breathing becomes superficial. Arterial pressure is almost not determined. The pulse is rapid, thready. Petechiae, extensive hemorrhages appear on the skin. The face becomes cyanotic, and then an earthy gray color, the nose is pointed, the eyes are sunken. The patient is afraid of death. Later develop prostration, coma. Death occurs on the 3-5th day of illness with increasing circulatory failure and, often, pulmonary edema.

Secondary pulmonary form. It develops as a complication of bubonic plague, clinically similar to primary pulmonary. Plague in vaccinated patients. It is characterized by a lengthening of the incubation period up to 10 days and a slowdown in the development of the infectious process. During the first and second days of the disease, subfebrile fever, general intoxication is mild, the condition of the patients is satisfactory. Bubo small sizes, without pronounced manifestations of periadenitis. However, the symptom of sharp soreness of the bubo always persists. If these patients do not receive antibiotic treatment within 3-4 days, then further development disease will be no different from clinical symptoms in unvaccinated patients.

Forecast. Almost always serious. Methods play a decisive role in recognizing the plague. laboratory diagnostics(bacterioscopic, bacteriological, biological and serological), carried out in special laboratories operating in accordance with the instructions on the mode of operation of anti-plague institutions.

Treatment. Plague patients are subject to strict isolation and mandatory hospitalization. The main role in etiotropic treatment belongs to antibiotics - streptomycin, tetracycline drugs, levomycetin, prescribed in large doses. Along with antibacterial treatment, detoxification pathogenetic therapy is carried out, including the introduction of detoxification fluids (polyglucin, reopoliglyukin, hemodez, neocompensan, albumin, dry or native plasma, standard saline solutions), diuretics (furosemide, or lasix, mannitol, etc.) - with fluid retention in the body, glucocorticosteroids, vascular and respiratory analeptics, cardiac glycosides, vitamins. Patients are discharged from the hospital with complete clinical recovery and negative results bacteriological control.

Prevention. In Russia, and earlier in the USSR, the only powerful anti-plague system in the world was created, which carries out preventive and anti-epidemic measures in natural foci of plague.

Prevention includes the following activities:

a) prevention of human diseases and outbreaks in natural foci;

b) prevention of infection of persons working with material infected or suspected of being infected with plague;

c) prevention of the importation of plague into the country from abroad.