Infections: general characteristics. History of the development of the doctrine of infectious diseases The role of infections

LITERATURE REVIEW

The role of INFECTIONS in URTICA IN CHILDREN

A. A. CHEBUKIN, L. N. MAZANKOVA, S. I. SALNIKOVA

GOU DPO RMAPO Roszdrav, Department of Children's Infectious Diseases, Moscow

Role of Infections of Urticaria in Children

A. A. Cheburkin, L. N. Mazankova, S. I. Saimkova

Russian MedicaL Academy of Postgraduate Education

The role of infectious and parasitic diseases in the genesis of urticaria in children has been studied and discussed for a long time, however it cannot be defined with certainty up to now. At the same time it is no doubt that in some patients urticaria is a symptom of infection and this is likely to be linked to genetically conditioned predisposing factors. The significance of infectious diseases and helminthisms in the pathogenesis of urticarious rash is most clearly identified in patients with acute urticaria; in chronic urticaria infections play a minimal role. Key words: urticaria, children, parasitosis, helminthisms, infectious diseases

Contact information: Mazankova Lyudmila Nikolaevna - Doctor of Medical Sciences, Prof., Head. department pediatric infectious diseases with a course in pediatric dermatovenerology at the Russian Medical Academy of Postgraduate Education; 125480, Moscow, st. Geroev Panfilovtsev, 28, Tushino Children's City Hospital; 949-17-22

UDC 616.514:616.9

Urticaria is a widespread disease among both adults and children. A single occurrence of urticaria during life is observed in 15-20% of both children and adults. The incidence of recurrent urticaria in children is estimated at two to three percent.

The primary element of the rash in urticaria is a wheal (igNsa); That's why the rash is called urticarial. Despite the different size and color of the blisters, the common features of such a rash are itching, erythema; elements of the rash rise above the surface of the skin. The blister turns pale when pressed, indicating dilation of the blood vessels and swelling of the surrounding tissue. Microscopic examination of the skin in patients with urticaria reveals dilation of small venules and capillaries of the superficial layers of the skin, spreading to the papillary layer and swelling of collagen fibers. In half of the patients, urticaria is accompanied by Quincke's edema (angioedema), in which similar changes develop in the deeper layers of the skin and subcutaneous tissue. There is no pattern in the localization of the rash with urticaria, while Quincke's edema most often occurs in the face, tongue, limbs and genitals. Urticarial rash is accompanied by itching and persists for several minutes to 48 hours, after which the elements of the rash disappear without a trace. With recurrent urticaria, new rashes may appear both on previously affected and other areas of the skin. According to the course, acute (up to 6 weeks) or chronic (more than 6 weeks) urticaria is distinguished. If urticaria rash appears repeatedly, recurrent urticaria (acute or chronic) is diagnosed.

The pathogenesis of urticaria is associated with the release of pro-inflammatory mediators from mast and mononuclear cells of the skin, activation of the complement system, Hagemann factor. Inflammatory mediators include histamine, prostaglandin D2, leukotrienes C and D, platelet activating factor, bradykinin. The “triggering” of inflammation can occur

to die in an immune and non-immune way. Accordingly, urticaria, according to the new nomenclature of allergic diseases, is divided into allergic (usually ^-mediated) and non-immune (non-allergic).

Acute urticaria in children is most often associated with food, drug, insect allergies, as well as viral infections. Moreover, in half of the patients the cause of the urticaria rash cannot be identified - such urticaria is designated as idiopathic. With chronic urticaria, in only 20-30% of children it is possible to establish its cause, which is most often represented by physical factors, infections, food allergies, food additives, inhaled allergens and medications. Thus, urticaria can be both a nosological entity and a syndrome, the causes and mechanisms of development of which are diverse. The most common causes of urticaria and angioedema in children are:

Allergic and non-immune reactions to medications, food and nutritional supplements

Allergic reactions to pollen, mold and dust allergens

Post-transfusion reactions

Insect bites and stings

Physical factors (cold, cholinergic, adrenergic, vibration, pressure, solar, dermographic, aquagenic urticaria)

Systemic connective tissue diseases Serum sickness

Malignant neoplasms accompanied by acquired deficiency of C1 and C1-complement inactivator

Mastocytosis (urticaria pigmentosa) Hereditary diseases (hereditary angioedema, familial cold urticaria, C3b complement inhibitor deficiency, amyloidosis with deafness and urticaria).

Group A streptococci are also considered as a possible factor playing a role in the occurrence of urticaria. In chronic urticaria, antibodies to these microorganisms are often detected, and the effect of treatment with erythromycin, amoxicillin, and cefuroxime is noted. However, these data also concern very small groups of pa-

Summarizing the above data, despite their inconsistency and ambiguity, we can state:

The development cycle of Giardia in the human body begins with the duodenum and proximal jejunum, where intensive parietal digestion occurs and there is an alkaline environment that is optimal for the life of Giardia. The most severe pathological syndrome of giardiasis is a violation of absorption processes due to the toxic effect of Giardia on the glycocalyx of the small intestine, enhanced by bacterial colonization. To date, strains and isolates of Giardia of different virulence have been isolated and the phenomenon of antigenic variation of Giardia has been identified, which allows trophozoites to exist inside the intestines of their hosts, creating conditions for chronicity and repeated invasion. IgA-1 proteases from Giardia trophozoites can destroy host IgA, which also promotes the survival of Giardia in the intestine. It is known that homogenate of Giardia trophozoites has a cytotoxic effect on the intestinal epithelium, causing both morphological and biochemical changes similar to manifestations of food allergy. It is believed that there is a connection between giardiasis infestation and allergies due to

A. A. CHEBURKIN et al. The role of INFECTIONS in URTISH in AETE

No blood is detected in the stool, and tenesmus is not described. Gastritis as a manifestation of giardiasis does not occur if the patient does not have disorders of the acid-forming function of the stomach, but often the source of infection is the duodenum, which is manifested by symptoms of damage to the upper gastrointestinal tract.

G. lamblia infection can be protracted and cause clinical symptoms over many weeks and months. This occurs in the absence of treatment. Chronic giardiasis is manifested by deep asthenia and abdominal pain. Most likely, asthenia is a consequence of malabsorption of fats, salts, carbohydrates and vitamins. Lactase deficiency is detected in 20-40% of patients with chronic giardiasis. When carrying out differential diagnosis, it should be borne in mind that malabsorption may be the only symptom of chronic infection caused by G. Lamblia.

Clinical observations of urticaria in giardiasis (observations by S. I. Salnikova at the Scientific Center for Children's Health of the Russian Academy of Medical Sciences).

In this case, 13% of these children had recurrent urticaria. In all cases, this invasion was accompanied by abdominal pain, loss of appetite, nausea, and stool disturbances (irregular, often with a tendency to constipation). Coprological studies revealed signs of inflammation and digestive disorders.

Toxocariasis - canine and feline ascariasis has a complex pathogenesis of allergic manifestations and immune response. Humans are an accidental host for Toxocara and therefore there is a high degree of pathological reactions to invasion. It has been established that toxocariasis is detected in 8-11% of children with chronic skin diseases, including recurrent urticaria. Invasion is accompanied by eosinophilia, hyperimmunoglobulinemia, tissue basophilia and an increase in the number of macrophages, which is due to the influence of migrating larvae of canine roundworms and the development of two phenomena: humoral (formation of specific antibodies) and cellular (eosinophilia). When meeting canine roundworm larvae, tissue basophils release active amines (heparin, histamine), which, in combination with leukotrienes and other inflammatory mediators, cause the main symptoms of allergy: hyperemia, skin itching, urticaria, bronchospasm. In children with allergic diseases, the severity of immunopathological reactions caused by toxocara increases.

Ascariasis, caused by a large nematode, in the acute migratory stage of larval development is characterized by various allergic manifestations, fever, pulmonary syndrome and hypereosinophilia. Typical skin rashes are itchy, urticarial papules and spots. The rash often has a migratory nature. Some researchers indicate that in recent years, acute urticaria has become more common with ascariasis.

In these cases, an erroneous diagnosis of photodermatitis or pruriginous dermatitis is often made.

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Immune system disorder

for HERPES VIRUS INFECTION

L. V. Kravchenko, A. A. Afonin, M. V. Demidova

Rostov Research Institute of Obstetrics and Pediatrics

Ministry of Health and Social Development of the Russian Federation, Rostov-on-Don

The importance of immune mechanisms in the pathogenesis of herpesvirus infection in children of the first year of life is shown. The balance of pro- and anti-inflammatory cytokines is a key factor determining the clinical condition of a child with herpes virus infection. The mechanism of intercellular interactions between the antigen-presenting cell, T-helper cells and B-lymphocytes is provided by costimulation molecules CO28 and CO40.

Key words: herpes virus infection, cytokines, costimulation molecules, children

The environment is filled with a huge number of “inhabitants”, among which there are various microorganisms: viruses, bacteria, fungi, protozoa. They can live in absolute harmony with humans (non-pathogenic), exist in the body without causing harm under normal conditions, but become activated under the influence of certain factors (conditionally pathogenic) and be dangerous to humans, causing the development of a disease (pathogenic). All these concepts relate to the development of the infectious process. What is an infection, what are its types and features - is discussed in the article.

Basic Concepts

An infection is a complex of relationships between different organisms, which has a wide range of manifestations - from asymptomatic carriage to the development of the disease. The process appears as a result of the introduction of a microorganism (virus, fungus, bacteria) into a living macroorganism, in response to which a specific protective reaction occurs on the part of the host.

Features of the infectious process:

1. Contagiousness is the ability to quickly spread from a sick person to a healthy person.
2. Specificity - a certain microorganism causes a specific disease, which has characteristic manifestations and localization in cells or tissues.
3. Periodicity - each infectious process has periods of its course.

Periods

The concept of infection is also based on the cyclical nature of the pathological process. The presence of periods in development is characteristic of each similar manifestation:

1. The incubation period is the time that passes from the moment a microorganism is introduced into the body of a living being until the first clinical signs of the disease appear. This period can last from several hours to several years.
2. The prodrome period is the appearance of a general clinic characteristic of most pathological processes (headache, weakness, fatigue).
3. Acute manifestations are the peak of the disease. During this period, specific symptoms of infection develop in the form of rashes, characteristic temperature curves, and tissue damage at the local level.
4. Convalescence is the time of fading of the clinical picture and recovery of the patient.

Types of infectious processes

To consider in more detail the question of what an infection is, you need to understand what it is like. There are a significant number of classifications depending on the origin, course, localization, number of microbial strains, etc.

1. According to the method of penetration of pathogens:

• - characterized by the penetration of a pathogenic microorganism from the external environment;
• endogenous process - activation of one’s own opportunistic microflora occurs under the influence of unfavorable factors.

2. By origin:

• spontaneous process - characterized by the absence of human intervention;
• experimental - the infection was bred artificially in a laboratory.

3. By the number of microorganisms:

• monoinfection - caused by one type of pathogen;
• mixed - several types of pathogens are involved.

4. By order:

• primary process - a newly emerging disease;
• secondary process - accompanied by the addition of additional infectious pathology against the background of the primary disease.

5. By localization:

• local form - the microorganism is found only in the place through which it entered the host’s body;
• - pathogens spread throughout the body with further settling in certain favorite places.

6. Downstream:

• acute infection - has a clear clinical picture and lasts no more than a few weeks;
• chronic infection - characterized by a sluggish course, can last for decades, has exacerbations (relapses).

7. By age:

• "children's" infections - affect children mainly aged 2 to 10 years (chicken pox, diphtheria, scarlet fever, whooping cough);
• There is no concept of “adult infections” as such, since the child’s body is just as sensitive to those pathogens that cause the development of the disease in adults.

There are concepts of reinfection and superinfection. In the first case, a person who has fully recovered, after an illness, becomes infected again with the same pathogen. With superinfection, re-infection occurs during the course of the disease (strains of the pathogen are layered on top of each other).

Paths of entry

There are the following routes of penetration of microorganisms that ensure the transfer of pathogens from the external environment to the host organism:

• fecal-oral (consists of nutritional, water and contact-household);
• transmissible (blood) - includes sexual, parenteral and through insect bites;
• aerogenic (airborne dust and airborne droplets);
• contact-genital, contact-wound.

Most pathogens are characterized by the presence of a specific route of penetration into the macroorganism. If the transmission mechanism is interrupted, the disease may not appear at all or may worsen in its manifestations.

Localization of the infectious process

Depending on the area affected, the following types of infections are distinguished:

1. Intestinal. The pathological process occurs in parts of the gastrointestinal tract, the pathogen penetrates through the fecal-oral route. These include salmonellosis, dysentery, rotavirus, and typhoid fever.
2. Respiratory. The process occurs in the upper and lower respiratory tract, microorganisms “move” in most cases through the air (influenza, adenoviral infection, parainfluenza).
3. External. Pathogens contaminate the mucous membranes and skin, causing fungal infections, scabies, microsporia, and STDs.
4. enters through the blood, spreading further throughout the body (HIV infection, hepatitis, diseases associated with insect bites).

Intestinal infections

Let us consider the features of pathological processes using the example of one of the groups - intestinal infections. What is an infection that affects the human gastrointestinal tract, and what is its difference?

Diseases of this group can be caused by pathogens of bacterial, fungal and viral origin. Viral microorganisms that can penetrate various parts of the intestinal tract are rotaviruses and enteroviruses. They can spread not only through the fecal-oral route, but also through airborne droplets, affecting the epithelium of the upper respiratory tract and causing herpes sore throat.

Bacterial diseases (salmonellosis, dysentery) are transmitted exclusively by the fecal-oral route. Infections of fungal origin occur in response to internal changes in the body that occur under the influence of long-term use of antibacterial or hormonal drugs, with immunodeficiency.

Rotaviruses

Rotavirus intestinal infection, the treatment of which must be comprehensive and timely, in principle, like any other disease, makes up half of the clinical cases of viral intestinal infectious pathologies. An infected person is considered dangerous to society from the end of the incubation period until complete recovery.

Intestinal rotavirus is much more severe than in adults. The stage of acute manifestations is accompanied by the following clinical picture:

• abdominal pain;
• diarrhea (the stool is light in color and may contain blood);
• bouts of vomiting;
• hyperthermia;
• runny nose;
• inflammatory processes in the throat.

Rotavirus in children is in most cases accompanied by outbreaks of the disease in school and preschool institutions. By the age of 5, most children have experienced the effects of rotaviruses. Subsequent infections are not as severe as the first clinical case.

Surgical infection

Most patients in need of surgical intervention are interested in the question of what a surgical-type infection is. This is the same process of interaction between the human body and a pathogenic pathogen, only occurring during surgery or requiring surgical intervention to restore functions in a certain disease.

There are acute (purulent, putrefactive, specific, anaerobic) and chronic processes (specific, nonspecific).

Depending on the location of the surgical infection, the following diseases are distinguished:

• soft tissues;
• joints and bones;
• brain and its structures;
• abdominal organs;
• organs of the chest cavity;
• pelvic organs;
• individual elements or organs (breast, hand, foot, etc.).

Pathogens of surgical infection

Currently, the most frequent “guests” of acute purulent processes are:

• staphylococcus;
• Pseudomonas aeruginosa;
• enterococcus;
• coli;
• streptococcus;
• Proteus.

The entrance gates for their penetration are various damage to the mucous membranes and skin, abrasions, bites, scratches, ducts of the glands (sweat and sebaceous). If a person has chronic foci of accumulation of microorganisms (chronic tonsillitis, rhinitis, caries), then they cause the spread of pathogens throughout the body.

Treatment of infection

The basis of getting rid of pathological microflora is aimed at eliminating the cause of the disease. Depending on the type of pathogen, the following groups of medications are used:

1. Antibiotics (if the causative agent is a bacterium). The choice of a group of antibacterial agents and a specific drug is made on the basis of bacteriological examination and determination of the individual sensitivity of the microorganism.
2. Antiviral (if the causative agent is a virus). At the same time, drugs are used that strengthen the human body’s defenses.
3. Antimycotic agents (if the pathogen is a fungus).
4. Antihelminthic (if the pathogen is a helminth or a protozoan).

Treatment of infections in children under 2 years of age is carried out in a hospital setting to avoid the development of possible complications.

Conclusion

After the occurrence of a disease that has a specific pathogen, the specialist differentiates and determines the need for hospitalization of the patient. The specific name of the disease must be indicated in the diagnosis, and not just the word “infection”. The medical history, which is taken for inpatient treatment, contains all the data about the stages of diagnosis and treatment of a specific infectious process. If there is no need to hospitalize the patient, all such information is recorded in the outpatient card.

Infection is the penetration and reproduction of a pathogenic microorganism (bacteria, virus, protozoa, fungus) in a macroorganism (plant, fungus, animal, human) that is susceptible to this type of microorganism. A microorganism capable of infection is called an infectious agent or pathogen.

Infection is, first of all, a form of interaction between a microbe and the affected organism. This process is extended over time and occurs only under certain environmental conditions. In an effort to emphasize the temporal extent of the infection, the term “infectious process” is used.

Infectious diseases: what are these diseases and how do they differ from non-infectious diseases

Under favorable environmental conditions, the infectious process takes on an extreme degree of manifestation, at which certain clinical symptoms appear. This degree of manifestation is called an infectious disease. Infectious pathologies differ from non-infectious pathologies in the following ways:

• The cause of infection is a living microorganism. The microorganism that causes a particular disease is called the causative agent of that disease;
• Infections can be transmitted from an affected organism to a healthy one - this property of infections is called contagiousness;
• Infections have a latent (hidden) period - this means that they do not appear immediately after the pathogen enters the body;
• Infectious pathologies cause immunological changes - they stimulate an immune response, accompanied by a change in the number of immune cells and antibodies, and also become the cause of infectious allergies.

Rice. 1. Assistants of the famous microbiologist Paul Ehrlich with laboratory animals. At the dawn of the development of microbiology, a large number of animal species were kept in laboratory vivariums. Nowadays they are often limited to rodents.

Factors of infectious diseases

So, for an infectious disease to occur, three factors are necessary:

1. Pathogen microorganism;
2. The host organism is susceptible to it;
3. The presence of environmental conditions in which the interaction between the pathogen and the host leads to the occurrence of the disease.

Infectious diseases can be caused by opportunistic microorganisms, which are most often representatives of normal microflora and cause disease only when the immune defense is reduced.

Rice. 2. Candida is part of the normal microflora of the oral cavity; they cause disease only under certain conditions.

But pathogenic microbes, while in the body, may not cause disease - in this case they speak of carriage of a pathogenic microorganism. In addition, laboratory animals are not always susceptible to human infections.

For an infectious process to occur, it is also important to have a sufficient number of microorganisms entering the body, which is called the infectious dose. The susceptibility of the host organism is determined by its biological species, gender, heredity, age, nutritional sufficiency and, most importantly, the state of the immune system and the presence of concomitant diseases.

Rice. 3. Malarial plasmodium can spread only in those areas where their specific carriers, mosquitoes of the genus Anopheles, live.

Environmental conditions are also important, in which the development of the infectious process is facilitated as much as possible. Some diseases are characterized by seasonality, some microorganisms can only exist in a certain climate, and some require vectors. Recently, the conditions of the social environment have come to the fore: economic status, living and working conditions, the level of development of healthcare in the state, religious characteristics.

Infectious process in dynamics

The development of infection begins with the incubation period. During this period, there are no manifestations of the presence of an infectious agent in the body, but infection has already occurred. During this time, the pathogen multiplies to a certain number or releases a threshold amount of toxin. The duration of this period depends on the type of pathogen.

For example, with staphylococcal enteritis (a disease that occurs when eating contaminated food and is characterized by severe intoxication and diarrhea), the incubation period takes from 1 to 6 hours, and with leprosy it can last for decades.

Rice. 4. The incubation period for leprosy can last for years.

In most cases it lasts 2-4 weeks. Most often, the peak of infectivity occurs at the end of the incubation period.

The prodromal period is a period of precursors of the disease - vague, nonspecific symptoms, such as headache, weakness, dizziness, changes in appetite, fever. This period lasts 1-2 days.

Rice. 5. Malaria is characterized by fever, which has special properties in different forms of the disease. Based on the form of the fever, one can assume the type of plasmodium that caused it.

The prodrome is followed by a period at the height of the disease, which is characterized by the appearance of the main clinical symptoms of the disease. It can develop either rapidly (then they speak of an acute onset) or slowly, sluggishly. Its duration varies depending on the state of the body and the capabilities of the pathogen.

Rice. 6. Typhoid Mary, who worked as a cook, was a healthy carrier of typhoid fever bacilli. She infected more than half a thousand people with typhoid fever.

Many infections are characterized by an increase in temperature during this period, associated with the penetration into the blood of so-called pyrogenic substances - substances of microbial or tissue origin that cause fever. Sometimes a rise in temperature is associated with the circulation of the pathogen itself in the bloodstream - this condition is called bacteremia. If at the same time the microbes also multiply, they speak of septicemia or sepsis.

Rice. 7. Yellow fever virus.

The end of the infectious process is called the outcome. The following outcome options exist:

• Recovery;
• Lethal outcome (death);
• Transition to chronic form;
• Relapse (reoccurrence due to incomplete cleansing of the pathogen from the body);
• Transition to healthy microbial carriage (a person, without knowing it, carries pathogenic microbes and in many cases can infect others).

Rice. 8. Pneumocystis are fungi that are the leading cause of pneumonia in people with immunodeficiencies.

Classification of infections

Rice. 9. Oral candidiasis is the most common endogenous infection.

By the nature of the pathogen, bacterial, fungal, viral and protozoal (caused by protozoa) infections are distinguished. Based on the number of pathogen types, they are distinguished:

• Monoinfections – caused by one type of pathogen;
• Mixed or mixed infections - caused by several types of pathogens;
• Secondary – occurring against the background of a pre-existing disease. A special case is opportunistic infections caused by opportunistic microorganisms against the background of diseases accompanied by immunodeficiencies.

By origin they distinguish:

• Exogenous infections, in which the pathogen enters from the outside;
• Endogenous infections caused by microbes that were in the body before the onset of the disease;
• Autoinfections are infections in which self-infection occurs by transferring pathogens from one place to another (for example, oral candidiasis caused by the introduction of fungus from the vagina with dirty hands).

According to the source of infection there are:

• Anthroponoses (source – humans);
• Zoonoses (source: animals);
• Anthropozoonoses (the source can be both humans and animals);
• Sapronoses (source - environmental objects).

Based on the location of the pathogen in the body, local (local) and general (generalized) infections are distinguished. According to the duration of the infectious process, acute and chronic infections are distinguished.

Rice. 10. Mycobacterium leprosy. Leprosy is a typical anthroponosis.

Pathogenesis of infections: general scheme of development of the infectious process

Pathogenesis is the mechanism for the development of pathology. The pathogenesis of infections begins with the penetration of the pathogen through the entrance gate - mucous membranes, damaged integument, through the placenta. The microbe then spreads throughout the body in various ways: through the blood - hematogenously, through the lymph - lymphogenously, along the nerves - perineurally, along the length - destroying the underlying tissues, along physiological paths - along, for example, the digestive or reproductive tract. The final location of the pathogen depends on its type and affinity for a particular type of tissue.

Having reached the site of final localization, the pathogen exerts a pathogenic effect, damaging various structures mechanically, with waste products or by releasing toxins. Isolation of the pathogen from the body can occur with natural secretions - feces, urine, sputum, purulent discharge, sometimes with saliva, sweat, milk, tears.

Epidemic process

The epidemic process is the process of spreading infections among the population. The links in the epidemic chain include:

• Source or reservoir of infection;
• Path of transmission;
• Receptive population.

Rice. 11. Ebola virus.

A reservoir differs from a source of infection in that the pathogen accumulates in it between epidemics, and under certain conditions it becomes a source of infection.

Main routes of transmission of infections:

1. Fecal-oral – with food contaminated with infectious secretions, hands;
2. Airborne - through the air;
3. Transmissible - through a carrier;
4. Contact – sexual, through touching, through contact with infected blood, etc.;
5. Transplacental - from a pregnant mother to a child through the placenta.

Rice. 12. H1N1 influenza virus.

Transmission factors are objects that contribute to the spread of infection, for example, water, food, household items.

Based on the coverage of a certain territory by the infectious process, the following are distinguished:

• Endemics are infections “tied” to a limited territory;
• Epidemics are infectious diseases covering large territories (city, region, country);
• Pandemics are epidemics that span several countries and even continents.

Infectious diseases make up the lion's share of all diseases facing humanity. They are special in that during them a person suffers from the vital activity of living organisms, albeit thousands of times smaller than himself. Previously, they often ended fatally. Despite the fact that today the development of medicine has made it possible to significantly reduce the mortality rate of infectious processes, it is necessary to be alert and aware of the peculiarities of their occurrence and development.

8.1. Infection. Forms of the infectious process

The terms “infection” and “infectious disease” are not synonymous.

Understanding infection as the interaction of a pathogenic (disease-causing) microorganism and a susceptible (sensitive) host under certain environmental conditions, it should be noted that an infectious disease is an extreme degree of manifestation of the infectious process, when a pathological focus is formed and specific clinical symptoms appear.

Various forms of the infectious process (infection) are classified depending on the nature of the pathogen, origin, conditions for the occurrence of the infection, the nature and duration of its course, etc.

Depending on the nature of the pathogen, belonging to a particular taxon, there is a classification of infections according to etiological principle: bacterial(dysentery, salmonellosis, diphtheria, tuberculosis, gonorrhea, etc.), viral(flu, HIV infection, smallpox, encephalitis, rabies, etc.), fungal(candidiasis, aspergillosis, trichophytosis, etc.), protozoans(malaria, toxoplasmosis, giardiasis), prion(kuru, Creutzfeldt-Jakob disease, scrapie).

If the genome of the pathogen is integrated (embedded) into the genome of the host chromosome, then the resulting infectious process can be inherited through the genetic material from generation to generation of the host. This is an integrative form of infection. An example of an integrative form of infection are infections

viral etiology (lysogeny in the microbial world, carcinogenesis - cancer lines of mice). Most infections that a person suffers from are not inherited (tuberculosis, cholera, influenza, etc.) and are called non-integrative. The integrative form of infection should not be confused with the congenital one, when the pathogen is transmitted from the mother to the fetus through the placenta (syphilis, HIV infection, etc.), or the newborn during childbirth becomes infected while passing through the mother’s birth canal (blenorrhea).

Based on their origin, infections are divided into exogenous and endogenous.

Exogenous infection occurs when a pathogen enters the body from the outside. For an exogenous infection, the presence of three elements of the epidemic process is required: the source of infection, the mechanism of transmission of the pathogen, and the susceptible organism. For example, for syphilis: the source of infection is a sick person, the mechanism of transmission of the pathogen is sexual, the susceptible organism is a person. Endogenous(opportunistic) infection is caused by representatives of normal microflora when the body's defenses are reduced (immunodeficiency states). The causative agents of endogenous infection belong to opportunistic types of microorganisms. An example of an endogenous infection is a nasal boil of staphylococcal etiology (Staphylococcus epidermidis). The infection occurred due to hypothermia of the body and the development of local immunodeficiency of the nasal mucosa. An endogenous infection can also develop when microorganisms move from one human biotope to another due to artificial transfer by hands, tools, or the natural transition of a microorganism - its translocation (migration). An example of this form is Escherichia cystitis, the causative agent Escherichia coli which got onto the mucous membrane of the genitourinary system from the intestines.

Based on the location of the pathogen in the body, local and generalized forms of infection are distinguished. Local or focal infection occurs when the pathogen is localized in a specific organ or tissue and does not spread throughout the body. For example, with a sore throat, the pathogen (most often Streptococcus pyogenes) located on the mucous membrane of the tonsils; with furunculosis the pathogen Staphylococcus aureus- in the hair follicle.

At generalized infection, the pathogen spreads throughout the body, overcoming various protective barriers: lymphoid-

nut tissue, blood-brain barrier, fascia, muscle tissue, connective tissue, etc. Blood is one of the common routes of pathogen spread - the hematogenous route. If the pathogen, spreading through the blood, does not multiply in it, then this phenomenon is called bacteremia or viremia (depending on the pathogen belonging to one or another taxonomic group). When bacteria multiply in the blood, one of the severe forms of generalized infection develops - sepsis. Sepsis can progress to septicopyemia, when the pathogen multiplies in the internal organs, causing the formation of purulent foci of inflammation in them. With a high concentration of bacteria and their toxins in the blood, toxic-septic shock can develop due to the massive intake of toxins. Due to the generalization of the infection, various organs and tissues of the body are affected (meningococcal meningitis, spinal tuberculosis).

The infectious process is classified depending on the number of pathogen species that have entered the body and the dynamics of their action. Monoinfection caused by a pathogen of one type (tuberculosis, diphtheria). Mixed (mixed) infection- simultaneous infection with two or more types of pathogens and the development of several diseases at once (HIV infection and hepatitis B when infected through a syringe in drug addicts; syphilis, gonorrhea and chlamydia during sexual infection). Reinfection- re-infection with the same type of pathogen after recovery. Reinfection is possible with diseases that do not leave lasting immunity: after gonorrhea, syphilis, dysentery. If re-infection occurs with the same pathogen before recovery, then superinfection(syphilis). Secondary infection occurs against the background of a developed primary disease and is caused by another type of pathogen. Secondary infection can be exogenous or endogenous. More often, a secondary infection develops as an endogenous one, when, due to the weakening of the body by a primary disease, representatives of the normal microflora of the human body cause a secondary disease as a complication of the primary one, for example, with influenza, staphylococcal pneumonia develops, with AIDS - Pneumocystis pneumonia.

According to the duration of the course, acute and chronic infections are distinguished. Acute infections last a short time, their duration is calculated in days, weeks (flu, measles, cholera, plague).

Features of the epidemiology of the infectious process make it possible to classify several forms of infection. Epidemic An infection is called when it covers the population of large territories (one or several countries), for example, influenza, cholera.

Endemic the infection is localized in a certain geographical area, where the pathogen circulates between certain species of animals in a given geographical area (plague, brucellosis, tularemia).

Depending on the sources of infection, people are classified as anthroponotic, zoonotic And sapronotic infections. At anthroponotic In infections, the only source of infection is humans (HIV infection, syphilis). At zoonotic In infections, the main source of infection is animals (rabies, anthrax, brucellosis). Pathogens sapronotic infections are saprophytes living in the external environment (legeonellosis, listeriosis). Consequently, sources of infection with sapronoses are environmental objects: soil (tetanus, gas gangrene), water (leptospirosis).

Currently, it has become widespread hospital(nosocomial) infection that occurs in medical institutions (hospitals, maternity hospitals, etc.). The source of hospital infections is often medical personnel: bacteria carriers of staphylococci, enterobacteria and other opportunistic or pathogenic microorganisms.

A typical infectious disease most often occurs in a manifest form and is characterized by certain clinical symptoms.

manifestations (symptom complex) and cyclic course. For example, in the typical course of typhoid fever, a typhoid status is observed, a roseola rash develops on the 8-10th day of illness, etc. The disease occurs in stages and lasts 3-4 weeks.

An atypical (erased) course of the disease without a characteristic symptom complex is possible. With the erased course of typhoid fever, the rash appears early (on the 4-6th day), scant; typhoid status is not expressed. In some cases, the disease can occur without any symptoms at all, and the result of the developed pathological process can only manifest itself in the form of deadly complications (pulmonary hemorrhage in asymptomatic pulmonary tuberculosis, peritonitis as a result of intestinal perforation from typhoid ulcers, heart disease as a consequence of rheumatic endocarditis ).

The infectious process can occur in the form of an asymptomatic infection: latent(hidden) or bacteria carriers(virus carriers). At latent form of infection, the pathogen resides in the body for a long time (persists), but does not exhibit its pathogenic effect. For example, the tuberculosis bacillus can persist for many years in the lung tissue of a healthy person, the herpes virus persists for life in the sensory ganglia of the trigeminal nerve, and the causative agent of brucellosis persists in the mesenteric lymph nodes. With a latent infection, the pathogen is not released into the external environment; a latent infection can develop into a manifest form (disease) when immunity decreases.

Bacterial carriage- long or short-term presence of the pathogen in the body of a healthy person. Unlike latent infection, bacterial carriers release the pathogen into the environment and are sources of spread of infection (typhoid fever, diphtheria, staphylococcal infection). Slow infection characterized by the persistence of the pathogen, in which there is a multi-month or multi-year incubation period, after which the symptoms of the disease slowly but steadily develop, always ending in death (HIV infection, rabies, leprosy).

There are 4 main periods in the development of an infectious disease: incubation, prodromal, height of illness And convalescent(recovery).

Incubation period - the period of adhesion of the pathogen to the sensitive cells of the body at the entrance gate. This could be the tonsils, upper respiratory tract, mucous membrane of the gastrointestinal, reproductive tract, etc. The pathogen is not released into the environment. The duration of the period ranges from several hours (influenza), days (plague, tularemia, diphtheria) to several months (rabies) and even years (AIDS, leprosy, spongiform encephalopathy).

IN premonitory period, colonization of sensitive cells and areas of the body by the pathogen takes place. Microorganisms settle in the host's biotope and nonspecific (general) symptoms of the disease begin to appear (temperature rises, headache, sweating, weakness, etc.). During this period, the pathogen is also, as a rule, not released into the environment.

Subsequent intensive reproduction of the pathogen in the host’s body marks the height of the disease with the appearance of specific symptoms (skin rashes with typhus, paralysis of the lower limbs with poliomyelitis, filmy deposits on the mucous membranes of the nose, pharynx, larynx with diphtheria, etc.). During this period, the patient is contagious, as the pathogen is released into the external environment. Finally, after the pathogen stops reproducing and as it is eliminated from the body, a period of convalescence (recovery) begins. At this point, restoration of impaired functions begins. As a rule, the release of microorganisms stops, but in some cases the formation of convalescent bacterial carriage is possible with a long stay of the pathogen in the body of the host who has suffered the infection.

A special place in characterizing an infection is its transmission routes, which is important for epidemiological purposes. There are three main options for transmitting the pathogen to humans: horizontal, vertical and artificial (artificial).

The horizontal option includes airborne transmission of the pathogen from a patient to a healthy one (influenza, diphtheria); fecal-oral (cholera, typhoid), contact (syphilis, gonorrhea) and transmissible (plague, encephalitis) routes.

For the vertical variant, the transplacental route of transmission of the pathogen from mother to fetus (syphilis, rubella) or during childbirth from mother to newborn (blennorrhea) is typical.

The artificial (man-made, artificial) version involves the transmission of the pathogen during an instrumental examination of the patient, injection, during surgical interventions (hepatitis, AIDS).

There are 4 levels of the infectious process: population, organismal, cellular and molecular.

The population level determines the interaction of the pathogen with susceptible individuals of the population. For organismal level, the complex (system) of reactions of a susceptible host to infection is important. The cellular or tissue-organ level is the selection by the pathogen of the corresponding target cells of the macroorganism. On molecular level, the competitive interaction of pathogen and host biomolecules under infection conditions is considered.

8.2. Driving forces of the infectious process

Based on the definition of the infectious process, at least 3 main participants in the infection are identified: pathogen, host And environmental factors.

Pathogen disease - a microbial cell - is characterized by quantitative and qualitative characteristics: pathogenicity (species characteristic) and virulence (individual characteristic of the strain).

The platform on which the infection unfolds is the human body -the owner, which must be susceptible to the infection (species characteristic) and be sensitive to it (individual characteristic), i.e. have infectious sensitivity. In this case, the physiological characteristics of the host and the state of its natural resistance play an important role.

And finally, the third participant in the infection - environmental conditions, in which the organism becomes infected with a pathogen. Various physical, chemical, biological and social environmental factors are essential for the formation and development of the infectious process. When the pathogen or host dies, the infectious process is interrupted. Under conditions of mutual adaptation of the pathogen and the host (persistence of the pathogen), the continuation of the infectious process takes place in the form of resistance.

dental bacterial carriage, latent infection or chronic disease. Environmental factors, although to varying degrees, participate in the formation of the infectious process, determining its development and outcome.

8.3. The role of the pathogen in the infectious process and its main biological characteristics

The pathogen as a participant in the infectious process is characterized by two main qualities: pathogenicity and virulence.

Pathogenicity - species characteristic: the ability of a certain type of microorganism to cause a corresponding infectious process in one or more species of the host organism. For example, pathogenic species Vibrio cholerae, S. Typhi, N. gonorrhoeae capable of causing the corresponding infection in humans, but not in other species.

But this range (spectrum) of pathogenicity varies among different microbes. If the named microorganisms (the sad “privilege” of the human race) are pathogenic only for humans, then the number of susceptible hosts for other microorganisms is much larger and is not limited only to humans. For Mycobacterium tuberculosis is 9 types, Y. pestis- 11 types, Br. abortus-

Pathogenic species of microbes realize their ability to cause an infectious process in the majority of individuals in the population of a susceptible species of macroorganism.

If the ability of a microbe to cause infection in a susceptible species of macroorganism is largely determined by the state of immunity of individuals in the population and, as a rule, the infection develops in conditions of immunodeficiency, then such types of microbes are called opportunistic, for example Escherichia coli, Staphylococcus epidermidis, Klebsiella pneumoniae.

Virulence - individual, strain trait: the degree (quantitative measure) of the realization of the pathogenicity of a species by each specific strain in relation to a specific individual - the host. If the strain Vibrio cholerae isolated from patient A, who died of cholera, which means that it turned out to be highly virulent in relation to this individual. The degree of virulence of a particular strain within a population of a pathogenic species of microorganisms can be assessed by the clinical course of the infectious process in the person from whom this strain was isolated; on the model in vivo by reproducing experimental infection in animals; on the model in vitro by qualitative and quantitative study of virulence factors of a particular strain (clinical and laboratory studies).

Using a model of experimental infection, a quantitative assessment of the virulence of the strain is carried out using conditionally

Common units of measurement of virulence: DLM and LD 50. DLM (from lat. Dosis letalis minima)- the smallest number of microbial cells capable of causing the death of 95% of animals of a susceptible species of a certain weight, sex and age with a certain method of infection and within a given time. LD 50 is the amount of bacteria that causes the death of 50% of the animals in the experiment. In some cases, DCL is determined for experimental purposes (from lat. Dosis certa letalis) - a lethal dose causing 100% death of infected animals.

The virulence of the pathogen can be adjusted in the direction of either decreasing or increasing it. At one time, French researchers Calmette and Gerin cultivated the causative agent of tuberculosis (bovine type) on potato-glycerin media with the addition of bile (an unfavorable factor for the pathogen) for 13 years. As a result, they managed to carry out about 230 cultures of the pathogen that had lost its virulence, and based on the avirulent strain, create a BCG vaccine (bacillus Calmette-Gerin) for the prevention of tuberculosis. In some cases, the virulence of microbes is reduced under the influence of various physicochemical factors, drugs, etc. A decrease in the virulence of strains is called attenuation(weakening).

On the other hand, it is known that by passage (passing) through the body of susceptible animals it is possible to increase the virulence of the pathogen, which is often necessary when carrying out experimental work.

The conditions that regulate the virulence of the pathogen include the chemical composition of the bacterial cell, the characteristics of its metabolism, the structure of the genome and the habitat (ecology).

8.3.1. Virulence factors

The classification of virulence factors depends on their structure, origin, mechanism of action and purpose.

Based on their structure and origin, virulence factors can be classified into two main groups: structural components of the bacterial cell and secreted factors.

8.3.1.1. Structural components of a bacterial cell

These include the capsule, pili, cell wall peptidoglycan, outer membrane proteins and gramtrium lipopolysaccharide.

healing bacteria, which are described in detail in the materials on the disc.

8.3.1.2. Secreted factors

In addition to the structures of the bacterial cell that contribute to the manifestation of its virulent qualities, a group of microbial secreted factors involved in the infectious process is known: bacteriocins, exotoxins, “defense and aggression” enzymes, secreted persistence factors.

Bacteriocins - proteins, mediators of intermicrobial interaction, are secreted by the bacterial cell as antagonistically active substances. Bacteriocins are released under conditions of closely related antagonism within a species or genus of bacteria. Bacteriocins ensure colonization of a certain biotope by a virulent strain, suppressing normal microflora: colicins Shigella flexneri suppress Escherichia coli staphylococcins S. aureus suppress S. epidermidis etc. Colicinogenic strains of Shigella more often cause protracted and more severe forms of the disease than non-colicinogenic strains. Bacteriocinogenic strains of staphylococci are much more often isolated from patients from pathological foci than from the skin and mucous membranes of healthy people. In chronic forms of streptococcal infection (rheumatism, chronic tonsillitis), bacteriocinogenic strains are detected 2 times more often than in healthy people.

Exotoxins - substances of protein nature, secreted by virulent strains of microorganisms and having a toxic effect on the cells and tissues of the host body.

Virulence factors also include enzymes produced by the bacterial cell. Virulence enzymes are figuratively called “defense and aggression” enzymes. Enzymes protection ensure the pathogen's resistance to the host's immunity: the coagulase enzyme coagulates blood plasma, as a result of which a protective capsule is formed around the bacterial cell; Immunoglobulin proteases destroy antibodies. Aggression enzymes ensure the spread of the pathogen throughout the body, they destroy the structures of cells and tissues of the body: hyaluronidase destroys connective tissue (S. аureus, S. рyogenes), neuraminidase breaks down sialic acids of cell membranes (influenza virus), fibrinolysin dissolves fibrin clots (S. pyogenes), DNase

destroys nucleic acids (S. aureus), elastase breaks down lysozyme in body cells (Pseudomonas).

Metabolic enzymes bacteria that cause the formation of toxic substances when breaking down substrates of the body are also considered as virulence enzymes: microbial urease forms toxic substances during the hydrolysis of urea (Helicobacter pylori), decarboxylase during protein destruction promotes the accumulation of biogenic amines (Salmonella Enteritidis). The virulence of bacteria is ensured by the enzymes superoxide dismutase and catalase, which inactivate highly active oxygen radicals during phagocytosis (Leg. pneumophila, M. tuberculosis).

Secreted bacterial persistence factors suppress specific and nonspecific host defense mechanisms, ensuring bacteria survival during infection. By chemical nature, these are mainly bacterial proteases that break down a specific substrate of the host, creating protection against the pathogen. They provide antilysozyme, antiinterferon, anticomplementary, antihistone, antilactoferrin and antihemoglobin activity. It is described in detail in the materials on the disc.

In realizing the virulence of a pathogen, the delivery of virulent proteins to the surface of the bacterial cell at the point of contact with the surface of the eukaryotic cell and/or the introduction of proteins into the cytosol of the host cell is important. During the process of evolution, bacteria have developed several types of secretory systems, which are described in detail in section 3.1.5. The term "secretion" is used to describe the active transport of proteins from the cytoplasm across the inner and outer membranes into the supernatant (environment) of a bacterial culture or to the surface of the bacterial cell. Secretion differs from export, which involves transporting proteins from the cytoplasm to the periplasmic space. Let us recall that type I secretory system is a sec-independent pathway (it is not under the control of the sec gene responsible for secretion). This route transports α-hemolysin E. coli, extracellular adenylate cyclase B. pertussis, proteases P. aeruginosa. Molecules transported by type I secretory system require 3-4 auxiliary molecules for transport, which participate in the formation of a transmembrane channel through which proteins are released.

Type II secretion is the main one for extracellular digestive enzymes of gram-negative bacteria. This system uses traditional sec-dependent pathways to clear exported molecules across the inner membrane into the periplasmic space. Type II secretory system is involved in the export of a huge number of different molecules, including virulence factors: pili P. aeruginosa(4 types) and related ones, enzyme-pullulanase y Klebsiella, pectic enzymes and cellulases y Erwinia, elastases, exotoxin A, phospholipases C and other proteins y Pseudomonas aeruginosa, amylase and protease Aeromonas hydrophila etc.

Type III secretory system is a large export system, independent of the sec system, which plays a significant role in the secretion of virulence factors in human and plant pathogens. Type III secretory system is responsible for the secretion of external proteins Yersinia spp., invasion and virulence factors of Salmonella and Shigella, signal transduction molecules of enteropathogenic Escherichia coli and virulence factors of some plant pathogens, and is also involved in the biosynthesis of surface organelles - flagellar proteins.

In contrast to the type I secretory pathway, which is a true secretory system in which secretory enzymes acquire activity in the extracellular space, type III is a mechanism for the translocation of proteins into the cytosol of a eukaryotic cell, because it ensures the assembly on the surface of the bacterial cell of supermolecular structures involved in transport proteins into a eukaryotic cell. The type III secretory system apparatus includes about 20 proteins, most of which are located in the inner membrane, and a cytoplasmic membrane-bound ATPase (ATPase).

Type V secretory system includes a group of so-called autotransporters - a family of secretory proteins that carry out their own transport from bacteria: gonococcal IgA protease and IgA protease H. influenzaece.

8.3.2. Pathogenetic factors of the pathogen during infection

Classification of pathogenicity factors by purpose and mechanism of action includes pathogenetically significant products

bacterial cell, determining the stages of development of the infectious process and its outcome. These factors are combined into 4 groups: colonization, invasion, toxigenicity and persistence.

8.3.2.1. Pathogen Colonization Factors

Colonization - settlement of microorganisms in a certain host biotope. This stage of infection of the body begins with adhesion - attachment of the pathogen to the cells of the body at the entrance gate of infection. Special structures - adhesins - are responsible for attaching the microbe. In gram-negative bacteria, this process involves pili (villi), proteins of the outer membrane, and in gram-positive microorganisms, teichoic acids, surface proteins. Adhesion is specific for each pathogen, taking into account its tropism to the tissues and cells of the host, where the receptor-ligand attachment of the pathogen occurs. The subsequent fixation of the pathogen on the eukaryotic cells of the body causes the settlement of microorganisms in the infected biotope of the host. This is facilitated by the participation of bacterial proteases that block the body’s secretory defense IgA, the production of bacteriocins, antioxidants, and the production of siderophores that compete with lactoferrin for Fe ions. Thus, adhesion and subsequent colonization are the initial (early) stages of the pathogenesis of the infectious process.

8.3.2.2. Factors of microbial invasion

Invasion is the penetration of a pathogen into the cells of the body (penetration), overcoming the natural barriers of the body (skin, mucous membranes, lymphatic system, etc.). This process is controlled by invasins - bacterial molecules that facilitate the penetration of the pathogen into the cell. During this period, the effect of toxic products increases - urease hydrolyzes urea with the formation of ammonia and toxic biogenic amines in the body. Microorganisms produce hemolysin, which destroys red blood cells, leukocidin, which destroys white blood cells, and spreading factors - enzymes of aggression that contribute to the generalization of infection due to the spread of the pathogen in the body. The following are included in the work: aggression enzymes, How lecithovitellase, cleaving lipoprotein of host cell membranes, fibrinolysin, eliminating fibrin clot for further spread of the microbe throughout the body; hyaluronidase,

breaking down hyaluronic acid - a substance of connective tissue; neuraminidase- pathogen propagation enzyme, IgA protease, which ensures the resistance of the pathogen to digestion by phagocytes and the action of antibodies, etc. The invasion process in some gram-negative bacteria is ensured by type III secretory system, which is responsible for the secretion of invasion factors, in particular in Salmonella and Shigella, signaling molecules transduction of enteropathogenic Escherichia coli. During the process of invasion into epithelial cells, the pathogen (S. Typhimurium) enters into intimate relationships with cells and uses physiological mechanisms to ensure their vital functions to serve its own needs, causing a massive rearrangement of the host cell cytoskeleton and activation of secondary messengers - a transit increase in the level of inositol triphosphate and the release of Ca 2+.

Both the surface structures of the bacterial cell and the substances it produces take part in protection against phagocytosis. Capsules (S. pneumoniae, N. meningitidis), surface proteins: A protein S. aureus, M protein S. pyogenes. Some bacteria, such as the causative agent of pertussis, produce extracellular adenylate cyclase, which inhibits chemotaxis, thereby allowing the bacteria to avoid capture by phagocytes. The enzymes superoxide dismutase and catalase inactivate highly reactive oxygen radicals during phagocytosis (Y. pestis, L. pneumophila, S. Typhi). The participation of the type III secretory system in some bacteria in the reorganization of the phagocyte cytoskeleton, preventing the formation of a phagolysosome, has been noted.

8.3.2.3. Toxigenic factors of bacteria

Toxigenicity is the production of toxic substances by bacteria that damage the cells and tissues of the host body.

The presence of a toxin in bacteria is pathogenetically significant during the development of the infectious process. The toxic component is present in almost any infection and exhibits its effect, although to varying degrees.

Toxins secreted by the pathogen into the environment are detected in the growth phase and accumulate in the cytoplasm. These are proteins - exotoxins. Endotoxins are part of the cell wall and are released only when the microbial cell dies.

Endotoxins include LPS from the cell wall of gram-negative bacteria, peptidoglycan, teichoic and lipoteichoic acids, and mycobacterial glycolipids. Endotoxins of enterobacteria (Escherichia, Shigella, Salmonella, Brucella) have been well studied. Some bacteria simultaneously produce both exo- and endotoxins (Vibrio cholera, some pathogenic E. coli, etc.).

Comparative characteristics of bacterial exotoxins and endotoxin LPS of the cell wall of gram-negative bacteria are presented in Table. 8.1.

Table 8.1. Comparative characteristics of bacterial toxins

Exotoxins are secreted by a living bacterial cell, are proteins, and are completely inactivated under the influence of high temperature (90-100 ° C). They are neutralized with formaldehyde at a concentration of 0.3-0.4% at 37 °C for 3-4 weeks, while retaining their antigenic specificity and immunogenicity, i.e. go to toxoid vaccine(tetanus, diphtheria, botulinum, staphylococcal, etc.).

Exotoxins have a specific effect on the cells and tissues of the body, determining the clinical picture of the disease.

The specificity of an exotoxin is determined by the mechanism of its action on certain targets (Table 8.2). The ability of microbes to produce exotoxins is mainly due to converting bacteriophages.

Table 8.2. Mechanisms of action of exotoxins

Information about endotoxins is contained in the chromosomal genes of bacteria, as in any other cellular component.

Endotoxins, unlike exotoxins, have less specificity of action. Endotoxins of all gram-negative bacteria (E. coli, S. Typhi, N. meningitidis, Brucella abortus etc.) inhibit phagocytosis, cause a decrease in cardiac activity, hypotension, increased temperature, and hypoglycemia. A large amount of endotoxin entering the blood leads to toxicoseptic shock.

Like virulence, the potency of toxins is measured by the lethal doses of DLM, LD 50, DCL, determined in animals.

Toxins that damage the CPM of body cells contribute to the lysis of cells: erythrocytes (hemolysins of staphylococci, streptococci, etc.), leukocytes (leukocidin of staphylococci).

There is a diverse group of toxins that disrupt the function of cell enzymes. Exotoxin C. diphtheriae being a cytotoxin, it blocks protein synthesis on the ribosome of myocardial cells, adrenal glands, nerve ganglia, and epithelial cells of the pharynx mucosa. Cell and tissue necrosis and inflammation develop: diphtheritic film, myocarditis, polyneuritis. Enterotoxins of Vibrio cholerae, enterotoxigenic strains E. coli, S. aureus and others activate adenylate cyclase in the epithelial cells of the mucous membrane of the small intestine, which leads to increased permeability of the intestinal wall and the development of diarrhea syndrome. Neurotoxins from tetanus and botulism bacilli block the transmission of nerve impulses in the cells of the spinal cord and brain.

A special group of staphylococcal and streptococcal toxins (exfoliatins, erythrogenins) disrupts intercellular interactions, which leads to damage to the skin (pemphigus of newborns, scarlet fever) and other organs.

Erythrogenic toxin is a superantigen that causes proliferation of T cells, thereby activating a cascade of components of the effector part of the immune system, the release of mediators with cytotoxic properties - interleukins, tumor necrosis factors, γ-interferon. Infiltration of lymphocytes and the local action of cytokines play an important role in the pathogenesis of invasive streptococcal infection in cellulitis, necrotizing fasciitis, septic skin lesions, and lesions of internal organs.

8.3.2.4. Pathogen persistence factors

Persistence of a pathogen is a form of symbiosis that promotes long-term survival of microorganisms in the infected host organism (from Lat. persistere- stay, persist).

The transition of bacteria from one environment of existence to another (the external environment - the host cell) is a forced movement of microorganisms, which ultimately allows them to survive as a species, therefore the persistence of bacteria in the body is considered as a strategy for the survival of the species. The change of ecological niche by a bacterial cell and its transition into the host organism is accompanied by the constant appearance of new biological characteristics in bacteria, facilitating the adaptation of the pathogen to new environmental conditions.

The survival of bacteria in host tissues is determined by the dynamic process of equilibrium between the destruction of bacteria by the body's protective factors and the accumulation (reproduction) of bacteria that inhibit or avoid the host's defense mechanisms.

When bacteria block the host's defense mechanisms, i.e. In their development of an ecological niche, the structural features of the pathogen play a certain role.

Unlike viruses or rickettsia, bacteria have their own persistence characteristics associated with the unique structure of the bacterial cell. The presence of peptidoglycan, which is present only in prokaryotes and absent in eukaryotic cells, makes it an excellent immunological target in the host body, which quickly detects foreign substances. Peptidoglycan is a marker of the foreignness of bacteria in an infected host. Therefore, any adaptive processes of a bacterial cell aimed at protecting (or isolating) the peptidoglycan structure of the cell wall can be considered as mechanisms of bacterial persistence.

In the process of interaction between both participants in the infection, the pathogen has evolutionarily established 4 ways to protect peptidoglycan from immune factors: shielding the bacterial cell wall; production of secreted factors that inactivate host defenses; antigenic mimicry; formation of forms with the absence (defect) of the bacterial cell wall (L-form, mycoplasma).

Persistence of microorganisms is the basic basis for the formation bacteria carriers.

In pathogenetic terms, bacterial carriage is one of the forms of the infectious process, in which a dynamic balance occurs between the micro- and macroorganism against the background of the absence of pathological changes, but with the development of immunomorphological reactions and antibody response.

marked status (immune imbalance, tolerance, deficiency of local immunity). As a result, conditions are created for the persistence (survival) of the pathogen, which leads to bacterial carriage. (The mechanism of development of persistence and formation of bacterial carriage is described in detail in the materials of the disk.)

8.3.3. Genetics of bacterial virulence

The life of a pathogen in an infected organism should probably be viewed as a series of steps of gene activation in response to a discrete set of environmental conditions. This gene regulation of bacterial virulence is environmentally dependent, ensuring the plasticity of microorganisms and their adaptive potential.

It is known that bacteria have one large evolutionary mechanism, due to which pathogenic representatives are formed. Virulence genes are most often found in large complex blocks designated as chromosomal insertions or pathogenic islands (see Section 5.1.5 for details). These islands and islets are linked by common sequences, indicating the acquisition of a DNA segment through events such as “illegal” recombinations, similar to phage transposition or insertion. These DNA blocks are most often inserted into chromosomal hot spots - areas most susceptible to invasion by foreign DNA or sites of phage insertion. For example, large segments of DNA encoding various virulence factors are inserted into the same place on the chromosome in both uropathogenic and enteropathogenic E. coli- pathogens of two different diseases, and the sequences located inside the pathogenic island do not show homology with those found in non-pathogenic clones like E. coli K-12, but sequences immediately adjacent to the pathogenic island show commonality between pathogenic and non-pathogenic strains.

Regions of chromosomal DNA encoding several clustered virulence genes, common among microorganisms from plant pathogens to Helicobacter pylori And Yersinia pestis. At the same time, despite a certain conservatism (in particular,

chromosomes E. coli, S. Typhimurium), Bacterial chromosomes are not constant, but constantly change. Phenotypic changes can modify pathogenicity within different clonal variants of the same species. For example, a chromosome S. Typhi, which causes disease only in humans, is subject to large genomic rearrangements during its evolution compared to non-typhoidal Salmonella, namely inversions, transpositions and insertions through homologous recombination events. Naturally, some of these events may alter virulence S. Typhi and increase its specific adaptive abilities to the human body. The regulation and expression of chromosomal virulence factors can also be altered by episodes such as shuffling of chromosomal genes.

It is believed that pathogenic microorganisms evolve not due to the slow adaptive evolution of pre-existing genes, but through a sum of leaps, as a rule, mastering genetic segments (which encode multiple virulence factors) not only related, but also unrelated organisms, and even include eukaryotic sequences (acquisition of tyrosine phosphatases Yersinia). Subsequently, the acquired genetic information is integrated into a chromosome or a stable plasmid. Appropriate selection of virulence factors ensures the safety of such sequences in pathogens, and the dissemination of this genetic information through mobile genetic elements (many virulence genes are encoded on mobile genetic elements of DNA) guarantees the possibility of any microorganisms receiving selective advantages. Information that is not necessary is mostly lost because there is no selective condition for its preservation.

The expression of virulence factors is closely related to various environmental signals, including temperature, ion concentration, osmolarity, iron levels, pH, presence of a carbon source, oxygen levels, and several others not yet identified. The pathogen is able to use both a single signal and a complex of them to “feel” what microenvironment it occupies inside the host or even inside a specialized compartment of a single host cell. Therefore, at each step of the infectious cycle (during

When bacteria achieve their biological goals), in response to a kaleidoscope of defensive responses from the host, various genes are dynamically turned on and off - a coordinated and interdependent process.

For example, the expression of one of the antiphagocytic factors of the plague pathogen, fraction F1, is expressed maximum at 35-37 °C when the pathogen is in the human body, and falls at 28 °C when it is in the flea body. Invasive genes are usually turned on early in infection but are repressed once the bacterium is inside the host cell. Disorganization of the expression of pathogenic factors over time can disrupt the process of bacterial invasion.

Thus, the regulation of pathogenicity is a complex event. All virulence factors can be controlled simultaneously by several regulatory systems that measure various environmental parameters, and at the same time, several regulatory systems can regulate one virulence factor. In addition, regulatory factors typically regulate themselves, which creates a hierarchy in the regulation and fine control of the expression of virulence factors. As a result, the level of virulence is determined by the average value of all signals (environment and regulation).

8.4. The role of the macroorganism in the infectious process

The host organism is the platform on which the infectious process with all its manifestations unfolds, and if the microbe determines the specificity of the infection, then the features of its course and form of manifestation are determined by the state of the macroorganism.

As with a microbe, two main characteristics should be distinguished here: species and individual. A species characteristic is the host's susceptibility to infection.

Receptivity - a species characteristic that characterizes the ability of a certain type of organism (host) to participate in the infectious process when interacting with a pathogen.

The human body is susceptible to Vibrio cholerae, but bats have innate resistance to this pathogen.

liu. For the causative agent of tularemia, the body of hares, mice, and hamsters is a suitable niche where bacteria multiply and cause infection, but cats, foxes, and ferrets are genetically resistant to this pathogen. A number of diseases are characteristic only of the human body - syphilis, gonorrhea, diphtheria, since it is practically impossible to select other candidates for reproducing the experimental infection due to the natural resistance of animals to these pathogens.

As for the individual characteristic that characterizes the measure of the body’s susceptibility to infection, it is defined as infectious sensitivity.

Infectious sensitivity is the individual susceptibility of the host organism to the pathogen that causes the disease. Often, instead of the term “infectious sensitivity”, a term with the opposite meaning is used - “natural resistance”, which makes these concepts synonymous. But in both cases we are talking about innate (natural) immunity, which, in addition to its non-specificity in relation to the infection, is always persistent and is inherited, since it is genetically programmed.

This natural immunity or natural resistance to the pathogen are aimed at maintaining homeostasis of the body. This nonspecific recognition of information (pathogens) foreign to the host is carried out according to a single program; the activity of the system is constant and does not depend on the specificity of the foreign agent. It has both a cellular (integument and internal barrier cells, phagocytic cells, natural killer cells) and a humoral (lysozyme, complement, β-lysines, acute phase proteins, etc.) basis. Among the factors that determine the body’s natural resistance to infection are: the age of the host, endocrinological and immune status, state of physical activity, central nervous system, endogenous biological rhythms, entrance gates of infection, etc.

Age significantly determines the level of nonspecific defense of the body. In newborns, the bactericidal activity of blood serum is significantly reduced during the first month of life. Children more often develop generalized forms of infection, sepsis, and many infectious diseases are more severe: salmonellosis, dysentery, tuberculosis, etc. Only

In newborns, colienteritis occurs, since their body does not yet produce secretory IgA - the main factor protecting the mucous membrane of the small intestine. The level of natural resistance in older people is reduced. Due to the dysfunction of lysosomes in the elderly, the activity of intracellular destruction of the pathogen is reduced, so they more often suffer from recurrent typhus (Brill's disease) and more often suffer from typhoid bacteria carriage.

A number of diseases are known - whooping cough, measles, diphtheria, which are typical for children. Elderly people are more likely to die from pneumonia. Tuberculosis infection affects people of mature age.

There are minor differences in the level of natural resistance rates between females and males. Women have a higher level of serum bactericidal activity than men. They are known to be more resistant to meningococcal and pneumococcal infections. However, it is difficult to give preference to any gender in terms of the body’s resistance to infection.

Endocrinological status human is important in regulating the level of natural resistance. The posterior pituitary hormone oxytocin stimulates the activity of phagocytes, T- and B-lymphocytes. Glucocorticoids reduce the level of natural resistance, and mineralcorticoids increase it. Patients with diabetes are sensitive to many infections, especially tuberculosis and furunculosis of staphylococcal etiology. Decreased function of the parathyroid glands often leads to the development of candidiasis. Thyroid hormones stimulate most natural resistance factors. They are successfully used to treat sepsis, viral hepatitis, and meningococcal infection.

Immune status of a person determines his individual sensitivity to certain infections. Persons with blood group II are more likely to suffer from pneumonia and sepsis of staphylococcal etiology, smallpox, and influenza. They have lower levels of interferon in their cells and blood compared to people with other blood types. Persons with blood group I are more likely to suffer from plague and leprosy. Availability in HLA-system (histocompatibility complex) of antigen A9 contributes to the resistance of these individuals to acute respiratory infections

diseases. Persons who have HLA-the system has antigens A10, B18, DR, and people get sick with them more often.

Physical activity status human regulates the level of his natural resistance. Professional athletes and members of national teams are highly susceptible to infections, since intensive training and participation in important sports competitions deplete the body's reserves and reduce its natural resistance: the level of bactericidal activity of serum, the phagocytic potential of neutrophils in elite athletes against the background of their high athletic form is reduced more than than 2 times compared to people involved in regular physical education. At the same time, physical education and increased physical activity are a means of strengthening the body’s natural resistance to infection, which is explained by normalizing the level of complement and lysozyme, and increasing the ability of the blood to self-purify.

Central nervous system takes an active part in regulating the level of the body’s natural resistance to infection. Rodents during hibernation are resistant to the plague pathogen, but as they wake up in the spring they die from plague infection. Rabbits during medicated sleep are resistant to the vaccinia virus, from which they die while awake. Under stress conditions, the body's natural resistance sharply decreases. After immobilization stress, mice developed a fatal form of influenza encephalitis, whereas under normal conditions the mice were resistant to the influenza virus. Interestingly, on the surface of lymphocytes and macrophages there are receptors for nervous system mediators: β-adrenergic receptors, cholinergic receptors, etc.

Endogenous biological rhythms. In a person, from the moment of his birth, all processes in the body occur with a certain cyclicity. A certain cyclicity in the dynamics of natural resistance to infection indicators was revealed (monthly and daily biorhythms were established).

Chronobiograms of immunological parameters of a healthy person have been determined, which reflects different time intervals of maximum values ​​of factors of the humoral and cellular nature of natural resistance. This turned out to be important for

choosing the time of optimal administration of drugs to patients with infectious pathology.

Its importance for the development of infection is also entrance gate. The entrance gate of infection - the place where the pathogen enters the human body - largely determines the possibility of developing the infectious process. The influenza virus, once in contact with the skin or mucous membrane of the gastrointestinal tract, is not able to cause disease. Influenza will occur only if the pathogen colonizes the mucous membrane of the upper respiratory tract. There is the concept of “colonization resistance,” which determines the body’s protective capabilities at the entrance gates of infection. In this regard, infections are divided into airborne (influenza, meningococcal infection, diphtheria), intestinal (cholera, dysentery, hepatitis A), external infections (tetanus, gas gangrene, rabies), and vector-borne (plague, malaria, tularemia).

8.4.1. Anatomical and physiological barriers of the body during infection

The natural resistance of the body includes a number of anatomical and physiological barriers that prevent both the penetration of the pathogen into the body and its spread throughout the body. Among the main anatomical and physiological barriers to the body’s natural defense during infection are: skin and mucous membranes (external barrier), normal microflora; lymph nodes, cells of the reticuloendothelial system, inflammation; blood - cellular and humoral factors; blood-brain barrier. (This section is described in detail in the materials on the disc.)

Leather not only is it a mechanical barrier to the pathogen, but also has a bactericidal property due to the secretions of the sebaceous and sweat glands. Clean skin increases its bactericidal properties. There is a known indicator of the bactericidal activity of the skin, which is determined in relation to indicator test strains E. coli. This indicator is one of the standard tests for assessing the resistance of the astronauts’ body before flying into space. Damage to the skin is a condition for the development of wound infections: gas gangrene, tetanus, rabies.

Mucous membranes provide protection not only as a mechanical barrier due to mucus, the integrity of the epithelial cover, and the function of the villi. Epithelial cells of the mucous membranes and glands of different biotopes secrete bactericidal secretions onto the surface: saliva, tear fluid, gastric juice, small intestinal juice, vaginal secretion, lysozyme, etc. When the barrier function is impaired, the mucous membranes become an entry point for infection for many pathogens: pathogens of intestinal and respiratory tract infections, pathogens of sexually transmitted diseases, etc.

An important role is played in protecting the body’s biotopes from pathogens. normal(resident or indigenous) microflora. The main representatives of the normal microflora of the colon are Escherichia coli and bifidobacteria, in the nasopharynx - coryneform bacteria and non-pathogenic Neisseria, on the skin - epidermal staphylococci.

The microflora of the mucous membrane of the gastrointestinal tract in children differs significantly from that in adults and varies depending on the age of the child, the conditions of his existence, the nature of his diet, etc. Thus, in children before teething, aerobic bacteria predominate in the microflora of the mouth. After teething, the microflora of a child’s mouth is similar to the microflora of adults, which is also associated with a change in the nature of nutrition.

A huge number of microorganisms are contained in the intestinal cavity. A study of the intestinal flora in children showed that microbes in meconium appear in the second half of the first day of life. First, cocci appear, then gram-positive rods with spores are detected in the intestines. Escherichia coli and Proteus vulgaris are also found in small quantities in meconium. From the 3rd day, when bifidobacteria appear, the spore rods disappear.

The basis of the intestinal microflora in breastfed children are bifidobacteria, which make up about 90% of all intestinal microbes. There are E. coli, enterococci, acidophilus and aerogenic bacteria. In formula-fed children, E. coli predominate, and the number of bifidobacteria decreases. The protective role of normal microflora is the release of antagonistic active substances (antibiotics,

bacteriocins, microcins) that suppress the pathogen and its ability to colonize the skin and mucous membranes. Normal microflora forms a film in the biotope. In addition to protective antagonism, the detoxifying, immunostimulating and vitamin-forming functions of normal microflora and their participation in digestion are known. Suppression of normal microflora due to disease or widespread use of antibiotics leads to the formation of dysbiosis, which can cause the development of various forms of pathology, including microbial origin. For the prevention and treatment of dysbacteriosis, eubiotics are used - preparations containing live antagonistically active strains - representatives of the normal microflora of the body (colibacterin, bifidumbacterin, lactobacterin).

The body's second defense barrier includes function of lymph nodes, cells of the reticuloendothelial system, development inflammation. Lymph nodes perform a barrier-fixing function and can retain a pathogen for a long time, preventing its penetration into the blood, for example, fixation of hemolytic streptococcus in the lymphoid tissue of the tonsils, retention of Brucella, the causative agent of plague, staphylococcus, tuberculosis bacilli in regional lymph nodes. Due to the lymph nodes, the development of a generalized form of infection is prevented. When the barrier function of the lymph nodes is suppressed, bacteremia (typhoid fever, brucellosis) and sepsis (plague, staphylococcal and streptococcal infections) can develop.

The liver, spleen, and endothelium of blood vessels, due to the cells of the reticuloendothelial system, are unique filters in which pathogens get stuck and thus prevent the generalization of infection (typhoid fever). Inflammation is basically a protective reaction of the body, since as a result of the inflammatory reaction, specialized cells are concentrated around the pathogen, which must either destroy the pathogen or limit its spread, for example, with purulent mastitis of staphylococcal etiology, a local purulent focus (abscess) is formed in the breast tissue, preventing the generalization of staphylococcal infection.

One of the methods of treating chronic infections is the prescription of drugs that enhance the body’s inflammatory response as a protective one (chronic gonorrhea, chronic dysentery).

teria). But sometimes inflammation can perform the opposite pathogenetic function, i.e. promote the development of a pathological process, disruption of the structure and function of an organ (tissue): pneumonia (pneumonia), kidney inflammation (nephritis). In this case, anti-inflammatory therapy is prescribed.

The third fairly powerful barrier to the spread of a pathogen throughout the body is blood. Bactericidal activity of blood, those. its ability to self-purify is ensured by a complex of humoral and cellular factors of the body’s natural resistance. If the blood ceases to perform its bactericidal function, then the pathogen unhinderedly resides and multiplies in the blood, and penetrates through the blood and is localized in various organs and tissues. In such cases, severe, generalized forms of infection, sepsis and septicopyemia develop, which pose a real threat to the life of the host organism (plague sepsis, anthrax sepsis, staphylococcal septicopyemia).

The fourth barrier of the body is hematoencephalic, which protects brain tissue (brain, spinal cord) from pathogen damage. The protective structures of the blood-brain barrier include the membranes of the brain and the walls of blood vessels that nourish brain tissue. Penetration of the pathogen into the brain tissue leads to the development of meningoencephalitis (meningococcus, Provacek's rickettsia, rabies and encephalitis viruses). Brain tissue is protected by neurosecreted hormones of the posterior lobe of the pituitary gland - oxytocin and vasopressin, which, along with antimicrobial activity, also suppress the persistent potential of many pathogens, which is used in clinical practice to combat infection.

8.4.2. Factors of natural resistance of the body

The section is presented in the materials on the disc.

8.5. The role of the external environment in the infectious process

External environment is an obligatory participant in the infectious process, its third driving force. Environmental factors (physical, chemical, biological and social)

can significantly influence the development, course and outcome of the infectious process.

An important physical factor is temperature. Classic experiments by Walker and Boring on a model of experimental viral infection showed that an increase in body temperature leads to the activation of natural resistance factors, in particular increased interferon production. At high temperatures, antiviral defense mechanisms are enhanced. Therefore, when treating patients with viral infections, reducing high temperature is not justified unless there are vital indications for this. On the other hand, a decrease in a person’s body temperature during the cold season (cold factor) leads to a weakening of natural resistance. Due to the effect of different temperatures, there is a seasonality in a number of infectious diseases. An increase in the incidence of airborne infections (acute respiratory viral infection - ARVI, influenza) occurs in the cold season (winter) under the influence of the cold factor, intestinal infections - in the summer-autumn period, when in conditions of high temperature the causative agents of intestinal infections (dysentery, cholera, hepatitis A, typhoid fever) multiply intensively in the external environment and are also spread through food and water.

Peculiarities nutrition, the presence of vitamins in food can significantly influence natural resistance. In the spring, due to vitamin deficiency, chronic infectious diseases (tuberculosis, rheumatism, etc.) worsen. Vitamin B 12 and other benzimidazole derivatives (dibazole), being stimulants of protein synthesis in the body, increase its natural resistance. Therefore, these drugs are used to prevent infectious diseases.

The sun controls life processes on our planet. A relationship has been identified between the activity of the Sun, its geomagnetic activity, infectious morbidity and mortality among people. The cyclical nature of pathological processes and indicators of natural resistance was revealed. A connection has been established between solar activity and the expression of microorganism virulence factors.

Social factor is a powerful environmental factor that influences the body's resistance to infection. Antibiotic

therapy and vaccine prophylaxis can effectively control the infectious process. Thanks to global anti-epidemic measures, humanity has gotten rid of smallpox and is successfully fighting polio. But there are diseases created by man (men made diseases): tuberculosis, viral hepatitis, HIV infection, sexually transmitted diseases.

Social diseases are a consequence of the vices of human society: drug addiction, prostitution, etc. Technogenic pollution of the external environment contributes to the development of infectious diseases. The high content of heavy metal salts, hydrogen sulfide-containing compounds, and radioactive elements in the air and water leads to the formation of immunodeficiencies in the body, and on the other hand, in some cases they stimulate the expression of pathogen virulence factors. Thus, natural hydrogen sulfide-containing gas from the Orenburg, Astrakhan, and Karachaganak natural fields sharply increased the persistent potential of staphylococci, making the population of these gas-bearing provinces hostage to the formation of resident staphylococcal bacteria carriers.

Thus, the forms, course and outcome of the infectious process depend both on the virulence of the pathogenic microorganism strain and on the state of natural resistance and immunity of the host organism, where the regulatory function is performed by environmental factors.

Tasks for self-preparation (self-control)

A. Name the form of the infectious process in which the pathogen resides in the body for a long time without exhibiting pathogenic properties and without being released into the environment:

1. Bacterial carriage.

2. Latent infection.

3. Slow infection.

4. Acute infection.

B. Name the factors contributing to the colonization of bacteria in the macroorganism:

1. Bacteriocins.

2. Adhesins.

3. Endotoxin.

4. IgA protease.

IN. Name the factors contributing to bacterial invasion:

1. Hyaluronidase.

2. Effector proteins of the type III secretory system.

3. Endotoxin.

G. In addition to the surface structures of the bacterial cell, substances secreted by this cell participate in protection against phagocytosis. Note the enzymes involved in the suppression of bacterial phagocytosis:

1. Extracellular adenylate cyclase.

2. IgA protease.

3. Catalase.

4. Superoxide dismutase.

D. Mark the positions characteristic of an exotoxin:

1. It is a weak antigen.

2. Has specificity of action.

3. Heat stable.

4. Stimulates the formation of neutralizing an-

E. A patient with influenza develops pneumonia caused by S. pneumoniae. Name the form of the infectious process that is caused by S. pneumoniae pneumonia.

AND. One of the methods for laboratory diagnosis of infectious diseases is the blood culture method, in which the pathogen is isolated from the patient’s blood. Name the conditions of the infectious process in which the pathogen can be isolated from the blood.

The study of infectious diseases goes back centuries. The idea of ​​the contagiousness of diseases such as plague, smallpox, cholera and many others originated among ancient peoples; Long before our era, some simple precautions were already taken against infectious patients. However, these fragmentary observations and bold guesses were very far from truly scientific knowledge.

Already in Ancient Greece, some philosophers, for example Thucydides, expressed the idea of ​​living pathogens (“contagions”) of infectious diseases, but these scientists did not have the opportunity to confirm their assumptions with any reliable facts.

Outstanding physician of the ancient world Hippocrates(about 460-377 BC) explained the origin of epidemics by the action of “miasma” - infectious fumes that supposedly could cause a number of diseases.

The progressive minds of mankind, even in the conditions of medieval scholasticism, rightly defended the idea of ​​​​the living nature of the causative agents of infectious diseases; for example, an Italian doctor Fracastoro(1478-1553) developed a coherent doctrine of contagious diseases and the methods of their transmission in his classic work “On contagious diseases and contagious diseases” (1546).

Dutch naturalist Anthony van Leeuwenhoek(1632-1723) made a very important discovery at the end of the 17th century, discovering under a microscope (which he personally made and gave a magnification of up to 160 times) various microorganisms in dental plaque, in stagnant water and infusions of plants. Leeuwenhoek described his observations in the book “Secrets of Nature Discovered by Anthony Leeuwenhoek.” But even after this discovery, the idea of ​​microbes as causative agents of infectious diseases for a long time did not receive the necessary scientific substantiation, although devastating epidemics repeatedly developed in various European countries, claiming thousands of human lives.

For many decades (in the 17th and 18th centuries), observations of epidemics of infectious diseases affecting large numbers of people convinced of the contagiousness of these diseases.

The works of the English scientist were of exceptionally important practical importance Edward Jenner(1749-1823), who developed a highly effective method of vaccination against smallpox.

Outstanding Russian epidemiologist D.S. Samoilovich(1744-1805) proved the contagiousness of the plague through close contact with a patient and developed the simplest methods of disinfection for this disease.

The great discoveries of the French scientist Louis Pasteur (1822-1895) convincingly proved the role of microorganisms in the processes of fermentation and decay, and in the development of infectious diseases.

Pasteur's works explained the actual origin of human infectious diseases; they were the experimental basis of asepsis and antiseptics, brilliantly developed in surgery by N.I. Pirogov, Lister, as well as their many followers and students.

Pasteur's great merit was the discovery of the principle of obtaining vaccines for preventive vaccinations against infectious diseases: weakening the virulent properties of pathogens by special selection of appropriate conditions for their cultivation. Pasteur produced vaccines for vaccination against anthrax and rabies.

German scientist Leffler proved in 1897 that the causative agent of foot-and-mouth disease belongs to the group of filterable viruses.

It should be noted that until the middle of the last century, many infectious diseases that were called “fevers” and “fever” were not differentiated at all. Only in 1813, a French doctor Brittany suggested that the disease of typhoid fever was independent, and in 1829 Charles Louis gave a very detailed description of the clinic of this disease.

In 1856, typhoid and typhus were isolated from the group of “fever diseases” with clear characteristics of these completely independent diseases. Since 1865, relapsing fever also began to be recognized as a separate form of infectious disease.

World science appreciates the merits of the famous Russian clinician-pediatrician N.F. Filatova ( 1847-1902), who made a significant contribution to the study of childhood infectious diseases, as well as

D.K. Zabolotny(1866-1929), who made a number of important observations in the field of epidemiology of especially dangerous diseases (plague, cholera).

In the works of our compatriot N.F. Gamaleya(1859-1949) reflected many issues of infection and immunity.

Thanks to the work of I.I. Mechnikov(1845-1916) and a number of other researchers, since the 80s of the last century, issues of immunity (immunity) in infectious diseases began to be resolved; the extremely important role of cellular (phagocytosis) and humoral (antibodies) defense of the body was shown.

In addition to purely clinical studies of infectious patients, laboratory methods began to be widely used to diagnose individual diseases from the end of the 19th century.

Works of a number of scientists ( I. I. Mechnikov, V. I. Isaev, F. Ya. Chistovich, Vidal, Ulengut) made it possible at the end of the last century to use serological tests (agglutination, lysis, precipitation) for laboratory diagnosis of infectious diseases.

X. I. Gelman and O. Kalning belongs to the honor of developing a method for allergic diagnosis of glanders (1892). Recognition of malaria was greatly facilitated thanks to the method of differential staining of the nucleus and protoplasm of the malarial plasmodium in blood smears, developed by D. L. Romanovsky (1892).

The meaning of the word "infection" varies. Infection is understood as a contagious principle, i.e. pathogen in one case, and in another case this word is used as a synonym for the concept of “infection, or contagious disease.” Most often, the word “infection” is used to refer to an infectious disease. Infectious diseases have the following distinctive features:

1) the cause is a living pathogen;

2) the presence of an incubation period, which depends on the type of microbe, dose, etc. This is the period of time from the penetration of the pathogen into the host’s body, its reproduction and accumulation to the limit that determines its pathogenic effect on the body (lasts from several hours to several months);

3) contagiousness, i.e. the ability of the pathogen to be transmitted from a sick animal to a healthy one (there are exceptions - tetanus, malignant edema);

4) specific reactions of the body;

5) immunity after illness.

Infection(Late Latin infektio - infection, from Latin inficio - introducing something harmful, infecting) - a state of infection of the body; an evolutionarily developed complex of biological reactions that arise during the interaction of an animal’s body and an infectious agent. The dynamics of this interaction is called the infectious process.

Infectious process is a complex of mutual adaptive reactions to the introduction and reproduction of a pathogenic microorganism in a macroorganism, aimed at restoring disturbed homeostasis and biological balance with the environment.

The modern definition of an infectious process includes interaction three main factors –

1) pathogen,

2) macroorganism

3) environment,

Each factor can have a significant impact on the outcome of the infectious process.

To cause disease, microorganisms must be pathogenic(pathogenic).

Pathogenicity microorganisms is a genetically determined trait that is inherited. In order to cause an infectious disease, pathogenic microbes must penetrate the body in a certain infectious dose (ID). Under natural conditions, for infection to occur, pathogenic microbes must penetrate certain tissues and organs of the body. The pathogenicity of microbes depends on many factors and is subject to large fluctuations in different conditions. The pathogenicity of microorganisms may decrease or, conversely, increase. Pathogenicity as a biological characteristic of bacteria is realized through their three properties:

· infectiousness,

invasiveness and

· Toxigenicity.

Under infectiousness(or infectivity) understand the ability of pathogens to penetrate the body and cause disease, as well as the ability of microbes to be transmitted using one of the transmission mechanisms, retaining their pathogenic properties in this phase and overcoming surface barriers (skin and mucous membranes). It is due to the presence of factors in the pathogen that promote its attachment to the cells of the body and their colonization.

Under invasiveness understand the ability of pathogens to overcome the body’s defense mechanisms, multiply, penetrate its cells and spread within it.

Toxigenicity bacteria is due to their production of exotoxins. Toxicity due to the presence of endotoxins. Exotoxins and endotoxins have a unique effect and cause profound disturbances in the functioning of the body.

Infectious, invasive (aggressive) and toxigenic (toxic) properties are relatively unrelated to each other; they manifest themselves differently in different microorganisms.

Infectious dose- the minimum number of viable pathogens necessary for the development of an infectious disease. The severity of the infectious process, and in the case of opportunistic bacteria, the possibility of its development, may depend on the magnitude of the infectious dose of the microbe.

The degree of pathogenicity or pathogenicity of microorganisms is called virulence.

The magnitude of the infectious dose largely depends on the virulent properties of the pathogen. There is an inverse relationship between these two characteristics: the higher the virulence, the lower the infectious dose, and vice versa. It is known that for such a highly virulent pathogen as the plague bacillus (Yersinia pestis), the infectious dose can vary from one to several microbial cells; for Shigella dysenteriae (Grigoriev-Shiga bacillus) - about 100 microbial cells.

In contrast, the infectious dose of low-virulent strains can be equal to 10 5 -10 6 microbial cells.

Quantitative characteristics of virulence are:

1) DLM(minimum lethal dose) - a dose that causes the death of single, most sensitive experimental animals over a fixed period of time; taken as the lower limit

2) LD 50 is the number of bacteria (dose) that causes the death of 50% of the animals in the experiment over a fixed period of time;

3) DCL(lethal dose) causes over a fixed period of time

100% death of animals in the experiment.

According to the degree of pathogenicity they are divided into:

Highly pathogenic (highly virulent);

Low pathogenic (low virulent).

Highly virulent microorganisms cause disease in a normal body, low-virulent microorganisms cause disease only in an immunosuppressed body (opportunistic infections).

In pathogenic microorganisms virulence due to factors:

1) adhesion– the ability of bacteria to attach to epithelial cells. Adhesion factors are adhesion cilia, adhesive proteins, lipopolysaccharides in gram-negative bacteria, teichoic acids in gram-positive bacteria, and in viruses - specific structures of protein or polysaccharide nature; These structures, responsible for adhesion to host cells, are called “adhesins.” In the absence of adhesins, the infectious process does not develop;

2) colonization– the ability to multiply on the surface of cells, which leads to the accumulation of bacteria;

4) penetration– ability to penetrate cells;

5) invasion– ability to penetrate into underlying tissues. This ability is associated with the production of enzymes such as

• neuraminidase is an enzyme that breaks down biopolymers that are part of the surface receptors of mucosal cells. This makes the shells accessible to microorganisms;

· hyaluronidase - acts on the intercellular and interstitial space. This promotes the penetration of microbes into body tissues;

· deoxyribonuclease (DNase) - an enzyme that depolymerizes DNA, etc.

6) aggression– the ability to resist factors of nonspecific and immune defense of the body.

TO factors of aggression include:

· substances of different nature that are part of the surface structures of the cell: capsules, surface proteins, etc. Many of them suppress the migration of leukocytes, preventing phagocytosis; capsule formation- this is the ability of microorganisms to form a capsule on the surface that protects bacteria from phagocyte cells of the host body (pneumococci, plague, streptococci). If there are no capsules, then other structures are formed: for example, staphylococcus has protein A, with the help of this protein staphylococcus interacts with immunoglobulins. Such complexes interfere with phagocytosis. Or microorganisms produce certain enzymes: for example, plasmacoagulase leads to the coagulation of a protein that surrounds the microorganism and protects it from phagocytosis;

· enzymes – proteases, coagulase, fibrinolysin, lecithinase;

· toxins, which are divided into exo- and endotoxins.

Exotoxins- these are protein substances released into the external environment by living pathogenic bacteria.

Exotoxins are highly toxic, have pronounced specificity of action and immunogenicity (in response to their administration, specific neutralizing antibodies are formed).

By type of action exotoxins are divided into:

A. Cytotoxins- block protein synthesis in the cell (diphtheria, shigella);

B. Membranotoxins- act on cell membranes (staphylococcal leukocidin acts on the membranes of phagocyte cells or streptococcal hemolysin acts on the membrane of erythrocytes). The most powerful exotoxins are produced by the causative agents of tetanus, diphtheria, and botulism. A characteristic feature of exotoxins is their ability to selectively affect certain organs and tissues of the body. For example, tetanus exotoxin affects the motor neurons of the spinal cord, and diphtheria exotoxin affects the heart muscle and adrenal glands.

For the prevention and treatment of toxinemic infections, toxoids(neutralized exotoxins of microorganisms) and antitoxic serums.

Rice. 2. The mechanism of action of bacterial toxins. A. Damage to cell membranes by S. aureus alpha toxin. B. Inhibition of cell protein synthesis by Shiga toxin. C. Examples of bacterial toxins that activate second messenger pathways (functional blockers).

Endotoxins- toxic substances that enter the structure of bacteria (usually the cell wall) and are released from them after lysis of the bacteria.

Endotoxins do not have such a pronounced specific effect as exotoxins, and are also less toxic. Do not turn into toxoids. Endotoxins are superantigens; they can activate phagocytosis and allergic reactions. These toxins cause general malaise in the body; their action is not specific.

Regardless of which microbe the endotoxin is obtained from, the clinical picture is the same: it is usually fever and severe general condition.

The release of endotoxins into the body can lead to the development of infectious-toxic shock. It is expressed in the loss of blood by capillaries, disruption of the circulatory centers and, as a rule, leads to collapse and death.

There are several forms of infection:

· A pronounced form of infection is an infectious disease with a specific clinical picture (overt infection).

· In the absence of clinical manifestations of infection, it is called latent (asymptomatic, latent, inapparent).

· A peculiar form of infection is microbial carriage unrelated to previous illness.

The occurrence and development of infection depends on the presence of a specific pathogen (pathogenic organism), the possibility of its penetration into the body of a susceptible animal, and the conditions of the internal and external environment that determine the nature of the interaction between the micro- and macroorganism.

Each type of pathogenic microbe causes a specific infection ( specificity of action). The manifestation of infection depends on the degree pathogenicity a specific strain of the infectious agent, i.e. on its virulence, which is expressed by toxigenicity and invasiveness.

Depending on the nature of the pathogen differentiate

· bacterial,

· viral,

· fungal

· other infections.

Entrance gates of infection– the place of penetration of the pathogen into the human body through certain tissues that lack physiological protection against a specific type of pathogen.

They may be skin, conjunctiva, mucous membranes of the digestive tract, respiratory tract, genitourinary system. Some microbes exhibit pathogenic effects only when they penetrate through strictly defined gates of infection. For example, the rabies virus causes disease only when introduced through damage to the skin and mucous membranes. Many microbes have adapted to a variety of ways of entering the body.

Source of infection(focal infection) – reproduction of the pathogen at the site of introduction

Depending from the transmission mechanism pathogens are distinguished

· nutritional,

· respiratory (aerogenic, including dust and airborne droplets),

· wounded,

· contact infections.

When microbes spread in the body, it develops generalized infection.

A condition in which microbes from the primary focus penetrate the bloodstream, but do not multiply in the blood, but are only transported to various organs, is called bacteremia. In a number of diseases (anthrax, pasteurellosis, etc.) septicemia: microbes multiply in the blood and penetrate all organs and tissues, causing inflammatory and dystrophic processes there.

The infection may be

spontaneous (natural) and

· experimental (artificial).

Spontaneous infection occurs in natural conditions during the implementation of the transmission mechanism characteristic of a given pathogenic microbe, or during the activation of conditionally pathogenic microorganisms that lived in the animal’s body ( endogenous infection or autoinfection). If a specific pathogen enters the body from the environment, it is said to be exogenous infection.

If, after suffering an infection and freeing the macroorganism from its causative agent, a repeated illness occurs due to infection with the same pathogenic microbe, we speak of reinfection And.

Celebrate and superinfection- a consequence of a new (repeated) infection that occurred against the background of an already developing disease caused by the same pathogenic microbe.

The return of the disease, the reappearance of its symptoms after clinical recovery has occurred, is called relapse. It occurs when the animal’s resistance weakens and the pathogens of the disease that remain in the body are activated. Relapses are characteristic of diseases in which insufficiently strong immunity is formed.

Mixed infections (mixed infections, mixed) develop as a result of infection by several types of microorganisms; Such conditions are characterized by a qualitatively different course (usually more severe) compared to monoinfection, and the pathogenic effect of pathogens does not have a simple summary nature. Microbial relationships in mixed (or mixed) infections are variable:

If microorganisms activate or aggravate the course of the disease, they are defined as activators, or synergists (for example, influenza viruses and group B streptococci);

If microorganisms mutually suppress the pathogenic effect, they are designated as antagonists (for example, E. coli suppresses the activity of pathogenic salmonella, shigella, streptococci and staphylococci);

Indifferent microorganisms do not affect the activity of other pathogens.

Manifest infections can occur typically, atypically or chronically.

Typical infection. After entering the body, the infectious agent multiplies and causes the development of characteristic pathological processes and clinical manifestations.

Atypical infection. The pathogen multiplies in the body, but does not cause the development of typical pathological processes, and clinical manifestations are unexpressed and erased. The atypicality of the infectious process can be caused by the reduced virulence of the pathogen, the active resistance of protective factors to its pathogenic potencies, the influence of antimicrobial therapy, and a combination of these factors.

Chronic infection usually develops after infection with microorganisms capable of long-term persistence. In some cases, under the influence of antimicrobial therapy or under the influence of protective mechanisms, bacteria are converted into L-forms. At the same time, they lose their cell wall, and along with it the structures that are recognized by AT and serve as targets for many antibiotics. Other bacteria are able to circulate in the body for a long time, “evading” the action of these factors due to antigenic mimicry or changes in the antigenic structure. Such situations are also known as persistent infections [from lat. persisto, persistens, survive, withstand]. At the end of chemotherapy, L-forms can return to the original (virulent) type, and species capable of long-term persistence begin to multiply, which causes a secondary exacerbation, a relapse of the disease.

Slow infections. The name itself reflects the slow (over many months and years) dynamics of the infectious disease. The pathogen (usually a virus) enters the body and remains latent in the cells. Under the influence of various factors, the infectious agent begins to multiply (while the reproduction rate remains low), the disease takes on a clinically pronounced form, the severity of which gradually increases, leading to the death of the patient.

In the vast majority of cases, pathogenic microorganisms find themselves in unfavorable conditions in various areas of the body, where they die or are exposed to protective mechanisms or are eliminated purely mechanically. In some cases, the pathogen is retained in the body, but is subjected to such “restraining” pressure that it does not exhibit pathogenic properties and does not cause the development of clinical manifestations ( abortive, hidden, “dormant” infections).

Abortion infection[from lat. aborto, not to bear, in this context - not to realize the pathogenic potential] is one of the most common forms of asymptomatic lesions. Such processes can occur during species or intraspecific, natural or artificial immunity (therefore, humans do not suffer from many animal diseases). Immunity mechanisms effectively block the vital activity of microorganisms, the pathogen does not multiply in the body, the infectious cycle of the pathogen is interrupted, it dies and is removed from the macroorganism.

Latent or hidden, infection [from lat. latentis, hidden] - a limited process with long-term and cyclical circulation of the pathogen, similar to that observed in obvious forms of the infectious process. The pathogen multiplies in the body; causes the development of protective reactions, is excreted from the body, but no clinical manifestations are observed. Such conditions are also known as inapparent infections (from the English inapparent, implicit, indistinguishable). Thus, viral hepatitis, polio, herpetic infections, etc. often occur in a latent form. Persons with latent infectious lesions pose an epidemic danger to others.

Dormant infections may be a type of latent infection or a condition after a clinically significant illness. Typically, this establishes a clinically invisible balance between the pathogenic potencies of the pathogen and the body’s defense systems. However, under the influence of various factors that reduce resistance (stress, hypothermia, nutritional disorders, etc.), microorganisms acquire the ability to exert a pathogenic effect. Thus, persons carrying dormant infections are the reservoir and source of the pathogen.

Microcarrier. As a consequence of a latent infection or after an illness, the pathogen “lingers” in the body, but is subjected to such “restraining pressure” that it does not exhibit pathogenic properties and does not cause the development of clinical manifestations. This condition is called microbial carriage. Such subjects release pathogenic microorganisms into the environment and pose a great danger to others. There are acute (up to 3 months), prolonged (up to 6 months) and chronic (more than 6 months) microbial carriage. Carriers play a large role in the epidemiology of many intestinal infections - typhoid fever, dysentery, cholera, etc.