Scientific electronic library. Infections: general characteristics Pathogenesis of infections: general scheme of development of the infectious process

An infectious process is unthinkable without its main causes - pathogens. Microorganisms can cause diseases of varying severity and manifestations. Infections are defined by virulence and pathogenicity.

There are a huge number of microorganisms living around that appeared on Earth long before the emergence of larger, multicellular living beings. Microbes are constantly trying to get the palm among all living things, so their number is growing rapidly, they occupy various ecological niches. The role of microorganisms in the infectious process is great, because they cause most of the known diseases of people, animals, plants, and even bacteria themselves.

First, it’s worth understanding what the term “germs” includes. In popular science literature, this group includes bacteria, protozoa (single-celled nuclear organisms), mycoplasmas and microscopic fungi (some also add viruses to this list, but this is a mistake, since they are not living). This group of microorganisms has several advantages in comparison with large macroorganisms: firstly, they multiply quickly, and secondly, their “body” is limited to one, or less often several cells, and this makes it easier to manage all processes.

Many microbes live deep in the earth, water, and on various surfaces and do not cause any harm. But there is a separate group of microorganisms that can cause infectious diseases in humans, animals, and plants. It can be divided into two subgroups: opportunistic and pathogenic organisms.

The role of microorganisms in the infectious process

The role of the microbe in the infectious process depends on several factors:

• pathogenicity;
• virulence;
• specifics of the choice of host organism;
• degree of organotropy.

Pathogenicity of microorganisms

• presence of a protective capsule;
• devices for active movement;
• attached receptors or enzymes for passage through the cell membranes of macroorganisms;
• devices for adhesion - attachment to the surface of cells of other organisms.

All of the above increases the likelihood that the microorganism will penetrate the host cell and cause an infectious process. The more pathogenicity factors a microbe combines, the more difficult it is to fight it, and the more acute the manifestations of the disease will be.

Based on the principle of pathogenicity, microbes are divided into opportunistic, pathogenic and non-pathogenic. The first group includes most of the bacteria living in the soil and on plants, as well as the normal microflora of the intestines, skin and mucous membranes. These microorganisms are capable of causing diseases only if they enter parts of the body that are not intended for them: the blood, the digestive tract, deep into the skin. Pathogenic microorganisms are most protozoa (there are especially many of them in two types: Sporozoans and Sarcoflagellates), some fungi, mycoplasmas and bacteria. These microbes can multiply and develop only in the host body.

Virulence

It is very easy to confuse the two concepts: pathogenicity and virulence, since the second is a phenotypic manifestation of the first. Simply put, virulence is the likelihood that an infectious agent will cause disease. Even if infected with a pathogenic microbe, a person can remain healthy, because the immune system tries to maintain “order” in the body.

The higher the virulence of microorganisms, the lower the chance of remaining healthy after they enter the body.

For example, E. coli has a low virulence rate, so many people ingest it with water daily, but do not have problems with the digestive system. But for Staphylococcus aureus, which is resistant to methicillin, this figure is above 90%, so when infected, people quickly develop a disease with severe symptoms.

The virulence of microbes has several quantitative characteristics:

• infectious dose (the number of microorganisms required to start the infectious process);
• minimum lethal dose (how many microbes must be in the body for it to die);
• maximum lethal dose (the number of microbes at which death occurs in 100% of cases).

The virulence of microorganisms is influenced by many external factors: temperature changes, treatment with antiseptics or antibiotics, ultraviolet irradiation, etc.

Specifics of host selection

The role of a microorganism in the infectious process largely depends on how specific it is in choosing a host microorganism. Dividing microbes according to this criterion, you can see that there are several groups:

Degree of organotropy

Organotropy is an indicator of the selectivity of a microorganism when choosing a “place of residence” in the body. Once in the body, the microbe rarely settles anywhere; more often it looks for certain tissues or organs in which conditions favorable for it are present.

For example, Vibrio cholera enters the body with dirty water, but it does not remain in the nasopharynx or oral cavity, it “reaches” the intestines, settles in its cells and causes severe digestive disorders: diarrhea, diarrhea.

A person inhales spores of the pathogenic fungus Aspergillus through the nose, but the pathogen can grow and multiply normally inside the cells of the lungs or brain.

Organotropy influences the specificity when choosing a host, because if a microorganism needs to get into hepatocytes - liver cells for normal development, but the infected macroorganism does not have it - the disease will not develop.

Macroorganism in the infectious process

The struggle between macro- and microorganisms has been going on since the very beginning of their cohabitation on Earth, therefore both have their own role in the infectious process. Each has its own advantages and weaknesses, which is why people, animals, and plants still exist together with bacteria, fungi, and protozoa.

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 sick person 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 typhoid fever was an independent disease, 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 the immunity is not strong enough.

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 a previous 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.

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 of 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 area of ​​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. When a urticarial 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, Hageman 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 herpesvirus infection. The mechanism of intercellular interactions between the antigen-presenting cell, T-helper cells and B-lymphocytes is provided by the costimulation molecules CO28 and CO40.

Key words: herpesvirus infection, cytokines, costimulation molecules, children

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, a sufficient number of microorganisms entering the body, which is called an infectious dose, is also important. 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

An 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 faced by 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.