Bacterial cytotoxins. Bacterial cell toxins. Separation according to the method of isolating poisons

Exotoxins are secretory protein substances that exhibit enzymatic activity. According to the mechanism of action of exotoxin on the cell, cytotoxins, membrane toxins, functional blockers, exfoliants and erythrohemines are distinguished. The mechanism of action of protein toxins is reduced to damage to vital processes in the cell: increased membrane permeability, blockade of protein synthesis and other biochemical processes in the cell, or disruption of interaction and mutual coordination between cells.

Exotoxins are powerful antigens that produce antitoxins in the body.

According to their molecular organization, they are divided into 2 groups: 1) exotoxins from two fragments 2) constituting a single polypeptide chain.

According to the degree of connection with the bacterial cell: 1) class A - toxins secreted into the external environment (diphtheria bacillus toxin) 2) class B - toxins partially secreted into the external environment and partially associated with a microbial cell (tetanospasmin of tetanus bacillus)

3) class C - toxins associated with the microbial cell and entering the environment when the cell is destroyed (enterobacterial exotoxins).

Classification by the nature of targets: neurotoxins, hemolysins (destroy erythrocytes), enterotoxins, dermatonecrotoxins, leukocidins (damage phagocytes)

Exotoxins are highly toxic. Under the influence of formalin and temperature, they lose their toxicity, but retain their immunogenic properties. Such toxins are called toxoids and are used to prevent tetanus, gangrene, botulism, diphtheria, and are also used as antigens in the immunization of animals in order to obtain anatoxic sera.

Exotoxins, consisting of two fragments - A and B. Each fragment itself is inactive. They possess the properties of a toxin, being associated with each other. In this case, fragment B performs two functions - acceptor (recognizes the receptor on the membrane and binds to it) and the formation of an intramembrane channel. Fragment A penetrates through it into the cell and exhibits toxic activity in it, affecting various metabolic processes of the cell. For example, enterotoxins of Vibrio cholerae and pathogenic gram-negative bacteria have such a structure.

Bacteria often synthesize several exotoxins with different effects (lethal, hemolytic, cytotoxic).

5. Endotoxins, chemical composition, properties, mechanism of action. Differences between exo- and endotoxins.

By their chemical structure, endotoxins are lipopolysaccharides, which are contained in the cell wall of gram-negative bacteria and are released into the environment during lysis of bacteria. Endotoxins have no specificity, are thermostable, less toxic, and have weak immunogenicity. When large doses enter the body, endotoxins inhibit phagocytosis, granulocytosis, monocytosis, increase capillary permeability, and have a destructive effect on cells. Microbial lipopolysaccharides destroy blood leukocytes, cause degranulation of mast cells with the release of vasodilators, activate the Hageman factor, which leads to leukopenia, hyperthermia, hypotension, acidosis, dessiminated intravascular coagulation (DVC). Endotoxins stimulate the synthesis of interferons, activate the complement system in the classical way, and have allergic properties. With the introduction of small doses of endotoxin, the body's resistance increases, phagocytosis increases, and B-lymphocytes are stimulated. The serum of an animal immunized with endotoxin has a weak antitoxic activity and does not neutralize endotoxin. The pathogenicity of bacteria is controlled by three types of genes: genes - by their own chromosomes, genes introduced by plasmids by temperate phages.

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Introduction

Toxins play an important role in the development of the infectious process. According to their biological properties, bacterial toxins are divided into exotoxins and endotoxins.

Exotoxins are produced by both gram-positive and gram-negative bacteria. By their chemical structure, these are proteins. According to the mechanism of action of exotoxin on the cell, several types are distinguished: cytotoxins, membrane toxins, functional blockers, exfoliants and erythrohemines. The mechanism of action of protein toxins is reduced to damage to vital processes in the cell: increased membrane permeability, blockade of protein synthesis and other biochemical processes in the cell, or disruption of interaction and mutual coordination between cells. Exotoxins are strong antigens that induce the formation of antitoxins in the body.

According to their molecular organization, exotoxins are divided into two groups:

* exotoxins, consisting of two fragments;

* exotoxins that make up a single polypeptide chain.

According to the degree of connection with the bacterial cell, exotoxins are conventionally divided into three classes.

* Class A - toxins secreted into the environment;

* Class B - toxins partially secreted and partially associated with the microbial cell;

* Class C - toxins associated with the microbial cell and entering environment when the cell is destroyed.

Exotoxins are highly toxic. Under the influence of formalin and temperature, exotoxins lose their toxicity, but retain their immunogenic properties. Such toxins are called toxoids and are used to prevent tetanus, gangrene, botulism, diphtheria, and are also used in the form of antigens for immunizing animals in order to obtain anatoxic sera.

Endotoxins stimulate the synthesis of interferons, activate the complement system in the classical way, and have allergic properties.

With the introduction of small doses of endotoxin, the body's resistance increases, phagocytosis increases, and B-lymphocytes are stimulated. The serum of an animal immunized with endotoxin has a weak antitoxic activity and does not neutralize endotoxin.

The pathogenicity of bacteria is controlled by three types of genes: genes - by their own chromosomes, genes introduced by plasmids and temperate phages.

1. Toxins. Concept

Toxins(Greek. toxikon poison) - biologically active substances of microbial, plant and animal origin, affecting a foreign eukaryotic cell and not acting on prokaryotic cells. The ability to form toxins is most widespread among microorganisms. Animal toxins are mostly produced by representatives of various taxonomic groups of invertebrates. In vertebrates, this property is most pronounced in reptiles, for example, in snakes. The ability to produce toxins has also been found in higher plants. The ability to produce toxins makes microbes pathogenic, and some fungi, plants and animals poisonous. toxin biological pathogenicity virulence

By chemical nature, most of the toxic microorganisms, plants and animals are represented by high molecular weight compounds (peptides, proteins, glycoproteins), and at the same time, toxic fungi are mainly components with low molecular weight. Examples include aflatoxins produced by species of the genera Aspergillus and trichothecene mycotoxins produced by species of the genera Fusarium, Trichoderma and Cephalosporium. These toxins are highly carcinogenic. The chemical nature of protozoan toxins is poorly understood, but there is evidence to suggest that species such as Trypanosoma cruzi, Giardia lamblia, and Entamoeba histolytica produce toxic proteins.

Some plant toxins (abrin, ricin, modecin, visculin) and toxic proteins (diphtheria toxin, Shigella dysenteriae enterotoxin) of some pathogenic bacteria have great similarity in molecular structure and mechanism of action.

Bacterial toxins are produced by both pathogenic and opportunistic bacteria and are the cause of various kinds of pathological conditions. Depending on the type of tissue affected, T. bacteria are divided into several groups; enterotoxins affecting the cells of the tissues of the gastrointestinal tract: neurotoxins affecting cells nervous system; leukotoxins (for example, leukocidin) that affect cells of the immune system: pneumotoxins that affect cells of the lung tissue; cardiotoxins affecting heart muscle cells .

According to the physicochemical properties, T. bacteria are classified as proteins and peptides. Some of them are synthesized by the bacterial cell in the form of an inactive precursor (diphtheria, botulinum toxins, etc.), which requires an activation stage to become active. Activation is carried out with the participation of proteolytic enzymes, which, under conditions of mild (limited) proteolysis, fragment the polypeptide target with the formation of two peptides (subunits A and B) that perform different functions when the toxin interacts with the target cell. Thus, fragmentation accompanied by activation leads to the emergence of a bifunctional (or binary) molecular structure.

T. bacteria in which the functionally active structure is represented by one polypeptide chain are called simple; T., having a subunit structure and consisting of several functionally different peptides, are complex. The T. structure of bacteria is closely related to the mechanism of their action on the eukaryotic cell.

According to the mechanism of action on the eukaryotic cell, T. bacteria are divided into two groups: those affecting the target cell through destruction of the cell membrane and T., affecting the target cell, affecting its vital regulatory systems. A classic example of T. of the first group, causing destruction of the cell membrane, are the so-called hemolysins (hemotoxins), which destroy the membranes of erythrocytes. This also includes thiol-dependent T., such as pneumolysin, streptolysin, tetanolysin, etc.

Thiol-dependent T. are proteins consisting of one polypeptide chain. The active state of these T. manifests itself only in a reduced form, when the disulfide group of a protein, in the presence of a thiol-reducing agent, is converted into a sulfhydryl group. Cholesterol is the membrane receptor for these T. on the eukaryotic cell. After binding with cholesterol, pores are formed in the membrane through which the contents of the cell flow out. When thiol-dependent T. acts on vascular cells, vascular permeability is disturbed, which, as a rule, is accompanied by the formation of edema.

T. of the second group, affecting vital regulatory systems, in order to hit the target cell, must overcome the membrane and penetrate into the cell. There they reach some important regulatory system and inactivate it. This group includes such toxins as diphtheria, cholera and cholera-like, exotoxin A Pseudomonas aeruginosa, enterotoxin Sh. dysenteriae, a part of Clostridial T. For T. of the indicated group, a characteristic feature is the bifunctionality of the structure. Sometimes these T. are called binary. Their molecular structure is based on the so-called type A-B the model that determines their bifunctionality. The first important property of such T. is the ability to recognize and bind to a sensitive eukaryotic cell. The function of recognition and binding in binary T. is performed by component B (subunit B). Thus, in cholera and cholera-like T., component B recognizes the complementary receptor of the sensitive cell, the ganglioside GMI. These T. do not bind to other structures of the membrane. Thus, the specificity of binding of T. to the surface of a sensitive cell is due to the presence on its surface of a receptor of a strictly defined chemical nature.

After the binding of T. through component B to the cell surface, the entire toxic molecule is delivered to the inside of the cell by endocytosis, where component A enters into action. Having enzymatic activity, component A interacts inside the cell with the corresponding substrate. Thus, for component A of cholera and cholera-like T., the substrate is one of the proteins of adenylate cyclase, the most important system of the eukaryotic cell. Carrying out enzymatic modification of the corresponding protein of the adenylate cyclase system, component A of choleragen (cholera T.) makes the entire system work in an abnormal manner. In the cells of the mucous membrane of the small intestine, which are affected by cholerogen, a dysfunction of the adenylate cyclase system leads to a violation of electrolyte metabolism and, as a consequence, to the development of changes characteristic of cholera.

The intracellular target for diphtheria T. is the system of protein biosynthesis of the eukaryotic cell. After passing through the membrane, the enzymatically active subunit A of diphtheria T. performs ribosylation of one of the transcription components and thereby stops protein biosynthesis.

Inactivation (neutralization) of T. bacteria is achieved by modifying their native structure. Exist different ways modifications of a toxic molecule, but they all boil down to a change in the function of individual parts of a toxic protein. Modification of T. bacteria can be achieved by genetic means, chemical and physicochemical action. The well-known neutralization of T. bacteria with formalin is reduced to a violation of the spatial configuration of a toxic protein due to the appearance of numerous cross-links between individual sections of the T. polypeptide chain or its individual subunits.

In connection with the deciphering of the molecular structure of many T. bacteria, the area of their application in practical medicine has expanded.

As before, T. remained important components vaccine preparations, however, data on the subunit structure, for example, choleragen, have allowed the development of a new generation of subunit vaccines. Such vaccines are devoid of reactogenicity, are not overloaded with unnecessary antigenic determinants and, which is especially important, are designed for a strictly defined area of the immune response.

The study of the nature and topography of antigenic determinants of T. bacteria contributed to the development of modern diagnostic methods (for example, the enzyme immunoassay method, or the method of molecular probes). The establishment of genes that control the production of certain protein toxins made it possible to develop DNA probes that are used to test toxigenic forms different types microorganisms.

T. bacteria are used to construct the so-called immunotoxins. In preparations of immunotoxins intended for the treatment of neoplasms, an enzymatically active T subunit (for example, subunit A of diphtheria T) is used as a damaging agent, and an antibody obtained to one of the antigens of the surface of a malignant cell is used as a component searching for a sensitive cell. cells. Models of such chimeric immunotoxins are being studied extensively.

Another area of practical application of T. is the use of their modified forms, subunits, or individual fragments for the purposes of competitive therapy based on blocking the corresponding receptor structures of the cell involved in the binding of active T.

After the discovery of diphtheria toxin by Emil Roux and Alexander Yersin in 1888, toxins are traditionally called protein substances, formed mainly by microorganisms and some animals, and having a toxic effect. Toxins determine the main symptoms of diphtheria, whooping cough, cholera, anthrax, botulism, tetanus, hemolytic uremic syndrome and some other infectious diseases of humans and animals. To date, data have been accumulated showing the possibility of toxins performing functions that are not related to infectious processes.

Among them:

The use of toxins by bacteria as a means of antagonism in microbial communities (cholera toxin has an inhibitory effect on a number of bacteria);

Achievements in genetic and protein engineering have opened the way for scientists to design new medical immunobiological preparations (MIBP) based on derivatives of bacterial toxins that have no analogues in nature. The aim of this work is to summarize data on the nature, mechanisms of action and the possibilities of constructing hybrid and modified bacterial toxins.

In the course of evolutionary development, pathogens have adapted to grow in various host tissues. The high degree of specificity inherent in many microorganisms reflects differences in the biochemical composition of organs. It was possible to identify a difference related to erythritol, the preferred carbon source for several species of the genus Brucella that cause miscarriage in ungulates. Erythritol is found in high concentrations only in the ungulate placenta and not in other tissues.

High concentrations of iron suppress the formation of toxin in Clostridium tetani, although they contribute to the invasiveness of the microorganism.

In tuberculosis, the factor limiting the growth of microbes is the availability of iron compounds. Both the body and the pathogen are used to transfer iron into cells, the chelating compounds secreted by them. As a result, a "battle" for iron arises, the outcome of which depends on the strength of binding and the concentration of chelating agents secreted by the body and mycobacterium tuberculosis. Therefore, the introduction into the body of compounds that reduce the concentration of free iron protects the animal from tuberculosis.

Pathogenicity is a qualitative characteristic of a species, determined by its genotype; it is the potential ability of a pathogen to cause an infectious process. Pathogenicity factors are associated with the structural elements of the microbial cell, its metabolism. They allow the pathogenic microorganism not only to penetrate and survive, but also to multiply, spread in the tissues and organs of the animal, and actively influence its functions.

Thus, pathogenicity is an evolutionarily fixed characteristic of a species. For example, among the vast genus Bacillus, only Bacillus anthracis (the causative agent of anthrax) is pathogenic for mammals.

Each type of pathogenic microbes is characterized by a specific set of pathogenic factors. This set determines the nature of the pathogenic action, that is, the ability to cause a certain infectious process. For example, artiodactyls are sick with foot and mouth disease, and one-hoofed, felines with glanders; infectious anemia - horses, swine fever - pigs. However, within a species, the pathogenicity of microorganisms can fluctuate.

The degree of pathogenicity, individual feature each variant and strain of microorganisms is called virulence.

This is a qualitative characteristic of a strain of microorganisms, a characteristic of its pathogenicity for animals of a certain species in certain unchanging conditions. In the process of evolution, pathogens have acquired a variety of abilities to penetrate a macroorganism, overcoming its protective barriers, resist the body's defenses, suppress them and cause changes in the morphology and function of cells, tissues and organs.

The virulence of any strain of a given pathogenic species is measured by two factors: toxigenicity (the ability to produce toxins-substances that damage tissues) and invasiveness (the ability to penetrate into body tissues, multiply in them and spread). Invasiveness and toxigenicity have their own genetic control in the bacterial cell.

Virulence is measured by the minimum number of microorganisms or micrograms of toxin that are fatal when a particular animal or bird is infected. Typically, this value is expressed as LD 50, i. E. the number of microorganisms or micrograms of toxin, causing the death of 50% of experimental individuals.

Some types of pathogenic microorganisms damage the vertebrate organism with the help of an indirect mechanism, which comes into effect only on condition of preliminary contact with the same pathogen or its metabolic products. This phenomenon is called hypersensitivity or allergy. The term "allergy" (allos-other, ergon-action) means change. Allergy should be considered a component of acquired immunity. The substances that cause it are called allergens.

Allergy is a state of increased sensitivity of the body to the reintroduction of an allergen.

2. Microbial toxins

The understanding of the nature of microbial toxins was obtained through studies of pathogenic bacteria.

By 1890, the first toxins of two pathogenic microorganisms were discovered: Corynebacterium diphtheriae and Clostridium tetani.

In both cases, the same experiments were performed: the bacterium was grown in a culture medium in vitro, and a sterile filtrate prepared from the grown culture was injected into the experimental animals. The latter died, and upon opening them, changes in organs characteristic of the corresponding natural infection were found. These toxic substances turned out to be proteins. Since they represented the metabolic products of bacteria and were not associated with bacterial cells, they were named exotoxins... Exotoxins form a number of other pathogenic bacteria (causative agent of botulism, infectious enterotoxemia, dysentery, etc.), mainly gram-positive. However, filtrates prepared from cultures of many other pathogenic microorganisms were not toxic. Boiling bacterial cultures proved that cells of almost all gram-negative pathogenic bacteria are toxic in themselves. Moreover, heat-killed cells of many pathogenic gram-negative bacteria have the same toxic effect. Heat-resistant toxins associated with the cell wall of gram-negative bacteria were named endotoxins.

However, for many pathogenic bacteria, including the causative agent of anthrax, these approaches did not allow the detection of any toxic products. The culture conditions in the laboratory are always different from those in the infected animal. Awareness of this obvious fact prompted a search for bacterial toxins formed directly in the body of an infected animal. This work led to the discovery of a specific exotoxin in Bacillus anthracis.

In addition to the enzymes of aggression and protection, microorganisms, multiplying, can produce biologically active substances that damage the cells and tissues of the macroorganism. - toxins. Some toxins (diphtheria, tetanus, botulinum-cKNP) are the leading factors in the development of the corresponding diseases. The action of others (staphylococcus hemolysins, leukocidins) is more limited.

The strength of toxins, as well as the virulence of the pathogens themselves, are measured by DLM or LD50-According to their properties, toxins are divided into 2 groups:

* endotoxins- lipopolysaccharides; thermostable, produced, as a rule, by gram-negative bacteria, have a general toxic effect, are weak antigens, do not pass into toxoid;

* exotoxins- proteins; are thermolabile, produced, as a rule, by gram-positive bacteria, have a specific action, strong antigens, with special treatment they turn into toxoids.

The most significant producers of exotoxins for medical practice are the following pathogens:

* among gram-positive bacteria - diphtheria, botulism, tetanus, gas gangrene, some types of staphylococci and streptococci;

* among gram-negative - cholera vibrio, some types of pseudomonads, shigella.

Exotoxins, depending on the strength of their connection with the microbial cell, are divided into:

* for completely secreted (actually exotoxins) into the environment;

* partially secreted;

* unclassified.

The latter are released only in the process of destruction of bacterial cells, which makes them similar in this property to endotoxins.

According to the mechanism of action on the cells of the macroorganism, bacterial toxins are divided into several types, although this division is rather arbitrary and some toxins can be attributed to several types at once:

* 1st type - membrane toxins (hemolysins, leukocidins);

* 2nd type - functional blockers, or neurotoxins (theta-nospasmin, botulinum toxin), - block the transmission of nerve impulses in synapses (in the cells of the spinal cord and brain);

* 3rd type - thermostable and thermolabile enterotoxins - activate cellular adenylate cyclase, which leads to impaired enterosorption and the development of diarrheal syndrome. Such toxins are produced by Vibrio cholerae (cholerogen), enterotoxigenic Escherichia coli;

* 4th type - cytotoxins - toxins that block protein synthesis at the subcellular level (enterotoxin staphylococcus aureus, dermatonecrotoxins of staphylococci, anthrax sticks, blue-green pus and whooping cough pathogen). This also includes antielongators - which prevent elongation (build-up) or translocation, i.e., the movement of i-RNA along the ribosome, and thereby blocking protein synthesis (diphtheria histotoxin, Pseudomonas aeruginosa toxin);

* 5th type - exfoliatins formed by some strains of Staphylococcus aureus, and erythrogenins produced by pyogenic streptococcus group A. They affect the process of interaction of cells with each other and with intercellular substances and completely determine the clinical picture of infection (in the first case, pemphigus occurs in newborns, during the second - scarlet fever).

Many bacteria form not one, but several protein toxins that have different effects - neurotoxic, cytotoxic, hemolytic: staphylococcus, streptococcus.

At the same time, some bacteria can simultaneously form both protein exotoxins and endotoxins: Escherichia coli, Vibrio cholerae.

3. All factors of pathogenicity according to their function are usually subdivided into 4 groups:

* 1st - bacteria with the epithelium of the corresponding ecological niches (biotopes);

* 2nd - interfering with the cellular and humoral defense mechanisms of the host and ensuring the reproduction of the pathogen in vivo;

* 3rd - bacterial modulins inducing the synthesis of certain cytokines and inflammatory mediators leading to immunosuppression;

* 4th - toxins and toxic products that have a damaging effect, associated, as a rule, with specific pathomorphological changes in various organs and tissues of the body.

Conclusion

The structure, mechanisms of action, and antiquity of the origin of bacterial toxins indicate that their evolution began in the communities of unicellular microorganisms, where they played the role of signaling molecules capable of acting at a great distance from the bacterial cell without weakening the signal strength. The evolution of toxins took place by increasing the complexity of their molecules, caused by duplications and fusions of genes encoding proteins of their individual domains. The antiquity of bacterial toxins makes it possible to call into question the anthroposic nature of certain infectious diseases, for example, cholera, whooping cough and diphtheria. Apparently it is advisable to search natural reservoirs pathogens of these diseases in communities of protozoa. The subunit structure of toxins, where one of the subunits plays the role of a ligand, the other causes a toxic effect, allows research aimed at obtaining a new generation of medical immunobiological preparations that have no analogues in nature. At present, approaches have been developed for interfering with the structure of toxin molecules, which make it possible to obtain immunotoxins for targeted therapeutic effects on malignant blood cells, and toxins with altered specificity and / or with higher toxicity to certain insect species. The toxicity of botulinum toxin is extreme not only for bacterial toxins, but also for natural toxic substances. Modification of toxins is most likely to change the spectrum of their targets. The LD 50 of hybrid and modified toxins, even with an increase in their toxicity for individual experimental animals, will be within the limits characteristic of toxic substances in a given molecular weight range.

Toxins are poisonous substances - waste products of microorganisms with high molecular weight and antigenic properties.

Bacterial toxins are divided into two groups - exotoxins and endotoxins, which differ in their properties and in the nature of their effect on the body.

Exotoxins are produced by the microbe into the environment and are highly toxic. For example, the minimum lethal dose of native (untreated) diphtheria toxin for guinea pig is 0.0002 ml, tetanus - 0.005 ml, and botulinum - 0.0001 ml. The activity of the purified toxins is several hundred times higher.

The effect of exotoxins on the body is manifested after a certain incubation period. Endotoxins act in a shorter period of time.

Endotoxins are structural components of the bacterial cell and enter the environment only after its destruction. In terms of their toxicity, endotoxins are significantly inferior to exotoxins. Exotoxins are thermolabile substances: most of them are destroyed at t ° 60-80 ° within 10-20 minutes. Endotoxins are highly resistant to heat: they are destroyed when more high temperature or with prolonged boiling. Exotoxins are less resistant to the action of various physicochemical factors in comparison with endotoxins. Freezing and thawing of toxins does not significantly affect their potency. Toxins are well kept dry.

The action of formalin and heat on exotoxins deprives them of their toxic properties, but retains their immunogenicity. On this principle, the production of so-called toxoids (see), used to prevent a number of infections, has been developed. Attempts to obtain toxoids from endotoxins have been unsuccessful. Most exotoxins are used in the titration of the corresponding antitoxic sera.

A characteristic feature of exotoxins is pronounced antigenicity - the ability to cause, when introduced into the body, the formation of antibodies that have high degree specificity. This circumstance allows the production of therapeutic and prophylactic sera against diseases caused by pathogens producing exotoxins under industrial conditions.

Most exotoxins are produced by gram-positive bacteria. However, according to a number of researchers, exotoxins are also capable of producing some gram-negative species (causative agents of plague, whooping cough, Grigoriev's dysentery bacillus - Shigi).

The biological properties of a number of animal products and vegetable origin are very close to microbial toxins (for example, plant poisons abrin, robin, ratsin; animal poisons of snakes, scorpions, spiders).

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Toxic substances synthesized by bacteria, by their chemical nature, belong to proteins (exotoxins) and LPS (endotoxins) - they are localized in wall B !! and are released only after their destruction.

Protein toxins. At present,> 80 are known, differ from each other in Mg, chemical structure, "targets" and biological activity. Depending on the connection with B! , they are subdivided into completely secreted (exotoxins), partially secreted and non-secreted (released when B is destroyed!). But protein toxins are not only intended to damage the hen; they can also participate in the metabolic reactions of the bacteria themselves. Divided into: thermolabile and thermostable.

They have 2 centers: 1 - fixes a toxin molecule on the corresponding cellular receptor, 2 - a toxic fragment - gets inside  and blocks vital metabolic reactions.

Cellular receptors for different toxins are not the same:

on gangliosides of a certain type - tetanospasmin, cholerogen, enterotoxins of intestinal bacteria, etc.

SPECIFICITY the action of protein toxins is determined by the selective fixation of the toxin on the receptors of - "targets" of certain tissues (epithelial, nervous, etc.). The mechanisms of action of toxins are:

"Cytotoxins" - block protein synthesis.

a group of antielongators (diphtheria histotoxin, Pseudomonas aeruginosa toxin, etc.), disable the enzyme transferase II, which is responsible for the elongation (build-up) of the polypeptide chain on the ribosome.

enteropathogenic toxins (Staph.aureus, Cl. perfringens)

dermonecrotoxins (Pseudomonas aeruginosa, B. Pertussis).

"Membrane toxins"

Erythrocyte membrane permeability (hemolysins) (Pseudomonas aeruginosa, Staph.aureus, streptococci, clostridia)

Permeability of the membrane of leukocytes (leukocidins) (Staph.aureus, streptococci (pyogenes), clostridia (perfringens et botulini)).

"Functional blockers"

Heat-labile (TL) and thermostable (TS) enterotoxins (cholerogen, heat-labile enterotoxins of E. coli and other enterobacteria) - activate adenylate cyclase → permeability of the wall of the small intestine and the release of fluid into its lumen (diarrhea).

Toxic blockers (anthrax and plague toxins - inactivate adenylate cyclase)

Neurotoxins (tetanospasmin, botulinum toxin) block the transmission of nerve impulses in the cells of the spinal cord and brain.

exfoliatins and erythrogens (formed by some strains of Staphylococcus aureus and scarlet fever streptococcus) - affect the interaction of cells with each other and with intercellular substances.

High TOXICITY protein toxins is explained by the peculiarity of the structure of the regions of their molecules, imitating the structure of subunits of hormones, enzymes and neurotransmitters MK  antimetabolites.

Toxicity is measured in the same units in which virulence is assessed - DLM and LD 50.

IMMUNOGENIC properties are manifested in the ability to induce an immune response from MK (to induce the synthesis of specific Ab – antitoxins).

ANATOXINS. A number of protein toxins under the action of formalin lose their toxicity, while maintaining immunogenic properties (tetanus, diphtheria, etc.), are used as vaccines for prophylaxis.

Many bacteria form not one, but several protein toxins that have different effects.

Table of contents of the subject "Pathogenicity of microorganisms. Virulence.":
1. Pathogenicity of microorganisms. Pathogenic microorganisms. Pathogenic microbes.
2. Conditionally pathogenic microorganisms. Conditionally pathogenic microbes. Opportunistic pathogens. Non-pathogenic microorganisms.
3. Obligate parasites. Optional parasites. Accidental parasites. Pathogenicity. What is pathogenicity?
4. Virulence. What is virulence? Virulence criteria. Lethal dose (DL, LD). Infectious Dose (ID).
5. Genetic control of pathogenicity and virulence. Genotypic reduction in virulence. Phenotypic decrease in virulence. Attenuation.
6. Factors of pathogenicity of microorganisms. Factors of pathogenicity of microbes. Colonization ability. Adhesion. Colonization factors.
7. Capsule as a factor of pathogenicity of microorganisms. Inhibiting enzymes of microbes as a factor of pathogenicity. Invasiveness of microorganisms.
8. Toxicity of microorganisms. Toxins. Partial toxins. Cytolysins. Protoxins.

10. Endotoxins. Endotoxins of microorganisms. Endotoxin shock. Endotoxinemia. Exozymes. Superantigens.

Exotoxins- secretory protein substances, usually showing enzymatic activity. Often, exotoxins serve as the only virulence factor of a microorganism, act remotely (far beyond the focus of infection) and are responsible for clinical manifestations infections (for example, enterotoxins cause diarrhea, neurotoxins cause paralysis and other neurological symptoms). Botulinum toxin exhibits the greatest toxicity - 6 kg of toxin could kill all of humanity.

High toxicity of exotoxins due to the peculiarity of the structure of their fragments, imitating the structure of the subunits of hormones, enzymes or neurotransmitters of the host. As a result, exotoxins exhibit the properties of antimetabolites, blocking the functional activity of natural analogs. Exotoxins exhibit high immunity; in response to their administration, specific neutralizing AT (antitoxins) are formed. According to the degree of connection with the bacterial cell, exotoxins are divided into three groups - A, B and C.

Group A exotoxins- toxins secreted into the environment (for example, diphtheria bacillus toxin).

Group B exotoxins- toxins partially secreted into the external environment and partially associated with the bacterial cell (for example, tetanospasmin of the tetanus bacillus).

Group C exotoxins- toxins associated with the bacterial cell and released after its death (for example, exotoxins of enterobacteria). Properties of exotoxins

Exotoxins usually contain bifunctional (ligand and effector) structures. The former recognize and bind a complementary receptor (gangliosides, proteins, glycoproteins) on the cell membrane, the latter provide an effector effect, most often hydrolysis of NAD to ADP-ribose and nicotinamide, followed by transfer of the ADP-ribosyl residue to the target.

Binding and penetration of exotoxins to a certain extent resembles the mechanism of action of peptide and glycoprotein hormones, which is due to the relationship of their molecular structures. The intracellular target for the effector part of the toxin molecule is usually a vital system, for example, protein biosynthesis (for the A-toxin of Pseudomonas aeruginosa and Shigella) or the adsnylate cyclase system (for cholerogen, thermolabile toxin of E. coli or exotoxin Bordetella pertussis).

The most common classification of exotoxins based on the nature of the targets for their effects: neurotoxins infect cells nervous tissue, hemolysins destroy erythrocytes, enterotoxins affect the epithelium of the small intestine, dermatonecro-toxins cause necrotic lesions of the skin, leukocidins damage phagocytes (leukocytes), etc.

By the mechanism of action among exotoxins release cytotoxins (eg enterotoxins or dermatonecrotoxins), membrane toxins (eg hemolysins and leukocidins), functional blockers (eg cholerogen), exfoliatins and erythrogens. Often, pathogenic bacteria synthesize several exotoxins that exhibit different effects (lethal, hemolytic, cytotoxic, etc.).

Bacterial toxins Bacterial toxins

constituents of the structures of a microbial cell or substances produced by it into the environment that have a damaging effect on the human and animal organism. They cause characteristic syndromes and, to a greater or lesser extent, determine the course and outcome of the disease. T.b. conventionally divided into: endotoxins(media exotoxins(cm.). Based on the structural and functional sv-in T. differentiate into simple and complex. Simple T. are proteins, one polypeptide chain to-rykh carries a toxic (activator), others - a transport (receptor) function. All of them belong to the group of exotoxins. Complex T. consist of several components of a proteinaceous and nonproteinaceous (polysaccharide, lipid) nature, and also have a receptor and an activator. A complex structure is characteristic of all endotoxins and some exotoxins. All T. have pronounced antigenic and protective sv-you, and in the specificity of the Ar endotoxins are close to the bacteria-producers, the Ar exotoxins differ from them. In this regard, antisera against endotoxins neutralize both endotoxin and the producing bacterium, against exotoxins - only exotoxin. The effect caused by T., as a rule, is a consequence of a number of progressive reactions, starting with the adsorption of the transport part of T. on the receptors of target cells. Receptors for exotoxins are located on a limited group of cells, so their action is manifested in a specific symptom complex; endotoxins are able to adsorb and damage cells of various organs, and therefore the wedge, the manifestations of the action of different endotoxins are close. Cm. Microbial toxicosis, food toxico-infections.

(Source: Glossary of Microbiology Terms)

See what "Bacterial toxins" are in other dictionaries:

Poisonous substances released by bacteria into the environment (exotoxins) or contained in microbial cells (endotoxins). Ecological encyclopedic dictionary. Chisinau: Main editorial board of the Moldavian Soviet Encyclopedia. I.I. Grandpa. 1989 ... Ecological Dictionary

Modern encyclopedia

Compounds (often of a protein nature) of bacterial, plant or animal origin, capable of causing disease or death when they enter the body of animals or humans. Contained in the venoms of snakes, spiders, scorpions. Bacterial ... ... Large encyclopedic Dictionary

TOXINS- TOXINS. The concept of "toxin" entered immunobiology at the end of the 19th century, when substances with the following basic properties were found in animals and plants, as well as in bacteria: 1) When introduced into the body of an animal, they cause ... ... Great medical encyclopedia

Toxins- TOXINS, compounds released by microorganisms, plants or animals that, if ingested, can cause illness or death. Contained in the venoms of snakes, spiders, scorpions, etc. Bacterial toxins cause ... ... Illustrated Encyclopedic Dictionary

- (from the Greek toxikon poison), poisonous substances formed by certain microorganisms, plants and animals. By chem. nature polypeptides and proteins. Sometimes the term "T." also applies to toxic substances of non-protein nature (in particular aflatoxins ... ... Biological encyclopedic dictionary

Compounds (often of a protein nature) of bacterial, plant or animal origin, capable of causing disease or death when ingested by animals or humans. Contained in the venoms of snakes, spiders, scorpions. Bacterial ... ... encyclopedic Dictionary

- (from the Greek toxikon poison) substances of bacterial, plant or animal origin, capable of inhibiting physiological functions, which leads to disease or death of animals and humans. By their chemical nature, all T. are proteins or ... ... Great Soviet Encyclopedia

TOXINS- (from the Greek toxikón - poison), poisonous metabolic products of microorganisms (bacteria, fungi), plants and animals. To T. of plant origin (phytotoxins) include abrin, ricin, crucine and other substances contained in plant seeds ... ... Veterinary encyclopedic dictionary

Compounds (often of a protein nature) of bacterial, grows. or of animal origin, capable of causing disease or death when ingested by animals or humans. Contained in the venoms of snakes, spiders, scorpions. Bacterial T. ... ... Natural science. encyclopedic Dictionary

Books

Forensic examination of food poisoning. Study guide, G.N. Zarafyants, M.I.Krut, S. Yu. Sashko Category: Textbooks for universities Publisher: Publishing House of St. Petersburg State University, Manufacturer: SPbSU Publishing House,
Forensic examination of food poisoning, Mikhail Krut, The manual sets out modern classifications of food poisoning (PO) of non-microbial (true and indirect), microbial etiology (food toxicoinfections, bacterial intoxication) and ... Category: Educational literature Publisher: