Microbiology. Cheat sheet: briefly, the most important

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Microbiology. Cheat sheet: briefly, the most important

Lecture notes, cheat sheets

Directory / Lecture notes, cheat sheets

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Table of contents

Subject and tasks of microbiology
Systematics and nomenclature of microorganisms
Nutrient media and methods for isolating pure cultures
Morphology of bacteria, main organs
Morphology of bacteria, additional organelles
Growth, reproduction, nutrition of bacteria
Types of bacterial metabolism
Genetics of macroorganisms
Bacteriophages
Morphology of viruses, types of interaction of the virus with the cell
Virus cultivation. Antiviral immunity
General characteristics of the form and periods of infection
Infectious agents and their properties
Normal human microflora
Dysbacteriosis
Classification of chemotherapy drugs
Major complications of chemotherapy
Subject of immunology. Types of immunity
immune system. Central and peripheral organs of the immune system
immune response. The concept of form
Classifications and types of antigens
Antibodies. Classifications and properties
Immunodeficiency conditions
Allergy, classification of allergens, features of infectious allergy
Autoimmune processes
Methods of immunodiagnostics
Immunoprophylaxis, immunotherapy, immunocorrection
General characteristics and classification of the Enterobacteriaceae family
Genus Escherichia, genus Shigella. Their characteristics
Salmonella genus, Yersinia genus. Their characteristics
Food poisoning and food poisoning
Plague. anthrax
Tularemia. Brucellosis
Staphylococci. Streptococci. Their characteristics
Meningococcus. Gonococcus. Their characteristics
Haemophilus influenzae. Pseudomonas aeruginosa
Klebsiella. Proteus
Diphtheria. Morphology and cultural properties. Diphtheria pathogenesis
Diagnostics. Prevention. Treatment of diphtheria
Tuberculosis
Tuberculosis. Diagnostics. Prevention. Treatment
Rickettsia group
Rickettsioses
Influenza viruses
ARVI pathogens
SARS pathogens (Adenoviruses)
ARVI pathogens (Rhinoviruses. Reoviruses)
Measles and mumps viruses
Herpes virus. rubella virus
Poliomyelitis virus, ECHO viruses, Coxsackie viruses
ВИЧ
HIV. Epidemiology. Diagnostics. Treatment
Rabies virus. Flaviviruses
Hepatitis A and B virus
Other causative agents of viral hepatitis
Plasmodium malaria

1. Subject and tasks of microbiology

microbiology - a science, the subject of which is microscopic creatures called microorganisms, their biological characteristics, systematics, ecology, relationships with other organisms.

organisms- the most ancient form of organization of life on Earth. In terms of quantity, they represent the most significant and most diverse part of the organisms inhabiting the biosphere.

Microorganisms include:

1) bacteria;

2) viruses;

3) mushrooms;

4) protozoa;

5) microalgae.

Bacteria are unicellular microorganisms of plant origin, devoid of chlorophyll and without a nucleus.

Mushrooms are unicellular and multicellular microorganisms of plant origin, devoid of chlorophyll, but having features of an animal cell, eukaryotes.

Viruses are unique microorganisms that do not have a cellular structural organization.

The main sections of microbiology: general, technical, agricultural, veterinary, medical, sanitary.

General microbiology studies the most general patterns inherent in each group of the listed microorganisms: structure, metabolism, genetics, ecology, etc.

The main task of technical microbiology is the development of biotechnology for the synthesis of biologically active substances by microorganisms: proteins, enzymes, vitamins, alcohols, organic substances, antibiotics, etc.

Agricultural microbiology deals with the study of microorganisms that participate in the cycle of substances, are used to prepare fertilizers, cause plant diseases, etc.

Veterinary microbiology studies the pathogens of animal diseases, develops methods for their biological diagnosis, specific prophylaxis and etiotropic treatment aimed at the destruction of pathogenic microbes in the body of a sick animal.

The subject of study of medical microbiology is pathogenic (pathogenic) and opportunistic microorganisms for humans, as well as the development of methods for microbiological diagnostics, specific prevention and etiotropic treatment of infectious diseases caused by them.

The subject of study of sanitary microbiology is the sanitary and microbiological state of environmental objects and food products, the development of sanitary standards.

2. Systematics and nomenclature of microorganisms

The main taxonomic unit of bacterial taxonomy is the species.

A species is an evolutionarily established set of individuals that has a single genotype, which under standard conditions is manifested by similar morphological, physiological, biochemical and other features.

The species is not the final unit of taxonomy. Within the species, variants of microorganisms are distinguished, differing in individual features:

1) serovars (by antigenic structure);

2) chemovars (according to sensitivity to chemicals);

3) fagovars (by sensitivity to phages);

4) fermenters;

5) bacteriocinovars;

6) bacteriocinogenovars.

Bacteriocins are substances produced by bacteria that have a detrimental effect on other bacteria. According to the type of bacteriocin produced, bacteriocinovars are distinguished, and according to sensitivity, bacteriocinogenovars are distinguished.

Bacteria properties:

1) morphological;

2) tinctorial;

3) cultural;

4) biochemical;

5) antigenic.

Species are grouped into genera, genera into families, families into orders. The higher taxonomic categories are classes, divisions, subkingdoms and kingdoms.

Pathogenic microorganisms belong to the kingdom of prokaryotes, pathogenic protozoa and fungi - to the kingdom of eukaryotes, viruses are combined into a separate kingdom - Vira.

All prokaryotes that have a single type of cell organization are combined into one department - Bacteria, in which:

1) actually bacteria;

2) actinomycetes;

3) spirochetes;

4) rickettsia;

5) chlamydia;

6) mycoplasmas.

For systematics of microorganisms are used:

1) numerical taxonomy. Recognizes the equivalence of all signs. The species affiliation is established by the number of matching characters;

2) serotaxonomy. Examines bacterial antigens using reactions with immune sera;

3) chemotaxonomy. Physico-chemical methods are used to study the lipid, amino acid composition of a microbial cell and certain of its components;

4) gene systematics. Based on the ability of bacteria with homologous DNA to transform, transduce and conjugate, on the analysis of extrachromosomal factors of heredity - plasmids, transposons, phages.

A pure culture is one species of bacteria grown on a nutrient medium.

3. Nutrient media and methods for isolating pure cultures

For the cultivation of bacteria, nutrient media are used, to which a number of requirements are imposed.

1. Nutrition. The bacteria must contain all the necessary nutrients.

2. Isotonic. Bacteria must contain a set of salts to maintain osmotic pressure, a certain concentration of sodium chloride.

3. Optimal pH (acidity) of the medium. The acidity of the environment ensures the functioning of bacterial enzymes; for most bacteria is 7,2-7,6.

4. Optimum electronic potential, indicating the content of dissolved oxygen in the medium. It should be high for aerobes and low for anaerobes.

5. Transparency (so that bacterial growth can be seen, especially for liquid media).

6. Sterility.

Classification of nutrient media.

1. By origin:

1) natural (milk, gelatin, potatoes, etc.);

2) artificial - media prepared from specially prepared natural components (peptone, aminopeptide, yeast extract, etc.);

3) synthetic - media of known composition, prepared from chemically pure inorganic and organic compounds.

2. By composition:

1) simple - meat-peptone agar, meat-peptone broth;

2) complex - these are simple with the addition of an additional nutrient component (blood, chocolate agar): sugar broth, bile broth, whey agar, yolk-salt agar, Kitt-Tarozzi medium.

3. By consistency:

1) solid (contain 3-5% agar-agar);

2) semi-liquid (0,15-0,7% agar-agar);

3) liquid (do not contain agar-agar).

4. By appointment:

1) general purpose - for the cultivation of most bacteria (meat-peptone agar, meat-peptone broth, blood agar);

2) special purpose:

a) elective - media on which bacteria of only one species (genus) grow, and the genus of others is suppressed (alkaline broth, 1% peptone water, yolk-salt agar, casein-charcoal agar, etc.);

b) differential diagnostic - media on which the growth of some types of bacteria differs from the growth of other species in one way or another, more often biochemical (Endo, Levin, Gis, Ploskirev, etc.);

c) enrichment environments - environments in which the reproduction and accumulation of pathogenic bacteria of any kind or species (selenite broth) occurs.

To obtain a pure culture, it is necessary to know the methods for isolating pure cultures:

1. Mechanical separation (stroke method by firing a loop, method of dilutions in agar, distribution over the surface of a solid nutrient medium with a spatula, Drygalsky method).

2. Use of elective nutrient media.

A colony is an isolated accumulation of bacteria visible to the naked eye on a solid nutrient medium.

4. Morphology of bacteria, main organs

The sizes of bacteria range from 0,3-0,5 to 5-10 microns.

According to the shape of the cells, bacteria are divided into cocci, rods and convoluted.

In a bacterial cell, there are:

1) main organelles: (nucleoid, cytoplasm, ribosomes, cytoplasmic membrane, cell wall);

2) additional organelles (spores, capsules, villi, flagella)

The cytoplasm is a complex colloidal system consisting of water (75%), mineral compounds, proteins, RNA and DNA.

Nucleoid is a nuclear substance dispersed in the cytoplasm of a cell. It does not have a nuclear membrane or nucleoli. It is pure DNA, it contains no histone proteins. The nucleoid encodes the basic genetic information, i.e. the cell genome.

The cytoplasm can contain autonomous circular DNA molecules with a lower molecular weight - plasmids.

Ribosomes are ribonucleoprotein particles 20 nm in size, consisting of two subunits - 30 S and 50 S. Ribosomes are responsible for protein synthesis.

Mesosomes are derivatives of the cytoplasmic membrane. Mesosomes can be in the form of concentric membranes, vesicles, tubules.

The cell wall is an elastic rigid formation with a thickness of 150-200 angstroms. Performs the following functions:

1) protective, the implementation of phagocytosis;

2) regulation of osmotic pressure;

3) receptor;

4) takes part in the nutritional processes of cell division;

5) antigenic;

6) stabilizes the shape and size of bacteria;

7) provides a system of communications with the external environment;

8) is indirectly involved in the regulation of cell growth and division.

Depending on the content of murein in the cell wall, Gram-positive and Gram-negative bacteria are distinguished.

In Gram-positive bacteria, the murein layer makes up 80% of the mass of the cell wall. According to Gram, they are colored blue. In gram-positive bacteria, the murein layer makes up 20% of the mass of the cell wall; according to Gram, they are stained red.

cytoplasmic membrane. It has selective permeability, takes part in the transport of nutrients, excretion of exotoxins, energy metabolism of the cell, is an osmotic barrier, participates in the regulation of growth and division, and DNA replication.

It has the usual structure: two layers of phospholipids (25-40%) and proteins.

According to their function, membrane proteins are divided into:

1) structural;

2) permiases - proteins of transport systems;

3) enzymes - enzymes.

The lipid composition of membranes is not constant. It may vary depending on the cultivation conditions and the age of the culture.

5. Morphology of bacteria, additional organelles

Villi (pili, fimbria) are thin protein outgrowths on the surface of the cell wall. Komon pili are responsible for the adhesion of bacteria to the surface of host cells. They are characteristic of Gram-positive bacteria. Sex pili provide contact between male and female bacterial cells during the conjugation process. Through them, genetic information is exchanged from the donor to the recipient.

Flagella- organelles of movement. These are special protein outgrowths on the surface of a bacterial cell containing a protein - flagelin. The number and location of flagella can be different:

1) monotrichous (have one flagellum);

2) lophotrichous (have a bundle of flagella at one end of the cell);

3) amphitrichous (have one flagellum at each end);

4) peritrichous (have several flagella, along the perimeter).

The motility of bacteria is judged by considering living microorganisms, or indirectly by the nature of growth in Peshkov's medium (semi-liquid agar). Non-motile bacteria grow strictly according to the injection, and mobile ones give diffuse growth.

Capsules are an additional surface layer. The function of the capsule is protection against phagocytosis and antibodies.

There are macro- and microcapsules. The macrocapsule can be identified using special staining techniques, combining positive and negative staining techniques. Microcapsule - thickening of the upper layers of the cell wall. It can only be detected with electron microscopy.

Bacteria include:

1) true capsular bacteria (genus Klebsiella) - retain capsule formation even when growing on nutrient media, and not only in the macroorganism;

2) pseudocapsular - form a capsule only when it enters the macroorganism.

Capsules can be polysaccharide and protein. They play the role of an antigen, they can be a virulence factor.

Spores are special forms of existence of some bacteria under adverse environmental conditions. Sporulation is inherent in Gram-positive bacteria. Unlike vegetative forms, spores are more resistant to chemical and thermal factors.

Most often, spores are produced by bacteria of the genusBacillusand Clostridium.

The process of sporulation consists in thickening of all cell membranes. They are impregnated with calcium dipicalinate salts, become dense, the cell loses water, and all its plastic processes slow down. When the spore gets into favorable conditions, it germinates into a vegetative form.

Gram-negative bacteria also have the ability to survive in unfavorable conditions in the form of non-culturable forms. At the same time, there is no typical sporulation, but metabolic processes in such cells are slowed down, it is impossible to immediately grow on a nutrient medium. But when they enter the macroorganism, they turn into their original forms.

6. Growth, reproduction, nutrition of bacteria

Bacterial growth - an increase in the size of a bacterial cell without increasing the number of individuals in the population.

Reproduction of bacteria - a process that ensures an increase in the number of individuals in a population. Bacteria are characterized by a high rate of reproduction.

Bacteria reproduce by transverse binary fission.

On dense nutrient media, bacteria form clusters of cells - colonies. On liquid media, bacterial growth is characterized by the formation of a film on the surface of the nutrient medium, uniform turbidity or sediment.

Phases of reproduction of a bacterial cell on a liquid nutrient medium:

1) the initial stationary phase (the number of bacteria that got into the nutrient medium and is in it);

2) lag phase (rest phase) (active cell growth begins, but there is no active reproduction yet);

3) the phase of logarithmic multiplication (the processes of cell multiplication in the population are actively going on);

4) maximum stationary phase (bacteria reach their maximum concentration; the number of dead bacteria is equal to the number of formed ones);

5) phase of accelerated death.

Under food understand the processes of entry and exit of nutrients into and out of the cell.

Organogens (carbon, oxygen, hydrogen, nitrogen, phosphorus, potassium, magnesium, calcium) are distinguished among the necessary nutrients.

Depending on the source of carbon production, bacteria are divided into:

1) autotrophs (use inorganic substances - CO2);

2) heterotrophs;

3) metatrophs (use organic matter of inanimate nature);

4) paratrophs (use organic substances of wildlife).

According to energy sources, microorganisms are divided into:

1) phototrophs (able to use solar energy);

2) chemotrophs (receive energy through redox reactions);

3) chemolithotrophs (use inorganic compounds);

4) chemoorganotrophs (use organic matter).

Ways of entry of metabolites and ions into the microbial cell.

1. Passive transport (without energy costs):

1) simple diffusion;

2) facilitated diffusion (along the concentration gradient).

2. Active transport (with the expenditure of energy, against the concentration gradient; in this case, the substrate interacts with the carrier protein on the surface of the cytoplasmic membrane).

7. Types of bacterial metabolism

There are two types of metabolism in the process of metabolism:

1) plastic (constructive):

a) anabolism (with energy costs);

b) catabolism (with the release of energy);

2) energy metabolism (occurs in the respiratory mesosomes):

a) breathing

b) fermentation.

Energy exchange

Depending on the acceptor of protons and electrons among bacteria, aerobes, facultative anaerobes and obligate anaerobes are distinguished. For aerobes, the acceptor is oxygen.

The following enzymes are isolated at the site of action:

1) exoenzymes (act outside the cell);

2) endoenzymes (act in the cell itself).

Depending on the chemical reactions catalyzed, all enzymes are divided into six classes:

1) oxidoreductases (catalyze redox reactions between two substrates);

2) transferases (carry out intermolecular transfer of chemical groups);

3) hydrolases (perform hydrolytic cleavage of intramolecular bonds);

4) lyases (attach chemical groups at two bonds);

5) isomerases (carry out isomerization processes, provide internal conversion with the formation of various isomers);

6) ligases, or synthetases (connect two molecules, resulting in the splitting of pyrophosphate bonds in the ATP molecule).

4. Types of plastic metabolism (protein, carbohydrate, lipid, nucleic).

Protein metabolism is characterized by catabolism and anabolism. In the process of catabolism, bacteria decompose proteins under the action of proteases with the formation of peptides. Amino acids are formed from peptides by the action of peptidases.

In carbohydrate metabolism in bacteria, catabolism prevails over anabolism. Polysaccharides are cleaved to disaccharides, which, under the action of oligosaccharidases, break down to monosaccharides.

Depending on the final products, the following types of fermentation are distinguished:

1) alcohol (typical for mushrooms);

2) propionic acid (typical for clostridia);

3) lactic acid (typical for streptococci);

4) butyric (typical for sarcin);

5) butyldenglycol (typical for bacilli).

Lipid metabolism is carried out with the help of enzymes - lipoproteinases, lecitinases, lipases, phospholipases.

Lipases catalyze the breakdown of neutral fatty acids. When fatty acids are broken down, the cell stores energy.

Nucleic metabolism of bacteria is associated with genetic metabolism. The synthesis of nucleic acids is important for the process of cell division. Synthesis is carried out with the help of enzymes: restriction enzyme, DNA polymerase, ligase, DNA-dependent RNA polymerase.

8. Genetics of macroorganisms

The hereditary apparatus of bacteria is represented by one chromosome, which is a DNA molecule.

The functional units of the bacterial genome, in addition to chromosomal genes, are: IS sequences, transposons, plasmids.

IS sequences are short pieces of DNA. They do not carry structural (protein-coding) genes, but contain only genes responsible for transposition.

Transposons are larger DNA molecules. In addition to the genes responsible for transposition, they also contain a structural gene. Transposons are able to move along the chromosome.

Plasmids are additional extrachromosomal genetic material. It is a circular, double-stranded DNA molecule, the genes of which encode additional properties, giving selective advantages to cells. Plasmids are capable of autonomous replication.

Depending on the properties of the features that encode plasmids, there are:

1) R-plasmids. Provide drug resistance; may contain genes responsible for the synthesis of enzymes that destroy medicinal substances, may change the permeability of membranes;

2) F-plasmids. Code for sex in bacteria. Male cells (F+) contain the F-plasmid, female cells (F-) do not;

3) Col-plasmids. Encode the synthesis of bacteriocins;

4) Tox-plasmids. Encode the production of exotoxins;

5) plasmids biodegradation. Encode enzymes by which bacteria can utilize xenobiotics.

Variation in bacteria:

1. Phenotypic variability - modifications - does not affect the genotype. They are not inherited and fade over time.

2. Genotypic variability affects the genotype. It is based on mutations and recombinations.

Mutations - a change in the genotype that persists over a number of generations and is accompanied by a change in the phenotype. A feature of mutations in bacteria is the relative ease of their detection.

Recombination is the exchange of genetic material between two individuals with the appearance of recombinant individuals with an altered genotype.

reaction mechanisms.

1. Conjugation - the exchange of genetic information through direct contact between the donor and the recipient.

2. Fusion of protoplasts - the exchange of genetic information through direct contact of sections of the cytoplasmic membrane in bacteria lacking a cell wall.

3. Transformation - the transfer of genetic information in the form of isolated DNA fragments when the recipient cell is in an environment containing donor DNA.

4. Transduction is the transfer of genetic information between bacterial cells with the help of moderate transducing phages. It is specific and non-specific.

9. Bacteriophages

Bacteriophages (phages) are viruses that infect bacterial cells. They do not have a cellular structure, they are unable to synthesize nucleic acids and proteins themselves, therefore they are obligate intracellular parasites.

Phage virions consist of a head containing the nucleic acid of the virus and an outgrowth.

The nucleocapsid of the phage head has a cubic type of symmetry, and the process has a spiral type, i.e., bacteriophages have a mixed type of symmetry.

Phages can exist in two forms:

1) intracellular (this is a prophage, pure DNA);

2) extracellular (this is a virion).

There are two types of phage-cell interaction.

1. Lytic (productive viral infection). This is the type of interaction in which the reproduction of the virus occurs in the bacterial cell. She dies at the same time. Phages are first adsorbed on the cell wall. Then comes the penetration phase. Lysozyme acts at the site of phage adsorption, and phage nucleic acid is injected into the cell due to the contractile proteins of the tail. This is followed by an average period during which the synthesis of cellular components is suppressed and the disconjunctive method of phage reproduction is carried out. In this case, the phage nucleic acid is synthesized in the nucleoid region, and then protein synthesis is carried out on the ribosomes. Phages that have a lytic type of interaction are called virulent.

In the final period, as a result of self-assembly, proteins fit around the nucleic acid and new phage particles are formed. They leave the cell, breaking its cell wall, i.e., lysis of the bacterium occurs.

2. Lysogenic. These are temperate phages. When a nucleic acid enters a cell, it integrates into the cell genome, and a long-term cohabitation of the phage with the cell is observed without its death. When external conditions change, the phage can leave the integrated form and develop a productive viral infection.

On the basis of specificity, they distinguish:

1) polyvalent phages (lyse cultures of one family or genus of bacteria);

2) monovalent (lyse cultures of only one type of bacteria);

3) typical (capable of causing lysis of only certain types (variants) of a bacterial culture within a bacterial species).

Phages can be used as diagnostic preparations to determine the genus and species of bacteria isolated during bacteriological examination. However, more often they are used for the treatment and prevention of certain infectious diseases.

10. Morphology of viruses, types of interaction of the virus with the cell

Viruses are microorganisms that make up the Vira kingdom.

Viruses can exist in two forms: extracellular (virion) and intracellular (virus).

The shape of the virions can be: round, rod-shaped, in the form of regular polygons, filamentous, etc.

Their sizes range from 15-18 to 300-400 nm.

In the center of the virion is a viral nucleic acid covered with a protein coat - a capsid, which has a strictly ordered structure. The capsid is made up of capsomeres.

Nucleic acid and capsid make up the nucleocapsid.

The nucleocapsid of complexly organized virions is covered with an outer shell - the supercapsid.

DNA can be:

1) double-stranded;

2) single-stranded;

3) ring;

4) double-stranded, but with one shorter chain;

5) double-stranded, but with one continuous and the other fragmented chains.

RNA can be:

1) single-strand;

2) linear double-strand;

3) linear fragmented;

4) ring;

5) containing two identical single-stranded RNA.

Viral proteins are divided into:

1) genomic - nucleoproteins. Provide replication of viral nucleic acids and virus reproduction processes;

2) proteins of the capsid shell - simple proteins with the ability to self-assemble. They add up to geometric structures in which several types of symmetry are distinguished: spiral, cubic or mixed;

3) supercapsid shell proteins are complex proteins. They perform protective and receptor functions.

Among the proteins of the supercapsid shell, there are:

a) anchor proteins (ensure the contact of the virion with the cell);

b) enzymes (can destroy membranes);

c) hemagglutinins (cause hemagglutination);

d) elements of the host cell.

Interaction of viruses with the host cell

There are four types of interaction:

1) productive viral infection (reproduction of the virus occurs, and the cells die);

2) abortive viral infection (reproduction of the virus does not occur, and the cell restores the impaired function);

3) latent viral infection (there is a reproduction of the virus, and the cell retains its functional activity);

4) virus-induced transformation (a cell infected with a virus acquires new properties).

11. Cultivation of viruses. Antiviral immunity

The main methods of cultivation of viruses:

1) biological - infection of laboratory animals. When infected with a virus, the animal becomes ill;

2) cultivation of viruses in developing chicken embryos. Chicken embryos are grown in an incubator for 7-10 days and then used for cultivation.

As a result of infection, the following can occur and appear:

1) death of the embryo;

2) developmental defects;

3) accumulation of viruses in the allantoic fluid;

4) propagation in tissue culture.

There are the following types of tissue cultures:

1) transplanted - cultures of tumor cells; have high mitotic activity;

2) primary trypsinized - subjected to primary treatment with trypsin; this treatment disrupts intercellular communication, resulting in the release of individual cells.

Special media are used to maintain tissue culture cells. These are liquid nutrient media of complex composition containing amino acids, carbohydrates, growth factors, protein sources, antibiotics and indicators for assessing the development of tissue culture cells.

The reproduction of viruses in tissue culture is judged by their cytopathic action.

The main manifestations of the cytopathic action of viruses:

1) virus reproduction may be accompanied by cell death or morphological changes in them;

2) some viruses cause cell fusion and the formation of multinuclear syncytium;

3) cells can grow but not divide, resulting in giant cells;

4) inclusions appear in the cells (nuclear, cytoplasmic, mixed). Inclusions may stain pink (eosinophilic inclusions) or blue (basophilic inclusions);

5) if viruses containing hemagglutinins multiply in tissue culture, then in the process of reproduction the cell acquires the ability to adsorb erythrocytes (hemadsorption).

Features of antiviral immunity

Antiviral immunity begins with the presentation of the viral antigen by T-helpers.

Immunity is aimed at neutralizing and removing the virus, its antigens and virus-infected cells from the body. There are two main forms of participation of antibodies in the development of antiviral immunity:

1) neutralization of the virus with antibodies;

2) immune lysis of virus-infected cells with the participation of antibodies.

12. General characteristics of the form and periods of infection

Infection - this is a set of biological reactions with which the macroorganism responds to the introduction of the pathogen.

For the occurrence of an infectious disease, a combination of the following factors is necessary:

1) the presence of a microbial agent;

2) susceptibility of the macroorganism;

3) the presence of an environment in which this interaction takes place.

The microbial agent is pathogenic and opportunistic microorganisms.

An epidemic is a widespread infection in a population covering large areas.

A pandemic is the spread of an infection to almost the entire territory of the globe.

Endemic diseases (with natural foci) are diseases for which territorial areas with an increased incidence of this infection are noted.

Classification of infections

1. By etiology: bacterial, viral, protozoal, mycoses, mixed infections.

2. By the number of pathogens: monoinfections, polyinfections.

3. According to the severity of the course: light, severe, moderate.

4. By duration: acute, subacute, chronic, latent.

5. By means of transmission:

1) horizontal:

a) airborne route;

b) fecal-oral;

c) contact;

d) transmissive;

e) sexual;

2) vertical:

a) from mother to fetus (transplacental);

b) from mother to newborn in the birth act;

3) artificial (artificial).

Depending on the location of the pathogen, there are:

1) focal infection;

2) generalized infection. The most severe form is sepsis.

The following periods of infectious diseases are distinguished:

1) incubation; from the moment the pathogen enters the body until the first signs of the disease appear;

2) prodromal; characterized by the appearance of the first unclear general symptoms. The causative agent multiplies intensively, colonizes the tissue, begins to produce enzymes and toxins. Duration - from several hours to several days;

3) the height of the disease; characterized by the appearance of specific symptoms;

4) outcome:

a) lethal outcome;

b) recovery (clinical and microbiological). Clinical recovery: the symptoms of the disease have subsided, but the pathogen is still in the body. Microbiological - complete recovery;

c) chronic carriage.

13. Infectious agents and their properties

Bacteria are distinguished by their ability to cause disease:

1) pathogenic species are potentially capable of causing an infectious disease;

Pathogenicity is the ability of microorganisms, entering the body, to cause pathological changes in its tissues and organs. This is a qualitative species feature.

2) conditionally pathogenic bacteria can cause an infectious disease with a decrease in the body's defenses;

3) saprophytic bacteria never cause disease.

The implementation of pathogenicity goes through virulence - this is the ability of a microorganism to penetrate into a macroorganism, multiply in it and suppress its protective properties.

This is a strain trait, it can be quantified. Virulence is the phenotypic manifestation of pathogenicity.

The quantitative characteristics of virulence are:

1) DLM (minimum lethal dose) is the amount of bacteria, when introduced into the body of laboratory animals, 95-98% of the death of animals in the experiment is obtained;

2) LD 50 is the number of bacteria that causes the death of 50% of the animals in the experiment;

3) DCL (lethal dose) causes 100% death of animals in the experiment.

Virulence factors include:

1) adhesion - the ability of bacteria to attach to epithelial cells;

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

3) penetration - the ability to penetrate cells;

4) invasion - the ability to penetrate into the underlying tissues. This ability is associated with the production of enzymes such as hyaluronidase and neuraminidase;

5) aggression - the ability to resist the factors of non-specific and immune defense of the body.

Aggressive factors include:

1) substances of various nature that make up the surface structures of the cell: capsules, surface proteins, etc. Many of them inhibit the migration of leukocytes, preventing phagocytosis;

2) enzymes - proteases, coagulase, fibrinolysin, lecithinase;

3) toxins, which are divided into exo- and endotoxins.

Exotoxins are highly toxic proteins. They are thermolabile, they are strong antigens, for which antibodies are produced in the body, which enter into toxin neutralization reactions. This trait is encoded by plasmids or prophage genes.

Endotoxins are complex complexes of lipopolysaccharide nature. They are thermostable, are weak antigens, have a general toxic effect. Encoded by chromosomal genes.

14. Normal human microflora

The normal human microflora is a combination of many microbiocenoses characterized by certain relationships and habitats.

Types of normal microflora:

1) resident - permanent, characteristic of a given species;

2) transient - temporarily trapped, uncharacteristic for a given biotope; She doesn't actively reproduce.

Factors affecting the state of normal microflora.

1. Endogenous:

1) secretory function of the body;

2) hormonal background;

3) acid-base state.

2. Exogenous conditions of life (climatic, domestic, environmental).

In the human body, blood, cerebrospinal fluid, articular fluid, pleural fluid, lymph of the thoracic duct, internal organs: heart, brain, parenchyma of the liver, kidneys, spleen, uterus, bladder, lung alveoli are sterile.

Normal microflora lines the mucous membranes in the form of a biofilm. This framework consists of polysaccharides of microbial cells and mucin. The thickness of the biofilm is 0,1-0,5 mm. It contains from several hundred to several thousand microcolonies.

Stages of formation of normal microflora of the gastrointestinal tract (GIT):

1) accidental seeding of the mucosa. Lactobacilli, clostridia, bifidobacteria, micrococci, staphylococci, enterococci, Escherichia coli, etc. enter the gastrointestinal tract;

2) the formation of a network of tape bacteria on the surface of the villi. Mostly rod-shaped bacteria are fixed on it, the process of biofilm formation is constantly going on.

The normal microflora is considered as an independent extracorporeal organ with a specific anatomical structure and functions.

Functions of normal microflora:

1) participation in all types of exchange;

2) detoxification in relation to exo- and endoproducts, transformation and release of medicinal substances;

3) participation in the synthesis of vitamins (groups B, E, H, K);

4) protection:

a) antagonistic (associated with the production of bacteriocins);

b) colonization resistance of mucous membranes;

5) immunogenic function.

The highest contamination is characterized by:

1) large intestine;

2) oral cavity;

3) urinary system;

4) upper respiratory tract;

5) skin.

15. Dysbacteriosis

Dysbacteriosis (dysbiosis) is any quantitative or qualitative changes in the normal human microflora typical for a given biotope, resulting from the impact of various unfavorable factors on a macro- or microorganism.

Microbiological indicators of dysbiosis are:

1) decrease in the number of one or more permanent species;

2) the loss of certain traits by bacteria or the acquisition of new ones;

3) increase in the number of transient species;

4) the emergence of new species unusual for this biotope;

5) weakening of the antagonistic activity of normal microflora.

Causes of development dysbacteriosis can be:

1) antibiotic and chemotherapy;

2) severe infections;

3) severe somatic diseases;

4) hormone therapy;

5) radiation exposure;

6) toxic factors;

7) deficiency of vitamins.

Phases of dysbacteriosis:

1) compensated, when dysbacteriosis is not accompanied by any clinical manifestations;

2) subcompensated, when local inflammatory changes occur as a result of an imbalance in the normal microflora;

3) decompensated, in which there is a generalization of the process with the appearance of metastatic inflammatory foci.

Laboratory diagnosis of dysbacteriosis

The main method is bacteriological research. At the same time, quantitative indicators prevail in the evaluation of its results.

An additional method is chromatography of the spectrum of fatty acids in the material under study. Each genus has its own spectrum of fatty acids.

Correction of dysbacteriosis:

1) elimination of the cause;

2) the use of eubiotics and probiotics.

Eubiotics are preparations containing live bactericinogenic strains of normal microflora (colibacterin, bifidumbacterin, bifikol, etc.).

Probiotics are substances of non-microbial origin and foods containing additives that stimulate their own normal microflora. Stimulants - oligosaccharides, casein hydrolyzate, mucin, whey, lactoferrin, dietary fiber.

16. Classification of chemotherapy drugs

Chemotherapeutic drugs are medicinal substances used to suppress vital activity and destroy microorganisms in the tissues and environments of the patient, which have a selective, etiotropic effect.

According to the chemical structure, several groups of chemotherapeutic drugs are distinguished:

1) sulfa drugs (sulfonamides). They disrupt the process by which microbes obtain growth factors - folic acid and other substances. This group includes streptocid, norsulfazol, sulfametizol, sulfamethaxazole, etc.;

2) derivatives of nitrofuran. The mechanism of action is to block several enzyme systems of the microbial cell. These include furatsilin, furagin, furazolidone, nitrofurazon, etc.;

3) quinolones. Violate various stages of DNA synthesis of a microbial cell. These include nalidixic acid, cinoxacin, norfloxacin, ciprofloxacin;

4) azoles - imidazole derivatives. They have antifungal activity. They inhibit the biosynthesis of steroids, which leads to damage to the outer cell membrane of fungi and an increase in its permeability. These include clotrimazole, ketoconazole, fluconazole, etc.;

5) diaminopyrimidines. Violate the metabolism of microbial cells. These include trimethoprim, pyrimethamine;

6) antibiotics are a group of compounds of natural origin or their synthetic analogues.

Principles of classification of antibiotics.

1. According to the mechanism of action:

1) violating the synthesis of the microbial wall (b-lactam antibiotics; cycloserine; vancomycin, teikoplakin);

2) disrupting the functions of the cytoplasmic membrane (cyclic polypeptides, polyene antibiotics);

3) disrupting the synthesis of proteins and nucleic acids (a group of levomycetin, tetracycline, macrolides, lincosamides, aminoglycosides, fusidine, ansamycins).

2. By type of action on microorganisms:

1) antibiotics with a bactericidal effect (affecting the cell wall and cytoplasmic membrane);

2) antibiotics with bacteriostatic action (affecting the synthesis of macromolecules).

3. According to the spectrum of action:

1) with a predominant effect on gram-positive microorganisms (lincosamides, biosynthetic penicillins, vancomycin);

2) with a predominant effect on gram-negative microorganisms (monobactams, cyclic polypeptides);

3) a wide spectrum of action (aminoglycosides, chloramphenicol, tetracyclines, cephalosporins).

4. By chemical structure:

1) b-lactam antibiotics;

2) aminoglycosides (kanamycin, neomycin);

3) tetracyclines (tetracycline, metacycline);

4) macrolides (erythromycin, azithromycin);

5) lincosamines (lincomycin, clindamycin);

6) polyenes (amphotericin, nystatin);

7) glycopeptides (vancomycin, teikoplakin).

17. Main complications of chemotherapy

1. Complications from the macroorganism:

1) allergic reactions. The severity can be different - from mild forms to anaphylactic shock. The presence of an allergy to one of the drugs in the group is a contraindication for the use of other drugs in this group, since cross-sensitivity is possible;

2) direct toxic effect. Aminoglycosides have ototoxicity and nephrotoxicity, tetracyclines disrupt the formation of bone tissue and teeth. Ciprofloxacin can have a neurotoxic effect, fluoroquinolones can cause arthropathy;

3) side toxic effects. These complications are not associated with a direct, but with an indirect effect on various body systems. Antibiotics that affect protein synthesis and nucleic acid metabolism always depress the immune system. Chloramphenicol can inhibit protein synthesis in bone marrow cells, causing lymphopenia. Furagin, penetrating the placenta, can cause hemolytic anemia in the fetus;

4) aggravation reactions. When using chemotherapeutic agents in the first days of the disease, mass death of pathogens can occur, accompanied by the release of a large amount of endotoxin and other decay products. This may be accompanied by a deterioration in the condition up to toxic shock. These reactions are more common in children. Therefore, antibiotic therapy should be combined with detoxification measures;

5) development of dysbiosis. It often occurs against the background of the use of broad-spectrum antibiotics.

2. Complications from the microorganism manifested by the development of drug resistance. It is based on mutations in chromosomal genes or the acquisition of resistance plasmids.

The biochemical basis of resistance is provided by the following mechanisms:

1) enzymatic inactivation of antibiotics;

2) a change in the permeability of the cell wall for the antibiotic or suppression of its transport into bacterial cells;

3) change in the structure of microbial cell components.

Methods for combating drug resistance:

1) creation of new chemotherapeutic drugs;

2) the creation of combined drugs, which include chemotherapeutic agents of various groups that enhance the effect of each other;

3) periodic change of antibiotics;

4) compliance with the basic principles of rational chemotherapy:

a) antibiotics should be prescribed in accordance with the sensitivity of pathogens to them;

b) treatment should be started as early as possible;

c) chemotherapeutic drugs must be prescribed in maximum doses, preventing microorganisms from adapting.

18. Subject of immunology. Types of immunity

Immunology is a science whose subject of study is immunity.

Infectious immunology studies the patterns of the immune system in relation to microbial agents, specific mechanisms of antimicrobial protection.

Immunity is understood as a set of biological phenomena aimed at maintaining the constancy of the internal environment and protecting the body from infectious and other genetically alien agents.

Types of infectious immunity:

1) antibacterial;

2) antitoxic;

3) antiviral;

4) antifungal;

5) antiprotozoal.

Infectious immunity can be:

1) sterile (there is no pathogen in the body);

2) non-sterile (the pathogen is in the body).

Innate immunity to infectious diseases is present from birth. It can be specific and individual.

Species immunity is the immunity of one species of animal or person to microorganisms that cause disease in other species. It is genetically determined in humans as a biological species. Species immunity is always active.

Individual innate immunity is passive, as it is provided by the transfer of immunoglobulins to the fetus from the mother through the placenta (placental immunity).

Acquired immunity is called such immunity of the human body to infectious agents, which is formed in the process of its individual development. It is always individual. It can be natural and artificial.

Natural immunity can be:

1) active. Formed after an infection;

2) passive. Immunoglobulins of class A and I are transmitted to the child with mother's milk.

Artificial immunity can be created actively and passively. Active is formed by the introduction of antigenic preparations, vaccines, toxoids. Passive immunity is formed by the introduction of ready-made sera and immunoglobulins, i.e. ready-made antibodies.

Non-specific protective factors

Anti-infective protection is carried out:

1) skin and mucous membranes;

2) lymph nodes;

3) lysozyme and other enzymes of the oral cavity and gastrointestinal tract;

4) normal microflora;

5) inflammation;

6) phagocytic cells;

7) natural killers;

8) complement system;

9) interferons.

19. Immune system. Central and peripheral organs of the immune system

Organs of the immune system divided into:

1) primary (central thymus, bone marrow);

2) secondary (peripheral spleen, lymph nodes, tonsils, intestinal and bronchial associated lymphoid tissue).

The thymus gland (thymus) plays a leading role in the regulation of the population of T-lymphocytes. The thymus supplies lymphocytes.

The cortical layer is densely filled with lymphocytes, which are affected by thymic factors. In the medulla there are mature T-lymphocytes that leave the thymus and are included in the circulation as T-helpers, T-killers, T-suppressors.

The bone marrow supplies progenitor cells for various populations of lymphocytes and macrophages. It serves as the main source of serum immunoglobulins.

The spleen is colonized by lymphocytes in the late embryonic period after birth. In the white pulp there are thymus-dependent and thymus-independent zones, which are populated by T- and B-lymphocytes. Antigens entering the body induce the formation of lymphoblasts in the thymus-dependent zone of the spleen, and in the thymus-independent zone, proliferation of lymphocytes and the formation of plasma cells are noted.

Lymphocytes enter the lymph nodes through afferent lymphatic vessels.

The lymphatic follicles of the digestive tract and respiratory system serve as the main entry gate for antigens.

Immunocompetent cells of the human body are T- and B-lymphocytes.

T cells are involved in:

1) cellular immunity;

2) regulation of B-cell activity;

3) delayed hypersensitivity (IV) type.

The following subpopulations of T-lymphocytes are distinguished:

1) T-helpers. Programmed to induce reproduction and differentiation of other cell types;

2) suppressor T cells. Genetically programmed for suppressive activity;

3) T-killers. They secrete cytotoxic lymphokines.

The main function of B-lymphocytes is that, in response to an antigen, they are able to multiply and differentiate into plasma cells that produce antibodies.

B-lymphocytes are divided into two subpopulations: B1 and B2.

B1-lymphocytes undergo primary differentiation in Peyer's patches, then they are found on the surface of serous cavities. During the humoral immune response, they are able to turn into plasma cells that synthesize only IgM.

B2-lymphocytes undergo differentiation in the bone marrow, then in the red pulp of the spleen and lymph nodes.

Memory B-cells are long-lived B-lymphocytes derived from mature B-cells as a result of antigen stimulation with the participation of T-lymphocytes.

20. Immune response. The concept of form

The immune response is a chain of successive complex cooperative processes that occur in the immune system in response to the action of an antigen in the body.

Distinguish:

1) primary immune response;

2) secondary immune response.

Any immune response consists of two phases:

1) inductive (representation and recognition of the antigen);

2) productive (products of the immune response are detected).

Further, the immune response is possible in the form of one of three options:

1) cellular immune response;

2) humoral immune response;

3) immunological tolerance.

The cellular immune response is a function of T-lymphocytes. There is the formation of effector cells - T-killers, capable of destroying cells that have an antigenic structure by direct cytotoxicity and by the synthesis of lymphokines, which are involved in the processes of cell interaction (macrophages, T-cells, B-cells) during the immune response. Two subtypes of T cells are involved in the regulation of the immune response: T-helpers enhance the immune response, T-suppressors have the opposite effect.

Humoral immunity is a function of B cells. T-helpers that have received antigenic information transmit it to B-lymphocytes. B-lymphocytes form a clone of antibody-producing cells. In this case, B-cells are converted into plasma cells that secrete immunoglobulins (antibodies) that have specific activity against the introduced antigen.

The resulting antibodies interact with the antigen with the formation of an AG-AT complex, which triggers nonspecific mechanisms of a protective reaction. These complexes activate the complement system. The interaction of the AG-AT complex with mast cells leads to degranulation and the release of inflammatory mediators - histamine and serotonin.

At a low dose of the antigen, immunological tolerance develops. In this case, the antigen is recognized, but as a result of this, neither cell production nor the development of a humoral immune response occurs.

The immune response is characterized by:

1) specificity (reactivity is directed only to a specific agent, which is called an antigen);

2) potentiation (the ability to produce an enhanced response with a constant intake of the same antigen in the body);

3) immunological memory (the ability to recognize and produce an enhanced response against the same antigen when it enters the body again, even if the first and subsequent hits occur at long intervals).

21. Classifications and types of antigens

Antigens are high molecular weight compounds. When ingested, they cause an immune reaction and interact with the products of this reaction.

Classification of antigens.

1. By origin:

1) natural (proteins, carbohydrates, nucleic acids, bacterial exo- and endotoxins, tissue and blood cell antigens);

2) artificial (dinitrophenylated proteins and carbohydrates);

3) synthetic (synthesized polyamino acids).

2. By chemical nature:

1) proteins (hormones, enzymes, etc.);

2) carbohydrates (dextran);

3) nucleic acids (DNA, RNA);

4) conjugated antigens;

5) polypeptides (polymers of a-amino acids);

6) lipids (cholesterol, lecithin).

3. By genetic relation:

1) autoantigens (from the tissues of one's own body);

2) isoantigens (from a genetically identical donor);

3) alloantigens (from an unrelated donor of the same species);

4) xenoantigens (from a donor of another species).

4. By the nature of the immune response:

1) thymus-dependent antigens;

2) thymus-independent antigens.

Also distinguish:

1) external antigens (enter the body from outside);

2) internal antigens; arise from damaged body molecules that are recognized as foreign;

3) latent antigens - certain antigens (for example, nervous tissue, lens proteins and spermatozoa); anatomically separated from the immune system by histohematic barriers during embryogenesis.

Haptens are low molecular weight substances that under normal conditions do not cause an immune response, but when bound to high molecular weight molecules become immunogenic.

Infectious antigens are antigens of bacteria, viruses, fungi, protozoa.

Varieties of bacterial antigens:

1) group-specific;

2) species-specific;

3) type-specific.

According to localization in a bacterial cell, they distinguish:

1) O - AG - polysaccharide (part of the cell wall of bacteria);

2) lipid A - heterodimer; contains glucosamine and fatty acids;

3) H - AG; is part of bacterial flagella;

4) K - AG - a heterogeneous group of surface, capsular antigens of bacteria;

5) toxins, nucleoproteins, ribosomes and bacterial enzymes.

22. Antibodies. Classifications and properties

Antibodies are proteins that are synthesized under the influence of an antigen and react specifically with it.

There are four structures in an immunoglobulin molecule:

1) primary - this is the sequence of certain amino acids;

2) secondary (determined by the conformation of polypeptide chains);

3) tertiary (determines the nature of the location of individual sections of the chain that create a spatial picture);

4) Quaternary. A biologically active complex arises from four polypeptide chains.

Most immunoglobulin molecules are composed of two heavy (H) chains and two light (L) chains linked by disulfide bonds. Light chains consist of either two k-chains or two l-chains. Heavy chains can be one of five classes (IgA, IgG, IgM, IgD and IgE).

Each circuit has two sections:

1) permanent;

2) variable (in this part of the chain, the reaction of the compound with the antigen occurs).

During the enzymatic cleavage of immunoglobulins, the following fragments are formed:

1) Fc-fragment contains sections of both permanent parts; does not have the property of an antibody;

2) Fab-fragment contains light and part of the heavy chain with a single antigen-binding site; has the property of an antibody;

3) F(ab)T2-fragment consists of two interconnected Fab-fragments.

There are five classes of immunoglobulins in humans.

1. Immunoglobulins G are monomers that include four subclasses (IgG1; IgG2; IgG3; IgG4).

Properties of immunoglobulins G:

1) The main role in humoral immunity;

2) form anti-infective immunity in newborns;

3) able to neutralize bacterial exotoxins.

2. Immunoglobulins M: (IgM1 and IgM2).

Properties of immunoglobulins M:

1) do not cross the placenta;

2) appear in the fetus and participate in anti-infective protection;

3) are able to agglutinate bacteria, neutralize viruses, activate complement;

4) play an important role in the elimination of the pathogen;

5) are formed in the early stages of the infectious process;

6) are highly active in the reactions of agglutination, lysis and binding of endotoxins of Gram-negative bacteria.

3. Immunoglobulins A are secretory immunoglobulins that include two subclasses: IgA1 and IgA2.

4. Immunoglobulins E. This class includes the bulk of allergic antibodies - reagins. The level of IgE is significantly increased in people with allergies and infected with helminths.

5. Immunoglobulins D are monomers.

23. Immunodeficiency states

Immunodeficiency states are called violations of the immune status and the ability to a normal immune response to various antigens.

Immunodeficiency states are divided into:

1) congenital;

2) acquired.

According to the level of the defect in the immune system, there are:

1) predominant defects in the B-system;

2) predominant defects of the T-system;

3) combined defects of T- and B-systems.

Main reasons immunodeficiency states:

1) infections accompanied by the reproduction of the pathogen directly in the cells of the immune system (AIDS virus, infectious mononucleosis). Infected immunocompetent cells can be destroyed under the action of the pathogen itself, its components or waste products (toxins, enzymes), as well as due to a specific immune response of the body directed against microbial agents included in the cell membrane;

2) violation of the processes of immunoregulation during the infection. At the same time, the ratio of regulatory subpopulations of T-helpers and T-suppressors is disturbed;

3) congenital or acquired metabolic and hormonal defects occurring in diseases such as diabetes mellitus, obesity, uremia, malnutrition, etc.;

4) immunoproliferative diseases;

5) the use of immunosuppressive drugs.

Immunodeficiency states lead to the emergence of opportunistic infections caused by opportunistic microorganisms, tumors, allergic and autoimmune processes.

For infectious diseases that have arisen against the background of immunodeficiency states, the following are characteristic:

1) recurrence of acute infections;

2) protracted, sluggish nature of diseases;

3) a pronounced tendency to generalize the infectious process;

4) high risk of chronic diseases with frequent subsequent exacerbations and steadily progressive course of the pathological process;

5) early, rapid accession of opportunistic microflora;

6) the leading role of mixed infection in the formation of the inflammatory process;

7) unusual pathogens;

8) atypical forms of diseases;

9) severe course of diseases;

10) opportunistic infections;

11) resistance to standard therapy.

24. Allergy, classification of allergens, features of infectious allergy

Allergy - this is a state of increased sensitivity of the body to re-sensitization by antigens.

Allergy occurs on the re-introduction of the allergen. Allergens are antigens to which an allergic reaction occurs in the body. Allergens can have different origin:

1) household;

2) medicinal;

3) animal origin;

4) vegetable;

5) food;

6) infectious.

Allergies may be based on a humoral and cellular immune response. According to the mechanisms and clinical manifestations, four types of allergies are distinguished.

1. Anaphylactic. Ag-AT complexes are formed, which are fixed on various target cells, mast cells, basophils, sensitizing them to the corresponding allergen. When the allergen enters the body again, allergy mediators are released.

2. Cytotoxic. With repeated sensitization, the resulting AG-AT complex leads to cytolysis - the death of one's own cells.

3. Immunocomplex. With the repeated introduction of the antigen, an excess of the AG-AT complex leads to a powerful activation of the complement.

4. Cellular. It is based on a cellular immune response. T-killers are responsible for the development of the reaction. Delayed-type hypersensitivity develops. Underlies infectious allergies.

infectious allergen - a weak allergen, the state of allergy develops only in its presence.

Infectious allergy develops:

1) in the chronic form of dysentery, gonorrhea, tuberculosis, in the tertiary period of syphilis; in this case, gummas are formed - tumor-like growths of lymphoid tissue;

2) with especially dangerous infections: plague, anthrax, tularemia, brucellosis;

3) with deep mycoses;

4) during the period of convalescence with typhoid and paratyphoid diseases.

With a number of infections, an allergological diagnostic method can be used,

1) for tuberculosis - Mantoux test with tuberculin;

2) in the chronic form of dysentery - Tsuverkalov's test;

3) in case of gonorrhea - test with gonovaccine;

4) with brucellosis - Burne test with brucellin;

5) with tularemia - a test with tularemine;

6) with anthrax - a test with anthraxin.

Positive allergic tests are given by patients, bacterial carriers and those vaccinated with a live vaccine.

25. Autoimmune processes

Autoimmune processes are such conditions in which the production of autoantibodies occurs (or the accumulation of a clone of sensitized lymphocytes to the antigens of the body's own tissues).

When autoimmune mechanisms cause a violation of the structure and functions of organs and tissues, they speak of autoimmune aggression and autoimmune diseases.

The mechanisms of immune tissue damage are similar to immune damage induced by exoallergens - according to the type of delayed and immediate types of hypersensitivity.

There are several mechanisms for the formation of autoantibodies. One of them is the formation of autoantibodies against natural, primary antigens of immunologically barrier tissues.

There are three mechanisms for inducing an autoimmune response (autosensitization):

1) the formation of autoantigens;

2) the emergence or depression of clones of T- and B-lymphocytes that carry receptors for the determinants of their own tissues (tolerance cancellation);

3) reproduction in the body of microorganisms containing cross-reacting antigens.

An autoimmune response can develop as a result of immunization with the body's own antigens, to which tolerance has not been developed (or it has been lost). As a result, the immune system, upon contact with autoantigens, reacts with them as if they were foreign.

Loss of natural immunological tolerance to certain antigens may be the result of:

1) antigenic stimulation with modified or cross-reacting antigens;

2) violations of immunoregulatory subpopulations of T-lymphocytes.

Autoimmunization is possible under the action of cross-reacting antigens, which are found in many bacteria and viruses. When they enter the body, they are recognized by the corresponding clones of T-helper cells, which activate B-lymphocytes to the immune response. This may result in self-aggression.

During infections and some destructive processes in the cells of the body, previously hidden antigenic determinants can be exposed (desquamated), against which the autoimmune process begins.

Autoimmune processes can occur with primary changes in the immune system - with lymphoproliferative diseases (leukemia). In this case, the reproduction of the "forbidden" clone of lymphocytes occurs.

26. Methods of immunodiagnostics

Immunodiagnostics is the use of immune reactions to diagnose infectious and non-infectious diseases.

Immunity reactions are the interaction of an antigen with the products of an immune response. In any immune reaction, two phases are distinguished:

1) specific - due to the interaction of the antigen with the antibody and the formation of the AG-AT complex;

2) non-specific.

All immune reactions are divided into:

1) simple; two components are involved (antigen and antibody);

2) complex; three or more components are involved (antigen, antibody, complement, etc.).

Also distinguish:

1) direct (the result is taken into account visually);

2) indirect (requires special indication systems).

The following immune responses are used.

1. An agglutination reaction is the adhesion and precipitation of a corpuscular antigen under the action of an antibody in the presence of an electrolyte.

There are the following modifications of the agglutination reaction:

1) passive hemagglutination reaction (RPHA);

2) latex agglutination;

3) co-agglutination;

4) antiglobulin test (Coombs reaction).

2. The precipitation reaction is the precipitation of an antigen from a solution under the action of an antibody of a precipitating serum in the presence of an electrolyte.

3. The complement fixation reaction (RCC) is a complex, multicomponent indirect immune response. Includes two systems:

1) the test, consisting of an antigen and an antibody (one of them is unknown), to which a complement is also introduced;

2) indicator, consisting of sheep erythrocytes and hemolytic serum containing antibodies to them.

If the antigen and antibody match each other in the system under study, then they form a complement-binding complex. In this case, there will be no changes in the indicator system. If the antigen and antibody do not correspond to each other in the system under study, then the AG-AT complex is not formed, the complement remains free. It binds to the AG-AT complex of the indicator system and thereby causes hemolysis of erythrocytes.

4. Reactions involving labeled antigens or antibodies:

1) radioimmunoassay (RIA) (based on the use of antibodies labeled with radioactive iodine or hydrogen);

2) immunofluorescence reaction (based on the fact that immune serum antibodies are labeled with fluorochromes);

3) enzyme immunoassay (ELISA) (the reaction component is labeled with an enzyme).

5. Toxin neutralization reaction (to determine the type of pathogen toxin). A mixture of toxin and antitoxic serum is injected into white mice, and if they match, i.e., are neutralized, the mice do not die.

27. Immunoprophylaxis, immunotherapy, immunocorrection

Immunoprophylaxis - this is the use of immunological patterns to create artificial acquired immunity (active or passive).

For immunoprophylaxis use:

1) antibody preparations (vaccines, toxoids), upon administration of which artificial active immunity is formed in a person;

2) antibody preparations (immune sera), with the help of which artificial passive immunity is created.

Vaccines are called antigenic preparations derived from pathogens or their structural analogues.

According to the method of preparation, they distinguish:

1) live vaccines (from avirulent strains of the pathogen);

2) killed vaccines. They are prepared from microorganisms inactivated by heating, UV rays, chemicals, under conditions that exclude the denaturation of antigens;

3) chemical vaccines. They contain chemically pure antigens of pathogens. Possess weak immunogenicity;

4) genetically engineered vaccines;

5) combined vaccines;

6) associated vaccines. They are a complex of killed vaccine and toxoid.

Anatoxins are antigenic preparations obtained from exotoxins during their sterilization treatment.

These sera are introduced into the human body fractionally according to the Bezredk method in order to avoid anaphylactic shock.

The unit of action of antitoxic serum is 1 IU.

1 IU is the minimum amount of antitoxic serum that can neutralize 100 lethal doses of the corresponding exotoxin.

Immunotherapy - is the use of immunological patterns for the treatment of patients. The goal of immunotherapy is to enhance specific defense mechanisms against microbial agents.

With chronic sluggish diseases. In this case, antigenic preparations are administered (therapeutic vaccines (always killed)).

In the treatment of acute severe generalized forms of infectious diseases, antibody preparations are used - antitoxic and antibacterial immune sera, immunoglobulins, plasma.

Immunocorrection - a modern trend in the treatment of infectious and non-infectious diseases. Use:

1) immunosuppressants (suppress immunity);

2) immunostimulants (stimulate the immune system);

3) immunomodulators.

These drugs may be:

1) exogenous origin;

2) endogenous origin;

3) synthetic.

28. General characteristics and classification of the Enterobacteriaceae family

The Enterobacteriaceae family includes numerous representatives that share a common habitat - the intestines.

Enterobacteria are divided into:

1) pathogenic (shigella, salmonella, escherichia, yersinia, etc.);

2) conditionally pathogenic (37 genera).

All pathogenic enterobacteria can cause acute intestinal infections in humans, opportunistic pathogens - purulent-inflammatory diseases and food poisoning.

Enterobacteria are gram-negative rods of medium size with rounded ends, arranged randomly. They are facultative anaerobes.

Colonies of the same type are formed on meat-peptone agar. (Medium size, round, smooth, convex, shiny, colorless). They grow in meat-peptone broth, giving a uniform turbidity.

All enterobacteria:

1) ferment glucose to acid or to acid and gas;

2) reduce nitrates to nitrites;

3) catalase +, oxidase -, OF-test ++.

Enterobacteria antigens consist of:

1) O-antigen, which is localized in the cell wall;

2) K-antigen (this is a surface, capsular antigen);

3) H-antigen (thermolabile, flagellar);

4) pilifimbrial antigen; it is present in bacteria that have villi, pili, fimbriae.

The classification of enterobacteria is based on their biochemical properties. According to Bergey's classification, the family of Enterobacteria is divided into 40 genera, genera - into species. In some cases, intraspecific differentiation into:

1) fermenters;

2) serogroups and serovars;

3) fagovars;

4) ringworms.

Intestinal infection is the result of the interaction of the pathogen with the corresponding structures of the macroorganism under the necessary environmental conditions. This process consists of several phases:

1) adhesion;

2) invasions;

3) colonization;

4) production of exo- and enterotoxins.

Adhesion occurs in two stages:

1) non-specific adhesion (approximation);

2) specific adhesion (as a result of ligand-specific interaction of the corresponding structures of enterobacteria (villi, fimbriae) and receptors of the plasmolemma of epithelial cells).

Invasion - the penetration of bacteria into epithelial cells with or without reproduction.

Invasion, colonization and production of toxins are expressed to varying degrees in different enterobacteria, so the pathogenesis and clinic of intestinal infections differ significantly.

29. Genus Escherichia, genus Shigella. Their characteristics

The genus Escherihia includes seven species. The most important species is E. coli, which are divided by pathogenicity into:

1) pathogenic (diarrheal);

2) conditionally pathogenic.

Diseases caused by Escherichia are divided into two groups:

1) endogenous co-infections;

2) exogenous coli infections - escherichiosis. Pathogenic E. coli are divided into four main classes.

1. ETEC - enterotoxigenic Escherichia coli. They have a tropism for the epithelium of the small intestine. Clinically, the disease proceeds as a mild form of cholera.

2. EIEC - enteroinvasive coli. They have a tropism for the epithelial cells of the large intestine.

3. EPEC - enteropathogenic Escherichia coli. Cause enterocolitis in children under one year old. The epithelium of the small intestine is affected.

4. EHEC - enterohemorrhagic Escherichia coli. They have a tropism for the epithelial cells of the large intestine. Cause hemocolitis.

The main diagnostic method is bacteriological examination.

Shigella belong to the genus Shigella. They are the causative agents of dysentery. The genus includes four species:

1) Sh. disenteriae; (within the species they are divided into 12 serovars; one of them is shigella Grigorieva-Shiga);

2) Sh. flexneri; (divided into 6 serovars);

3) Sh. boydii; (divided into 18 serovars);

4) Sh. sonnei; (antigenically, the species is homogeneous; fermentovars, fagovars, and koletsinovars are distinguished within the species).

Shigella enter the large intestine. They attach to colonocyte membrane receptors and penetrate through the outer membrane protein. Cell death leads to the formation of erosions and ulcers surrounded by perifocal inflammation.

Pathogenic factors:

1) outer membrane proteins;

2) contact hemolysin;

3) exotoxin;

4) endotoxin.

Clinical forms of dysentery:

1) Grigoriev-Shiga dysentery. Pathogen - Sh. disenteriae, serovar - Shigella Grigorieva-Shiga. Ways of transmission - alimentary, contact-household. It proceeds hard, bloody diarrhea with blood, symptoms of CNS damage are characteristic;

2) Flexner's dysentery. Pathogens - Sh. flexneri and Sh. boydii. Water transmission route. It proceeds like a typical dysentery;

3) Sonnei dysentery. food transmission route. There may be symptoms of food poisoning, vomiting.

Diagnostics:

1) bacteriological examination;

2) immunoindication (ELISA);

3) serodiagnosis (has a retrospective value).

30. Salmonella genus, Yersinia genus. Their characteristics

The bacteria are motile and do not form spores or capsules.

on simple nutrient media. They form small transparent colonies.

Antigenic structure:

1) O-antigen;

2) H-antigen.

Salmonella can cause two groups of diseases:

1) anthroponotic - typhoid fever and paratyphoid A and B; pathogens: S. typhi, S. paratyphi A, S. paratyphi B;

2) zooanthroponic - salmonellosis; pathogens: S. typhimurium, S. haifa, S. anatum, S. panama, S. infantis.

Typhoid fever and paratyphoid A and B are combined into one group - typhoid and paratyphoid diseases. The source of infection is a patient (or a bacteriocarrier).

The disease includes five phases.

1. The phase of the introduction of the pathogen into the body (corresponds to the incubation period of the disease).

2. Phase of primary localization (corresponds to the prodromal period).

3. The phase of bacteremia (the onset of the disease).

4. Phase of secondary localization: (height of the disease).

5. The excretory-allergic phase (ulcers form on the mucous membrane).

The outcome of the disease can be different:

1) recovery;

2) formation of carriage;

3) lethal.

Etiotropic therapy: antibiotics.

Specific prophylaxis: killed typhoid vaccine.

Salmonellosis. Sources of infection - sick animals, infected food. The route of infection is alimentary. Runs like a food poisoning.

The genus Yersinia contains seven species, of which Y. pestis (the causative agent of plague), Y. pseudotuberculesis (the causative agent of pseudotuberculosis), Y. enterocolitica, the causative agent of acute intestinal infections, intestinal yersiniosis, are pathogenic for humans.

Y. enterocolitica is a Gram-negative motile rod that does not form spores or capsules. Cultivated on simple nutrient media at a temperature of 20-26 °C.

yersiniosis - zooanthroponic diseases. Reservoir - various rodents that excrete bacteria in feces and urine. The route of infection is alimentary.

Y. enterocolitica are facultative intracellular parasites.

There are four phases in pathogenesis.

1. Implementation.

2. Enteral (enterocolitis and lymphadenitis).

3. Bacteremia: (sepsis and scarlet fever).

4. Secondary focal and allergic manifestations. (hepatitis, arthritis, urticaria).

31. Food poisoning and food toxicosis

Food poisoning (FTI) is a large group of acute intestinal infections that develop after eating foods contaminated with pathogens and their toxins.

Food poisoning can be caused by:

1) salmonella;

2) shigella;

3) conditionally pathogenic microorganisms;

4) enterotoxic strains of staphylococcus;

5) streptococci;

6) spore anaerobes (Clostridium perfringens);

7) spore aerobes (Bac. cereus);

8) halophilic vibrios (Vibrio parahaemolyticus), etc.

Most often they are caused by salmonella and opportunistic pathogens that are widespread in the environment.

In general, this group of diseases is characterized by a short incubation period, acute onset and rapid development, a combination of signs of damage to the gastrointestinal tract and severe intoxication.

There are some features of the clinical picture, depending on the type of pathogen.

Diagnostics:

1) bacteriological examination of excretions of patients, food products;

2) serodiagnosis.

Food toxicosis is a disease that occurs when eating food containing exotoxins of the pathogen, while the pathogen itself does not play a decisive role in the development of the disease.

Cl. botulinum are Gram-positive large rods. They form subterminally located spores. Capsules do not. Strict anaerobes.

The natural habitat of Clostridium botulism is the intestines of fish, animals, microorganisms enter the soil with feces. Able to persist and multiply in the external environment for a long time in the form of spore forms.

According to the antigenic structure of the produced toxins, serovars A, B, C1, D, E, F, Q are distinguished. The antigenic specificity of the bacteria themselves is not determined.

Clostridium botulism produces the most powerful of the exotoxins - botulinum. Botulinum toxin accumulates in the food product, multiplying in it. Such products are usually home-made canned food, raw smoked sausages, etc.

The toxin has a neurotropic effect, it affects the medulla oblongata and the nuclei of the cranial nerves, it is quickly absorbed into the bloodstream and enters the neuromuscular synapses.

There are general intoxication, signs of damage to the organ of vision - double vision, accommodation disorder, dilated pupils, damage to the oculomotor muscles. At the same time, swallowing becomes difficult, aphonia, headache, dizziness, and vomiting appear.

Treatment: antitoxic anti-botulinum serum.

32. Plague. anthrax

Plague belongs to the genus Yersinia, species Y. pestis.

These are gram-negative polymorphic small rods with rounded ends. They are motionless. Dispute does not form.

They are facultative anaerobes.

Yersinia plague can remain viable for a long time in the environment and in the body.

Plague wand antigens:

1) O-antigen;

2) F-antigen;

3) V- and W-antigens (have antiphagocytic activity).

The main hosts of Yersinia plague in nature are rodents (ground squirrels, tarbagans, etc.). Infection of a person occurs transmissible (carriers - fleas), contact and alimentary routes. Patients with the pneumonic form of plague infect others by aerogenic means.

The clinical manifestations of plague depend on the entrance gate of infection. There are the following forms of the disease:

1) skin-bubonic;

2) primary pulmonary;

3) secondary pulmonary;

4) primary septic;

5) secondary septic.

The main breeding site of the pathogen is the lymph nodes.

After the illness, a strong long-term immunity remains.

anthrax

The causative agent belongs to the genus Bacillus, species B. anthracis.

They are Gram-positive, large, non-motile rods. Outside the body in the presence of oxygen form spores.

The causative agent is an aerobe or a facultative anaerobe. It reproduces well on simple nutrient media.

Pathogenicity factors (Toxin, Capsule).

Under natural conditions, anthrax affects animals: large and small cattle, horses, pigs, deer, camels. The pathological process develops in the intestine.

A person becomes infected from sick animals through direct contact, through infected objects, products from contaminated raw materials, meat of sick animals. Transmissible transmission is possible.

Clinical forms of the disease:

1) skin - the formation of a carbuncle;

2) intestinal - intoxication, vomiting, nausea, diarrhea with blood;

3) pulmonary - severe bronchopneumonia.

In those who have been ill, a strong immunity is created.

33. Tularemia. Brucellosis

Tularemia belongs to the genus Francisella, species F. tularensis.

These are very small polymorphic, coccoid or rod-shaped gram-negative bacteria. Dispute does not form.

facultative anaerobes. They do not grow on simple nutrient media. Reproduction requires the introduction of cysteine into the medium.

In the environment, the pathogen remains viable for a long time. Not resistant to high temperatures.

The pathogenicity factor is endotoxin.

The natural hosts of the pathogen are rodents (water rats, voles, house mice, hamsters, hares).

Human infection occurs through direct contact with sick animals or dead bodies, through contaminated water and food. Carriers of the disease can be ticks, mosquitoes, horseflies.

Clinical forms of tularemia:

1) bubonic;

2) anginal-bubonic;

3) intestinal;

4) pulmonary;

5) primary septic.

After that, immunity remains.

Treatment: antibiotics are used - streptomycin, tetracycline, chloramphenicol.

Specific prophylaxis: Gaisky-Elbert live vaccine; immunity is created for 5-6 years.

Brucellosis

The causative agent belongs to the genus Brucella.

Three species are pathogenic for humans: B. melitensis, B. abortus, B. suis.

These are small Gram-negative coccobacilli. They do not have flagella. Dispute does not form.

Brucella are demanding on nutrient media. (media with the addition of blood serum, glucose, thiamine, biotin).

They are strict aerobes.

They are highly resistant to environmental factors.

Brucella antigens:

1) Vi-antigen (surface);

2) somatic species-specific antigens A and B.

Pathogenic factors:

1) endotoxin;

2) aggression and defense enzymes: hyaluronidase, etc.;

3) the ability to multiply in the cells of the lymphoid-macrophage system.

The natural hosts of the pathogen are different depending on the species: B. melitensis causes the disease in small cattle, B. abortus in cattle, B. suis in pigs. A person becomes infected by contact, alimentary and airborne droplets.

More often, the disease is of a professional nature - livestock breeders, workers of meat-packing plants, livestock specialists get sick.

The pathogen is able to enter the body through intact mucous membranes.

34. Staphylococci. Streptococci. Their characteristics

Staphylococci. Family Staphilococcoceae, genus Staphilicoccus.

They are the causative agents of staphylococcal pneumonia, neonatal staphylococcus, sepsis, pemphigus.

According to biochemical properties are divided into types:

1) St. aureus (has many pathogenicity factors);

2) St. epidermidis (affects the skin);

3) St. saprophiticus (genitourinary tract parasite).

Staphylococcal antigens are divided into:

1) extracellular (variant-specific proteins of exotoxins and exoenzymes);

2) cellular:

a) surface (glycoproteins);

b) deep (teichoic acids).

Factors of pathogenicity of staphylococci.

1. The role of adhesins is performed by complexes of surface proteins of the cell wall with teichoic acids.

2. Hyaluronidase is an invasion factor.

3. Enzymes of aggression: plasmacoagulase, fibrinolysin, lecithinase, phosphatases, phosphotidase, exonucleases, proteases.

4. Toxins:

1) hematolysins (a, b, g, d, e);

2) hemotoxins (responsible for the development of toxic shock);

3) leukocidin;

4) exofoliative exotoxin;

5) enterotoxins (A, B, C, D, E).

1. Chemotherapy - antibiotics, sulfonamides.

2. Phage therapy - polyvalent phages.

3. Immunotherapy:

1) staphylococcal toxoids;

2) therapeutic autovaccines;

3) finished antibody preparations.

Specific prevention: staphylococcal toxoid (active).

Streptococcus

They belong to the family Streptococcaceae, genus Streptococcus.

These are gram-positive cocci, arranged in chains or in pairs in smears. They are facultative anaerobes.

streptococcal antigens.

1. Extracellular - proteins and exoenzymes.

2. Cellular: superficial, deep.

pathogenicity factors.

1. Teichoic acid complexes with surface proteins.

2. M-protein (possesses antiphagocytic activity).

3. OF-protein - an enzyme that causes hydrolysis of blood serum lipoproteins, reducing its bactericidal properties:

1) OF+ strains (rheumatogenic);

2) OF-strains (nephritogenic); primary adhesion to the skin.

4. Enzymes of aggression and defense: hyaluronidase, streptokinase, streptodornase, proteases, peptidases,

5. Exotoxins:

1) hemolysins: O- and S-streptolysin;

2) erythrogenin (has a pyrogenic effect).

35. Meningococcus. Gonococcus. Their characteristics

meningococcibelong to the genus Neisseria, genus N. meningitidis.

These are bean-shaped diplococci, in smears they look like coffee beans. They do not form spores, they do not have flagella, they form a capsule in the body. Gram negative. Strict aerobes.

Meningococci are demanding on nutrient media - they grow only on media containing human protein.

Meningococcal virulence factors:

1) adhesins - fimbriae (drank);

2) endotoxin;

3) aggression enzymes - hyaluronidase, neuraminidase;

4) surface proteins with anti-lysozyme activity;

5) siderophores are cellular inclusions that actively bind ferric iron, competing with erythrocytes.

Meningococci are pathogenic only for humans.

Meningococcal infection is an anthroponotic infection, the source is a patient (or a bacteriocarrier). The main route of transmission is airborne.

After the disease, a stable species-specific antimicrobial immunity is formed. Young children have passive immunity due to IgG obtained from the mother.

Treatment: etiotropic therapy: sulfonamides, penicillins, chloramphenicol.

Specific prevention:

1) chemical meningococcal vaccine;

2) human immunoglobulin.

Gonococci

They belong to the genus Neisseria, species N. gonorrhoeae.

These are bean-shaped diplococci.

They do not form spores, are immobile, form a microcapsule, Gram-negative. They are obligate aerobes.

Gonococci are extremely demanding on nutrient media; they grow only on media containing human proteins.

Gonococcal infection is an anthroponotic infection, the source of infection is a sick person, there is no carriage. The path of sexual transmission, it is possible to infect a newborn when passing through the birth canal of a sick mother.

Clinical forms of gonococcal infection:

1) gonorrhea (urogenital, extragenital);

2) gonococcal septicopyemia;

3) specific conjunctivitis of newborns.

Distinguish:

1) fresh gonorrhea (lasting no more than 2 months):

a) sharp;

b) subacute;

c) torpid;

2) chronic gonorrhea (sluggish disease lasting more than 2 months or with an unspecified period).

According to the clinical course, there are:

1) uncomplicated gonorrhea;

2) complicated gonorrhea.

Treatment: etiotropic antibiotic therapy.

Specific prophylaxis has not been developed.

36. Haemophilus influenzae. Pseudomonas aeruginosa

Haemophilus influenzae. Family Pasterellaceae, genus Haemophilus, species H. influenza.

These are straight rods, non-spore-forming, immobile, gram-negative, aerobes. In the body form a capsule.

For cultivation, nutrient media containing blood (blood agar) or its preparations (chocolate agar) are required.

Pathogenic factors:

1) endotoxin;

2) capsular polysaccharide with antiphagocytic activity.

Does not produce exotoxin.

Haemophilus influenzae can be part of the normal microflora of the mucous membrane of the oropharynx and upper respiratory tract, so the infection can occur as endogenous.

With exogenous infection, it causes infections of the ENT organs and respiratory organs (otitis media, pneumonia), meningitis. The route of transmission is airborne. The source of infection is a patient or a bacteriocarrier (anthroponotic infection).

Most often, the disease develops as a secondary infection with a decrease in the overall resistance of the organism.

Bacterial meningitis caused by Haemophilus influenzae occurs most often in children aged 6 months to 3 years.

Pseudomonas aeruginosa

Belongs to the family Pseudomonadaceae, genus Pseudomonas, species P. aerugenosa. These are straight or slightly curved rods of medium size, mobile, gram-negative, obligate aerobes. They do not form spores, they have a thin mucous capsule.

Pseudomonas aeruginosa is undemanding to nutrient media, grows well on artificial nutrient media. The ability of pseudomonads to form pigments is the most characteristic differential diagnostic feature.

The culture of Pseudomonas aeruginosa when cultivated on nutrient media has a specific smell of jasmine.

Stable in the external environment. It is naturally resistant to antibiotics.

Pseudomonas aeruginosa can live in the human intestine, found on the skin and mucous membranes.

Most often, Pseudomonas aeruginosa infection is nosocomial. Source - the patient (or bacteriocarrier). Can cause various diseases. Especially often allocated with purulent-inflammatory complications of burn wounds.

Etiotropic therapy:

1) antibiotics (cephalosporins, aminoglycosides);

2) Pseudomonas aeruginosa bacteriophage;

3) Pseudomonas aeruginosa immune plasma;

4) killed therapeutic staphylo-Protein-Pseudomonas aeruginosa vaccine.

37. Klebsiella. Proteus

Klebsiella. The genus Klebsiella includes several species pathogenic to humans. The most significant are K. pneumoniae, K. ozaenae, K. rhinoscleromatis.

These are gram-negative rods of medium size that do not form spores. facultative anaerobes. In preparations, they are arranged singly, in pairs or in short chains. They do not have flagella, are immobile. Dispute does not form.

These are truly capsular bacteria.

Undemanding to nutrient media.

Klebsiella are resistant to environmental factors.

Pathogenic factors:

1) have pronounced adhesive properties;

2) a capsule that protects against phagocytosis;

3) have a K-antigen that suppresses phagocytosis;

4) secrete endotoxin.

Sources of infection can be a patient, a bacteriocarrier, objects of the external environment. Ways of transmission - airborne, contact-household.

K. pneumoniae can cause pneumonia in humans, damage to the joints, meninges, urinary organs, purulent postoperative complications, and sepsis.

K. ozaenae infects the mucous membrane of the upper respiratory tract and paranasal sinuses, causing them to atrophy.

K. rhinoscleromatis affects the nasal mucosa, trachea, bronchi, pharynx, and larynx.

Post-infection immunity is unstable.

Etiotropic therapy:

1) antibiotics, fluoroquinolones;

2) killed therapeutic vaccine Solko-Urovak;

3) VP-4 vaccine (for the treatment of respiratory tract infections).

Specific prophylaxis: IRS19 vaccine.

Proteus

Genus Proteus. The causative agent of purulent-inflammatory diseases is the species P. mirabilis.

These are polymorphic gram-negative rods with rounded ends, facultative anaerobes. There is no capsule formation. They have peritrichous flagella. Undemanding to nutrient media. During cultivation, a putrefactive odor is characteristic.

Resistant to the environment.

Pathogenic factors:

1) adhesins - drank;

2) endotoxin;

3) pathogenic amines - indole, skatole;

4) enzymes of aggression - proteases.

Their main habitat is objects of the external environment, rotting products, sewage, soil. Sources of infection for a person can be a patient and a bacteriocarrier.

Bacteria are involved in the development of purulent-inflammatory diseases of the urinary tract, quickly spread over the burn surface, giving a characteristic putrid odor.

Etiotropic therapy:

1) antibiotics, nitrofurans, fluoroquinolones;

2) Proteus or coliproteus bacteriophage;

3) killed therapeutic staphylo-Protein-Pseudomonas aeruginosa vaccine.

38. Diphtheria. Morphology and cultural properties. Diphtheria pathogenesis

The causative agent belongs to the genus Carinobacterium, the species C. difteria.

These are thin rods, straight or slightly curved, gram-positive. They are characterized by pronounced polymorphism. Club-shaped thickenings at the ends. In smears, bacteria are arranged at an angle in the form of a V or X.

Spores and capsules do not form. Motionless. They have fimbriae. They are facultative anaerobes or aerobes.

Being released into the external environment with saliva, films, diphtheria bacilli are able to remain viable on objects for several days. They tolerate drying well.

Carinobacteria are demanding on nutrient media; serum media or media with the addition of blood are used for their cultivation. Roux medium (clotted serum) is used. For isolation, elective nutrient media with the addition of potassium tolurite are used. Carinobacteria are divided into three biovars: gravis, mitisintermedius.

Virulence factors:

1) villi, fimbria or pili;

2) colonization and invasion (due to enzymes);

3) cord factor (impairs phosphorylation of the processes of respiration of macroorganism cells);

4) the leading factor is exotoxin.

Pathogenesis

Ways of transmission - airborne, contact-household.

The causative agent penetrates through the mucous membranes of the oropharynx, less often - the eyes, genitals, skin, wound surface.

The pathogen itself remains at the site of the entrance gate of infection, and the pathogenesis and clinical picture are determined by the action of exotoxin, which has a general and local effect.

The pathomorphological manifestation of the interaction of macro- and microorganism in diphtheria is fibrinous inflammation. In the exudate leaving the vessels, fibrinogen is detected, during the coagulation of which, grayish-white membranous plaques are formed on the surface of the mucous membrane, tightly soldered to the surrounding tissue. They are difficult to remove; when they are torn off, an erosive surface is exposed. The growth of these films lead to the development of a true croup.

Then the following are involved in the inflammatory process:

1) regional lymph nodes (lymphadenitis);

2) vessels;

3) heart (paralysis of the heart muscle);

4) adrenal cortex;

5) kidneys (nephritis);

6) peripheral nervous system - polyneuritis, paresis;

7) immune system (antibodies are absent on the 5-7th day).

The strength of a toxin is measured in DLM. 1 DLM is the minimum amount of toxin that, when administered subcutaneously to a guinea pig weighing 250 g, causes her death on the 4-5th day with a characteristic pathological and anatomical picture.

39. Diagnostics. Prevention. Treatment of diphtheria

Microbiological diagnostics

1. The main method is bacteriological examination.

2. Determination of the toxigenicity of the species culture (Vagai precipitation reaction).

Methods for determining toxigenicity:

1) biological sample;

2) setting ELISA;

3) use of DNA probes;

4) Wagai precipitation reaction.

Subject to research:

1) persons with suspected diphtheria;

2) patients with various diseases of the ENT organs.

Features of bacteriological research in diphtheria:

1) inoculation of material on elective nutrient media;

2) the mucous membranes of the nose, pharynx, genitals, skin as part of the normal microflora contain various representatives of the genus Carinobacterium. They are conditionally pathogenic, united by the concept of diphtheroids. In debilitated patients, with secondary immunodeficiency, in cancer patients, various purulent-inflammatory processes can be caused. In the course of a bacteriological study, it is necessary to differentiate diphtheria carinobacteria from diphtheroids.

Differences between diphtheroids and diphtheria pathogens:

1) differences in morphological properties. Diphtheroids in smears are arranged randomly or in the form of a palisade. There are no volutin grains in the cytoplasm;

2) differences in biochemical activity;

3) to identify differences in antigenic properties, an agglutination reaction is used for identification with a species differentiated serum;

4) sensitivity to bacteriophage.

Cultural properties do not differ.

Etiotropic therapy: antitoxic antidiphtheria serum; administered at a dose of 10-000 AU (depending on the age and severity of the disease).

1 AU is the minimum amount of serum that will neutralize 100 DLF diphtheria toxin.

Serotherapy is effective in the early period of the disease, until the toxin is fixed in the cells of the body and the tissues are not significantly damaged.

Prevention:

1) active. Vaccines are used: AD (diphtheria toxoid), ADS, ADSM, DTP. DTP vaccination is carried out three times for children at the age of 3 months. Revaccination is carried out under the control of determining the content (titer) of serum antitoxins using the reaction of RPHA with diphtheria toxoid erythrocyte diagnosticum;

2) passive. It is carried out in the foci of the disease with antitoxic serum, the dose of which is determined by the form and severity of the disease.

40. Tuberculosis

The causative agent belongs to the genus Mycobacterium, species M. tuberculesis.

These are thin sticks, slightly curved, do not form spores or capsules.

T Gram-positive.

Tuberculosis bacillus has features - the cell wall contains a large amount of lipids (up to 60%). Most of them are mycolic acids, which are included in the framework of the cell wall, where they are in the form of free glycopeptides that are part of the cord factors. Cord factors determine the nature of growth in the form of bundles.

Mycobacterium tuberculosis stained by Ziehl-Neelsen. This method is based on the acid resistance of mycobacteria.

As a result of treatment with anti-tuberculosis drugs, the pathogen may lose acid resistance.

Mycobacterium tuberculosis is characterized by pronounced polymorphism. In their cytoplasmic membrane, characteristic inclusions are found - Fly grains. Mycobacteria in the human body can transform into L-forms.

Mycobacteria are demanding on nutrient media. Growth factors - glycerin, amino acids. They grow on potato-glycerin, egg-glycerin and synthetic media.

On dense nutrient media, characteristic colonies are formed: wrinkled, dry, with uneven edges.

Pathogenesis

The causative agent of tuberculosis enters the body as part of fine aerosols. The pathogen must enter the alveoli, where they are engulfed by resident macrophages.

As a result of the interaction of mycobacteria and macrophages, inflammation of the granulomatous type develops under the influence of virulence factors.

From the lungs, the tubercle bacillus enters the regional lymph nodes, then into the bloodstream.

The route of infection is airborne. The source is a sick person who, in the acute period, excretes tubercle bacilli with sputum.

Pulmonary tuberculosis is most common, but the intestines, the musculoskeletal system, and the genitourinary system, etc. can also be affected. There are two pathogenetic variants of tuberculosis.

1. Primary tuberculosis. Occurs in individuals who have not previously had contact with the pathogen. Infection occurs during childhood or adolescence.

After 2-3 weeks, a primary tuberculous complex is formed (primary affect, lymphadenitis, lymphangitis).

Most often, it heals itself, undergoes fibrosis and calcification (Gon's focus). In other cases, acute tuberculosis develops.

2. Secondary tuberculosis. Runs chronically. It occurs when the primary focus is reactivated (after 5 years or more).

The development of secondary tuberculosis is facilitated by unfavorable living conditions, chronic diseases, alcoholism, etc.

Features of immunity in tuberculosis:

1) non-sterile;

2) unstable.

41. Tuberculosis. Diagnostics. Prevention. Treatment

Diagnostics:

1) microscopic examination. Two smears are made from sputum. One is stained by Ziehl-Neelsen, the second is treated with fluorochrome and examined using direct fluorescence microscopy;

2) bacteriological examination. Is required. During the study, sensitivity to tuberculostatic drugs is determined.

Apply accelerated methods for the detection of mycobacteria in crops, for example, according to the Price method. Microcolonies make it possible to see the presence of the cord factor, when the bacteria that formed it are folded into braids, chains, bundles;

3) polymer chain reaction (PCR). It is used for extrapulmonary forms;

4) serodiagnosis - ELISA, RPHA, fluorescence reaction. Not a leading method;

5) Mantoux test with tuberculin - an allergological method. Tuberculin is a preparation from a killed culture of mycobacteria. The sample is placed during the selection of persons for revaccination to assess the course of the tuberculosis process;

6) microculturing on slides in Shkolnikov's medium;

7) biological method. It is rarely used when the pathogen is difficult to isolate from the test material. Material from the patient infects laboratory animals (guinea pigs, rabbits). Observation is carried out until the death of the animal, and then the punctate of its lymph nodes is examined.

Specific prevention: live BCG vaccine. Vaccination is carried out in the maternity hospital on the 4th-7th days of life by the intradermal method.

Revaccination is carried out for persons with a negative tuberculin test with an interval of 5-7 years until the age of 30. In this way, infectious immunity is created, in which a delayed-type hypersensitivity reaction occurs.

Treatment

Most antibiotics have no effect on Mycobacterium tuberculosis, so tuberculostatic drugs are used.

There are two types of drugs used:

1) first-line drugs: isoniazid, pyrazinamide, streptomycin, rifampicin, ethambutol, ftivazid;

2) second-line drugs (with the ineffectiveness of first-line drugs): amikacin, kanomycin, sodium aminosalicylate (PAS), dapsone, cycloserine, etc.

Features of therapy for tuberculosis:

1) treatment should be started as early as possible, immediately after the detection of the disease;

2) therapy is always combined - at least two drugs are used;

3) it is carried out for a long time (4-6 months), which is associated with a long life cycle of mycobacteria;

4) must be continuous, since interruptions lead to the formation of resistance of the pathogen and the chronization of the process.

42. Rickettsia group

Rickettsia is divided into subclasses a1, a2, b and g.

a1 includes the family Rickettsiaceae.

1. Genus Rickettsia, species are divided into two groups:

1) a group of typhus:

a) R. provacheka - the causative agent of epidemic (lousy) typhus;

b) R. typhi - the causative agent of endemic (rat-flea) typhus;

2) a group of tick-borne rickettsiosis:

a) R. rickettsi - the causative agent of rocky mountain fever;

b) R. conori - the causative agent of hemorrhagic fever;

c) R. sibirika is the causative agent of North Asian rickettsiosis.

2. The genus Erlihia, isolated species: E. canis and E. sennetsu (may be the causative agents of infectious mononucleosis).

a2 includes the family Bartonellaceae, genus Bartonella, subdivided into species:

1) B. kvintana - the causative agent of five-day (trench) fever;

2) B. hensele - the causative agent of "cat-scratch disease".

Includes the genus Coxiella, the species C. burneti - the causative agent of Q fever.

Rickettsiae are bacteria whose hallmark is obligate intracellular parasitism. They are similar in structure to Gram-negative bacteria. They have their own enzyme systems. Motionless, no spores or capsules.

Rickettsia are characterized by pronounced polymorphism. There are four forms:

1) form A - coccal, oval, located singly or in the form of dumbbells;

2) form B - sticks of medium size;

3) form C - bacillary rickettsia, large sticks;

4) form D - filiform, can give branches.

Morphology depends on the stage of the infectious process. In the acute form, forms A and B are mainly found, in the chronic, sluggish form - C and D.

The interaction of rickettsia with the cell includes several stages.

1. Adsorption on the receptors of the corresponding cells.

2. After attachment, the membrane invaginates, the rickettsia sinks into the cell as part of the vacuole.

3. Then there are two options:

1) some types of rickettsia continue to remain inside the vacuole and multiply there;

2) others lyse the membrane and lie freely in the cytoplasm.

4. Rickettsia multiply intensively, the membrane is destroyed, and they leave the cell.

Obligate intracellular parasitism of rickettsia is realized at the cellular level.

For their cultivation, the same methods are used as for the cultivation of viruses:

1) tissue infection;

2) infection of chicken embryos;

3) in the body of experimental animals;

4) in the body of ectoparasites.

43. Rickettsioses

The most common rickettsiosis is epidemic typhus. The causative agent is R. Provacheka. The source of infection is a sick person. The carrier is body and head lice.

These are polymorphic microorganisms. Reproducing in host cells, they form a microcapsule. Aerobes.

They have two antigens:

1) group-specific;

2) corpuscular, species-specific.

The disease begins after the pathogen enters the bloodstream. Rickettsiae adhere to capillary endotheliocytes. In the cytoplasm of these cells, they multiply. After the cells are destroyed, a new generation of rickettsiae enters the bloodstream. Damage to the capillaries leads to the formation of blood clots and granulomas. The most dangerous localization of the lesion is the central nervous system. A rash appears on the skin. In addition to direct action, rickettsia secrete endotoxin, which causes capillary paresis.

After the disease, intense antimicrobial immunity remains.

Diagnostics:

1) serodiagnosis - the main method (RPHA, RSK with a diagnosticum from R. Provacheka);

2) bacteriological examination;

3) PCR diagnostics.

Specific prophylaxis: live typhoid vaccine.

Etiotropic therapy: antibiotics - tetracyclines, fluoroquinolones.

The most common rickettsioses include endemic (rat-flea) typhus. Pathogen - R. typhi. The source of infection is rat fleas, lice, gamasid mites. Ways of infection - transmissible, airborne.

The pathogenesis and clinical manifestations of the disease are similar to epidemic typhus.

Diagnostics:

1) biological sample;

2) serodiagnosis - RSK, IF.

It is necessary to say about the cooler. The causative agent is C. burneti. The source of infection is livestock. Ways of transmission - alimentary, contact-household.

These are small rod-shaped or coccoid formations, stained according to Romanovsky-Giemsa in a bright pink color. They form L-shapes.

Resistant to environmental factors.

Rickettsemia occurs after C. burneti enters the body. In the process of infection, a delayed-type hypersensitivity reaction develops, and a tense immunity is formed.

The disease is characterized by an unclear clinical picture.

Diagnostics:

1) serological examination (RSK, RPGA);

2) skin-allergic test.

Specific prophylaxis: live vaccine M-44.

Treatment: antibiotics - tetracyclines, macrolides.

44. Influenza viruses

They belong to the family of orthomyxoviruses. Influenza viruses of types A, B and C are isolated.

The influenza virus has a spherical shape, with a diameter of 80-120 nm. The nucleocapsid of helical symmetry is a ribonucleoprotein strand (NP protein) folded in the form of a double helix that makes up the core of the virion. RNA polymerase and endonucleases are associated with it. The core is surrounded by a membrane consisting of protein M, which connects the ribonucleoprotein strand to the lipid double layer of the outer shell. Among the proteins of the supercapsid envelope, two are of great importance:

1) neuraminidase;

2) hemagglutinin.

The virus genome is represented by a minus-strand fragmented RNA molecule. Replication of orthomyxoviruses is primarily realized in the cytoplasm of the infected cell. Synthesis of viral RNA is carried out in the nucleus.

Influenza A, B, and C viruses differ from each other in type-specific antigen associated with M and NP proteins. A narrower specificity of type A virus is determined by hemagglutinin (H-antigen). The variability of the H-antigen determines:

1) antigenic drift - changes in the H-antigen caused by point mutations in the gene that controls its formation;

2) antigenic shift - a complete replacement of a gene, which is based on recombination between two genes.

Initially, the pathogen replicates in the epithelium of the upper respiratory tract, causing the death of infected cells. Through damaged epithelial barriers, the virus enters the bloodstream. Viremia is accompanied by multiple lesions of the capillary endothelium with an increase in their permeability. In severe cases, extensive hemorrhages are observed in the lungs, myocardium and various parenchymal organs.

The main symptoms include a rapid increase in body temperature with concomitant myalgia, runny nose, cough, headaches.

The main route of transmission of the pathogen is airborne.

Laboratory diagnostics:

1) express diagnostics - determination of virus antigens in the cytoplasm of the epithelium of the nose and nasopharynx in smears-prints by ELISA;

2) infection of cell cultures or chicken embryos with nasal discharge, sputum or swabs from the nasopharynx (obtained in the first days of illness);

3) serodiagnostics (RCC, RTGA, enzyme activity inhibition reaction).

Specific prevention:

1) human anti-influenza immunoglobulin;

2) live and inactivated vaccines.

Treatment: amantadine derivatives (remantadine).

45. ARVI pathogens

Parainfluenza virus and RS virus belong to the Paramyxoviridae family.

These are spherical viruses with helical symmetry. The average size of the virion is 100-800 nm. They have a supercapsid membrane with spiny processes. The genome is represented by a linear non-segmented RNA molecule. The RNA is associated with a major (NP) protein.

The shell contains three glycoproteins:

1) HN, which has hemagglutinating and neuraminidase activity;

2) F, responsible for fusion and exhibiting hemolytic and cytotoxic activity;

3) M-protein.

Virus replication is fully realized in the cytoplasm of host cells. The human parainfluenza virus belongs to the genus Paramyxovirus. Viruses are characterized by the presence of their own RNA-dependent RNA polymerase (transcriptase).

Based on differences in the antigenic structure of HN, F and NP proteins of human parainfluenza viruses, four main serotypes are distinguished.

The pathogen reproduces in the epithelium of the upper respiratory tract, from where it enters the bloodstream.

Clinical manifestations in adults most often occur in the form of catarrhs of the upper respiratory tract. In children, the clinical picture is more severe.

The main route of transmission of the parainfluenza virus is airborne. The source of infection is the patient (or virus carrier).

Laboratory diagnostics:

1) express diagnostics (ELISA);

2) isolation of the pathogen in monolayer cultures of the kidneys of the embryo of humans or monkeys;

3) serodiagnosis (RSK, RN, RTGA with paired sera).

PC virus is the main causative agent of lower respiratory tract infections in newborns and young children. Belongs to the genus Pneumovirus.

It is characterized by low resistance, virions are prone to self-decay.

The pathogen replicates in the epithelium of the airways, causing the death of infected cells, and exhibits pronounced immunosuppressive properties.

PC virus causes annual epidemic respiratory tract infections in newborns and young children; adults may be infected, but the course of infection is mild or asymptomatic. The main route of transmission is airborne.

After recovery, unstable immunity is formed.

Laboratory diagnostics:

1) express diagnostics - determination of virus antigens in the nasal discharge using ELISA;

2) specific antigens are detected in RSK and RN.

Etiotropic therapy has not been developed.

46. ARVI pathogens (Adenoviruses)

The family Adenoviridae includes two genera - Mastadenovirus (mammalian viruses) and Aviadenovirus (avian viruses); the first includes about 80 species (serovars), the second - 14.

The family includes viruses with a naked capsid (there is no outer shell), a cubic type of symmetry. The size of the virion is 60-90 nm. The genome is represented by a linear double-stranded DNA molecule.

The mature virus consists of 252 capsomeres, including:

1) hexons responsible for the manifestation of the toxic effect;

2) pentons causing the hemagglutinating properties of viruses.

Antigenic structure:

1) surface antigens of structural proteins;

2) hexon antigens (group-specific);

3) complement-fixing antigen.

The main routes of transmission are airborne and contact.

The symptomatology of lesions is due to the reproduction of the pathogen in sensitive tissues. According to the type of lesions of sensitive cells, three types of infections are distinguished:

1) productive (lytic). Accompanied by cell death after the release of the daughter population;

2) persistent. It is observed when the rate of reproduction slows down, which makes it possible for tissues to compensate for the loss of infected cells due to the normal division of uninfected cells;

3) transforming. In tissue culture, cells are transformed into tumor cells.

The main clinical manifestations of adenovirus infections.

1. Most often - SARS, occurring as flu-like lesions. The peak incidence occurs in the cold season. Outbreaks are possible throughout the year.

2. Pharyngoconjunctivitis (pharyngoconjunctival fever). The peak incidence occurs in the summer months; the main source of infection is the water of pools and natural reservoirs.

3. Epidemic keratoconjunctivitis. Lesions are caused by infection of the cornea during injuries or medical manipulations. Possible erosion of the cornea up to loss of vision.

4. Infections of the lower respiratory tract.

Laboratory diagnostics:

1) isolation of the pathogen by inoculation into cultures of human epithelial cells; the investigated material - discharge of the nose, pharynx, conjunctiva, feces;

2) detection of virus antigens in cells by immunofluorescence microscopy;

3) RSK, RTGA and RN of the cytopathic effect in cell culture.

Treatment: no specific drug therapy is available.

Specific prophylaxis: live vaccines containing attenuated viruses of the dominant serotypes.

47. ARVI pathogens (Rhinoviruses. Reoviruses)

Rhinoviruses belong to the Picornaviridae family.

Virions have a spherical shape and a cubic type of symmetry. Size 20-30 nm. The genome is formed by a positive RNA molecule that is not segmented. The capsid membrane consists of 32 capsomeres and 3 large polypeptides. There is no supercapsid membrane.

Virus replication takes place in the cytoplasm.

Viruses lose their infectious properties in an acidic environment. Well preserved at low temperatures. The temperature required for replication is 33 °C.

Rhinoviruses are divided into two groups:

1) group H viruses. They multiply and cause cytopathic changes in a limited group of diploid cells, the human embryo;

2) viruses of group M. They multiply and cause cytopathic changes in the cells of the kidneys of monkeys, the human embryo.

After the illness, there is a short immunity.

Laboratory diagnostics:

1) isolation of viruses in cell cultures infected with nasal discharge;

2) express diagnostics - immunofluorescent method.

Treatment: symptomatic.

Reoviruses belong to the Reoviridae family.

Virions are spherical, 60-80 nm in diameter. The capsid is built according to the icosahedral type of symmetry. Double-stranded RNA consists of ten fragments. There are eight separate proteins in the inner and outer capsids. One of the proteins of the outer capsid is responsible for binding to specific cell receptors, with the help of another, the virus enters the cell.

Virus replication occurs in the cytoplasm of host cells.

There are three serotypes of reoviruses. They have a common complement-fixing antigen and type-specific antigens (outer capsid protein). Viruses have hemagglutinating activity.

The main route of transmission is airborne.

Reoviruses primarily reproduce in the epithelial cells of the mucous membrane of the mouth, pharynx, small intestine, regional lymph nodes, from where they enter the lymph and blood. Viruses are able to pass through the placenta and have an embryopathic effect.

Laboratory diagnostics:

1) isolation of the virus in cell culture and in newborn mice;

2) identification of the virus - in the neutralization reaction and RTGA;

3) serodiagnosis (RTGA).

Specific prophylaxis and etiotropic therapy have not been developed.

48. Measles and mumps viruses

The mumps virus and the measles virus belong to the Paramixoviridae family.

Virions have a spherical shape with a diameter of 150-200 nm. In the center of the virion is a nucleocapsid with a helical symmetry type, surrounded by an outer shell with spiny processes. Viral RNA is represented by a single-stranded negative strand. The nucleocapsid is covered with a matrix protein.

The mumps virus belongs to the genus Paramyxovirus. Viral infection is characterized by a predominant lesion of the parotid salivary glands.

Antigenic structure:

1) internal NP protein;

2) surface NH- and F-glycoproteins.

Initially, the pathogen reproduces in the epithelium of the nasopharynx, then penetrates into the bloodstream and during the period of viremia penetrates into various organs: parotid glands, testicles, ovaries, pancreas, thyroid glands, head and other organs. Primary reproduction in the epithelium of the parotid glands is also possible.

The main route of transmission is airborne.

Laboratory diagnostics: isolation of the virus from the cerebrospinal fluid, saliva and punctate glands and cultivation on chicken embryos and chicken fibroblast cell cultures.

Means of specific drug therapy are absent.

Specific prevention:

1) live and killed vaccine;

2) specific immunoglobulin.

The measles virus belongs to the genus Morbillivirus.

Antigenic structure:

1) hemagglutinin (H);

2) peptide (F);

3) nucleocapsid protein (NP).

The main ways of transmission are airborne, less often contact.

Initially, the virus multiplies in the epithelium of the upper respiratory tract and regional lymph nodes, and then penetrates into the bloodstream. Viremia is short-lived. The causative agent is hematogenously distributed throughout the body, fixing in the reticuloendothelial system. The activity of immune mechanisms aimed at the destruction of infected cells leads to the release of the virus and the development of a second wave of viremia. The tropism of the pathogen to epithelial cells leads to secondary infection of the conjunctiva, mucous membranes of the respiratory tract and oral cavity. Circulation in the bloodstream and emerging protective reactions cause damage to the walls of blood vessels, tissue edema and necrotic changes in them.

Laboratory diagnostics:

1) detection of multinuclear cells and pathogen antigens in the discharge of the nasopharynx;

2) isolation of the virus on primary trypsinized cultures of monkey kidney cells or human embryo.

Treatment: no specific therapy is available.

Specific prevention:

1) human measles immunoglobulin;

2) live attenuated vaccine.

49. Herpes virus. rubella virus

Herpes virus. The Herpesviridae family includes subfamilies:

1) a-herpesviruses (types I and II, herpes zoster);

2) b-herpesviruses;

3) g-aherpesviruses.

They belong to DNA viruses. DNA is double-stranded, linear. The capsid shell is a cubic type of symmetry. There is a supercapsid membrane that forms spiny processes.

Herpes viruses are relatively unstable.

a-herpes type I causes aphthous stomatitis in early childhood, labial herpes.

a-herpes type II causes genital herpes, herpes of newborns. Herpes zoster is the causative agent of shingles and chickenpox.

After an infection, lifelong immunity remains.

The virus persists for life in the nerve ganglia. With a decrease in the body's defenses, a viral infection develops.

B-herpes (cytomegalovirus) during reproduction in culture cells causes cytopathic changes. It has an affinity for the cells of the salivary glands and kidneys, causing the formation of large multinuclear inclusions in them. With the development of the disease, viremia, damage to internal organs, bone marrow, central nervous system, and the development of immunopathological diseases take place.

g-herpes virus (Epstein-Bar virus) causes infectious mononucleosis.

rubella virus

Belongs to the family Togaviridae, genus Rubivirus.

They are spherical enveloped viruses with an icosahedral nucleocapsid enclosed in a lipid envelope.

The genome is formed by a single-stranded +RNA molecule.

In humans, the virus causes rubella. The main route of transmission of the pathogen is airborne. Upon recovery, lifelong immunity is formed.

A characteristic sign of the disease is a maculopapular rash of a pale pink color, most abundant on the extensor surfaces of the limbs, back and buttocks. After 2-3 days, the skin elements disappear, leaving no pigmentation and peeling. Adults tolerate rubella more severely: the temperature can reach 39 ° C, severe headaches and myalgia, pronounced catarrhs of the nasal mucosa and conjunctiva are possible.

The greatest danger is the infection of the fetus during pregnancy.

The virus is unstable in the external environment, it dies when exposed to physical and chemical factors.

Treatment:

1) there are no means of etiotropic therapy;

2) pregnant women who have been in contact with the patient are prophylactically injected with a specific immunoglobulin.

Specific prophylaxis: live attenuated vaccine; immunization of women of childbearing age should be carried out only in the absence of pregnancy.

50. Poliomyelitis virus, ECHO viruses, Coxsackie viruses

Polio virus. Belongs to the family Picornaviridae, a genus of enteroviruses.

They are relatively small viruses with icosahedral symmetry. The genome is formed by an unsegmented +RNA molecule.

Each viral particle consists of a capsid built of 60 subunits and containing 4 polypeptides of one VPg molecule connected to RNA.

The pathogens are highly contagious, the main transmission mechanism is fecal-oral.

Poliomyelitis is an acute infection that affects the neurons of the medulla oblongata and anterior horns of the spinal cord.

The primary breeding site is localized in the epithelium of the mouth, pharynx, small intestine, as well as in the lymphoid tissues of the Pirogov ring and Peyer's patches. Possible secondary penetration of the virus from the epithelium of the mucous membranes into the lymphoid tissues and bloodstream, and then into various organs, excluding the central nervous system.

Neurons of the anterior horns of the spinal cord, medulla oblongata, and pons varolii carry receptors for polioviruses.

Treatment: symptomatic and prevent the development of secondary bacterial infections.

Specific prevention:

1) live (attenuated) vaccine;

2) killed viral vaccine.

ECHO viruses. Coxsackie viruses

They belong to the family Picornaviridae, a genus of enteroviruses.

The structure of the virion is the same as that of the polio virus.

ECHO viruses are isolated in a special group of intestinal viruses due to the complete absence of pathogenic effects on laboratory animals.

Infection with ECHO viruses occurs by the fecal-oral route, less often by inhalation.

ECHO viruses cause:

1) SARS and fever of unknown origin;

2) aseptic meningitis (occur relatively easily);

3) ascending paralysis and encephalitis.

After a disease, immunity is formed, the duration of which varies within different limits.

Treatment is symptomatic.

Coxsackieviruses are typical picornaviruses.

According to biological properties, they distinguish:

1) group A viruses. They cause diffuse myositis with inflammation and focal necrosis of striated muscles;

2) viruses of group B. Cause lesions of the central nervous system (focal degeneration, paralysis), necrosis of skeletal muscles and sometimes myocardium, inflammatory lesions of the spleen, etc.

The main transmission mechanisms are fecal-oral and contact (through the discharge of the nasopharynx).

51. HIV

HIV belongs to the retrovirus family.

The virion has a spherical shape, with a diameter of 100-150 nm. Cubic type of symmetry.

Each RNA molecule contains nine HIV genes:

1) structural (three genes);

2) regulatory (three genes);

3) additional (three genes).

There are three groups of structural genes:

1) gag (encode the formation of structural proteins of the core of the virus);

2) pol (direct the synthesis of proteins - viral enzymes);

3) ent (encode the synthesis of envelope proteins gp 120 and gp 41).

In addition to RNA, viral enzymes are also located there:

1) reverse transcriptase;

2) protease;

3) endonuclease (integrase).

In conventional cell cultures, HIV is not cultivated. For cultivation, a culture of T-lymphocytes with a helper function is used.

Pathogenesis and immunological disorders

In the body, viruses interact with CD-4 receptors, which are located on the surface of immunocompetent cells - lymphocytes, macrophages. The interaction of a virus with a target cell includes four stages:

1) adsorption to CD-4 receptors;

2) cell puncture and endocytosis;

3) deproteinization with the participation of host cell protein kinases;

4) DNA synthesis on an RNA template with the participation of reverse transcriptase.

The DNA of the virus is included in the cell genome, then the synthesis of viral components - proteins occurs, then - the self-assembly of the virion and its budding, during which the virus acquires a supercapsid.

Infection begins with the introduction of the virus into the human body. The pathogenesis of HIV infection includes five main periods:

1) incubation period (7 to 90 days);

2) the stage of primary manifestations Clinically, this stage resembles any acute infection: the only alarming symptom is an increase in the cervical and axillary lymph nodes. This stage lasts 2-4 weeks;

3) latent period. During this period, the virus slows down its replication and enters a state of persistence. The latent period lasts 5-10 years. The only clinical symptom is lymphadenopathy;

4) AIDS-associated complex (pre-AIDS);

5) AIDS itself. There is a complete lack of immune response. Duration - approximately 1-2 years, secondary infections are the direct cause of death.

52. HIV. Epidemiology. Diagnostics. Treatment

Sources of the virus are sick and virus carriers.

Ways of transmission of the virus:

1) infection through sexual contact;

2) parenteral infection with blood during blood transfusions, medical manipulations, operations;

3) transmission to newborns through the placenta, in the birth canal, during breastfeeding.

HIV is present in a sick person in all cells where there are CD-4 receptors - these are T-helpers, tissue macrophages, in intestinal cells, mucous membranes, etc. In an infected person, the virus is excreted with all biological fluids: the maximum amount is in the blood and in seminal fluid. The average amount of virus is in the lymph, cerebrospinal fluid, vaginal discharge.

Even less virus in the milk of a nursing mother, saliva, tears, sweat. The content of the virus in them is such that it is not enough to cause an infection.

The main risk groups are drug addicts, patients with hemophilia, homosexuals, prostitutes.

HIV is characterized by low resistance to physical and chemical factors. Heating at 560°C for 30 minutes reduces the infectious titer of the virus by 100 times, and higher temperatures quickly and completely inactivate the virus. Sensitive to detergents and disinfectants. HIV is resistant to desiccation. Its infectivity persists for 4-6 days at room temperature. Not sensitive to UV radiation.

Laboratory diagnostics:

1) screening of antibodies against HIV using enzyme immunoassay (from the beginning of the second period until the death of the infected person). If the reaction is positive, it is repeated with another serum and on a more advanced system. Then immunobloding is carried out;

2) HIV-2 diagnosticum (with suspected HIV infection and with negative reactions to HIV-1);

3) infection of T-helper cultures. The virus is detected by cytopathic action, in serological reactions, by reverse transcriptase activity;

4) hybridization tests using virus-specific nucleic probes.

Treatment:

1) etiotropic therapy. Use the following drugs:

a) azidothymizine (;

b) a-interferon (prolongs the latent period, suppressing replication);

2) immunostimulation: interleukin-2, interferons and immunoglobulins are administered;

3) treatment of tumors, secondary infections and invasions.

Specific prophylaxis has not been developed. A genetically engineered vaccine containing viral surface glycoproteins is being tested.

53. Rabies virus. Flaviviruses

Rabies virus. Belongs to the family Rhabdoviridae, genus Lyssavirus.

Rhabdoviruses are distinguished by their bullet shape, the presence of a shell, and helical symmetry; the genome is made up of RNA.

Rabies is an acute infection of the central nervous system, accompanied by degeneration of neurons in the brain and spinal cord. Mortality for humans in the absence of timely treatment is 100%.

The virus enters the human body through damage to the skin, usually through the bites of sick animals. The virus migrates along the axons of peripheral nerves to the basal ganglia and the central nervous system, where it multiplies in cells, resulting in the appearance of cytoplasmic bodies of Babes-Negri. The virus then migrates back along the centrifugal neurons to various tissues.

The time for the virus to move along the nerve trunks corresponds to the incubation period of the disease. Its duration can be different: minimal (10-14 days) with a bite in the head and face, and longer (a month or more) with bites in the limbs.

The reservoir of the virus in nature are various warm-blooded animals.

Treatment:

1) broad-spectrum antibiotics;

2) specific anti-rabies immunoglobulin;

3) horse anti-rabies serum;

4) anti-rabies vaccine.

Specific prophylaxis: rabies vaccine.

Flaviviruses

The family includes about 50 viruses.

They are spherical enveloped viruses with an icosahedral nucleocapsid enclosed in a lipid envelope.

The genome is formed by a single-stranded +RNA molecule.

Flaviviruses are cultivated in chicken embryos and tissue cultures.

The flavivirus family includes various representatives that cause the corresponding diseases:

1) yellow fever virus. The reservoir of infection is monkeys, the carrier is mosquitoes. Found in South African countries;

2) Dengue fever virus. The reservoir of infection is sick people and monkeys, the carrier is mosquitoes;

3) Japanese encephalitis virus. Pathogen reservoir - wild birds, rodents, cattle, horses and pigs; a person is a dead-end host (in epidemics, transmissible transmission from person to person is possible). Carriers - mosquitoes of the genus Culex;

4) tick-borne encephalitis virus. The reservoir and carrier of the virus are ixodid ticks. Additional tank - various animals and birds.

For the specific prevention of tick-borne encephalitis, an inactivated vaccine is used. When a tick bites, a specific immunoglobulin is injected.

54. Hepatitis A and B virus

Hepatitis A virus belongs to the picornavirus family, the genus Enterovirus.

The hepatitis A virus is morphologically similar to other members of the enterovirus genus. The genome is formed by a single-stranded +RNA molecule. It does not have a supercapsid shell.

The main mechanism of transmission of the hepatitis A virus is fecal-oral. The patient secretes the pathogen within 2-3 weeks before the onset of the icteric stage and 8-10 days after its completion. The virus is pathogenic only for humans.

The hepatitis A virus enters the human body with water or food, reproduces in the epithelium of the mucous membrane of the small intestine and regional lymphoid tissues.

Then the pathogen enters the bloodstream with the development of short-term viremia. The main target for cytopathogenic action is hepatocytes.

The defeat of hepatocytes is accompanied by the development of jaundice and an increase in the level of transaminases.

Further, the pathogen with bile enters the intestinal lumen and is excreted with feces, in which there is a high concentration of the virus.

After the transfer of infection, lifelong humoral immunity is formed.

Specific prophylaxis: killed vaccine based on strain CR 326.

Hepatitis B virus

Belongs to the Hepadnaviridae family. These are icosahedral, enveloped DNA-containing viruses, the genome forms an incomplete (with a break in one strand) circular double-stranded DNA molecule.

Efficient replication requires the synthesis of virus-induced reverse transcriptase.

Antigenic structure:

1) HBsAg (includes two polypeptide fragments):

a) preS1 polypeptide;

b) preS2 polypeptide;

2) HBcorAg;

3) HBeAg.

Infection occurs by injection of infected blood or blood products; through contaminated medical instruments, sexually and intranatally, intrauterine infection is possible.

Clinical manifestations range from asymptomatic and anicteric forms to severe liver degeneration. The course of hepatitis B is more severe, with a gradual onset, a long infectious cycle, a higher mortality rate than with hepatitis A. Chronization of the process is possible.

Laboratory diagnostics.

Serological studies include the determination of antigens and antibodies using reagents - HBsAg, HBeAg; antigens to HBsAg, HBcorAg, HBeAg and IgM to HBcorAg.

Specific prevention:

1) specific immunoglobulin (HBIg);

2) recombinant vaccines.

55. Other causative agents of viral hepatitis

Hepatitis C virus - RNA-containing virus. Its taxonomic position is currently not precisely defined; it is close to the flavivirus family.

It is a spherical particle consisting of a nucleocapsid surrounded by a protein-lipid membrane. The size of the virion is 80 nm. RNA has zones encoding the synthesis of structural and non-structural proteins of the virus. The synthesis of structural proteins is encoded by the C and E zones of the RNA, and the synthesis of non-structural proteins of the virus is encoded by the NS-1, NS-2, NS-3, NS-4 and NS-5 zones of the RNA.

The hepatitis C virus is characterized by antigenic variability, there are seven main variants of the virus.

The source of infection are patients with acute and chronic hepatitis C and virus carriers. The virus is transmitted parenterally, sexually and from mother to fetus (with peri- and postnatal infection).

The predominance of anicteric forms and the frequent transition to the chronic form of the disease are characteristic. The virus is one of the factors in the development of primary hepatocellular carcinoma.

Laboratory diagnostics:

1) detection of RNA virus by PCR;

2) determination of antibodies to the virus in ELISA.

hepatitis D virus does not belong to any of the known families of animal viruses. It is a spherical particle with an average diameter of 36 nm. The genome is represented by a single-stranded, cyclic RNA molecule, which forms a rod-shaped unbranched structure. RNA encodes a virus-specific polypeptide - HDAg (nucleocapsid own antigen). The outer shell forms a surface antigen.

Hepatitis D RNA virus replication occurs in the nucleus of an infected hepatocyte.

Sources of infection - a sick person and a virus carrier. The route of transmission is parenteral. The hepatitis D virus cannot participate in the development of hepatitis infection without simultaneous replication of the hepatitis B virus. This fact determines two possible forms of their interaction:

1) simultaneous infection with viral hepatitis B and D (conversion);

2) infection of the carrier of the hepatitis D virus with the hepatitis B virus (superinfection).

With superinfection, rapid damage to the liver parenchyma occurs with massive necrosis.

Diagnosis: detection of antibodies to the virus in ELISA.

Hepatitis E virus belongs to the Calicinovirus family. This is a spherical RNA virus, 20-30 nm in size. Ways of transmission - water, food, contact is possible. The source of infection is a patient with an acute or chronic form. The clinical picture is close to hepatitis A.

Diagnosis: detection of antibodies in ELISA.

56. Plasmodium malaria

They belong to the genus Plasmodium. There are four types of human parasites: P. vivax - the causative agent of three-day malaria, P. malariae - the causative agent of four-day malaria, P. falciparum - the causative agent of tropical malaria, P. ovale - the causative agent of malaria-ovale.

There are two phases of development of malarial plasmodia.

1. Phase of sexual reproduction. Occurs in the body of the final host - a mosquito of the genus Anopheles. It ends with the formation of a large number of sporozoites - long thin mononuclear cells that are concentrated in the salivary glands. When bitten by a mosquito, sporozoites enter the bloodstream of the vertebrate host.

2. Phase of asexual reproduction - schizogony. Carried out in the body of the intermediate host - humans. It proceeds in two stages:

1) exoerythrocytic schizogony. Sporozoites are brought into the liver with blood flow, invade its cells, in which they are transformed into tissue trophozoites, and then into tissue schizonts. As a result of the division of tissue schizonts, tissue merozoites are formed, which are released into the blood;

2) erythrocyte schizogony. Merozoites are introduced into erythrocytes. After the destruction of red blood cells, merozoites enter the bloodstream. Some of the parasites undergo phagocytosis, while others infect new red blood cells, and the cycle repeats.

The pathogenesis of the disease: the release of erythrocyte merozoites, malarial pigment, metabolic products of parasites and structural components of erythrocytes into the blood leads to the development of a feverish reaction. It is characterized by a cyclicity corresponding to the cyclicity of erythrocyte schizogony.

Foreign plasmodium proteins cause an anaphylactic reaction.

When this happens:

1) increased capillary permeability;

2) hyperplasia of the reticuloendothelial elements of the spleen;

3) inhibition of hematopoiesis;

4) the appearance of allergic symptoms (bronchitis, bronchial asthma).

IgM and IgG accumulate in the blood.

Malaria is seasonal. The prevalence is associated with the presence of specific carriers - mosquitoes of the Anopheles genus.

Diagnostics:

1) microscopy of blood smears of the patient, stained by the Romanovsky-Giemsa method;

2) serodiagnosis - immunofluorescence reactions, passive hemagglutination, enzyme immunoassay.

Etiotropic therapy: schizocidal action is possessed by chloroquine, amodiaquine; gamontocidal action - pyrimethamine, proguanil, quinocide, primaquine.

Author: Tkachenko K.V.

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Economical biofuel from cellulose 27.06.2015

A bright dream of biotechnologists is an economical biofuel from cellulose. Of course, sawdust and other garbage are supposed to be used for biofuel, and not timber. Cellulose, as you know, is a polymer of glucose, however, it is beta-glucose, not alpha-glucose, which is part of sugar and starch, but bacteria or yeast fungi may well make some alcohols or other energetically valuable molecules from it. It would be much more profitable than spending potential food raw materials on fuel. However, it is difficult to break down cellulose into monomers; it is not for nothing that plant mass and wood are malnourished, unlike starchy tubers. This is the bottleneck on the way to biofuels.

But some people in nature eat wood, like some bacteria. And if they eat, then they know how to break down cellulose. Aerobic (oxygen-loving) microorganisms do this with the help of free enzyme molecules, while anaerobic, living in an oxygen-free environment, use enzyme complexes called "cellulosomes". Cellulase enzymes, which cleave bonds between glucose molecules, and specific proteins that attach to cellulose, are assembled into a construct that is significantly more efficient than free enzymes.

Recently it has been shown that the activity of cellulases is significantly enhanced by other enzymes, lytic polysaccharide monooxygenases - LPMO. But these enzymes are available only in aerobic bacteria (which is understandable: oxygen is needed to carry out the redox reaction).

Researchers from the Weizmann Institute (Israel) have managed to combine single molecules of cellulases and LPMO of the aerobic bacterium Thermobifida fusca into a cellulosome. Proteins were combined "in the Lego principle," as the authors of the article put it. But it would be more accurate to say that all the necessary proteins - cellulases, LPMO and the cellulose binding site - were genetically engineered with connectors borrowed from proteins of anaerobic bacteria that can assemble into cellulosomes. The connectors were chosen so that the complex included one molecule of each of the proteins. The activity of modified proteins, taken separately, did not change compared to the initial one, but cellulosomes containing LPMO cleaved cellulose 1,6 times better than a mixture of free-floating proteins, and 2,6 times better than a cellulase solution without LMPO.

Israeli scientists will not stop there: they plan to include enzymes that break down lignin into new designer cellulosomes. And you get a multi-enzyme complex that turns solid wood into a solution of sugars and phenol derivatives.

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