How can we explain the different levels of bacteria? Bacteria

Bacteria are relatively simple microscopic single-celled organisms.

Bacteria shape(Fig. 28). Depending on the shape of the cell, bacteria are distinguished: spherical cocci, rod-shaped bacilli, comma-shaped vibrios, spiral spirilla. Very often, bacteria form clusters in the form of long curved chains, groups and films. Some bacteria have one or more flagella. Among bacteria there are mobile and immobile forms. Motile ones move due to wave-like contractions or with the help of flagella.

Rice. 28. Shape and size of bacterial cells

Most bacteria are colorless. Only a few are purple or green.

Structure of bacteria. Bacterial cells are surrounded by a dense membrane, thanks to which they maintain a constant shape. In composition and structure, the cell walls of bacteria differ significantly from the membranes of plants. The cell does not have a formed nucleus, separated from the cytoplasm by a nuclear envelope. The nuclear substance in most bacteria is distributed in the cytoplasm (Fig. 29).

Rice. 29. Structure of a bacterial cell

Spread of bacteria. There is practically no place on Earth where bacteria are not found. They live in the ice of Antarctica at a temperature of -83 °C and in hot springs, the temperature of which reaches +85-90 °C. There are especially many of them in the soil. 1 g of soil can contain hundreds of millions of bacteria.

The number of bacteria is different in the air of ventilated and unventilated rooms. Thus, in the classroom after ventilation before the start of the lesson, there are 13 times less bacteria than in the same room after the lesson.

The living conditions of bacteria are varied. Some of them require atmospheric oxygen, others do not need it and are able to live in an oxygen-free environment.

Nutrition of bacteria. Most bacteria feed on ready-made organic substances. Only some of them, for example blue-green bacteria, or cyanobacteria, are capable of creating organic substances from inorganic ones. They played an important role in the accumulation of oxygen in the Earth's atmosphere.

Bacteria reproduction. Bacteria reproduce by dividing one cell into two. At favorable conditions Cell division in many bacteria can occur every 20-30 minutes. With such rapid reproduction, the offspring of one bacterium in 5 days is capable of forming a mass that could fill all the seas and oceans. However, this does not happen in nature, since most bacteria quickly die under the influence of sunlight, during drying, lack of food, heating to 65-100 ° C, under the influence of disinfectants, as a result of struggle between species, etc.

Only some types of bacteria form special cells - spores (from the Greek “spore” - seed), with the help of which they can reproduce.

IN unfavorable conditions(with a lack of food, moisture, sudden changes in temperature), the cytoplasm of the bacterial cell, shrinking, moves away from the mother shell, becomes rounded and forms a new, denser shell inside it on its surface (Fig. 30). like this bacterial cell also called spore (from the Greek word “spore” - seed). Spores of some bacteria persist for a very long time in the most unfavorable conditions. They can withstand drying, heat and frost, and do not die immediately even in boiling water. Spores are easily spread by wind, water, etc. There are many of them in the air and soil. Under favorable conditions, the spore germinates and becomes a living bacterium. Spores in the vast majority of bacteria are an adaptation to survival in unfavorable conditions.

Rice. 30. Formation of dispute

New concepts

How can we explain the widespread distribution of bacteria on our planet?

Tasks

1. Wash the potato tuber without peeling it, cut into slices. Rub the slices with chalk and place in a Petri dish. Place the cup in a warm place with a temperature of 25-30 °C. After 2-3 days, a dense, wrinkled film forms on the surface of the slices. Rub a small piece of film in a drop of water and examine the potato stick bacteria under a microscope. They are motile, have flagella and can form spores.
2. To obtain a culture of Bacillus subtilis, put some hay in a flask with water, cover the neck of the flask with cotton wool and boil the contents for 15 minutes to destroy other bacteria that may be in the flask. Bacillus subtilis does not die when boiled. Filter the resulting hay infusion and place it in a room with a temperature of 20-25 ° C for several days. Bacillus subtilis will multiply, and soon the surface of the infusion will be covered with a film of bacteria.

   Using a glass rod, transfer a piece of film onto a glass slide, cover it with a coverslip and examine it under a microscope. Add a drop of methylene blue or ink diluted with water under the cover slip. Bacteria are much more visible against a blue background. Some of them are mobile, while the non-moving ones have shiny oval formations inside. This is a debate.

3. Most bacteria die at temperatures of +65-100 °C, but the spores of some of them can withstand heating up to +140 °C and cooling down to -253 °C.

   Heat the filtered infusion. Find out at what temperature Bacillus subtilis bacteria die.

Do you know that...

There are so-called predatory bacteria. These are colonial bacteria. Their cells are connected by bridges and form a kind of trapping net. While moving, such a colony captures and digests small living organisms.

People who survive more than 48 hours after an injury are most likely to die from sepsis (Wilson, 1985). In many cases of death of severely injured patients due to sepsis, the source of infection cannot be identified. Most often, bacteriological examination shows the presence of gram-negative microorganisms. On this basis, many researchers are inclined to assume that the intestine is a reservoir pathogenic bacteria and endotoxins, which initiate a general host response that leads to shock and failure internal organs (BealandCerra, 1994).

Pathogenesis

Bacterial spread refers to the movement of viable microorganisms present in the body from the gastrointestinal tract to the mesenteric lymph nodes, liver, spleen and bloodstream. (Deitchetal., 1996). Numerous studies of animal and human diseases have clearly shown that microorganisms and toxins normally found in the gastrointestinal tract can move from the intestinal lumen to the outside of the intestine ( Deitchetal., 1985, 1987, 1988). However clinical significance the spread of bacteria was called into question when researchers were unable to detect the presence of microorganisms in the portal vein or circulatory system when examining people who died as a result of injuries (Mooretal., 1991). In addition, disappointing results from examinations of seriously ill patients in several medical centers to evaluate the possibility of selective intestinal decontamination did not meet expectations (VanSaeneetal., 1992).When antimicrobial agents were used to intensively cleanse the intestines of pathogenic gram-negative bacteria and fungi, the survival rate did not increase, although these patients showed a 50% decrease in the number of infectious complications.

It is now believed that many microorganisms that enter the intestinal lymphatic tissue are killed by the body's defenses, thereby initiating a massive inflammatory response characterized by the release of cytokines, vasoactive substances, complement and other immunomodulators (Deitchetal., 1996). Moreover, the presence of intestinal endotoxins in the blood may be a factor that causes, irreversibly, or enhances the hypermetabolic reaction observed in systemic inflammatory response syndrome. Endotoxins are known to stimulate the release of cytokines and can lead to decreased function of the immune system, blood coagulation system, and the protective barrier of the gastrointestinal mucosa. Therefore, it is not necessary to isolate viable bacteria from the bloodstream or peripheral organs to conclude that the intestine is the most probable cause systemic inflammatory response syndrome.

Visceral ischemia may play a role main role in the development of failure of several internal organs, since there is a close relationship between a decrease in the pH value of the mucous membrane and the likelihood of disease and death (Silverman and Tita, 1992). It is believed that intestinal ischemia leads to a decrease in the protective function of the barrier, leaving the lymphoid tissue associated with the intestine exposed to microorganisms and toxins. In addition, a large number of cytokines and endotoxins are released. A consequence of suppression of the reticuloendothelial system may be the presence of endotoxins or bacteria in the circulatory system.

Protective barrier of the gastrointestinal mucosa
Under normal conditions, the intestine is an effective mechanical and functional protective barrier that prevents the absorption of bacteria and toxins found in its cavity. The condition for the spread of bacteria is their adhesion to the intestinal mucosa. Bacterial adhesion is reduced by intestinal peristalsis and mucus production. Research shows that increased bacterial proliferation occurs in diseases and disorders associated with decreased motility, such as ileus and intestinal obstruction. The use of vasoconstrictors, corticosteroids and non-steroidal anti-inflammatory drugs can cause a decrease in mucus production and destruction of the protective mechanical barrier. Insufficient perfusion, such as in visceral ischemia associated with shock, also leads to decreased epithelial cell turnover, cell destruction, and increases the risk of mucosal destruction. Stress gastritis and ulcers often develop in seriously ill patients.

The intestine is the largest immunological and endocrine organ. Lymphoid tissue associated with the intestine consists of Peyer's patches, lymphatic follicles, laminapropria lymphocytes, intraepithelial lymphocytes and mesenteric lymph nodes. Secretory IgA is produced by sensitized (effector) lymphocytes of the surface layer of the intestinal mucosa. These immune mechanisms play an important role in protecting the host from microbial invasion. Therefore, when the immune system is suppressed, there is a predisposition to the spread of bacteria. Poor nutrient supply of enterocytes may also lead to decreased IgA production and weakened gastrointestinal immune defenses.

Another factor contributing to the preservation of the protective barrier of the gastrointestinal mucosa is the natural microflora, which performs a protective function. The vast majority of microorganisms contained in the gastrointestinal tract are anaerobes. These bacteria compete with potential pathogenic microorganisms in the fight for nutrients and sites of attachment to the mucous membrane, thereby preventing the excessive development of the microflora of gram-negative bacteria. Antibiotic therapy often disrupts the delicate balance of the microflora of the gastrointestinal tract by suppressing more sensitive anaerobic microorganisms (Deitchetat., 1985). In addition, the use of Hg receptor blockers, which can stimulate excessive development of microflora and the formation of colonies of microorganisms in the stomach, as well as the use of hyperosmolar nutrient solutions for enteral nutrition, can disrupt the normal microflora in the intestines of seriously ill patients.

The importance of proper nutrition

For many years, the gastrointestinal tract has been neglected in the treatment of seriously ill patients. The main function of the gastrointestinal tract was considered to be absorption nutrients, which according to popular belief is necessary to ensure adequate wound healing and the body's response to injury or infection. Because of the potential for aspiration, vomiting, ileus, or lack of enteral access, many clinicians have chosen to “leave the bowel alone.” We now know that such “rest” can cause atrophy of the mucous membrane, changes in permeability and loss of the nutritional effect of gastrointestinal hormones. Experimental models have shown that fasting and poor nutrition alone do not cause the spread of bacteria. However, they may predispose them to mucosal damage and the development of fatal sepsis of intestinal origin during periods of systemic inflammation. Currently, experts are paying considerable attention to this problem and are conducting research to determine the role of various nutrients, and are also trying to use enteral nutrition to influence metabolism and inflammatory processes.

Clinical significance

Experiments on animals revealed three main mechanisms for activating the spread of bacteria:

1. excessive development of intestinal microflora;
2. weakening of the body's defenses;
3. damage to the protective barrier of the gastrointestinal mucosa. Therefore, intensive bacterial prevention should primarily focus on preventing these problems, as well as providing the intestines with essential nutrients.

Results from human clinical studies indicate that the spread of bacteria may be promoted by thermal injury, immunosuppression, trauma, hemorrhagic shock, endotoxins, acute pancreatitis causing necrosis, total parenteral feeding, neutropenia, intestinal obstruction and ischemia. Animal studies suggest that the same diseases and disorders may contribute to the spread of bacteria in the bodies of seriously ill veterinary hospital patients. In addition, dogs with severe parvovirus enteritis are particularly predisposed to the spread of bacteria in the body, sepsis and the appearance of endotoxins in the blood due to a combination of neutropenia and destruction of the protective barrier of the gastrointestinal mucosa.

Prevention

Prevention of bacterial spread, sepsis, and multi-organ failure is the subject of ongoing research. Most important factor To prevent the spread of bacteria is to maintain the integrity of the protective barrier of the gastrointestinal mucosa, since experimental studies show that the spread of bacteria can be largely prevented by reducing the degree of damage to the mucosa. For this reason, therapeutic measures are aimed at:

1. reducing the likelihood of mucosal rupture,
2. limiting undesirable consequences in case of rupture,
3. maintaining intestinal function for rapid healing of mucosal defects. In this regard, the following recommendations can be made.

Improved intestinal oxygenation. Apparently, ischemia plays a major role in damage to the mucous membranes in seriously ill patients. The size of the damage increases as a result of reperfusion injury. It is necessary to maximize the supply of oxygen to the intestines through effective and intensive restoration of hemodynamics. To maintain adequate blood pressure and gastrointestinal perfusion, sufficient volumes of crystalloid and/or colloid solutions should be administered. Positive myotropic agents such as dobutamine or dopamine may be necessary to maintain blood pressure in sepsis. (Silverman and Tita, 1992). Oxygen should be additionally administered if oxygemometry parameters do not exceed 90-95%. If the hemoglobin concentration drops below 10-12 g/100 ml, then a blood transfusion or bovine hemoglobin solution can be administered to improve the ability of blood to transport oxygen. To monitor the pH of the mucous membranes and determine the adequacy of perfusion of the gastrointestinal tract, it is best to use the method of gastric tonometry, if possible. With clinical signs of sepsis, bactericidal antibiotics must be administered in any case. wide range actions. Early diagnosis and surgical correction of dead bowel or drainage of an abscess are of paramount importance for successful completion of treatment.

In experimental settings, reperfusion injury has been prevented by the use of allopurinol or peroxide dismutase. The components of the body's antioxidant defense system are vitamins C, E and A, selenium, beta-carotene, as well as amino acids such as cystine, glycine and glutamine. Adding antioxidants to your food may also be beneficial. Research is currently underway to identify substances that selectively improve gastrointestinal perfusion, but so far they have not been successful. Catecholamines such as norepinephrine and adrenaline, which induce constriction of the blood vessels of internal organs, should not be used.

Limitation negative consequences damage to mucous membranes. The use of antacids and H2 blockers to limit the development of stress ulcers and gastritis in critically ill patients may lead to overgrowth of microflora and increase the likelihood of pneumonia in hospitalized ventilated patients (VanSaeneetal., 1992) To reduce the size of gastric damage without increasing gastric pH, the use of sucralfate and nasogastric aspiration is currently recommended.

The method of selective intestinal decontamination appears to reduce the likelihood of developing an infectious disease in a clinical setting, but there is no documented evidence of an increase in the chances of survival of seriously ill people (VanSaeneetal., 1992).For human treatment, a combination of amikacin, amphotericin B and polymyxin B is usually used (Cockerille et al., 1992). The literature provides evidence that oral neomycin prevented death and reduced the spread of bacteria after thermal injury. (Osa et al., 1993). A combination of polymyxin B, activated charcoal and kaopectate administered orally was used to bind lipopolysaccharide endotoxin. In addition, there are anecdotal reports of success using diluted chlorhexidine or betadine (povidone-iodine) administered by enema to treat parvovirus enteritis in puppies.

A polyvalent equine antiserum is currently available to neutralize lipopolysaccharide endotoxin in domestic animals. (SEPTI-serum, Immac, Inc., Columbia, MO 75201). It is administered slowly over 30-60 minutes at a dose of 4.4 ml/kg along with intravenous crystalloid solutions in a 1:1 ratio. Currently, the results of clinical studies of the use of this drug are not known, but it should be assumed that it is most effective when used before antibiotic therapy, since after the destruction of bacteria, the concentration of endotoxin in the circulating blood increases sharply. When equine antiserum is used, patients should be monitored closely as signs of anophylaxis may occur.

Maintaining bowel function through enteral feeding
Meaning proper feeding seriously ill patients is beyond doubt. However, in recent years, the important role of “gut filling” through enteral feeding, which should be started as early as possible, has become increasingly clear. Studies have shown that, compared with enteral feeding, total parenteral feeding results in an increased likelihood of infectious disease and death. Total parenteral feeding leads to mucosal atrophy. In addition, practice shows that lipid emulsions increase immune suppression by suppressing lymphocyte blastogenesis. In addition, omega-6 fatty acids are “precursors” to prostaglandins and leukotrines, which can cause inflammation. Currently, it is recommended that total parenteral feeding be used only when there are serious contraindications to enteral nutrition.

Enteral feeding has a beneficial effect on intestinal function by strengthening the immune system (lymphocytes and macrophages), increasing the secretion of IgA and mucin, and maintaining intestinal mass through nutritional action.

The most suitable metabolic source for the cells lining the inner surface of the small intestine is glutamine. Glutamine is considered a "conditionally essential" nutrient for critically ill patients. He has great importance for lymphocyte mitogenesis and strengthens the intestinal protective barrier. The results of many studies support the advisability of adding glutamine to solutions for enteral or parenteral nutrition (slowing the spread of bacteria, thickening the gastrointestinal mucosa, increasing the chances of survival). At the same time, in some cases, the use of glutamine did not produce a positive effect. Glutamine is safe for the patient's health, however, this substance is very unstable, and therefore it must be added to the nutrient solution immediately before administration. If there is significant damage to the mucous membrane, adding glutamine may have a beneficial effect. This drug is available in powder form (CambridgeNeutraceuticals), which can be used at a dose of 10 mg/kg per day. Glutamine can be added to water given to convalescent animals or enteral feeding solutions administered through nasogastric, gastrostomy, or jejunostomy tubes. In addition, other factors may help reduce the spread of bacteria. nutritional supplements, such as omega-3 fatty acids (fish oil products), arginine, nucleic acid and antioxidants.

The most suitable metabolic source for colonocytes is short-chain fatty acids. They are produced by the fermentation of indigestible carbohydrates commonly called “fermentable fibers” (pectin, betaglycan and lactulose). Insoluble fibers, such as cellulose, have nutritional effects on the gastrointestinal mucosa by increasing mucus production and epithelial cell growth, as well as supporting the growth of normal microflora. Insoluble fiber is thought to stimulate the secretion of nutritional gut hormones that strengthen the intestinal protective barrier. There are currently no recommendations regarding the optimal fiber type or dose, but research is ongoing. A number of preliminary studies and experiments conducted on animals show that the addition of crude fiber to enteral nutritional solutions can reduce the rate of bacterial spread, prevent mucosal atrophy and excessive development of microflora in the cecum. In addition, the subject of research is hormones such as bombesin, which have a protective nutritional effect on the mucous membrane of the gastrointestinal tract. To develop specific recommendations regarding animal feeding, it is necessary to await the results of research conducted in this promising and interesting area.

Microorganisms are ubiquitous. The only exceptions are the craters of active volcanoes and small areas at the epicenters of exploded atomic bombs. Neither low temperatures Antarctica, neither boiling streams of geysers, nor saturated salt solutions in salt pools, nor strong insolation of mountain peaks, nor harsh radiation nuclear reactors do not interfere with the existence and development of microflora. All living beings - plants, animals and people - constantly interact with microorganisms, often being not only their repositories, but also their distributors. Microorganisms are the natives of our planet, the first settlers, actively exploring the most incredible natural substrates.

Soil microflora. The number of bacteria in the soil is extremely large - hundreds of millions and billions of individuals per 1 g (Table 5). There are much more of them in soil than in water and air. The total number of bacteria in soils changes. By B. C. Winogradsky, microflora-poor soils contain 200-500 million bacteria per 1 g, medium - up to a billion, rich - two or more billion individuals per 1 g. The number of bacteria depends on the type of soil, their condition, and the depth of the layers (Table 6) .

On the surface of soil particles, microorganisms are located in small microcolonies (20-100 cells each). They often develop in the thickness of clots organic matter, on living and dying plant roots, in thin capillaries and inside lumps.

The soil microflora is very diverse. Various physiological groups of bacteria are found here: rotting bacteria, nitrifying bacteria, nitrogen-fixing bacteria, sulfur bacteria, etc. Among them are aerobes and anaerobes, spore and non-spore forms. Microflora is one of the factors in soil formation.

Region active development microorganisms in the soil is the zone adjacent to the roots of living plants. It is called the rhizosphere, and the totality of microorganisms contained in it is called the rhizosphere microflora.

Microflora of water bodies. Water is a natural environment where large quantities microorganisms develop. The bulk of them enters the water from the soil. Factor that determines the number of bacteria in water, - availability it contains nutrients. The cleanest waters are from artesian wells and springs. Open reservoirs and rivers are very rich in bacteria. Largest quantity bacteria are found in the surface layers of water, closer to the shore. The water in the suburban area is very polluted due to wastewater. Co wastewater pathogenic microorganisms enter water bodies: brucellosis bacillus, tularemia bacillus, polio virus, foot-and-mouth disease virus, pathogens of intestinal infections (bacillus typhoid fever, paratyphoid fever, dysentery bacillus, vibrio cholera, etc.). Bacteria persist in water for a long time, so it can be a source of infectious diseases. As you move away from the shore and increase in depth, the number of bacteria decreases.

Pure water contains 100-200 bacteria per ml, and polluted water contains 100-300 thousand or more. There are many bacteria in bottom sludge, especially in its surface layer, where bacteria form a film. This film contains a lot of sulfur and iron bacteria, which oxidize hydrogen sulfide to sulfuric acid and thereby prevent fish from dying. There are nitrifying and nitrogen-fixing bacteria. There are more spore-bearing forms in the silt (about 75%), while non-spore-bearing forms predominate in the water (about 97%).

By species composition The microflora of water is similar to the microflora of soil, but specific bacteria are also found in water (You. fluorescens, You. aquatilisand etc.). By destroying various waste that gets into the water, microorganisms gradually carry out the so-called biological purification of water.

Air microflora. The microflora of the air is less numerous than the microflora of soil and water. Bacteria rise into the air with dust, can remain there for some time, and then settle on the surface of the earth and die from lack of nutrition or under the influence of ultraviolet rays. The number of microorganisms in the air depends on geographical area, terrain, time of year, dust contamination, etc. Each speck of dust is a carrier of microorganisms, so there are a lot of them in enclosed spaces (from 5 to 300 thousand in 1 m 3). Most bacteria are in the air above industrial cities. Air rural areas cleaner. Most fresh air over forests, mountains, snowy areas. The upper layers of air contain fewer microbes. The air microflora contains many pigmented and spore-bearing bacteria, which are more resistant than others to ultraviolet rays. Very much attention is paid to the microbiological study of air, since infectious diseases (influenza, scarlet fever, diphtheria, tuberculosis, tonsillitis, etc.) can spread through airborne droplets.

Microflora of the human body. The human body, even a completely healthy one, is always a carrier of microflora. When the human body comes into contact with air and soil, various microorganisms, including pathogenic ones (tetanus bacilli, gas gangrene, etc.), settle on clothing and skin. The number of microbes on the skin of one person is 85 million - 1212 million. The exposed parts of the human body are most often contaminated. E. coli and staphylococci are found on the hands. There are over 100 types of microbes in the oral cavity. The mouth with its temperature, humidity, and nutrient residues is an excellent environment for the development of microorganisms.

The stomach has an acidic reaction, so the bulk of microorganisms in it die. Starting from the small intestine, the reaction becomes alkaline, i.e. favorable for microbes. The microflora in the large intestines is very diverse. Each adult excretes about 18 billion bacteria daily in excrement, i.e., more individuals than there are people on the globe.

Internal organs not connected to external environment(brain, heart, blood, liver, bladder, etc.) are usually free of germs. Microbes enter these organs only during illness.

Microorganisms that cause infectious diseases, are called pathogenic or pathogenic (Table 7). They are able to penetrate tissue and release substances that destroy the body's protective barrier. Permeability factors

highly active, act in small doses, have enzymatic properties. They enhance the local effect of pathogenic microorganisms and infect connective tissue, contribute to the development of general infection. These are the invasive properties of microorganisms.

Substances that inhibit the body's defenses and enhance the pathogenic effect of pathogens are called aggressins. Pathogenic microorganisms also produce toxins - poisonous waste products. Most strong poisons secreted by bacteria in environment, are called exotoxins. They are formed by diphtheria and tetanus bacilli, staphylococcus, streptococcus, etc. In most bacteria, toxins are released from cells only after their death and destruction. Such toxins are called endotoxins. They are formed by tuberculosis bacillus, Vibrio cholerae, pneumococci, pathogen anthrax and etc.

There are bacteria that are called opportunistic because under normal conditions they live as saprophytes, but when the resistance of the human or animal body weakens, they can cause serious diseases. For example, E. coli - a common intestinal saprophyte - under unfavorable conditions can cause inflammatory processes in the kidneys, bladder, intestines and other organs.

Louis Pasteur made a great contribution to the fight against infectious diseases of animals and humans.

Pasteur Louis (1822-1895) - French microbiologist and chemist. Founder of microbiology and immunology. He proposed a method of preventive vaccinations with vaccines that have saved and are saving millions of people from infectious diseases.

- Source-

Bogdanova, T.L. Handbook of biology / T.L. Bogdanov [and others]. – K.: Naukova Dumka, 1985.- 585 p.

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The emergence of bacterial diseases in a certain area for the first time in a season (primary infection) is mainly due to the presence of a surviving bacterial infection, and the spread of bacterial diseases during the growing season (secondary infection) is carried out by various natural and artificial factors.

Bacterial infection may persist different ways, But highest value have seeds and planting material, living plants and plant debris, insects and soil.

Seeds and planting material. Seeds, tubers and other planting material are the most common place for the preservation of phytopathogenic bacteria and a source of plant infection with bacterioses. Seeds can serve as a source of the appearance of some kind of bacteriosis where it did not exist before, i.e. they can spread diseases throughout to the globe. The causative agent of cotton gommosis, Xanthomonas malvacearum Dowson, was introduced with the seeds into cotton-growing areas where this disease had not previously been encountered. Bacteria can be found both on the surface of seeds, where they get during threshing (for example, tobacco pods Pseudomonas tabaci Stapp.) and extracting seeds from fruiting organs (for example, tomato fruits when infected with black spot Xanthomonas vesicatoria Dowson), and in their internal tissues, where enter during plant growth. For example, the causative agent of bean bacteriosis, Xanthomonas phaseoli Dowson, is transmitted from beans to seeds.

Infection of plants from infected seeds occurs in various ways: the movement of bacteria through the vessels of seedlings (black bacteriosis of wheat - Xanthomonas translucens Dowson, ring rot of potatoes - Corynebacterium sepedonicum Scapt. et Burch.); the removal of bacteria from the cotyledons, which become diseased and serve as a source of leaf infection and damage (cotton blight - Xanthomonas malvacearum Dowson); the removal of the seed coat to the soil surface upon emergence and the transfer of bacteria to plant leaves, causing their infection (bacterial tobacco grouse - Pseudomonas tabaci Stapp.).

Plant remains. Dead remains diseased plants are one of the main places where bacteria persist and a source of infection of healthy plants with bacteriosis. This is how many phytopathogenic bacteria are preserved. Therefore, plant debris (fallen leaves, dry branches, etc.) must be destroyed. Phytopathogenic bacteria can also persist in living plants, for example, during bacteriosis of tree species.

Insects. Some types of phytopathogenic bacteria overwinter in insects, which can serve as a source of primary plant infection in the spring. This has been proven for the causative agent of cucumber wilting - Erwinia tracheifila (Sm.) Holl., which overwinters in the intestines of some leaf beetles (Diabrotia vittata). Here the causative agent of the disease is completely dependent on the leaf beetle, and fighting it is tantamount to fighting the disease itself. Insects serve as the main agents of spread for many types of phytopathogenic bacteria. They play an important role in the spread of the potato blackleg pathogen, Pectobacterium phytophthorum Dowson. For example, the sprout fly (Hylemya trichodactyla) harbors the pathogen, which then serves as a source of infection for potatoes. The burn of apple, pear and other fruit trees - Pseudomonas cerasi Griff, spreads in the garden with the participation of bees and wasps, on which the possibility of insects carrying bacteriosis was first proven. Bacterial wilt of corn (Aplanobacter stewarti McCul) is transmitted by the stem beetles Chaetocnema pulicoria and Ch. denticulata, as well as the larvae of the beetle Diabrotica duodecempunctata. The bread bug spreads bacteriosis of corn cobs - Bacillus mesentericus vulgatus Flugge.

The soil. Until recently, soil was considered one of the main places for the preservation and accumulation of bacterial infection. It has now been established that most phytopathogenic bacteria in the soil die very quickly. Their death is caused by soil microorganisms - antagonists or bacteriophages. Therefore, even if soil serves as a source of infection of plants with bacterioses, it is only very short term(no more than 10-15 days). At the same time, phytopathogenic bacteria can persist in the rhizosphere of roots, which is probably explained by the smaller number of their antagonists in the rhizosphere than in the soil. The possibility of overwintering of the causative agent of bacterial tobacco grouse - Pseudomonas tabaci Stapp - has been proven on the roots of winter crops. and black spot of tomatoes - Xanthomonas vesicatoria Dowson.

The spread of phytopathogenic bacteria from diseased plants to healthy ones and from the site of primary infection of one area to another can occur both with the help of various natural factors - air, water, insects, and by artificial introduction of infection as a result economic activity person.

Air currents. Microscopically small bacteria and tiny particles Diseased plants are also spread by air movement. However, most phytopathological bacteria are nonsporeless and die rather quickly in dry air and from exposure to direct sunlight.

Water. Water is of great importance in the spread of bacteria. Raindrops fall on the ground or diseased plants and with splashes of water the infection is transferred to healthy plants. The spread of bacteriosis is facilitated by irrigation waters and river flows, when the remains of diseased plants enter the water. An example of such a transfer is the spread of cotton fungus - Xanthomonas malvacearum Dowson with ditch waters.

In the process of cultivating agricultural crops, humans can also spread certain bacterial diseases. For example, when pinching tomatoes from one plant to another, the bacterial tomato cancer - Corynebacterium michiganense Jens - is transferred, while when topping shag, the grouse - Pseudomonas tabaci Stapp - spreads.

When introducing into culture important economically and productive plants, as well as when transporting plants from one country to another (wheat, corn, potatoes, tobacco, etc.), various pathogens were also imported. At the same time, they found themselves in the most favorable conditions, since the crops they affected were susceptible to this disease.

For example, the causative agent of citrus canker, Xanthomonas citri Dowson, was brought from Japan to Florida in 1911. In Japan, this bacteriosis did not cause harm, but in Florida it turned out to be so dangerous that to eradicate the disease it was necessary to destroy 15 million trees in nurseries and plantations. This came at a huge cost, amounting to millions of dollars. The causative agent of bacterial blight of fruits is Pseudomonas cerasi Griff., found in North America back in 1870, was transferred around 1911 to Japan, in 1919 - to New Zealand and in 1924 to Italy, and then the disease spread to other countries. In our country, the disease occurs on apricots, plums and peaches.

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