– an infectious process caused by spore-forming or non-spore-forming microorganisms under conditions favorable for their life. Characteristic clinical signs of anaerobic infection are the predominance of symptoms of endogenous intoxication over local manifestations, the putrefactive nature of the exudate, gas-forming processes in the wound, and rapidly progressing tissue necrosis. Anaerobic infection is recognized on the basis of the clinical picture, confirmed by the results of microbiological diagnostics, gas-liquid chromatography, mass spectrometry, immunoelectrophoresis, PCR, ELISA, etc. Treatment of anaerobic infection involves radical surgical treatment of the purulent focus, intensive detoxification and antibacterial therapy.

General information

Anaerobic infection is a pathological process caused by anaerobic bacteria that develop under conditions of anoxia (lack of oxygen) or hypoxia (low oxygen tension). Anaerobic infection is a severe form of the infectious process, accompanied by damage to vital organs and a high mortality rate. In clinical practice, specialists in the field of surgery, traumatology, pediatrics, neurosurgery, otolaryngology, dentistry, pulmonology, gynecology and other medical fields have to deal with anaerobic infection. Anaerobic infection can occur in patients of any age. The proportion of diseases caused by anaerobic infection is not precisely known; from purulent foci in soft tissues, bones or joints, anaerobes are sown in approximately 30% of cases; anaerobic bacteremia is confirmed in 2-5% of cases.

Causes of anaerobic infection

Anaerobes are part of the normal microflora of the skin, mucous membranes, gastrointestinal tract, and genitourinary system and, due to their virulent properties, are opportunistic. Under certain conditions, they become causative agents of endogenous anaerobic infection. Exogenous anaerobes are present in soil and decomposing organic matter and cause a pathological process when they enter a wound from the outside. Anaerobic microorganisms are divided into obligate and facultative: the development and reproduction of obligate anaerobes is carried out in an oxygen-free environment; facultative anaerobes are able to survive both in the absence and presence of oxygen. Facultative anaerobic bacteria include Escherichia coli, Shigella, Yersinia, streptococci, staphylococci, etc.

Obligate pathogens of anaerobic infection are divided into two groups: spore-forming (clostridia) and non-spore-forming (non-clostridial) anaerobes (fusobacteria, bacteroides, veillonella, propionibacteria, peptostreptococci, etc.). Spore-forming anaerobes are causative agents of clostridiosis of exogenous origin (tetanus, gas gangrene, botulism, foodborne toxic infections, etc.). Non-clostridial anaerobes in most cases cause purulent-inflammatory processes of an endogenous nature (abscesses of internal organs, peritonitis, pneumonia, phlegmon of the maxillofacial area, otitis media, sepsis, etc.).

The main factors of the pathogenicity of anaerobic microorganisms are their quantity in the pathological focus, the biological properties of the pathogens, and the presence of associated bacteria. In the pathogenesis of anaerobic infection, the leading role belongs to enzymes produced by microorganisms, endo- and exotoxins, and nonspecific metabolic factors. Thus, enzymes (heparinase, hyaluronidase, collagenase, deoxyribonuclease) can enhance the virulence of anaerobes and the destruction of muscle and connective tissue. Endo- and exotoxins cause damage to the vascular endothelium, intravascular hemolysis and thrombosis. In addition, some clostridial toxins have nephrotropic, neurotropic, and cardiotropic effects. Nonspecific factors in the metabolism of anaerobes - indole, fatty acids, hydrogen sulfide, ammonia - also have a toxic effect on the body.

Conditions favorable to the development of anaerobic infection are damage to anatomical barriers with the penetration of anaerobes into tissues and the bloodstream, as well as a decrease in the redox potential of tissues (ischemia, bleeding, necrosis). The entry of anaerobes into tissues can occur during surgical interventions, invasive manipulations (punctures, biopsies, tooth extraction, etc.), perforation of internal organs, open injuries, wounds, burns, animal bites, long-term compartment syndrome, criminal abortions, etc. Factors Contributing to the occurrence of anaerobic infection are massive contamination of wounds with soil, the presence of foreign bodies in the wound, hypovolemic and traumatic shock, concomitant diseases (collagenosis, diabetes mellitus, tumors), and immunodeficiency. In addition, irrational antibiotic therapy aimed at suppressing the accompanying aerobic microflora is of great importance.

Depending on the location, anaerobic infection is distinguished:

• central nervous system (brain abscess, meningitis, subdural empyema, etc.)
• head and neck (periodontal abscess, Ludwig's angina, otitis media, sinusitis, cellulitis of the neck, etc.)
• respiratory tract and pleura (aspiration pneumonia, lung abscess, pleural empyema, etc.)
• female reproductive system (salpingitis, adnexitis, endometritis, pelvioperitonitis)
• abdominal cavity (abdominal abscess, peritonitis)
• skin and soft tissues (clostridial cellulitis, gas gangrene, necrotizing fasciitis, abscesses, etc.)
• bones and joints (osteomyelitis, purulent arthritis)
• bacteremia.

Symptoms of anaerobic infection

Regardless of the type of pathogen and the location of the focus of anaerobic infection, various clinical forms share some common features. In most cases, anaerobic infection has an acute onset and is characterized by a combination of local and general symptoms. The incubation period can range from several hours to several days (on average about 3 days).

A typical sign of anaerobic infection is the predominance of symptoms of general intoxication over local inflammatory phenomena. A sharp deterioration in the patient's general condition usually occurs even before the onset of local symptoms. The manifestation of severe endotoxemia is high fever with chills, severe weakness, nausea, headache, lethargy. Characterized by arterial hypotension, tachypnea, tachycardia, hemolytic anemia, icterus of the skin and sclera, acrocyanosis.

In case of anaerobic wound infection, the early local symptom is severe, increasing pain of a bursting nature, emphysema and crepitus of soft tissues caused by gas-forming processes in the wound. Constant signs include the fetid and ichorous odor of exudate associated with the release of nitrogen, hydrogen and methane during anaerobic oxidation of the protein substrate. The exudate has a liquid consistency, serous-hemorrhagic, purulent-hemorrhagic or purulent in nature, heterogeneous color interspersed with fat and the presence of gas bubbles. The putrefactive nature of the inflammation is also indicated by the appearance of the wound, containing gray-green or gray-brown tissue, sometimes black scabs.

The course of an anaerobic infection can be fulminant (within 1 day from the moment of surgery or injury), acute (within 3-4 days), subacute (more than 4 days). Anaerobic infection is often accompanied by the development of multiple organ failure (renal, hepatic, cardiopulmonary), infectious-toxic shock, severe sepsis, which causes death.

Diagnostics

For the timely diagnosis of anaerobic infection, the correct assessment of clinical symptoms is of great importance, allowing timely provision of the necessary medical care. Depending on the location of the infectious focus, the diagnosis and treatment of anaerobic infection can be performed by clinicians of various specialties - general surgeons, traumatologists, neurosurgeons, gynecologists, otolaryngologists, maxillofacial and thoracic surgeons.

Methods for express diagnosis of anaerobic infection include bacterioscopy of wound discharge with Gram staining of a smear and gas-liquid chromatography. In the verification of the pathogen, the leading role belongs to bacteriological culture of the discharged wound or abscess contents, analysis of pleural fluid, blood culture for aerobic and anaerobic bacteria, enzyme immunoassay, and PCR. Biochemical blood parameters during anaerobic infection reveal a decrease in protein concentration, an increase in the level of creatinine, urea, bilirubin, transaminase and alkaline phosphatase activity. Along with clinical and laboratory tests, radiography is performed, which detects gas accumulation in the affected tissues or cavities.

Anaerobic infection must be differentiated from erysipelas of soft tissues, polymorphous exudative erythema, deep vein thrombosis, pneumothorax, pneumoperitoneum, perforation of hollow abdominal organs.

Treatment of anaerobic infection

An integrated approach to the treatment of anaerobic infection involves radical surgical treatment of the purulent focus, intensive detoxification and antibacterial therapy. The surgical stage must be performed as early as possible - the patient’s life depends on it. As a rule, it consists of a wide dissection of the lesion with removal of necrotic tissue, decompression of surrounding tissue, open drainage with washing of cavities and wounds with antiseptic solutions. Features of the course of anaerobic infection often require repeated necrectomies. The outcome of anaerobic infection largely depends on the clinical form of the pathological process, premorbid background, timely diagnosis and initiation of treatment. The mortality rate for some forms of anaerobic infection exceeds 20%. Prevention of anaerobic infection consists of timely and adequate PSO of wounds, removal of foreign bodies of soft tissue, compliance with the requirements of asepsis and antisepsis during operations. In case of extensive wound damage and a high risk of developing anaerobic infection, specific immunization and antimicrobial prophylaxis are necessary.

Anaerobic infection is caused by anaerobic microorganisms that do not require oxygen to obtain energy and function. Ailments caused by this type of bacteria include diseases such as botulism, tetanus, gas cellulitis and gangrene. Aerobic infection, unlike anaerobic infection, is provoked by microorganisms that need oxygen to maintain their vital functions.

Brief classification of anaerobes

Microorganisms in this category are divided into clostridia (spore-forming) and non-clostridial types. There are also exogenous and endogenous anaerobes. The latter are considered a component of the normal human microflora and are usually detected in the genitourinary system and intestines. They are also found on mucous membranes, skin, and are released from the respiratory tract. Exogenous microorganisms are found in soil and decaying organic matter.

This type of infection occurs quickly and is characterized by rapidly progressing necrotic changes in tissues, as well as the formation of gases and severe intoxication. In this case, there are no pronounced inflammatory phenomena. Anaerobic infection is considered one of the most severe. It leads to the development of endogenous intoxication and damage to important systems and organs. Anaerobic infection has a high mortality rate. Its development can be subacute (from 4 days), acute (3-4 days), fulminant (1 day from the moment pathogens enter the body). The probability and rate of development of anaerobic infection, as a rule, depend on the number of microorganisms that have entered the wound, the degree of their pathogenicity and the individual characteristics of the human body. The appearance of pathology is facilitated by weakened immunity, the presence of tissue areas deprived of blood supply, and chronic intoxication. Anaerobic infection in surgery is one of the most severe postoperative complications.

Treatment

The main method of treating wound anaerobic infection is surgical, namely large-scale dissection of the affected area and complete removal of necrotic tissue with good drainage and antiseptic treatment. The leading role in postoperative therapy is the use of antibacterial drugs.

As a rule, broad-spectrum antibiotics are used: cephalosporins, semi-synthetic penicillins, aminoglycosides, etc. Antibacterial drugs are also used that selectively act on anaerobic microorganisms (Metronidazole, Clindamycin, Dioxidin, etc.). In difficult cases, patients are prescribed the maximum allowable dose of antibiotics every day. Infusion therapy is actively used: amino acid solutions, blood products, blood substitutes. Detoxifying the body and increasing immunity is of great importance. Prevention of anaerobic infections consists of careful and timely treatment of wounds and compliance with antiseptic and aseptic measures during surgical interventions.

A surgical infection is a type of disease that affects human tissues and organs. It is caused by a huge number of pathogenic bacteria. Among them there are aerobic and anaerobic bacteria.

What type of microbes are these - anaerobes? Why did doctors separate them into a separate group? The clinic, treatment and prevention of anaerobic infection will be discussed in our article.

What is an anaerobic infection? This is a disease caused by microbes that live without oxygen. Such microorganisms are called anaerobes (an-negation, aero-air). They are ubiquitous in nature. Their usual habitat is the hollow organs of animals and humans (stomach, intestines, respiratory tract). In unfavorable conditions (in the air), they form a spore - a form of life that is resistant to aggressive external environmental factors. And when the spore enters the patient’s body, the bacterium is activated and begins to actively multiply.

Anaerobes - who are they?

Anaerobic infection is caused by two types of pathogens:

1. non-clostridial microorganisms;
2. clostridial organisms.

Non-clostridial pathogens include peptococci and bacteroides. They cause a so-called putrefactive infection. Clostridia include the causative agents of gas gangrene and tetanus.

Why is anaerobic infection identified as a special type? This surgical pathology occurs with severe intoxication, has a specific course of the disease, reacts only to strong antibacterial agents and, without treatment, often leads to death. Before the era of antibiotics, anaerobes claimed many human lives.

Non-clostridial infection

Putrefactive infection most often affects the subcutaneous tissue or synovial tendon sheaths. Also, a similar infectious process is detected in the lungs and abdominal cavity. For an anaerobic infection to enter the tissue, there must be some kind of injury that damages the integrity of the skin. The microbe can enter the body from the outside. For example, a deep wound leads to inflammation of the subcutaneous tissue, muscle or tendon. Or the microbe penetrates from the inside (through damaged organs in which it is localized). Then the source of infection is located next to the gastrointestinal tract, oral cavity, perineum, genitals, and respiratory tract. The most common cases are endogenous lung abscess and peritonitis.

In soft tissues, putrefactive infection begins with severe swelling of the skin and redness. Intoxication of the body (weakness, drowsiness, loss of appetite) sharply increases against the background of low-grade fever.

A characteristic feature of this infection is very severe swelling. A thread tied loosely around a patient's sore limb will dig deep into the skin within two hours.

This is a reason to immediately consult a surgeon. If the visit is postponed, the disease begins to gain momentum. The temperature reaches the level of fever, the infection spreads throughout the tissues, and the skin lesions soften. A crunching sound (crepitus) is detected under the fingers. These are crunchy gas bubbles released by microorganisms. The patient's condition is classified as serious. To treat the patient, urgent surgical treatment of the wound (or surgery) will be required. The patient's recovery is carried out in a hospital, accompanied by active antibiotic therapy and detoxification.

Gas gangrene

This anaerobic infection occurs as a result of clostridia (Clostridium perfringens, Clostridium novi, Clostridium septicum) getting into deep wounds, burns and open fractures.

The mortality rate from gas gangrene during World War II was 60%.

Suitable conditions must be created for them:

1. blind pockets in the wound;
2. a large amount of damaged tissue;
3. blind wounds;
4. heavily contaminated wounds.

In confined conditions with a lack of oxygen, clostridium multiplies quickly. The patient has severe fever, swelling, and intoxication. Later, a characteristic discharge from the wound (“meat slop”) and the crunch of gas bubbles appear.

Treatment of any wounds should be under the supervision of a physician. When providing first aid, it is better to wash small wounds with oxygen-releasing solutions (hydrogen peroxide, potassium permanganate).

Tetanus

The anaerobic infection tetanus is caused by Clostridium tetani. The microbe enters the body from the external environment. Tetanus spores are found in soil rich in manure. The rod lives in the intestines of animals. Tetanus still has a high morbidity rate and a high mortality rate.

Rural residents suffer from tetanus more often than urban residents.

The symptoms of tetanus are not caused by the growth of the bacterium itself, but by the toxins it produces. The first toxin is called tetanospasmin. It causes a convulsive picture of tetanus. The second toxin is called tetanolysin. It destroys red blood cells and white blood cells.

Tetanospasmin is the second most potent neurotoxin. In terms of potency, it is second only to botulinum toxin.

From the moment of penetration into the body until the onset of the disease, 5-15 days pass. The shorter the incubation period, the more microbes enter the body, the more pronounced the tetanus clinical picture will be.

A tetanus wound has the following characteristics:

• closed;
• blind;
• inflicted with a piercing object;
• contaminated with foreign bodies.

Tetanus can enter the wound through animal and insect bites. Infection is possible even after a bite from a tarantula spider.

If the wound is not treated in time, signs of illness appear:

1. heavy sweating;
2. muscle twitching in the wound area;
3. severe pain;
4. swallowing disorder;
5. difficulty urinating and defecating.

After a few days, a clinical picture develops with convulsions, spasm of the glottis, respiratory failure and cardiac arrest. Death occurs from cessation of breathing and heartbeat. Less commonly, the cause of mortality is developed pulmonary complications.

Tetanus is treated in a hospital. Along with wound treatment (anaerobic infection in surgery requires abundant oxygen), toxins are neutralized with tetanus toxoid (and serum) and symptomatic therapy.

Prevention of tetanus

The first direction in tetanus prevention is to work with the population. It is important to explain to people that any wound needs careful treatment. After all, tetanus can penetrate both a large laceration and a tiny scratch. The wound should be treated with oxygen-releasing solutions - hydrogen peroxide or potassium permanganate.

The second direction of prevention is coverage of the population with preventive vaccinations. Specific prevention of tetanus is carried out from 2-3 months. A baby at this age is given the associated vaccine DTP (adsorbed pertussis-diphtheria-tetanus vaccine) or Pentaxim (vaccine against diphtheria, tetanus, whooping cough, polio and hemophilius influenza). For persons over 17 years of age, tetanus prevention is carried out using ADS. Revaccination is carried out every 10 years.

Emergency tetanus prophylaxis is also carried out in hospitals and clinics. Vaccines and serums used for emergency prophylaxis are selected depending on the completeness of the patient’s previous vaccination course. Indications for emergency prophylaxis:

1. open wounds;
2. frostbite and burns above 1st degree;
3. criminal abortions;
4. childbirth outside the hospital;
5. penetrating wounds of the gastrointestinal tract;
6. necrosis;
7. gangrene;
8. animal bites.

Dennis L. Kasper

Definition. Anaerobic bacteria are microorganisms that require low oxygen tension for growth and cannot grow on the surface of a dense nutrient medium in the presence of 10% carbon dioxide. Microaerophilic bacteria can grow when its content in the atmosphere is 10%, as well as under anaerobic or aerobic conditions. Facultative bacteria grow both in the presence and absence of air. This chapter focuses on infections caused by non-spore-forming anaerobic bacteria. In general, anaerobes that cause infections in humans are relatively aerotolerant. Microorganisms can survive in the presence of oxygen for 72 hours, although they usually do not reproduce in this case. Less pathogenic anaerobic bacteria, which also form part of the normal flora of the human body, die after short-term contact with oxygen, even at low concentrations.

Non-spore-forming anaerobic bacteria are part of the normal microflora of mucous membranes in humans and animals. The main reservoirs of these bacteria are located in the oral cavity, in the gastrointestinal tract, on the skin and in the female genital tract. Anaerobes predominate in the microflora of the oral cavity. Their concentration is 1/2 ml of saliva and up to 1/2 ml in scrapings from the gums. In the oral cavity, the ratio of anaerobic to aerobic bacteria on the surface of the teeth is 1:1. At the same time, in the crevice spaces between the gum and the tooth surface, the number of anaerobic bacteria is 100-1000 times higher than the number of aerobes. In a normally functioning intestine, anaerobic bacteria are not found until the distal ileum. In the large intestine, the proportion of anaerobes increases significantly, as does the total number of bacteria. For example, in the large intestine, 1 g of feces contains 10 11 - 10 12 microorganisms with a ratio of anaerobes to aerobes of approximately 1000:1. 1 ml of secretion from the female genital organs contains approximately 10 9 microorganisms with an anaerobic to aerobic ratio of 10:1. Several hundred species of anaerobic bacteria have been identified in the normal human microflora. The diversity of anaerobic flora is reflected by the fact that up to 500 species of anaerobes have been identified in human feces. However, despite the diversity of bacteria that make up the normal human microflora, a relatively small number of them are detected in infectious diseases.

Anaerobic infections develop when the harmonious relationship between macro- and microorganisms is destroyed. Any organ is sensitive to these microorganisms that constantly grow in the body when mucous barriers or skin are damaged during operations, after injuries, in tumors or conditions such as ischemia or necrosis, which contribute to a decrease in the local redox potential of tissues. Due to the fact that various types of bacteria grow in areas of bacterial growth, damage to anatomical barriers creates opportunities for the penetration of many microorganisms into tissues, which often leads to the development of mixed infections with different types of anaerobes, facultative or microaerophilic bacteria. Similar mixed infections occur in the head and neck area (chronic sinusitis and otitis media, Ludwig's tonsillitis, periodontal abscess). The most common anaerobic infections of the central nervous system include brain abscess and subdural empyema. Anaerobes cause pleuropulmonary diseases, such as aspiration and necrotizing pneumonia, abscesses or empyema. Similarly, anaerobes play an important role in the development of intra-abdominal processes such as peritonitis, abscesses, and liver abscesses. They are often found in infectious diseases of the female genital organs: salpingitis, pelvioperitonitis, tubo-ovarian (tubo-ovarian) and vulvovaginal abscesses, septic abortions and endometritis. Anaerobic bacteria are often identified in infections of the skin, soft tissues, bones, and also cause bacteremia.

Etiology. The classification of these microorganisms is based on their Gram staining ability. Among the anaerobic gram-positive cocci that most often cause diseases, peptostreptococci should be noted. Of the gram-negative anaerobic bacteria, the main role is played by representatives of the Bacteroides family, including Bacteroides, Fusobacteria and pigmented Bacteroides. The B. fragilis group includes pathogenic anaerobic bacteria that are most often isolated in clinical infections. Representatives of this group of microorganisms are part of the normal intestinal flora. It includes several species, including Bacteroides, B. thetaiotaomicron, B. distasonis, B. vulgaris and B. ovatis. B. fragilis is of most clinical importance in this group. However, they are found less frequently in the normal intestinal flora than other types of bacteroids. The second large group forms part of the normal flora of the oral cavity. These are primary pigment-producing bacteria that were originally assigned to the species B. melaninogenicus. Modern terminology to define this group has changed: B. dingivalis, B. asaccharolyticus, and B. melaninogenicus. Fusobacteria have also been isolated from clinical infections, including necrotizing pneumonia and abscesses.

Infections caused by anaerobic bacteria are more often caused by mixed flora. Infection may be caused by one or more species of anaerobes or a combination of anaerobic and aerobic bacteria acting synergistically. The concept of mixed infections requires a revision of Koch's postulates, since the position of “one microbe - one disease” for many infections is not acceptable for diseases caused by many strains of bacteria acting synergistically.

Approaches to the management of patients with anaerobic bacterial infections. It is necessary to remember some important points when approaching the management of a patient with suspected anaerobic infection.

1. Most of the microorganisms are harmless commensals and only a few of them cause disease.

2. In order for them to cause infection, they must penetrate the mucous membranes.

3. Conditions are necessary that favor the proliferation of these bacteria, especially a reduced redox potential; therefore, infections occur in the area of ​​injury, tissue destruction, impaired blood supply, or as complications of previous infections that contributed to tissue necrosis.

4. A characteristic feature of anaerobic infections is the diversity of the infecting flora; for example, up to 12 types of microorganisms can be isolated from individual foci of suppuration.

5. Anaerobic microorganisms are found mainly in abscess cavities or in necrotic tissues. The discovery of an abscess in a patient, from which a microorganism cannot be isolated during routine bacteriological examination, should alert the doctor to the fact that anaerobic bacteria are likely growing in it. However, often in smears of such “sterile pus”, a large number of bacteria are determined by Gram staining. The stench of pus is also an important sign of anaerobic infection. Although some facultative organisms, such as Staphylococcus aureus, can also cause abscesses, an abscess in an organ or deep tissue should suggest an anaerobic infection.

6. Treatment does not necessarily have to be aimed at suppressing all microorganisms located in the inflammatory focus. However, when infested by certain types of anaerobic bacteria, specific treatment is required. An example is the need to treat a patient with an infection caused by B. fragilis. Many of these synergists can be suppressed by antibiotics that affect only certain, and not all, representatives of the microflora. The hypothesis is that treatment with antibacterial drugs while draining the abscess disrupts the interdependent relationships between bacteria and that microorganisms resistant to antibiotics cannot survive without the accompanying flora.

7. Manifestations of disseminated intravascular coagulation in patients with infections caused by anaerobic bacteria are usually absent.

Epidemiology. Difficulties in obtaining appropriate cultures, contamination of crops with aerobic bacteria or normal microflora and the lack of easily feasible, accessible and reliable methods of bacteriological research lead to insufficient information about the incidence of anaerobic infections. However, it can be stated that they are often found in hospitals in which surgical, traumatological, obstetric and gynecological services are actively functioning. In some centers, anaerobic bacteria are cultured from the blood of approximately 8-10% of patients. In these cases, B. fragilis predominates. The frequency of isolation of anaerobes when inoculating various clinical material can reach 50%.

Pathogenesis. Due to the specific growth conditions of these microorganisms and their presence as commensals on the surface of mucous membranes, for the development of infection, it is necessary that the microorganisms be able to penetrate the mucous membranes and invade tissues with a reduced redox potential. Consequently, tissue ischemia, trauma, including surgical perforation of internal organs, shock or aspiration provide conditions conducive to the proliferation of anaerobes. Highly demanding anaerobes do not contain the enzyme superoxide bismutase (SOB), which allows other microorganisms to break down toxic superoxide radicals, thereby reducing their effect. A correlation has been noted between the intracellular concentration of SOM and the tolerance of anaerobic bacteria to oxygen: microorganisms containing SOM have a selective advantage after exposure to aerobic conditions. For example, when an organ is perforated, several hundred species of anaerobic bacteria enter the abdominal cavity, but many of them do not survive, since the richly vascularized tissue is sufficiently supplied with oxygen. The release of oxygen into the environment leads to the selection of aerotolerant microorganisms.

Anaerobic bacteria produce exoenzymes that enhance their virulence. These include heparinase produced by B. fragilis, which can be involved in intravascular coagulation and determine the need for increased doses of heparin in patients receiving it. Collagenase produced by B. meianinogenicus can enhance tissue destruction. Both B. fragilis and B. meianinogenicus produce lipopolysaccharides (endotoxins) that lack some of the biological potency of endotoxins produced by aerobic gram-negative bacteria. This biological inactivity of endotoxin may explain the rare incidence of shock, disseminated intravascular coagulation, and purpura in Bacteroides bacteremia compared with bacteremia due to facultative and aerobic Gram-negative rod-shaped bacteria.

B. fragiiis is a unique species of pathogenic anaerobic bacteria in its ability to cause abscess formation, acting as the sole pathogenic agent. This microorganism has polysaccharides in its capsule that determine its virulence. They directly cause abscess formation in experimental models of intra-abdominal sepsis. Other types of anaerobes can cause abscess formation only in the presence of synergistically acting facultative microorganisms.

Clinical manifestations. Anaerobic infections in the head and neck area. Infections of the oral cavity can be divided into those originating from dental structures, localized above the gums and below them. Supragingival plaques begin to form when Gram-positive bacteria adhere to the surface of the tooth. Plaques are susceptible to the influence of saliva and food components, their formation depends on compliance with the rules of oral hygiene and local protective factors. Once they occur, they eventually lead to the development of gum inflammation. Early bacteriological changes in plaques located above the gums provoke inflammatory responses in the gums. These changes are manifested by swelling, swelling of the gums and an increase in the amount of fluid in them. They cause the development of caries and intradental infection (pulpitis). These changes also contribute to the development of subsequent lesions in the plaques located under the gums, which form due to poor oral hygiene. Plaques localized under the gums are directly related to periodontal lesions and disseminated infections emanating from the oral cavity. Bacteria growing in subgingival areas are represented mainly by anaerobes. The most important of them include black pigment-forming gram-negative anaerobic bacteria from the bacteroid group, in particular B. gingivalis and B. meianinogenicus. Infections in this area are often mixed; both anaerobic and aerobic bacteria take part in their development. After the development of a local infection either in the root canal of a tooth or in the periodontal area, it can spread to the lower jaw with the subsequent development of osteomyelitis, as well as to the sinuses of the upper jaw or into the soft tissues of the submandibular spaces of the upper or lower jaw, depending on the tooth that serves as the source of infection . Periodontitis can also cause infection to spread to adjacent bone or soft tissue. This form of infection can be caused by bacteroides or fusobacteria vegetating in the oral cavity.

Inflammation of the gums. Gingivitis can be complicated by a necrotic process (Vincent spirochetosis, Vincent stomatitis) - The disease usually begins unexpectedly and is accompanied by the development of bleeding seals on the gums, bad breath, and loss of taste. The mucous membrane of the gums, especially the papillae between the teeth, become ulcerated and may be covered with gray exudate, which is easily removed with a little effort. The disease can take a chronic course; in this case, patients have an increase in body temperature, cervical lymphadenopathy and leukocytosis. Sometimes ulceration from the gums can spread to the buccal mucosa, teeth, lower or upper jaw, leading to extensive destruction of bone and soft tissue. This infection is called acute necrotizing ulceration of the mucous membrane (water cancer, noma). It causes rapid tissue destruction, accompanied by tooth loss and the transformation of large areas of bone and even the entire lower jaw into scabs. It is often accompanied by a putrid odor, although the lesions are painless. Sometimes healing of gangrenous foci occurs, after which large shapeless defects remain. Most often, the disease is caused by debilitating diseases or severe malnutrition of children in undeveloped countries of the world. It is known to complicate leukemia or develop in individuals with genetically determined catalase deficiency.

Acute necrotizing infections of the pharynx. These infections are combined with ulcerative hypgivitis, although they can develop independently. The main complaints presented by patients include severe sore throat, difficulty breathing and an unpleasant taste in the mouth against the background of difficulty swallowing and a feverish state. When examining the pharynx, you can see the arches, swollen, hyperemic, ulcerated and covered with a grayish, easily removable film. Typically, lymphadenopathy and leukocytosis are noted. The illness may last for just a few days or persist if left untreated. The process is usually unilateral, but can spread to the other side of the pharynx or larynx. Aspiration of infectious material by a patient can lead to the development of a lung abscess. Orofacial soft tissue infections can be of odontogenic or non-odontogenic origin. Ludwig's tonsillitis, a periodontal infection usually originating from the third molar, can cause submandibular cellulitis, manifested by severe local swelling of the tissues, accompanied by pain, trismus and anterior and posterior displacement of the tongue. Submandibular swelling develops, which can lead to difficulty swallowing and airway obstruction. In some cases, tracheostomy is required for health reasons. A mixed anaerobic and aerobic infection emanating from the oral cavity plays a role in the etiology of the disease.

Fascial infections. These infections develop as a result of the spread of microorganisms found in the upper respiratory tract through the hidden spaces formed by the fascia of the head and neck. Despite the lack of confirmed reports on the microbiology of these diseases, according to many bacteriological studies, anaerobes living in the oral cavity are involved in its development. In severe skin infections, such as furunculosis or impetigo, Staphylococcus aureus and Streptococcus pyogenes may be involved in the infection of fascial spaces. At the same time, anaerobic infection is usually associated with damage to the mucous membranes and dental procedures or occurs spontaneously.

Sinusitis and otitis. Despite the lack of information about the role of anaerobic bacteria in acute sinusitis, it is likely that, due to the inadequate nature of the pathological material studied, the frequency with which anaerobes cause them is often underestimated. Samples for culture are obtained by aspiration through the lower nasal passage without decontamination of the mucous membranes of the nasal cavity. In contrast, there is no controversy regarding the importance of anaerobes in chronic sinusitis. Anaerobic bacteria were detected in 52% of samples obtained from external frontoethmoidotomy or radical antrotomy through the canine fossa. These methods avoid contamination of samples with bacteria that live on the mucous membranes of the nasal cavity. Likewise, anaerobic bacteria are more likely to cause chronic suppurative inflammation of the middle ear than acute otitis media. It has been established that with chronic otitis media, purulent discharge from the ear contains anaerobes in almost 50% of patients. During these chronic infections, a wide variety of anaerobes, mainly the genus Bacteroides, were isolated. In contrast to other head and neck infections, B. fragilis was isolated in 28% of cases in chronic otitis media.

Complications of anaerobic head and neck infections. The spread of these infections in the cranial direction can lead to osteomyelitis of the bones of the skull or mandible, or to the development of an intracranial infection such as a brain abscess or subdural empyema. Caudal spread of infection can cause mediastinitis or pleuropulmonary processes. Anaerobic head and neck infections can spread hematogenously. There are known cases of bacteremia, when the etiological factor is numerous types of bacteria, in which endocarditis or another distant source of infection can develop. With purulent phlebitis of the internal jugular vein, caused by the spread of infection, a destructive syndrome may develop with a prolonged increase in body temperature, bacteremia, purulent embolism of the vessels of the lungs and brain, and multiple metastatic purulent foci. This syndrome with septicemia caused by fusobacteria is caused by exudative pharyngitis. However, in the era of antibiotics, this disease, known as Lameer's postanginous septicemia, is rare.

Infections of the central nervous system. Of the many infectious diseases of the central nervous system, anaerobes most often cause brain abscesses. When using the most effective methods of bacteriological research, anaerobic flora can be detected in 85% of abscesses, especially gram-positive anaerobic cocci, less often fusobacteria and certain types of bacteroides. Facultative or microaerophilic streptococci or Escherichia coli are often found in the mixed flora of brain abscesses. A brain abscess is formed as a result of the spread of purulent processes through contact from the paranasal cavities, mastoid process or middle ear, or from foci of infection in distant organs, especially in the lungs, spreading hematogenously. Brain abscesses are discussed in more detail in Chap. 346.

Diseases of the pleura and lungs. These diseases are caused by aspiration of oropharyngeal contents, most often with impaired consciousness or absence of a gag reflex. There are four known clinical syndromes associated with anaerobic infections of the pleura and lungs that develop as a result of aspiration: simple aspiration, necrotizing pneumonia, abscess and pulmonary empyema.

Anaerobic aspiration pneumonia. Anaerobic aspiration pneumonia must be differentiated from aspiration pneumonia of two other types of non-bacterial origin. One of the aspiration syndromes is caused by the aspiration of solid masses, usually food. In these cases, obstruction of the main airways occurs due to developing atelectasis. Moderately expressed nonspecific inflammation develops. Treatment consists of removing the foreign body.

Another aspiration syndrome is more easily mistaken for aspiration of infected masses. This is the so-called Mendelssohn syndrome as a result of reflux of gastric contents and aspiration of chemical compounds, most often gastric juice. In this case, inflammation of the lungs develops very quickly, causing destruction of the alveolar structures with transudation of fluid into their lumen. The syndrome usually develops within a few hours, often after anesthesia, when the gag reflex is suppressed. The patient develops tachypnea, hypoxia and febrility. The white blood cell count may increase and the x-ray picture may suddenly change within 8-24 hours (from normal to complete bilateral darkening of the lungs). Sputum is produced in minimal quantities. With symptomatic treatment, changes in the lungs and symptoms can quickly disappear, or respiratory failure develops within a few days, followed by bacterial superinfection. Antibiotic treatment is not indicated until a bacterial infection has developed. Its signs include sputum, persistent fever, leukocytosis, and clinical manifestations of sepsis.

In contrast to these syndromes, bacterial aspiration pneumonia develops more slowly, and in hospitalized patients with a suppressed gag reflex, in elderly patients or with transient impairment of consciousness as a result of a nervous attack or alcohol intoxication. Persons hospitalized with this syndrome usually have been sick for several days by this point, they complain of a slight increase in body temperature, a feeling of malaise and sputum production. There is usually a history of factors predisposing to aspiration, such as alcohol overdose or nursing home stays. It is typical that during at least the first week of the disease the sputum does not have an unpleasant odor. Her Gram-stained smear reveals a mixed bacterial flora with a large number of polymorphonuclear leukocytes. Reliable data on the causative agent of the disease can only be obtained by inoculating samples that are not contaminated with oral microflora. These samples can be obtained by tracheal aspiration. X-ray of the chest cavity can reveal compaction of certain segments of the lungs. These include the hilar areas of the lower lobes, if aspiration occurred while the patient was in an upright or sitting position (usually in the elderly), or in the posterior segment of the upper lobe, usually on the right, or in the upper segment of the lower lobe, if aspiration occurred while position of the patient on his back. The microorganisms released in this case reflect the normal composition of the microflora of the pharynx (B. melaninogenicus, fusobacteria and anaerobic cocci). In patients whose aspiration occurred in a hospital, mixed microflora may be isolated, including facultative intestinal gram-negative bacilli.

Necrotizing pneumonia. This form of pneumonia caused by anaerobes is characterized by numerous but small abscesses spreading over several lung segments. The process can be sluggish or lightning fast. It is less common than aspiration pneumonia or lung abscess and may present as such. same as them.

Anaerobic lung abscesses. They develop in connection with a sub-acute pulmonary infection. Typical features of clinical symptoms include a feeling of malaise, weight loss, fever, chills, and foul-smelling sputum, sometimes for several weeks. The patient usually suffers from infectious dental diseases or periodontitis, but there is information about the development of lung abscesses in patients who have no teeth. Abscesses can be single or multiple, but are usually localized to the affected segment of the lung. Despite the similarity in clinical symptoms with other abscesses, anaerobic abscesses can be differentiated from tuberculous, neoplastic, etc. The microflora is dominated by anaerobes of the oral cavity, although in almost 10% of patients B. fragilis and sometimes Staphylococcus aureus are cultured. Although B. fragilis is resistant to penicillin in vitro, it is usually used successfully for anaerobic lung abscesses with vigorous debridement. The effect of penicillin is likely due to the synergistic nature of the infection. Bronchoscopy is indicated only to establish airway obstruction, but it should be delayed until the therapeutic effect of antibiotics has been demonstrated so that bronchoscopy does not contribute to the mechanical spread of infection. Bronchoscopy does not increase the drainage function. Surgical treatment is almost never indicated and can even be dangerous due to the possibility of abscess contents getting into the lung tissue.

Empyema. With prolonged anaerobic infection of the lungs, empyema develops. Clinical manifestations, including the production of foul-smelling sputum, resemble other anaerobic lung infections. The patient may complain of pleural pain and severe chest tenderness.

Empyema may be masked by severe pneumonia and may be suspected whenever fever persists for a long time despite treatment. A thorough physical examination and ultrasound are important for diagnosis to determine the location of the localized empyema. Thoracentesis usually produces an exudate with an unpleasant odor. It is necessary to drain the cavity. Recovery, normalization of the condition and resolution of the inflammatory process can occur after several months of treatment for both empyema and lung abscess.

Anaerobic empyema can also be caused by the spread of infection from the subphrenic space. Septic pulmonary emboli can originate from foci of infection located in the abdominal cavity or in the female genital organs. These emboli can cause the development of anaerobic pneumonia.

Infections of the abdominal organs. Due to the fact that in the normal intestinal flora the number of anaerobic bacteria is 100-1000 times higher than the number of aerobic bacteria, it is not surprising that damage to the intestinal wall leads to peritonitis of predominantly anaerobic etiology. Perforation of the colon wall allows large numbers of these bacteria to enter the abdominal cavity and is therefore associated with a high risk of intra-abdominal sepsis. As a consequence of peritonitis, abscesses can develop in any part of the abdominal cavity and retroperitoneal space. The peritoneum reacts with a pronounced inflammatory reaction and is effectively freed from infection in a short time. If the intra-abdominal abscess is localized, then its typical signs and symptoms appear (see Chapter 87). For example, a subdiaphragmatic abscess can cause the formation of a sympathetic pleural effusion on the corresponding side, and the patient on the same side may experience pleural-type pain and flattening of the dome of the diaphragm. Typical symptoms include fever, chills, and malaise. There is a history of surgery on the abdominal organs, trauma, or other reasons predisposing to disruption of the integrity of the intestinal wall. If the intra-abdominal abscess forms gradually, the clinical signs of its development may be more subtle. Peritonitis and abscess formation are two closely related processes. Often, after an operation aimed at eliminating perforation of the intestinal wall, the patient may maintain a febrile body temperature for a long period without local signs of an abdominal process or general deterioration of the condition. Persistent leukocytosis may be associated directly with surgery and/or resolving peritonitis. The doctor's attention should be directed to the wound discharge. If it is copious, cloudy, or foul-smelling, an anaerobic infection may be suspected. A Gram-stained smear, which reveals mixed intestinal flora, often helps in diagnosis. B. fragilis is cultured in approximately 70% of cases of surgical wounds after trauma, accompanied by perforation of the wall of the lower intestine; the percentage of their detection is similar after surgical interventions on the large intestine. Antibiotics play an important role in treatment; they are effective against infection with B. fragilis and facultative bacteria, although they cannot replace surgical or percutaneous drainage of the lesion. The most common source of intra-abdominal anaerobic infection is perforated appendicitis, leading to the formation of an abscess. Diverticulitis, which involves nonspore-forming anaerobes, can lead to perforation followed by generalized peritonitis, but it usually involves small, unrestricted foci of infection that do not require surgical drainage. In order to clarify the location of abscesses in the abdominal cavity, ultrasound examination of the abdominal organs, a gallium or indium scan, computed tomography, or a combined scan of the liver, spleen and lungs may be useful. However, surgical exploration of the abdominal cavity may be necessary to determine the exact location of the infection.

Of the infections of the internal abdominal organs caused by non-spore-forming anaerobic bacteria, liver abscesses are the most common. Liver abscess can be caused either by bacteremic spread of infection (sometimes after blunt trauma with localized infarction of liver tissue) or by contact, especially within the abdominal cavity. The infection can spread from the biliary tract or portal vein system (purulent pylephlebitis), into which it enters during sepsis in the pelvic or abdominal cavity. Symptoms and signs suggest infection, which can be quickly localized, but many patients develop fever, chills, and weight loss accompanied by nausea and vomiting. Only in half of the patients the size of the liver increases, pain in the right upper quadrant of the abdomen and jaundice appear. The diagnosis can be confirmed using ultrasound, computed tomography or radioisotope scanning. Sometimes it is necessary to resort to several diagnostic procedures. In more than 90% of patients with liver abscesses, leukocytosis and increased levels of alkaline phosphatase and aspartate transaminase in the serum are determined, in 50% there is concomitant anemia, hypoalbuminemia and increased levels of serum bilirubin. On a chest x-ray, one can see an infiltrate in the basal parts of the lung, pleural effusion and an increase in the dome of the diaphragm on the corresponding side. 1/3 of patients develop bacteremia. If the abscess is associated with other purulent foci that require drainage, open surgical drainage is indicated. Otherwise, percutaneous drainage with ultrasound or computed tomographic assessment of catheter position is used. Percutaneous drainage can be performed during antibiotic treatment. If a liver abscess develops as a result of infection spreading from the gallbladder, cholecystectomy is very effective.

Pelvic organ infections. The vagina of a healthy woman is one of the main reservoirs of both anaerobic and aerobic flora. In the normal flora of the female genital tract, the number of anaerobes exceeds the number of aerobic bacteria in a ratio of approximately 10:1. The predominant anaerobes are gram-positive cocci and Bacteroides sp. In case of severe infections of the upper parts of the female genital tract, microorganisms that make up the normal vaginal flora are isolated. Most patients produce anaerobes, the main pathogenic representatives of which are B. fragilis, B. melaninogenicus, anaerobic cocci and clostridia. Anaerobic bacteria are often found in tubo-ovarian abscesses, septic abortions, pelvic abscesses, endometritis and post-operative wound infections, especially after hysterectomy. Although these functions are often mixed (anaerobes and intestinal bacteria), “pure” anaerobic infection (without intestinal flora or other facultative bacteria) is much more common in pelvic infections than in intra-abdominal infections. These infections are characterized by the discharge of foul-smelling pus or blood from the uterus, widespread tenderness in the uterine area or local tenderness in the pelvic cavity, prolonged fever and chills. Infections of the pelvic organs can be complicated by purulent thrombophlebitis of the pelvic veins, which leads to recurrence of septic embolism in the lungs.

Skin and soft tissue infections. Damage to the skin, bones or soft tissues due to trauma, ischemia or surgery provides a favorable environment for the development of anaerobic infection. The latter most often develop in areas most susceptible to contamination by feces or secretions of the upper respiratory tract. These include wounds associated with intestinal surgery, bedsores and human bites. Anaerobic bacteria can be isolated from patients with crepitant cellulitis, synergistic cellulitis or gangrene and necrotizing fasciitis. Moreover, these microorganisms have been isolated from abscesses of the skin, rectum and sweat glands (hidradenitis suppurativa). Anaerobes are often isolated from foot ulcers in diabetic patients. In these types of skin and soft tissue infections, a mixed flora is usually found. On average, several bacterial species are isolated from each purulent lesion with a ratio of anaerobes and aerobes of the order of 3:2. Most often these are Bacteroides spp., anaerobic streptococci, group D streptococci, clostridia and Proteus. Anaerobic infection is often accompanied by an increase in body temperature, the appearance of foci with foul-smelling discharge, and visible ulcers on the feet.

Typically, a few days after surgery, anaerobic bacterial synergistic gangrene of Meleni develops. This disease is manifested by a focus of wound infection with acute pain, hyperemia, swelling with subsequent thickening. Erythema surrounds the central zone of necrosis. A granulomatous ulcer forms in the center of the lesion, which can heal, while necrosis and erythema spread along the periphery of the lesion. Symptoms are limited to pain. A febrile state is not typical. The causative agent is most often an association of anaerobic cocci and Staphylococcus aureus. Treatment consists of surgical removal of necrotic tissue and administration of antibiotics.

Necrotizing fasciitis. It is a rapidly spreading destruction of the fascia, usually caused by group A streptococci, but sometimes by anaerobic bacteria, including peptostreptococci and bacteroides. Similarly, myonecrosis may be associated with mixed anaerobic infection. Fournier's gangrene is an anaerobic cellulitis that spreads to the scrotum, perineum and anterior abdominal wall, in which mixed anaerobic microflora spreads through deep fascial spaces and causes extensive skin lesions.

Bone and joint infections. Despite the fact that actinomycosis (see Chapter 147) is considered throughout the world to be the basis (background) of most anaerobic infections of bone tissue, other microorganisms are often isolated during these infections. Particularly widespread are anaerobic or microaerophilic cocci, Bacteroides spp., Fusobacteria and Clostridia. Soft tissues adjacent to the foci of infection often become infected. Bacteroides that live in the oral cavity are often found during an infectious process in the upper and lower jaws, while clostridia are considered the main anaerobic pathogen in osteomyelitis after a fracture or injury of long tubular bones. Fusobacteria can be isolated in pure culture from osteomyelitis localized in the paranasal sinuses. In the pre-antibiotic era, they were isolated for mastoiditis that ended in the death of the patient. It has been established that anaerobic and microaerophilic cocci are the main causative agents of infections of the bone tissue of the skull and mastoid process.

In anaerobic septic arthritis, Fusobacterium spp. is more often isolated. In most patients, peritonsillar infections remain undetected, and as they progress, septic thrombophlebitis of the neck veins develops. The latter is characterized by a tendency to hepatogenic dissemination with predominant damage to the joints. Most of these infections occurred in the pre-antibiotic era. After the introduction of antibiotics into medical practice, fusobacteria from joints began to be sown much less frequently. Unlike anaerobic osteomyelitis, in most cases, purulent arthritis caused by anaerobes does not have a polybacterial etiology; it may be due to hematogenous spread of infection. Anaerobes are important pathogenic agents of infectious lesions of joint prostheses. In this case, the causative agents of infection are usually representatives of the normal microflora of the skin, in particular anaerobic gram-positive cocci and P. acnes.

In patients with osteomyelitis, the most informative method for determining the etiological agent is a bone biopsy performed through uninfected skin and subcutaneous tissue. If mixed flora is detected in a bone biopsy, treatment is prescribed with a drug that affects all isolated microorganisms. If the primary or only pathogenic agent isolated from the affected joint is an anaerobe, treatment should be no different than that of a patient with arthritis caused by aerobic bacteria. It should be aimed at stopping the underlying disease, using appropriate antibiotics, temporary immobilization of the joint, percutaneous drainage of the joint cavity and, usually, removal of infected prostheses or internal fixation devices. In treatment, surgical drainage and removal of affected tissue (such as sequestrectomy), which can support anaerobic infection, is essential.

Bacteremia. Transient bacteremia is a well-known condition in a healthy person when anatomical mucosal barriers are damaged (for example, when brushing teeth). These episodes of bacteremia, often caused by anaerobes, usually have no pathological consequences. However, with adequate culture techniques, anaerobic bacteria in a person with clinical manifestations of bacteremia account for 10-15% of microorganisms isolated from the blood. The single most frequently isolated microorganism is B. fragilis. The entry gates of infection can be established by identifying the microorganism and determining its habitat from which it enters the bloodstream. For example, bacteremia caused by mixed anaerobic microflora, including B. fragilis, usually develops with pathology of the large intestine with damage to its mucous membrane (malignant neoplasms, diverticulitis or other inflammatory processes). The initial manifestations of the disease are determined by the site of infection and the body’s response. However, if microorganisms enter the bloodstream, the patient may develop an extremely serious condition with chills and a hectic body temperature reaching 40.5°C. The clinical picture may be no different from that of aerobic sepsis caused by gram-negative bacteria. However, other complications of anaerobic bacteremia are also known, such as septic thrombophlebitis and septic shock, the frequency of which is low in anaerobic bacteremia. Anaerobic bacteremia often causes death, so rapid diagnosis and initiation of appropriate treatment is necessary. The source of bacteremia should also be identified. The choice of antibiotic depends on the results of identification of the microorganism.

Endocarditis (see Chapter 188). Endocarditis caused by anaerobes is rare. However, anaerobic streptococci, which are often misclassified, cause this disease much more often than is thought, although its overall frequency is unknown. Gram-negative anaerobes rarely cause endocarditis.

Diagnostics. Because of the difficulties associated with isolating anaerobic bacteria and the period required for this, the diagnosis of anaerobic infections must often be based on speculation. Infections caused by these non-spore-forming anaerobic bacteria have characteristics that greatly facilitate diagnosis. The diagnosis of anaerobic infection is facilitated by the identification of certain clinical signs, in particular nonvascularized necrotic tissue with reduced redox potential. When identifying the pathogen in foci of inflammation distant from mucous surfaces that are normally populated by anaerobic microflora (gastrointestinal tract, female genital tract or oropharynx), anaerobes should be considered a potential etiological agent. In anaerobic infections, an unpleasant odor often appears because certain organic acids are produced in necrotic tissues during the process of proliferation. Despite the pathognomonicity of the odor for an anaerobic infection, its absence does not exclude the possibility that anaerobes cause the disease. In 50% of cases with anaerobic infection, there is no characteristic unpleasant odor. Due to the fact that anaerobes are often associated with other bacteria, causing a mixed or synergistic infection, numerous pleomorphic cocci and bacteria suspicious for anaerobes are often detected in Gram-stained exudate. Sometimes these microorganisms have morphological characteristics characteristic of certain bacterial species.

Gas in tissues is a sign that is highly suspicious of anaerobic infection but has no diagnostic value. The results of bacteriological studies of samples from obviously infected foci, in which bacterial growth is not detected or only steptococci or one type of aerobe, for example Escherichia coli, are found, and mixed microflora is found in smears from the same material stained by Gram, mean that anaerobic microorganisms do not grow due to inadequate transport conditions or inoculation method. Likewise, the failure of antibacterial drugs that do not have activity against anaerobes, such as aminoglycosides or sometimes penicillin, cephalosporins, or tetracyclines, suggests the possibility of anaerobic infection.

In the diagnosis of anaerobic infection, three decisive conditions are distinguished: 1) obtaining appropriate samples; 2) their rapid delivery to the microbiological laboratory, preferably in an environment designed for the transport of anaerobes; 3) appropriate sample processing in the laboratory. Samples for research are taken with special care directly from the affected area with maximum protection from contamination by normal flora. If a sample is suspected of being contaminated with normal flora of the body, it should not be sent for examination to a bacteriological laboratory. Samples that are not suitable for bacteriological examination to detect anaerobic microflora include: 1) sputum obtained through spontaneous discharge, or discharge from the nose or trachea; 2) samples obtained during bronchoscopy; 3) samples obtained directly from the vaginal vaults; 4) urine obtained during free urination; 5) feces. Specimens that can be cultured include blood, pleural fluid, transtracheal aspirates, pus obtained by direct aspiration from the abscess cavity, fluid obtained by centesis, aspirate obtained by suprapubic puncture of the bladder, cerebrospinal fluid, and pulmonary punctures. .

Due to the fact that even short-term exposure to oxygen can cause the death of these microorganisms and prevent their isolation in the laboratory, air must be removed from the abscess cavities from which the contents are taken with a syringe for examination, and the needle should be closed with a sterile rubber cap. The resulting sample can be placed in sealed containers with a reduced nutrient medium or immediately transferred in a hermetically sealed syringe to the laboratory for direct bacteriological examination. Swab sampling should not be practiced. However, if a smear is needed, the sample is placed in a reduced semi-solid medium for delivery to the laboratory. It is important to remember that delay in transportation may result in failure to isolate anaerobes due to exposure to oxygen or excessive growth of facultative microorganisms that can suppress the growth or completely destroy the anaerobes contained in the sample. If an anaerobic infection is suspected, Gram-stained smears are prepared from all samples and examined to identify microorganisms with a morphology typical of anaerobes. This is important for microorganisms that are detected by Gram staining but are not cultured. If the examination of the pus is considered “sterile” or if the Gram stain reveals microorganisms that do not grow on the nutrient medium, an anaerobic infection and a violation of the conditions of transportation or the method of examination should be suspected.

Treatment. Effective treatment for anaerobic infections is achieved with a combination of appropriate antibiotics, surgical resection and drainage. Although surgery alone can be decisive, it may not be sufficient. Drainage of abscess cavities should be carried out immediately as soon as the focus is localized or fluctuation appears. Perforations should be immediately closed, nonviable tissue or foreign bodies should be removed, closed spaces should be drained, areas of tissue compression should be decompressed, and adequate blood supply should be ensured. At the same time, appropriate antibiotics should be used, since anaerobic sepsis can continue after surgery, manifested by intermittent symptoms and hidden progression of the process. Often there is a need to start treatment with antibiotics based only on suspicion of an anaerobic infection, without waiting for the results of bacteriological examination and determination of the sensitivity of the microorganism. The choice of antibiotic for initial treatment should be based on knowledge of the pathogen that causes certain clinical manifestations, as well as on bacterioscopic examination of Gram-stained smears, suggesting the participation of certain types of microorganisms in the process. Due to the fact that mixed microflora, in particular intestinal bacteria and other facultative microorganisms, are actively involved in the development of many anaerobic infections, it is advisable to use drugs that act on both anaerobic and aerobic pathogens. In general, if an anaerobic infection is suspected, the choice of antibiotic can be justified with complete certainty, since the sensitivity of some types of anaerobes to drugs is already known. Because B. fragilis is resistant to penicillin, the main question is whether it is involved in the inflammatory process. In general, B. fragilis does not play a significant role in infections located above the level of the diaphragm, including infections of the head and neck, pleura and lungs, and the central nervous system.

However, in septic processes developing below the level of the diaphragm, including in the pelvic and abdominal cavities, B. fragilis often takes an active part, and therefore requires treatment with antibiotics that have a detrimental effect on this microorganism.

Since B. fragilis is rarely isolated or has a questionable role in infections in which the primary focus is located above the level of the diaphragm, penicillin G is most widely used. Recommended doses vary depending on the location of the infection and its severity. Thus, for lung abscesses, 6-12 million units/day is recommended for at least 4 weeks (see Chapter 205). Infections caused by microorganisms growing in the oral cavity are often insensitive to penicillin. In such cases, drugs that are effective against penicillin-resistant anaerobes should be used, in particular clindamycin, chloramphenicol, (chloramphenicol) or cefoxitin. Failures of this type of treatment may explain reports of increasing resistance of B. mclaninogenicus to penicillin.

Infections originating in the large intestine are probably caused by B. fragilis and present another problem. Numerous therapeutic failures have been reported in patients with confirmed B. fragilis infection who were treated with penicillin or first-generation cephalosporins. When conducting basic studies of septic processes in the abdominal cavity, it was shown that antibiotics effective against infection with anaerobic bacteria significantly reduced the incidence of postoperative infectious complications, including severe ones. Based on these data, it is obvious that if bacteroids are suspected of being involved in the pathological process, appropriate treatment should be started immediately. Despite the fact that the number of antibacterial drugs that are effective against B. fragilis is insufficient, there is always a choice, but no one method has a clear advantage over the other. In general, with appropriate antibiotic therapy, more than 80% of patients with B. fragilis infection can recover.

Many drugs regularly available to the physician may be considered potentially useful for infections caused by B. fragilis. These include clindamycin, metronidazole and cefoxitin. At the same time, although it is known that chloramphenicol (chloramphenicol) is effective against some intra-abdominal infections and infectious diseases of the pelvic organs in women, there are isolated reports of treatment failures, including persistent bacteremia caused by B. fragilis. Cefamandole, cefocerazone, cefotaxime and moxalactam, in significantly lower concentrations than the other antibiotics mentioned, suppress this microorganism.

The treatment regimen for specific infections must strictly correspond to the primary localization of the process and the clinical picture. For example, a patient with intra-abdominal sepsis should be treated with either clindamycin (600 mg IV over 8 hours) or metronndazole (7.5 mg/kg over 8 hours). Aminoglycosides (gentamicin, tobramycin) are recommended to be included in the treatment regimen for gram-negative bacterial infections. Cefoxitin is more effective than clindamycin and amipoglycosides for severe mixed infections of the abdominal organs and skin, the etiology of which [often involves B. fragilis. However, for patients who are receiving or have previously received antibacterial drugs or for nosocomial infections, an aminoglycoside must be added to cefoxitin. This is due to the fact that the patient in this case is at high risk of infections caused by cefoxitine-resistant microorganisms, such as Enterobacteriaceae, Pseudomonas or Serratia.

Chloramphenicol (chloramphenicol) can be used to treat patients with infections of the abdominal cavity or central nervous system at a dose of 30-60 mg/kg per day, depending on the severity of the infection. The drug is effective against infections of the central nervous system caused by anaerobic bacteria. Penicillin G and metronidazole also easily penetrate the vascular wall and the spinal barrier and have bactericidal properties against bacteria that cause the development of brain abscesses. Patients with meningitis or endocarditis caused by anaerobic bacteria are also preferably treated with bactericidal drugs.

Although other semisynthetic penicillinase-resistant penicillins are inactive against anaerobes, carbenicillin, ticarcillin and piperacillin, which have the same spectrum of action as penicillin G, are active against B. fragilis and are effective when used in higher doses. Although this group of antibiotics is not recommended as first-line drugs for anaerobic infections, in some cases their treatment has been effective.

Almost all of the antibiotics mentioned cause some toxic reactions. Chloramphenicol (chloramphenicol) causes aplastic anemia that ends in death in one out of 40,000-100,000 patients. Clindamycin, cephalosporins, nenicillins, and sometimes metronidazole have been implicated in the development of pseudomembranous colitis caused by clostridia. Because diarrhea may precede the development of pseudomembranes, the use of these drugs should be discontinued immediately.

Due to widespread drug resistance, tetracycline and doxycycline should not be used for anaerobic infections. Erythromycin and vancomycin have some activity against infections with gram-positive anaerobes, but they are not recommended for severe infections.

For infections caused by anaerobes, in which treatment is ineffective or a relapse occurs after initial treatment, a repeat bacteriological examination is mandatory. The need for surgical drainage and excision of dead tissue should also be reconsidered. If a superinfection develops, it can be assumed that it is caused by drug-resistant gram-negative facultative or anaerobic bacteria. It is also necessary to take into account the drug resistance of the pathogen, especially if treatment is carried out with chloramphenicol (chloramphenicol). During repeated bacteriological examination, it is necessary to isolate the causative agent of infection.

Other additional measures for the treatment of patients with anaerobic infection include careful monitoring of electrolyte and water balance, since the development of severe local edema can cause hypovolemia, as well as hypodynamic measures in the development of septic shock, if necessary, immobilization of the limbs, maintaining appropriate nutrition for chronic infections by enteral or parenteral administration of nutrients, administration of painkillers, anticoagulants (heparin for thrombophlebitis). Hyperbaric oxygen therapy is of no value for anaerobic infection.

Anaerobic infection is a severe toxic wound infection caused by anaerobic microorganisms, primarily affecting connective and muscle tissue.

Anaerobic infection is often called anaerobic gangrene, gas gangrene, or gas infection.

The causative agents are clostridia - CI. perfringens, CI. oedomatien, C.I. septicum, CI. hystolyticus. These bacteria are anaerobic spore-bearing rods. Pathogenic anaerobes are common in nature, saprophyte in the intestines of mammals, and enter the soil with feces. Together with the soil, they can get into the wound. Pathogens are resistant to thermal and chemical factors. Anaerobic bacteria produce strong toxins that cause necrosis of connective tissue and muscles. They also cause hemolysis, vascular thrombosis, damage to the myocardium, liver, and kidneys. For the development of anaerobic infection, the lack of free access of oxygen with impaired blood circulation in injured tissues is of great importance.

The reasons contributing to the development of anaerobic infection in the wound are: extensive damage to muscles and bones; deep closed wound channel; the presence of a wound cavity that has poor communication with the external environment; impaired tissue circulation due to vascular damage; large necrotic areas with poor oxygenation.

Clinically, anaerobic infection is divided into the following forms: classical; edematous-toxic; gas-purulent mixed.

Clinical picture. The patient's condition is serious, intoxication is progressing, manifested by weakness, nausea, vomiting, poor sleep, lethargy, delirium, the skin is pale with a jaundiced tint, facial features become sharpened. The pulse is significantly increased and does not correspond to the temperature, blood pressure is reduced, body temperature ranges from low-grade to high. A blood test reveals anemia, high leukocytosis with a shift in the leukocyte formula to the left. Diuresis is reduced, leukocytes, casts and protein are detected in the urine.

In the area of ​​the wound, the patient notes the appearance of severe arching pain. The skin around it is cyanotic, cold to the touch, with dilated bluish veins. The limb is swollen; upon palpation, crepitus of the soft tissues is determined (due to the presence of air in them). When dressing or opening a wound, a scanty discharge with an unpleasant odor and air bubbles is released from it. An X-ray examination reveals areas of gas accumulation and disintegrating muscles.

To clarify the diagnosis, it is necessary to conduct a bacteriological study.

Treatment. The patient is urgently hospitalized in the purulent-septic department of the surgical hospital in a separate box.

After the diagnosis is made, surgical intervention is performed - wide and deep opening of the wound, excision of necrotic tissue and drainage. A bandage with hydrogen peroxide is applied to the wound. If the general condition worsens and local symptoms increase, they resort to radical surgery - amputation of the limb.

General treatment includes the use of mixtures of anti-gangrenous serums, infusion therapy, blood transfusions, plasma and blood substitutes, antibacterial therapy, high-calorie nutrition, and symptomatic treatment. Hyperoxybarotherapy (pressure chamber for saturating the body with oxygen) is highly effective.

To prevent anaerobic infection, early and radical primary surgical treatment of wounds is necessary; drainage of crushed, contaminated, gunshot and festering wounds; good transport and therapeutic immobilization on a limb with damaged tissues; early antibiotic therapy for large wounds.

Rules for patient care. The patient is hospitalized in a specialized box and medical personnel are assigned to care for him. When entering the room, the nurse puts on a clean gown, scarf, mask, shoe covers and rubber gloves. Dressings are made with separate instruments intended only for a given patient, which are then immersed in a disinfectant solution. The dressing material is burned after disinfection. The ward is cleaned 2-3 times a day using a 6% hydrogen peroxide solution and a 0.5% detergent solution, after which the bactericidal irradiator is turned on. Bed and underwear are disinfected in a 2% solution of soda ash, followed by boiling and sending to the laundry.

After use, dishes are disinfected in a 2% solution of sodium bicarbonate, boiled and washed in running water.

The paramedic monitors the patient’s condition hourly on the first day, and 3-4 times a day on the following days: measures blood pressure, body temperature, counts pulse, and respiratory rate. An oilcloth with a diaper is placed under the affected limb, which is changed as often as possible. The wound with drainage is left open. If it becomes very wet with blood or bursting pain appears, immediately inform the doctor.

Putrid infection

Putrefactive infection is caused by various representatives of anaerobic non-clostridial microflora in combination with anaerobic microorganisms.

Clinical picture. Putrefactive infection is observed with lacerations, crushed wounds, and open fractures. The general condition worsens in the same way as with an aerobic infection. In the wound area, the process of necrosis prevails over the processes of inflammation. The edges and bottom of the wound with necrotic areas of tissue of a hemorrhagic, dirty gray color and foul-smelling discharge. There is pronounced swelling and hyperemia around the wound. Lymphangitis and lymphadenitis are often observed.

Treatment. Treatment is carried out in the purulent-septic department of a surgical hospital without isolating the patient in a box.

Urgent radical surgical treatment of the wound with wide dissection of tissue and removal of necrosis, antibacterial, detoxification therapy, and immunotherapy are carried out.

Tetanus

Tetanus is an acute specific infection. According to the World Health Organization (WHO), more than 1 million people fall ill with tetanus every year, and the mortality rate reaches 50–80%.

The causative agent of tetanus (CL tetani) - tetanus bacillus - is an anaerobic, spore-forming, gram-positive microorganism, the spores of which are very resistant to environmental factors. Bacteria can exist under normal conditions for many years. The toxin released by the tetanus bacillus damages the nervous system and destroys red blood cells.

Infection occurs only through damaged tissue. The incubation period lasts from 4 to 40 days. During the incubation period, a person complains of headache, insomnia, increased irritability, general malaise, profuse sweating, pain and twitching of tissue in the wound area. Tendon reflexes increase and pathological reflexes appear on the injured side.

Clinical picture. The leading symptom of the disease is the development of toxic and clonic spasms of skeletal muscles. First, muscle spasms and cramps begin around the site of injury, then move to the chewing and facial muscles. The patient's face twists into a so-called “sardonic smile.” The spread of spasms to the neck muscles leads to throwing back the head. Convulsive contractions of the respiratory muscles cause breathing problems up to asphyxia, and contractions of the heart muscles cause it to stop. Due to tonic contraction of all skeletal muscles, opisthotonus develops - the torso arches, and the patient touches the bed only with the back of the head and heels (Fig. 10.5). Such convulsions can be accompanied by retraction of the tongue, fractures of bones, spine, ruptures of organs, muscles, and neurovascular bundles.

Frequent cramps are combined with profuse sweating, high body temperature, respiratory and cardiovascular disorders. The severity of the disease is determined not only by convulsions, but also by intoxication, suppuration of the wound, the characteristics of the course of the wound process, the number and virulence of the pathogen, and the reactivity of the body.

Treatment. Necrotic tissue in and around the wound is carefully removed, leaving the wound open to allow air access to the tissue.

For local treatment, proteolytic enzymes are used, which accelerate necrolysis, clean the wound, and stimulate the regeneration process.

General treatment consists of specific serotherapy (administration of PSS, tetanus toxoid, antitetanus human immunoglobulin), anticonvulsant therapy (aminazine, droperidol, muscle relaxants with mechanical ventilation), hyperbaric oxygenation, antibiotic therapy, symptomatic therapy aimed at maintaining the functions of the cardiovascular and respiratory systems, infusion therapy to compensate for fluid loss and normalize water and electrolyte balance. In severe forms of the disease, when providing first aid, the patient during hospitalization is placed horizontally on a stretcher with straps attached to it, aminazine with diphenhydramine is administered intravenously, an air duct is inserted into the oral cavity, and, if necessary, mechanical ventilation is performed.

Rules for patient care. A patient with tetanus is treated in the same conditions as a patient with sepsis, but the room must be darkened to eliminate unnecessary irritation to the patient. The patient must be provided with a medical and protective regime, an individual nursing station, constant medical supervision and careful care. The patient is placed on a soft bed. Staff must maintain silence: sharp sounds and bright lights cause seizures in the patient. All manipulations and feeding are carried out after the administration of anticonvulsants. Significant dehydration of the patient, administration of large amounts of fluid and the inability to urinate on his own necessitates the need to release urine with a catheter 2 times a day after preliminary anesthesia of the urethra (dicaine, novocaine), if the patient is not under anesthesia.

You can give fluids enterally and feed via a sippy cup, through a thin gastric tube inserted through the nose, or as a nutritional enema. Food should be liquid. All measures must be carried out carefully, since any careless impact on the patient can lead to the development of a convulsive attack.

When the frequency and duration of seizures increases, long-acting muscle relaxants are administered and the patient is transferred to mechanical ventilation through an endotracheal tube or tracheostomy.

When monitoring a patient, it is necessary to measure blood pressure, count pulse, respiratory rate, monitor renal function (calculate daily diuresis), gastrointestinal tract, blood composition (general analysis).

Emergency prevention. Emergency prevention of tetanus is carried out in case of injury with violation of the integrity of the skin and mucous membranes, frostbite and burns of II - IV degrees; penetrating wounds, out-of-hospital abortions, childbirth outside of medical institutions, gangrene or tissue necrosis of any type, long-term abscesses, carbuncles and other purulent infections, animal bites.

Emergency prevention of tetanus consists of primary surgical treatment of the wound and simultaneous immunoprophylaxis. Prevention should be carried out as early as possible. Contraindications to the use of specific means of emergency prophylaxis of tetanus are hypersensitivity to the drug and pregnancy.

When a patient consults a doctor about an injury, the issue of emergency tetanus prophylaxis must be decided.

Prevention is not carried out for patients who have documented evidence of routine preventive vaccinations in accordance with age or a full course of immunization no more than 5 years ago in an adult; patients in whom, according to emergency immunological control, the titer of tetanus antitoxin in the blood serum is higher than 1: 160 according to the passive hemagglutination reaction. The titer of tetanus antitoxin in the blood serum can be determined within 1.5 -2.0 hours from the moment the patient contacts the health care facility for assistance.

For emergency immunoprophylaxis, adsorbed tetanus toxoid, adsorbed diphtheria-tetanus toxoid with reduced antigen content (ADS-m), purified concentrated horse PSS, and human tetanus immunoglobulin (HAT) are used. If the patient's tetanus antitoxin titer is within the range of 1: 20... 1: 80 (0.01-0.1 IU/ml), then for the purpose of prevention, only 0.5 ml of tetanus toxoid or 0.5 ml of ADS- m.

If the patient's tetanus antitoxin titer is less than 1:20 (0.01 IU/ml), then 1 ml of tetanus toxoid and 3,000 IU PSS are administered after the test (or 250 IU PSS).

Antitetanus serum is administered according to the usual method: 0.1 ml intradermally, if there is no reaction within 20 - 30 minutes - another 0.1 ml subcutaneously, after 20 - 30 minutes if there is no reaction - the entire dose is intramuscular. Revaccination at a dose of 0.5 ml of tetanus toxoid is carried out after 1 month and 1 year. In this case, immunity is developed for 10 years.

Before administering the drugs, the paramedic carefully examines the ampoule (label, expiration date, presence of sediment in the ampoule or cracks), shakes until a homogeneous suspension is obtained, and treats the skin at the injection site with 70% alcohol. The drugs are taken with one needle, and another needle is used for injection. Antitetanus serum is stored covered with a sterile napkin for no more than 30 minutes.

Osteoarticular tuberculosis

Tuberculosis of bones and joints occurs in patients of any age, is characterized by a long chronic course and is a manifestation of general tuberculosis. It is caused by the tuberculosis bacillus. With bone tuberculosis, flat and short bones are most often affected, as well as small tubular ones - fingers and toes, ribs, vertebrae, wrist joints.

The process begins in the spongy bone and gradually leads to the destruction of the bone structure, the formation of small sequesters, fistulas and cavities, from which pus leaks into the soft tissue. Tuberculous abscesses are called “cold”, since they have no signs of inflammation, and the pus contains almost no leukocytes. When thinned, the abscess wall can break through and a long-term non-healing fistula is formed.

Clinical picture. Symptoms of the disease appear gradually, so it is difficult to determine the onset of the disease. From the moment of infection to the symptoms of the disease, it takes from 3 months to 3 years, depending on the location of the process. The process can move from the bones to the joints, or it can remain only in the bones.

If the process is localized in the spine (tuberculous spondylitis), then the focus is in the spongy substance of the anterior part of the vertebral body. The muscles in the area of ​​the affected vertebra become tense and it collapses. Several vertebrae may also be destroyed, causing the spine to bend and form a hump. This creates a danger to the spinal cord, the likelihood of developing paresis and paralysis.

Tuberculosis most often affects the hip joint, causing tubular coxitis. When the knee joint is damaged, tubular gonitis occurs. An effusion forms in the joint cavity, the contours of the joint are smoothed out, and it takes the shape of a spindle. The skin becomes white and shiny, muscle atrophy occurs above and below the joint. This process happens very slowly. The joint capsule, ligaments, and cartilage are destroyed, and the function of the joint is impaired. In this case, the patient has no inflammatory symptoms. The body temperature is normal, pain is characteristic of the later stages of the disease, although sometimes it can be present in the initial stages. They occur during movement and stress on the joint (the patient is asked to stand on one leg). The diagnosis is confirmed by x-ray.

Treatment. Treatment is carried out in anti-tuberculosis dispensaries. It can be specific and non-specific. Anti-tuberculosis antibiotics, vitamins, restoratives and immunity boosters are prescribed. The regimen and proper nutrition of the patient are very important. The joint must be

at rest, so the patient is prescribed bed rest and special orthopedic devices or a plaster cast.

Surgical treatment is indicated in the final period of treatment to correct the deformity and restore joint function.

In case of abscesses, pus is removed by puncture of the joint cavity. Treatment of abscesses lasts several months. As a complication, bone deformation, curvature, and pathological fractures may occur.

After inpatient treatment, patients are recommended to undergo sanatorium-resort treatment. General treatment of patients with osteoarticular tuberculosis lasts several years.

Professional examinations and fluorographic examination are of great importance for identifying early forms of the disease.