Dormant anaerobic infection. Anaerobic surgical infection

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 a ratio of anaerobes to aerobes 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 a complication 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 disease. 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 can 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 a 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 tissue swelling, 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 anthrotomy 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 with a prolonged increase in body temperature, bacteremia, purulent embolism of the vessels of the lungs and brain and multiple metastatic purulent foci can develop. 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 pneumonia, 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 in whom 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 diseases of the teeth 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. Despite the fact that B. fragilis exhibits resistance to penicillin in vitro, it is usually used successfully for anaerobic lung abscesses against the background of 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 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 entering 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 because they help 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 subphrenic 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. Often, a Gram-stained smear, which reveals mixed intestinal flora, 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 tomography 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 Meleny 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 questionable involvement 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 none of the methods 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 cavity 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 in 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, 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 pronounced 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.

is one of the most severe complications of wounds. The most common causes of this infection are gunshot wounds and extensive tissue damage. In addition, anaerobic infection can occur after surgery, invasive medical procedures, and injections. The number of cases increases sharply during military operations.

The causative agents of anaerobic infection are microbes whose vital activity occurs without access to oxygen. Depending on the type of pathogen and the characteristics of the clinical picture, clostridial and non-clostridial anaerobic infections are distinguished.

Anaerobic clostridial infection.

In most cases, the causative agents of anaerobic clostridial infection are: Cl. perfringens /up to 80% of observations/, Cl. oedematiens, Cl. septicum, Cl. hystoliticum are spore-forming rods widely distributed in the external environment. The listed microorganisms are found in large numbers in the intestines of mammals. The spores of the causative agents of this infection are highly resistant to external factors, but the microbes themselves cannot exist for a long time in an oxygen environment. The causative agents of anaerobic clostridial infection produce exotoxins that cause necrosis of fatty tissue, connective tissue, and muscles; hemolysis and vascular thrombosis. Exotoxins also affect the myocardium, liver, kidneys, and nervous tissue.

The risk of developing an anaerobic infection increases significantly with significant damage to muscles and bones, especially when access of oxygen to the depth of the wound channel is difficult (gunshot wounds). Predisposing factors are trauma to the wound during transportation, impaired blood supply to tissues, and a decrease in the immunobiological resistance of the body.

Anaerobic clostridial infection is characterized by gas formation in the area of ​​the pathological focus, swelling and tissue necrosis. Gas is one of the waste products of anaerobes. The main components included in its composition are hydrogen and carbon dioxide. Edema leads to an increase in pressure inside the fascial sheaths, which causes muscle ischemia with subsequent necrosis. Gas and edematous fluid, along with toxins and microbes, quickly spread throughout the intermuscular and perivascular tissue. After saturating the skin, the edematous fluid exfoliates the epidermis with the formation of blisters filled with serous-hemorrhagic contents. Depending on the characteristics of the course of wound infection, in some cases there is a predominant lesion of muscle tissue (clostridial myositis), in others - subcutaneous fatty tissue (clostridial cellulitis). Hemolyzed blood, together with muscle breakdown products, imbibes the subcutaneous tissue, which is visually determined by the appearance of brown or bluish spots on the skin. The entry of toxins and tissue breakdown products into the systemic circulation leads to the development of severe general intoxication of the body and multiple organ failure.

Classification.

Based on the speed of the pathological process, fulminant, rapidly progressing and slowly progressing forms of infection are distinguished;

by the nature of local changes - forms with a predominance of gas formation (gas), forms with a predominance of edema (malignant edema) and mixed forms;

according to the depth of the process - subfascial (deep) and epifascial (superficial).

Clinic.

The duration of the incubation period depends on the forms of the disease and lasts from several hours (with fulminant forms) to several days, and, as a rule, the earlier the disease begins, the more severe it is.
The disease often begins with severe arching pain in the wound area.
A typical complaint is the patient's complaint of a feeling of tightness from the previously applied bandage, which is associated with a rapid increase in swelling of the affected tissues. The patient's general condition is rapidly deteriorating. The victim is concerned about general weakness, loss of appetite, sleep disturbance, thirst, and nausea. In some cases, patients show anxiety. Upon examination, attention is drawn to the pallor of the skin, sometimes with a jaundiced or earthy tint; increase in body temperature from low-grade to significant levels; tachycardia; decreased blood pressure; sharpened facial features.
By palpation and percussion of the affected area, crepitus and tympanic sound (subcutaneous emphysema) can be detected.
If there is gas in the wound channel during dressing, small bubbles in the exudate can be observed.

Diagnostics.

During clinical and laboratory studies, a general blood test shows a decrease in red blood cells and hemoglobin, leukocytosis is observed with a shift in the leukocyte formula to the left (in especially severe cases, leukopenia is observed, which is an unfavorable criterion); Protein and casts are detected in the urine, diuresis decreases. An important diagnostic method is x-ray examination, which makes it possible to detect gas formation in soft tissues in the early stages (irregular clearing zones are determined on x-rays).

In all cases, it is necessary to perform a bacteriological examination of the exudate and affected tissues. A complete bacteriological examination of the material with identification of the pathogen takes 5-7 days. A bacterioscopic examination confirms an anaerobic infection by the presence in the preparation of a large number of microbial rods among the fragmented muscle fibers.

Treatment of anaerobic infection can only be complex.

Its main component is surgical intervention, which in most cases is performed according to one of three options:

wide dissection of tissue in the area of ​​the pathological process (lamp incisions);

wide dissection combined with excision of non-viable tissue;

amputation and disarticulation of limbs.

Anaerobic non-clostridial infection.

Among the non-clostridial microbial flora, the most important for clinicians are bacteroids (B. fragilis, B. melaninogenicus/, Fusobacterium - gram-negative bacilli; gram-positive cocci - Peptococcus, Peptostreptococcus; gram-positive bacilli - Actinomyces, Eubacterium, Propionibacterium, Bifidobacterium, Arachnia; gram-negative cocci - Veilonella. As a rule, the development of anaerobic non-clostridial infection is polymicrobial in nature with the participation of several types of anaerobes and aerobes (hemolytic streptococcus, enterobacteria, staphylococci, etc.), acting synergistically.

This infection can affect the lungs (abscesses), abdominal cavity (anaerobic peritonitis), and soft tissues.

There are 4 types of non-clostridial anaerobic infection: anaerobic non-clostridial cellulitis, anaerobic non-clostridial fasciitis, anaerobic non-clostridial myositis and a mixed form.

The disease can develop gradually without being accompanied in the early stages by pronounced disturbances in the general condition of the patient. In the later stages of the disease, symptoms of severe intoxication are characteristic, up to the development of multiple organ failure. Patients complain of general weakness, lack of appetite, hyperthermia. General symptoms precede local manifestations of the pathological process. Patients are bothered by pain in the wound area. When examining the affected area, attention is drawn to swelling of the tissues and pallor of the skin. As a rule, the dynamics of the increase in edema are less pronounced compared to anaerobic clostridial infection. Often the classic signs of inflammation are not detected. The vital activity of some types of non-clostridial anaerobic microorganisms may be accompanied by gas formation, but in general, this is not typical for this type of infection.

The main treatment method for anaerobic non-clostridial soft tissue infection is surgery. The operation consists of radical surgical sanitation of the pathological focus, with mandatory excision of all non-viable tissue. The effectiveness of surgical treatment can be increased through the use of ultrasonic cavitation; treating tissues with a high-pressure antiseptic flow; exposure of the wound surface to an air-plasma flow containing nitric oxide; vacuuming the wound surface).

In the presence of anaerobic non-clostridial myositis involving several muscle groups in the pathological process, indications for limb amputation arise.

Symptoms depend on the location of the infection. Anaerobes are often accompanied by the presence of aerobic organisms. Diagnosis is clinical, along with Gram staining and culture to identify anaerobic cultures. Treatment with antibiotics and surgical drainage and debridement.

Hundreds of varieties of non-spore-forming anaerobes are part of the normal flora of the skin, mouth, gastrointestinal tract and vagina. If these relationships are disrupted (eg, by surgery, other trauma, compromised blood supply, or tissue necrosis), some of these species can cause infections with high morbidity and mortality. Once established at a primary site, organisms can reach distant sites hematogenously. Because aerobic and anaerobic bacteria are often present in the same infected site, appropriate identification and culture procedures are necessary to avoid overlooking anaerobes. Anaerobes may be a major cause of infection in the pleural cavities and lungs; in the intrabdominal area, gynecological area, central nervous system, upper respiratory tract and skin diseases, and in bacteremia.

Causes of anaerobic infections

The major anaerobic gram-negative bacilli include Bacteroides fragilis, Prevotella melaninogenica, and Fusobacterium spp.

Pathogenesis of anaerobic infections

Anaerobic infections can usually be characterized as follows:

• They tend to appear as localized collections of pus (abscesses and cellulitis).
• The reduction in O2 and low oxidation reduction potential that predominates in avascular and necrotic tissues are critical for their survival,
• When bacteremia occurs, it does not usually lead to disseminated intravascular coagulation (DIC).

Some anaerobic bacteria have obvious virulence factors. The virulence factors of B. fragilis are likely to be somewhat exaggerated due to their frequent detection in clinical specimens, despite their relative rarity in normal flora. This organism has a polysaccharide capsule, which apparently stimulates the formation of a purulent focus. An experimental model of intraabdominal sepsis showed that B. fragilis can cause an abscess on its own, while other Bactericides spp. a synergistic effect of another organism is required. Another virulence factor, a potent endotoxin, has been implicated in septic shock associated with severe Fusobacterium pharyngitis.

Morbidity and mortality in anaerobic and mixed bacterial sepsis are as high as in sepsis caused by a single aerobic microorganism. Anaerobic infections are often complicated by deep tissue necrosis. The overall mortality rate in severe intraabdominal sepsis and mixed anaerobic pneumonia is high. B. fragilis bacteremia has a high mortality rate, especially among the elderly and patients with cancer.

Symptoms and signs of anaerobic infections

Fever, chills, and severe critical illness are common in patients; incl. infectious-toxic shock. DIC can develop with Fusobacterium sepsis.

For specific infections (and symptoms) caused by mixed anaerobic organisms, see GUIDELINES and Table. 189-3. Anaerobes are rare in urinary tract infections, septic arthritis, and infective endocarditis.

Diagnosis of anaerobic infections

• Clinical suspicion.
• Gram stain and culture.

Clinical criteria for anaerobic infections include:

• Infection adjacent to mucosal surfaces that have anaerobic flora.
• Ischemia, tumor, penetrating trauma, foreign body or perforated internal organ.
• Spreading gangrene affecting the skin, subcutaneous tissue, fascia and muscles.
• Unpleasant odor of pus or infected tissue.
• Abscess formation.
• Gas in tissues.
• Septic thrombophlebitis.
• Lack of response to antibiotics that do not have significant anaerobic activity.

Anaerobic infection should be suspected when the wound has a foul odor or when a Gram stain of pus from the infected site reveals mixed pleomorphic bacteria. Only samples collected from normally sterile sites are used for culture because other organisms present can easily be mistaken for pathogens.

Gram stains and aerobic cultures should be obtained for all specimens. Gram stains, especially in the case of bacteroides infection, and cultures for all anaerobes may be falsely negative. Antibiotic susceptibility testing of anaerobes is difficult and data may not be available >1 week after initial culture. However, if the variety is known, the susceptibility pattern can usually be predicted. Therefore, many laboratories do not routinely test anaerobic organisms for sensitivity.

Treatment of anaerobic infections

• Drainage and sanitation
• The antibiotic is selected depending on the location of the infection

When infection is established, the pus is drained and dead tissue, foreign bodies and necrotic tissue are removed. Organ perforations should be treated by wound closure or drainage. If possible, blood supply should be restored. Septic thrombophlebitis may require vein ligation along with antibiotics.

Since test results for anaerobic flora may not be available for 3-5 days, antibiotics are started. Antibiotics sometimes work even when several bacterial species in a mixed infection are resistant to the antibiotic, especially if surgical debridement and drainage are adequate.

Oropharyngeal anaerobic infections may not respond to penicillin and thus require a drug effective against penicillin-resistant anaerobes (see below). Oropharyngeal infections and lung abscesses should be treated with clindamycin or β-lactam antibiotics with β-lactamase inhibitors such as amoxicillin/clavulanate. For patients allergic to penicillin, it is good to use clindamycin or metronidazole (plus a drug active against aerobes).

Gastrointestinal tract infections or female pelvic anaerobic infections are likely to contain anaerobic gram-negative bacilli such as B. fragilis plus facultative gram-negative bacilli such as Escherichia coir; the antibiotic must be active against both species. The resistance of B. fragilis and other obligatory gram-negative bacilli to penicillin and 3rd and 4th generation cephalosporins differs. However, the following drugs have superior activity against B. fragilis and in vitro efficacy: metronidazole, carbapenems (eg, imipenem/cilastatin, meropenem, ertapenem), combination inhibitor, tigecycline, and moxiflocacin. No single drug can be given preference. Drugs that appear to be somewhat less active against B. fragilis in vitro are generally effective, including clindamycin, cefoxitin, and cefotetan. All but clindamycin and metronidazole can be used as monotherapy because these drugs also have good activity against facultative anaerobic gram-negative bacilli.

Metronidazole is active against clindamycin-resistant B. fragilis, has unique anaerobic bactericidal ability, and is not usually prescribed for the pseudomembranous colitis sometimes associated with clindamycin. Concerns about the potential mutagenicity of metronidazole have not been clinically supported.

Because many options are available for the treatment of gastrointestinal or female pelvic anaerobic infections, the use of a combination of a potentially nephrotoxic aminoglycoside (to target intestinal gram-negative bacilli) and an antibiotic active against B. fragilis is no longer advocated.

Prevention of anaerobic infections

• Metronidazole plus gentamicin or ciprofloxacin.

Before undergoing colorectal surgery, patients must have their intestines prepared for the procedure, which is achieved by the following:

• Laxative.
• Enema,
• Antibiotic.

Most surgeons give both oral and parenteral antibiotics. For emergency colorectal surgery, only parenteral antibiotics are used. Examples of oral are neomycin plus erythromycin or neomycin plus metronidazole; these drugs are given no more than 18-24 hours before the procedure. Examples of preoperative parenterals are cefotetan, cefoxitin, or cefazolin plus metronidazole. Preoperative parenteral antibiotics control bacteremia, reduce secondary or metastatic suppurative complications, and prevent the spread of infection around the surgical site.

For patients with documented allergy or adverse reaction to β-lactams, clindamycin plus gentamicin, aztreonam, or ciprofloxacin is recommended; or metronidazole plus gentamicin or ciprofloxacin.

Anaerobic infection is a pathology caused by bacteria that can grow and multiply in the complete absence of oxygen or its low voltage. Their toxins are highly penetrating and are considered extremely aggressive. This group of infectious diseases includes severe forms of pathologies, characterized by damage to vital organs and a high mortality rate. In patients, manifestations of intoxication syndrome usually prevail over local clinical signs. This pathology is characterized by predominant damage to connective tissue and muscle fibers.

Anaerobic infection is characterized by a high rate of development of the pathological process, severe intoxication syndrome, putrid, foul-smelling exudate, gas formation in the wound, rapid necrotic tissue damage, and mild inflammatory signs. Anaerobic wound infection is a complication of injuries - wounds of hollow organs, burns, frostbite, gunshot, contaminated, crushed wounds.

Anaerobic infection in origin can be community-acquired and; by etiology – traumatic, spontaneous, iatrogenic; by prevalence - local, regional, generalized; by localization - with damage to the central nervous system, soft tissues, skin, bones and joints, blood, internal organs; along the flow - lightning, acute and subacute. According to the species composition of the pathogen, it is divided into monobacterial, polybacterial and mixed.

Anaerobic infection in surgery develops within 30 days after surgery. This pathology is hospital-acquired and significantly increases the patient’s time in the hospital. Anaerobic infection attracts the attention of doctors of various specialties due to the fact that it is characterized by a severe course, high mortality and disability of patients.

Causes

The causative agents of anaerobic infection are inhabitants of the normal microflora of various biocenoses of the human body: skin, gastrointestinal tract, genitourinary system. These bacteria are opportunistic due to their virulent properties. Under the influence of negative exogenous and endogenous factors, their uncontrolled reproduction begins, bacteria become pathogenic and cause the development of diseases.

Factors causing disturbances in the composition of normal microflora:

1. Prematurity, intrauterine infection,
2. Microbial pathologies of organs and tissues,
3. Long-term antibiotic, chemotherapy and hormonal therapy,
4. Radiation, taking immunosuppressants,
5. Long-term hospital stays of various profiles,
6. Prolonged presence of a person in a confined space.

Anaerobic microorganisms live in the external environment: in the soil, at the bottom of reservoirs. Their main characteristic is lack of oxygen tolerance due to insufficiency of enzyme systems.

All anaerobic microbes are divided into two large groups:

Pathogenicity factors of anaerobes:

1. Enzymes enhance the virulent properties of anaerobes and destroy muscle and connective tissue fibers. They cause severe microcirculation disorders, increase vascular permeability, destroy red blood cells, promote microthrombosis and the development of vasculitis with generalization of the process. Enzymes produced by bacteroids have a cytotoxic effect, which leads to tissue destruction and the spread of infection.
2. Exotoxins and endotoxins damage the vascular wall, cause hemolysis of red blood cells and trigger the process of thrombus formation. They have nephrotropic, neurotropic, dermatonecrotizing, cardiotropic effects, disrupt the integrity of epithelial cell membranes, which leads to their death. Clostridia secrete a toxin, under the influence of which exudate is formed in the tissues, the muscles swell and die, become pale and contain a lot of gas.
3. Adhesins promote the attachment of bacteria to the endothelium and its damage.
4. The anaerobic capsule enhances the virulent properties of microbes.

Exogenous anaerobic infection occurs in the form of clostridial enteritis, post-traumatic cellulite and myonecrosis. These pathologies develop after the penetration of the pathogen from the external environment as a result of injury, insect bites, or criminal abortion. Endogenous infection develops as a result of the migration of anaerobes within the body: from their places of permanent residence to foreign loci. This is facilitated by operations, traumatic injuries, therapeutic and diagnostic procedures, and injections.

Conditions and factors that provoke the development of anaerobic infection:

• Contamination of the wound with soil, excrement,
• Creation of an anaerobic atmosphere by necrotic tissues deep in the wound,
• Foreign bodies in the wound,
• Violation of the integrity of the skin and mucous membranes,
• Penetration of bacteria into the bloodstream,
• Ischemia and tissue necrosis,
• Occlusive vascular diseases,
• Systemic diseases
• Endocrinopathies,
• Oncology,
• Great blood loss
• Cachexia,
• Neuropsychic stress,
• Long-term hormone therapy and chemotherapy,
• Immunodeficiency,
• Irrational antibiotic therapy.

Symptoms

Morphological forms of clostridial infection:

Non-clostridial anaerobic infection causes purulent inflammation of internal organs, the brain, often with abscess formation of soft tissues and the development of sepsis.

Anaerobic infection begins suddenly. In patients, symptoms of general intoxication prevail over local inflammation. Their health deteriorates sharply until local symptoms appear, the wounds become black in color.

The incubation period lasts about three days. Patients experience fever and chills, they experience severe weakness and weakness, dyspepsia, lethargy, drowsiness, apathy, blood pressure drops, heart rate increases, and the nasolabial triangle turns blue. Gradually, lethargy gives way to excitement, restlessness, and confusion. Their breathing and heart rate increase. The condition of the gastrointestinal tract also changes: patients' tongue is dry, coated, they experience thirst and dry mouth. The skin of the face turns pale, acquires an earthy tint, and the eyes become sunken. The so-called “mask of Hippocrates” – “fades Hippocratica” - appears. Patients become inhibited or sharply agitated, apathetic, and depressed. They cease to navigate space and their own feelings.

Local symptoms of pathology:

• Severe, unbearable, increasing pain of a bursting nature, not relieved by analgesics.
• Swelling of the tissues of the limb progresses quickly and is manifested by sensations of fullness and distension of the limb.
• Gas in affected tissues can be detected using palpation, percussion and other diagnostic techniques. Emphysema, soft tissue crepitus, tympanitis, slight crackling, box sound are signs of gas gangrene.
• The distal parts of the lower extremities become inactive and practically insensitive.
• Purulent-necrotic inflammation develops rapidly and even malignantly. If left untreated, soft tissues are quickly destroyed, which makes the prognosis of the pathology unfavorable.

Diagnostics

Diagnostic measures for anaerobic infection:

• Microscopy of smears from wounds or wound discharge makes it possible to determine long polymorphic gram-positive “rough” rods and the abundance of coccal microflora. Bacteriods are polymorphic, small gram-negative rods with bipolar coloring, mobile and immobile, do not form spores, strict anaerobes.
• In the microbiological laboratory they carry out bacteriological examination of wound discharge, pieces of affected tissue, blood, urine, liquor. The biomaterial is delivered to the laboratory, where it is inoculated on special nutrient media. The dishes with the crops are placed in an anaerostat, and then in a thermostat and incubated at a temperature of +37 C. In liquid nutrient media, microbes grow with rapid gas formation and acidification of the environment. On blood agar, colonies are surrounded by a zone of hemolysis and in air they acquire a greenish color. Microbiologists count the number of morphologically different colonies and, after isolating a pure culture, study the biochemical properties. If the smear contains gram+ cocci, check for the presence of catalase. When gas bubbles are released, the sample is considered positive. On Wilso-Blair medium, clostridia grow in the form of black colonies in the depths of the medium, spherical or lenticular in shape. Their total number is counted and their belonging to clostridia is confirmed. If microorganisms with characteristic morphological signs are detected in the smear, a conclusion is made. Bacteriodes grow on nutrient media in the form of small, flat, opaque, grayish-white colonies with jagged edges. Their primary colonies are not reseeded, since even short-term exposure to oxygen leads to their death. When bacteriodes grow on nutrient media, a disgusting smell attracts attention.
• Express diagnostics – study of pathological material in ultraviolet light.
• If bacteremia is suspected, the blood is inoculated onto nutrient media (Thioglycolate, Sabouraud) and incubated for 10 days, periodically inoculating the biomaterial onto blood agar.
• Enzyme immunoassay and PCR help to establish a diagnosis in a relatively short time.

Treatment

Treatment of anaerobic infection is complex, including surgical treatment of the wound, conservative and physical therapy.

During surgical treatment, the wound is widely dissected, non-viable and crushed tissue is excised, foreign bodies are removed, and then the resulting cavity is treated and drained. The wounds are loosely packed with gauze swabs with a solution of potassium permanganate or hydrogen peroxide. The operation is performed under general anesthesia. When decompressing edematous, deeply located tissues, a wide fasciotomy is performed. If an anaerobic surgical infection develops against the background of a limb fracture, it is immobilized with a plaster splint. Extensive tissue destruction can lead to amputation or disarticulation of the limb.

Conservative therapy:

Physiotherapeutic treatment consists of treating wounds with ultrasound and laser, conducting ozone therapy, hyperbaric oxygenation, and extracorporeal hemocorrection.

Currently, specific prevention of anaerobic infection has not been developed. The prognosis of the pathology depends on the form of the infectious process, the state of the macroorganism, the timeliness and correctness of diagnosis and treatment. The prognosis is cautious, but most often favorable. Without treatment, the outcome of the disease is disappointing.

plan lectures:

/Kremen V.E./

1. 
   Anaerobic infection (definition, classification);
2. 
   Anaerobic non-clostridial infection (ANI):

1. 
   Etiology, pathogenesis of ANI;
2. 
   Signs of ANI;

3. ANI soft tissues:

3.1. ANI Soft Tissue Clinic;

3.2. Anaerobic non-clostridial peritonitis /clinic/;

3.3. Anaerobic non-clostridial lung infection /clinic/.

4. Diagnostics of ANI:

4.1. bacteriological examination;

4.2. gas-liquid chromatography.

5. Principles of treatment of ANI:

5.1. surgical treatment;

5.2. conservative treatment.

1. 
   Anaerobic clostridial infection.

Anaerobic:

1. 
   gangrene (gas gangrene):
   1. 
      Etiopathogenesis of hypertension;
   2. 
      Stages of the process;
   3. 
      Clinic of limited gas phlegmon;
   4. 
      Clinic of common gas phlegmon;
   5. 
      Gas gangrene clinic;
   6. 
      Prevention of anaerobic (gas) gangrene:

a) nonspecific;

b) specific.

1. 
   Treatment for anaerobic gangrene.

1. 
   Tetanus:
   1. 
      Etiopathogenesis;
   2. 
      Classifications;
   3. 
      General tetanus clinic:

a) in the initial period;

b) during the peak period;

c) during the recovery period.

1. 
   Local Tetanus Clinic;
2. 
   Causes of death due to tetanus;
3. 
   Principles of treatment for tetanus;
4. 
   Prevention of tetanus:

a) nonspecific;

b) specific /indications for emergency specific prevention, drugs/.

1. 
   Diphtheria wounds:

1. 
   The causative agent of infection;
2. 
   Clinical picture;
3. 
   Treatment for diphtheria wounds.

Anaerobic infection is an acute severe surgical infection caused by anaerobic microorganisms.

Classification of anaerobic surgical infection:

1. 
   anaerobic non-clostridial infection
2. 
   anaerobic clostridial infection:
   1. 
      anaerobic (gas) gangrene;
   2. 
      tetanus.

Lecture “Anaerobic surgical infection”.
Anaerobic non-clostridial infection (ANI) is an acute anaerobic surgical infection accompanied by putrefactive tissue destruction.

Pathogens:

1. 
   Gram-negative rods: Bacteroides (B. Fragilis, B. Melaninogenicus, ovatus, distasonis, vulgatus, etc.), Fusobacterium.
2. 
   Gram-positive rods: Propionibacterium, Eubacterium, Bifidobacterium, Actinomyces.
3. 
   Gram-positive cocci: Peptococcus, Peptostreptococcus.
4. 
   Gram-negative cocci: Veilonella.

In addition, opportunistic anaerobes can take part in the development of putrefactive infection: Escherichia coli, Proteus and the symbiosis of anaerobes with aerobes.

Contamination from an exogenous source occurs through wounds contaminated with soil, scraps of clothing, shoes, and other foreign bodies.

The main endogenous sources of anaerobes are the large intestine, oral cavity, and respiratory tract.

Signs of ANI:

1. 
   The most common symptom of anaerobic non-clostridial infection is the putrid odor of the exudate, resulting from anaerobic oxidation of protein substrates. In this case, foul-smelling substances are formed: ammonia, indole, skatole, volatile sulfur compounds. Therefore, the foul odor of exudate always indicates its anaerobic origin. The absence of a putrefactive odor cannot serve as a basis for removing the diagnosis of anaerobic non-clostridial infection, since not all anaerobes form substances that have a fetid odor.
2. 
   The second sign of an anaerobic infection is the putrefactive nature of the exudate. The lesions contain nonstructural detritus, but with accompanying aerobic flora there may be an admixture of pus. These lesions are surrounded by dead tissue of gray or dark color. The skin over the areas of tissue decay is brown or black.
3. 
   The third sign is the color of the exudate: gray-green, brown or hemorrhagic.
4. 
   The fourth sign of an anaerobic infection is gas formation. During anaerobic metabolism, gases that are poorly soluble in water are formed: nitrogen, hydrogen, methane, hydrogen sulfide, etc. Therefore, when soft tissue is damaged, emphysema (accumulation of gas in the form of bubbles) is observed, which is clinically defined as crepitus. However, not all anaerobes cause gas formation to the same extent, so in the early stages and certain associations, crepitus may be absent. In these cases, gas can be detected by x-ray or during surgery.
5. 
   Endogenous foci of anaerobic non-clostridial infection are characterized by proximity to natural habitats (digestive tract, oral cavity, respiratory tract, perineum and genitals).

The presence of two or more of the described signs indicates the undoubted participation of anaerobes in the pathological process.
ANI SOFT TISSUE INFECTION.

This pathology occurs in the form of phlegmon and more often affects the subcutaneous fatty tissue (non-clostridial anaerobic cellulite), fascia (non-clostridial anaerobic fasciitis) or muscle (non-clostridial anaerobic myositis). Putrefactive infection of soft tissues very often complicates circulatory disorders of the lower extremities with atherosclosis, endarteritis and diabetic angiopathy. The spread of non-clostridial anaerobic infection occurs along the length, lymphogenously and along the synovial tendon sheaths (the latter indicates specific tenosynovitis.

With the relatively limited focus of infection, in the early stage there are symptoms of moderate intoxication: general weakness, weakness, loss of appetite, persistent low-grade fever, periodic pain in the area of ​​a bursting nature, increasing anemia, moderate leukocytosis and toxic granularity of neutrophils. As putrefactive phlegmon progresses, the pain becomes intense, depriving sleep. Body temperature rises to 38 0 -39 0 C, chills, increased sweating, and shortness of breath appear. The phenomena of endotoxicosis are increasing, the condition of patients is becoming severe.

Local signs of putrefactive cellulite are expressed by dense swelling of the skin. Its color is initially unchanged, then hyperemia appears without a clear boundary. Subcutaneous emphysema (a symptom of crepitus) can be detected.

Subcutaneous fatty tissue is gray or dirty brown in color with areas of hemorrhage. The exudate is brown or hemorrhagic in nature and often has an unpleasant odor.

With non-clostridial anaerobic fasciitis, rapidly progressing swelling of the skin and subcutaneous tissue, widespread hyperemia, and early foci of skin necrosis are very characteristic. Foci of softening are palpated, and a symptom of crepitus may be present. When tissue is dissected, necrosis of the fascia and adjacent tissue is noted. Detritus is brown in color and has an unpleasant odor.

With non-clostridial anaerobic myositis, swelling of the limb occurs, and bursting pain is very intense. The skin, as a rule, is significantly unchanged; there is practically no necrosis. Distinct lymphangitis, lymphadenitis. Body temperature rises sharply, chills are noted. The condition of the patients is serious. Palpation: dense swelling of the skin and subcutaneous tissue, pain in the area of ​​greatest damage, fluctuation is determined only when the process is advanced. When tissue is dissected, after opening the fascia, dirty-brown detritus is released, often with an unpleasant odor, as well as air bubbles. The muscles disintegrate easily and do not bleed. The boundaries of the lesion are almost impossible to determine.

ANAEROBIC DISEASES OF THE PERITONEUM

Peritonitis, occurring with a predominance of the anaerobic component (putrefactive peritonitis), as a rule, is a consequence of destructive processes of the hollow organs of the abdominal cavity.

The microbial landscape in putrefactive peritonitis is represented by associations consisting of anaerobic and aerobic bacteria. The most common anaerobes found are gram-negative bacilli (E. Coli, bacteroides, Fusobacterium) and gram-positive cocci (Peptococcus, Peptostreptococcus); clostridia are periodically sown. On average, for each case of an infectious process there are 2 aerobes and 3 anaerobes. Of the facultative anaerobes, Escherichia coli is found in the vast majority of cases (85%).

There is a certain dependence of the frequency of different bacteria isolated on the localization of the pathological focus.

Thus, B. fragilis is sown 5 times more often if the process is located in the lower part of the gastrointestinal tract, clostridia, respectively, 4 times, while anaerobic cocci are sown from pus almost equally, regardless of the location of the process.

The clinical picture of peritonitis, which occurs with a predominance of the anaerobic component, has its own characteristics. Abdominal pain is the earliest symptom of peritonitis; during a putrefactive process, it is usually not intense; Spontaneous pain is less pronounced than pain that occurs during palpation. Pain of a constant nature, palpation tenderness is first determined in the area of ​​the source of peritonitis, and then in the areas of spread of the inflammatory process. Vomiting is a very common symptom of peritonitis. The body temperature during putrefactive peritonitis in the early stages is subfebrile; however, as the process spreads and the duration of the course increases, the temperature becomes hectic in nature and chills appear.

The general condition of the patients does not change significantly within 2-3 days, euphoria is noted; then the condition quickly and progressively worsens.

An objective examination reveals early scleral icterus, tachycardia, shortness of breath, and symptoms of paralytic obstruction.

Abdominal wall tension is usually mild, and there are no symptoms of peritoneal irritation at an early stage. The not entirely typical course of acute peritonitis very often causes diagnostic errors. A repeated blood test helps clarify the diagnosis, which reveals progressive anemia, moderate leukocytosis with a shift to the left, pronounced toxic granularity of neutrophils, increasing ESR, dysproteinemia, hypoproteinemia, bilirubinemia.

Intraoperative diagnosis is based primarily on the nature and smell of the exudate. On the first day of development of putrefactive peritonitis, the exudate is serous-fibrinous (cloudy) or serous-hemorrhagic with the presence of droplets of fat; later it takes on the appearance of greenish or brownish-brown pus. Fibrinous deposits are dirty green in color and represent jelly-like masses that are easily separated from the peritoneum and are found in the exudate in the form of many fragments. The peritoneum is dull, the walls of the underlying tissues are infiltrated and are easily injured.

Peritonitis, pathogenetically associated with the gastrointestinal tract, usually leads to the formation of exudate with a foul odor.

Postoperative anaerobic peritonitis is often diagnosed late after surgery, since the symptoms of paralytic obstruction are regarded as a postoperative condition. Under these conditions, anaerobic phlegmon of the surgical wound often occurs. The pathological process from the abdominal cavity spreads to the preperitoneal tissue, and then to other layers of the abdominal wall. The skin is not involved in the process for a long time. Late diagnosis of phlegmon of a surgical wound ends with eventeration - the exit of abdominal organs through the surgical wound to the outside or under the skin.

NONCLOSTRIDIAL ANAEROBIC INFECTION OF THE LUNG
Putrefactive lung abscesses are usually associated with atelectasis due to aspiration and obstruction of small bronchi or with severe pneumonia. The occurrence of such abscesses is facilitated by chronic diseases of the oral cavity and nasopharynx (alveolar pyorrhea, periodontal disease, chronic tonsillitis, etc.), as well as a decrease in the body's resistance.

An early sign of putrefactive lung abscess is an acute onset: chills, increased body temperature to 39-40 0 C, chest pain, shortness of breath. The cough is dry at first, but then sputum appears, the amount of which is constantly increasing. The sputum changes from mucous to purulent in nature, a fetid odor of exhaled air appears, which is especially strong at the moment the abscess breaks into the bronchus, which is accompanied by immediate copious discharge of sputum (150-500 ml) of a dirty gray or gray-brown color. Subsequently, sputum is released especially abundantly at a certain position of the body, its amount reaches 100-300 ml per day. The general condition is progressively worsening.

Objectively, pallor of the skin with icterus, tachycardia, and a tendency to hypotension are noted. Severe shortness of breath (30-40 respiratory excursions). The respiratory excursion of the chest on the affected side is limited, dullness over the affected area is noted by percussion, and wet and dry rales are heard.

When examining peripheral blood, anemia, leukocytosis, shift to the left, toxic granularity of neutrophils, accelerated ESR are revealed; with a long course of the process - leukopenia, aneosinophilia, neutropenia, hypoproteinemia, dysproteinemia, bilirubinemia, azotemia.

During an X-ray examination, at the onset of the disease there is intense darkening with foci of clearing; after the abscess breaks into the bronchus, a cavity with a fluid level and perifocal infiltration of the lung tissue without clear boundaries are determined.

The diagnosis of non-clostridial anaerobic infection is based on medical history, clinical symptoms, morphological examination of biopsy material, bacteriological and chromatographic examination.

Bacteriological research is implemented in the form of a three-stage scheme:

The first stage is microscopy of the native material, Gram-stained and microscopy in ultraviolet light immediately after receiving the material;

The second stage (after 48 hours) - assessment of the growth of microbes grown under anaerobic conditions, morphology of the colony and cells, examination of cells in ultraviolet light;

The third stage (after 5-7 days) is the identification of grown microorganisms.

Gas-liquid chromatography is based on the fact of accumulation in exudate and tissues during putrefactive infection of volatile fatty acids (acetic, propionic, butyric, caproic) and derivatives of phenol, indole, pyrol, which are produced by anaerobic microorganisms. The method allows you to detect these substances in 1 cm 3 of tissue or 1 ml of exudate.

Principles of treatment of non-clostridial anaerobic infection

The results of treatment of putrefactive infection depend on a complex treatment system, including surgery (local treatment), detoxification, antibacterial therapy, stimulation of the body’s natural and immunological resistance and correction of morphofunctional disorders of organs and systems (general treatment).

Surgical treatment of putrefactive infection of soft tissues involves radical surgical treatment. Tissue dissection begins with intact skin, the incision passes through the entire affected area and ends at the border of intact tissue. Then a wide, thorough excision of the affected tissue is performed, regardless of the extent of the defect formed after surgical treatment.

The edges of the wound are spread widely, the remaining unaffected skin flaps are turned out and fixed to the nearest areas of the skin.

The resulting wound is washed with a pulsating stream of chlorhexidine or dioxidine and thoroughly dried, removing small pieces of necrotic tissue using an electric suction device or other vacuum device.

Further wound management is carried out using:

Fractional irrigation through tubes with oxygen-releasing solutions or solutions of dioxidine, metronidazole;

Loose tamponing with gauze napkins moistened with water-soluble ointment (levamicol, levasin, dioxidine).

After stopping the process and the appearance of granulations, skin grafting of the resulting defects is often used. In cases where there is total damage to the soft tissues of a limb segment, there is a need for amputation.
Treatment of anaerobic peritonitis is surgical: laparotomy, sanitation of the abdominal cavity, drainage.

Surgical treatment of patients with anaerobic lung abscesses is carried out in cases where there is inadequate natural drainage through the bronchus or with “blocked” abscesses. In case of poor natural drainage, the main method of treatment is sanitary bronchoscopy and microtracheostomy to deliver antiseptics and antibiotics to the lesion.

The main causative agents of non-clostridial anaerobic infection (bacteroides, cocci, fusobacteria) are very sensitive to the following antibiotic-bacterial drugs: thienam, clindamycin (Dalacin C), metronidazole, lincocin, tricanix (tinidozole) and dioxidine; have average sensitivity to cephalosporins and chloramphenicol.
ANAEROBIC (GAS) GANGRENE -

Severe wound infection with predominant damage to connective and muscle tissue, caused by strict anaerobes (clostridia).

Preferential localization

1. Lower limbs - 70%

2. Upper limbs - 20%

3. Other parts of the body - 10%

Mortality during the Great Patriotic War was 50-60%.

Pathogens: clostridia: Cl.perfringens-50-90%; Cl. novi - 20-50%; Cl.septicum - 10-15%; other clostridia - 5-6%. Along with clostridia, facultative anaerobes, as well as a wide variety of aerobes, can take part in the development of gas gangrene.

Pathogenesis. The incubation period for 90% of cases is 2-7 days, for 10% it is 8 or more days.

Factors contributing to the development of gas gangrene: microbiological, local, general:

1. Microbial associations

In 80-90% of patients, the disease develops as a result of the introduction of 2 or more types of anaerobic microorganisms and 2-3 aerobes.

2. Local factors contributing to the development of gangrene

2.1. Blind deep wounds in the area of ​​powerful muscle layers are especially dangerous - shrapnel wounds.

2.2. Open, especially gunshot fractures.

2.3. The presence of foreign bodies in the wound (pieces of clothing, shoes, wood, etc.), soil contamination.

2.4. Damage to the great vessels of the limb.

3. Reduced body resistance:

3.1. Acute blood loss.

3.2. Traumatic shock.

3.3. Chronic anemia.

3.4. Hypovitaminosis.

3.5. General hypothermia.

3.6. Nutritional exhaustion.

Stages of the process

1. Limited gas phlegmon (within the wound canal and surrounding tissues).

2. Widespread gas phlegmon (within a limb segment or more).

3. Gas gangrene (starts in the distal parts of the limb, spreading in the proximal direction).

4. Sepsis (usually caused by aerobic or facultative anaerobic microorganisms).

Clinic of limited gas phlegmon

1. Mental agitation, severe weakness, fatigue against the background of low-grade fever.

2. Bursting pain in the wound after a certain period of disappearance (calming) of it.

3. Swelling, rapidly progressing in the wound area, feeling of tightness of the applied bandage.

4. Severe tachycardia (110-120 beats per minute), shortness of breath.

5. When examining the wound, a dirty gray coating appears; there is a little discharge, the color of meat slop; swelling of the wound edges; unpleasant, sometimes sickly-sweet odor. There are no other signs of acute purulent inflammation (skin hyperemia, local fever).

6. The symptom of crepitus in the tissues surrounding the wound canal is determined by palpation (a kind of crunch, creaking of air bubbles).

7. Positive Melnikov’s symptom (ligature symptom): a silk thread tied around a limb near the wound after 1-2 hours, due to rapidly progressing swelling and an increase in the volume of the limb, sinks into the swollen skin.

8. Moderate leukocytosis with a shift to the left

Clinic of common gas phlegmon

1. The patient’s condition is serious, high fever, insomnia, agitation, shortness of breath.

2. Pain of a bursting nature intensifies, spreading along the limb to proximal direction from the wound.

3. Pale skin with an icteric or earthy tint.

4. Blood pressure is reduced, pulse is 120-130 beats. per minute, low filling.

5. Sudden swelling of the limb. The skin of the affected limb is pale, with a bluish pattern of translucent veins, in places blisters, with serous or serous-hemorrhagic contents.

6. Inspection of the wound: its edges bulge (turn out) above the surface of the skin; The discharge is light, bloody-dirty in color, and often has a foul odor.

7. Widespread crepitus (the presence of gas in the tissues) is determined by palpation.

8. X-rays (on pictures) reveal gas bubbles in tissues located away from the wound in the form of a chain.

9. High leukocytosis with a shift to the left, toxic granularity of neutrophils, anemia.

Gas gangrene stage clinic

1. The patient’s condition is serious or extremely serious. Consciousness is inhibited, delirium, motor agitation, high fever, severe shortness of breath, decreased diuresis (oliguria).

2. The pain is intense throughout the entire limb, but especially in the distal parts (fingers, feet).

3. The skin is pale with an earthy tint, facial features are sharpened, the tongue is dry, covered with a brown coating.

4. Blood pressure is reduced, pulse is 120-140 beats. per minute, low filling.

5. The skin of the affected limb is pale, sometimes with a bluish or brown tint. Severe swelling, the volume of the affected limb is 3-4 times greater than the healthy one, on the skin in the affected area there are blisters with hemorrhagic or brown contents.

6. The limb is cold, especially in the distal parts; there is no sensitivity at a certain level; severe disturbances in active movements; There is no vascular pulsation in the periphery. All these 4 symptoms indicate gangrene of the limb.

7. The wound is lifeless, the damaged muscles bulge from the wound, their color is gray-brown (“dirty”), the discharge is bloody-dark in color, and has an unpleasant, sometimes fetid odor.

8. The widespread accumulation of gases in the tissues of the affected limb is determined by palpation and x-ray.

Depending on the nature of the microbes and the reactivity of the body, the following forms of anaerobic infection occur:

1. 
   Edema
2. 
   Mixed
3. 
   Emphysematous
4. 
   Necrotic
5. 
   Phlegmanous
6. 
   Fabric melting

The given forms of gas gangrene reflect the local features of the process.

Prevention of anaerobic gangrene

1. 
   Early adequate surgical treatment of open injuries, wide drainage of the wound with tubular drainages and flow-through rinsing (continuous or fractional) with oxygen-releasing solutions (oxidizing agents: potassium permanganate, hydrogen peroxide). Immobilization.
2. 
   Administration of large doses of antibiotics: thienam (1.5-2.0 g per day), penicillin (3-5 million units 6 times a day), semi-synthetic penicillins (ampicillin, oxacillin, ampiox - up to 6-8 g) ; lincomycin (1.8 – 2.0 g).
3. 
   Administration of polyvalent anti-gangrenous serum, prophylactic dose of 30 thousand IU (10 thousand units each against Cl. Perfringens, Cl. Novi, Cl. Septicum).
4. 
   Bacteriophage anaerobic 100 ml. diluted with 100 ml. 0.5% novocaine solution infiltrates the tissue around the wound.

Treatment of anaerobic gas gangrene

1. Surgical treatment is determined by the stage of the process.

1.1. In case of limited gas phlegmon - wide dissection of the wound with excision of all non-viable tissues, if necessary, counter-openings are performed. Drainage: tubular drainages, continuous flow irrigation of the wound with oxygen-releasing solutions (potassium permanganate 1:1000; hydrogen peroxide 1-2% solution). Immobilization.

1.2. With widespread gas phlegmon - wide dissection of the wound with excision of all non-viable tissue; strip dissection of the tissues of the limb with fasciotomy within the affected segment. Drainage: tubular drainages, continuous flow irrigation of the wound with oxygen-releasing solutions. Immobilization.

1.3. At the stage of gangrene - amputation of the limb, if possible, within the limits of healthy tissue. Amputation is performed without applying a tourniquet. Primary sutures are never placed. Drainage of the wound is done in the same way as with phlegmon.

In case of amputation at the level of questionable tissues, a strip dissection of the soft tissues of the stump of the amputated limb is performed, drainage with tubular drainages with continuous irrigation with oxygen-releasing solutions. Immobilization.

2. Specific treatment

2.1. Antibiotics intravenously and intramuscularly: penicillin 40-60 million units. per day; semisynthetic penicillins (ampicillin, oxacillin, ampiox) up to 8-10 g per day; lincomycin 2.0-2.4 g per day.

2.2. Polyvalent anti-gangrenous serum 5-6 prophylactic doses.

2.3. Anti-gangrenous bacteriophage 100-150 ml is diluted with 400-500 ml of physiological sodium chloride solution, administered intravenously, slowly.

3. Oxybarotherapy (HBO - hyperbaric oxygenation): repeated sessions in a pressure chamber with oxygen under a pressure of 2.5-3.0 atmospheres.

4. Symptomatic therapy, including a detoxification system.

TETANUS (tetanus)
Acute severe specific wound infection caused by the tetanus bacillus (Cl. tetani).

Every year, 1.5-1.7 million people worldwide suffer from tetanus, and about 1.0 million people die. Mortality ranges from 30 to 45%, in elderly people it reaches 60-70%, and in newborns - 90-95%.

Etiology- tetanus stick; it is little mobile, forms spores that are very resistant to the influence of the external environment. Saprophyte under normal conditions lives in the intestines of animals (100%) and humans (20-30%). Soils fertilized with manure are extremely dangerous as a source of infection, since they contain 100% tetanus bacillus (spores). Apparently, this circumstance can explain the significant incidence of tetanus in rural residents (75%).

Pathogenesis. The disease can develop only when the rod is introduced into the tissue and if anaerobic conditions are created.

During the process of reproduction under anaerobic conditions, the tetanus bacillus releases a strong exotoxin, consisting of two fractions: tetanospasmin- causing the typical convulsive picture of tetanus and tetanolysin, which causes hemolysis of red blood cells and inhibits phagocytosis. Thus, the clinical picture of tetanus is caused not by microorganisms, but by their toxins entering the blood and central nervous system.

Tetanospasmin itself does not directly cause the convulsive component, but by binding to the nervous tissue, it blocks the inhibitory effect of interneurons. Thus, it removes all types of inhibitory regulation, blocking the differential function of central neurons. Under these conditions, under the influence of a nonspecific stimulus or spontaneously, excitation arises in the motor neurons, which in the form of impulses of various types arrives at the striated muscles. This causes their rigidity and the development of clonic and tonic convulsions.

Due to metabolic and thermoregulation disorders and respiratory disorders, hypoxia and acidosis arise and progress in the body.

Pathological changes with tetanus they do not have specific symptoms.

Classification depending on the mechanism of penetration of the microorganism and the occurrence of tetanus.

1. Wound. 2. Post-burn. 3. Postpartum. 4 Tetanus of newborns. 5. Postoperative. 6. For diseases accompanied by destruction of the large intestine.

Clinical classification

1. General tetanus

1.1. Primarily general. 1.2. Descending general. 1.3. Rising general.

2. Local tetanus (vaccinated and rare forms).

In humans, the disease, as a rule, proceeds like general tetanus.

Depending on the severity of the course, the following forms are distinguished:

1) very heavy, 2) heavy, 3) moderate, 4) light.

General Tetanus Clinic

The incubation period is most often 5-15 days, but the disease may develop 30 days after injury or even later. The shorter the incubation period, the more severe the tetanus.

Clinic tetanus in unvaccinated or vaccinated people, but more than 10 years ago, is very typical. N.I. Bereznyagovsky wrote: “Whoever has observed such a disease once will never forget the clinical picture of tetanus.”

There are an initial period, a peak period and a recovery period.

Initial period (early signs of tetanus): weakness, weakness, irritability, difficulty opening the mouth and swallowing, muscle pain, extremely severe sweating, increased temperature, severe tachycardia, muscle twitching in the wound area, stool retention, urination. The initial period lasts from 1 to 6 days. The duration of the initial period determines the severity of tetanus; the shorter this period, the more severe the tetanus and the higher the mortality rate.

High period- clear signs of tetanus. Against the background of the previously listed symptoms, the following appear: a sardonic smile - a tonic contraction of the facial muscles creates the appearance of a smile, but at the same time there is a pained expression in the eyes; increased muscle tone, including plank belly; clonic and tonic local, and then generalized convulsions. In humans, general tetanus most often occurs in a descending form: trismus of the masticatory muscles, rigidity of the neck (pronounced increase in the tone of the neck muscles), upper extremities, torso, lower extremities. Generalized tonic convulsions cause opisthotonus: arching of the patient's body anteriorly (predominance of extensor strength) and the patient touches the bed with the back of the head, heels and elbows. If during tonic convulsions you can hold a fist under the patient’s back, this indicates the presence of opisthotonus (G.N. Tsibulyak).

The most important disorder associated with the convulsive component is respiratory failure, since this causes tonic contraction of the intercostal muscles and the diaphragm, which often leads to apnea (cessation of breathing).

Tonic convulsions are so intense that patients moan and cry in pain. Sometimes, as a result of muscle contraction, avulsion fractures and muscle tears develop. The period of the height of the disease continues until the end of the second - beginning of the third week.

Recovery period characterized by gradual extinction of cramps and decreased muscle tone. Due to the presence of developed complications, the restoration of homeostasis parameters occurs very slowly.

Local tetanus a rare phenomenon, it develops in cases where a small amount of tetanus bacillus gets into the wound, and the wound contains a small amount of necrotic tissue, or when the patient has a relatively tense immune system.

Clinically, local tetanus is manifested by increased muscle tone, and sometimes by local convulsions, often clonic in nature, localized mainly near the entrance gates of the infection. A characteristic type of local tetanus is facial paralytic tetanus (“facial tetanus of Rose”), which occurs with unilateral or bilateral contraction of the facial and masticatory muscles. Local tetanus is not accompanied by endotoxicosis and fever: the disease passes quickly (3-5 days), but at any time it can turn into generalized convulsions.

Main causes of death due to tetanus

1. External respiration disorder - asphyxia.

2. Cardiac arrest (asystole) or cardiovascular failure.

3. Metabolic exhaustion.

4. Pulmonary complications (pneumonia, atelectasis, abscess, lung gangrene).

Principles of treatment

Treatment of patients with tetanus is carried out in intensive care units; transportation is carried out in a specialized vehicle accompanied by a resuscitator or anesthesiologist.

The following tasks are solved in the hospital:

1. STOP the release of toxin into the blood

For these purposes, the following activities are carried out:

Under anesthesia, surgical treatment of the wound is performed (wide dissection with excision of necrotic tissue);

Drainage of the wound with tubular drainages with flow-through irrigation with oxygen-releasing solutions;

Limb immobilization;

Administration of antibiotics intravenously, intramuscularly: penicillin (40-60 million units per day), semisynthetic penicillins (ampicillin, oxacillin, ampiox - 8-10 g per day), lincomycin (2.0-2.4 g per day);

HBO (hyperbaric oxygenation) - oxygen therapy sessions in a pressure chamber under a pressure of 2.5-3.0 atmospheres.

2. Neutralize the toxin circulating in the blood, lymph, interstitial fluid (it is impossible to neutralize the toxin associated with the nervous tissue).

Various drugs are used to neutralize the toxin.

2.1. Antitetanus serum (TSS) - horse immune serum is administered 100 thousand IU on the first day of treatment, and then 50 thousand IU for 2 days intramuscularly, extremely rarely intravenously. In severe cases, the total dose of PSS increases to 300 thousand IU.

2.2. Human tetanus immunoglobulin (HTI) is administered intramuscularly or intravenously in the amount of 30-40 thousand IU.

1. 
   Adsorbed tetanus toxoid 1.0 ml (20 EU) is administered intramuscularly, 3 times every other day. Anatoxin, competing with tetanospasmin, can theoretically displace it from nervous tissue.

3. Eliminate (stop) the convulsive component

To treat the convulsive component, anesthesia (sodium hydroxybutyrate, neuroleptanalgesia, sodium thiopental) and the administration of non-depolarizing muscle relaxants with artificial ventilation are used. In case of severe prolonged convulsive crisis, patients undergo tracheostomy, which significantly reduces the likelihood of developing severe pulmonary failure and pulmonary complications.

For mild cases of tetanus, it is possible to use antipsychotics(aminazine 2.5% - 2 ml intramuscularly 3 times a day), tranquilizers(Relanium 0.5% - 4-6 ml intramuscularly 3 times a day), sleeping pills(barbamyl 10% - 5 ml intravenously 2 times a day, chloral hydrate 2% - 100 ml in enema).

4. Correction of the function of the cardiovascular system.

5. Prevention of complications, especially pulmonary ones (sanitation of the oral cavity, bronchial tree, administration of antibiotics), careful care.

6. Ensuring energy needs, correcting water and electrolyte balance. Replenishment of energy expenditure, loss of fluid and electrolytes is carried out through parenteral and enteral (if necessary through tube) administration of protein and energy substrates, fluids and electrolytes.

Prevention of tetanus

1. Non-specific prophylaxis

1.1. The basis of nonspecific prevention is primary surgical treatment of the wound.

2. S p e c t i c a l prophylactic

2.1. Active immunization.

CHILDREN AND TEENAGERS

1. Adsorbed pertussis-diphtheria-tetanus toxoid (DTP) from three months three times with an interval of 1.5 months. Revaccination after 1.5-2 years.

2. Adsorbed diphtheria-tetanus toxoid (ADS) - at six and eleven years old.

3. Adsorbed tetanus toxoid (AS) (1 ml of AS contains 20 units of tetanus toxoid - EC) - at 16 years of age.

Such immunization ensures the maintenance of strong immunity against tetanus (antitoxin in the blood serum more than 0.1 IU/ml) until the age of 25.

ADULTS

AS is administered intramuscularly - 0.5 ml; after 30-40 days, AC - 0.5 ml is re-injected intramuscularly, vaccination is completed.

The first revaccination is carried out after 9-12 months: AC - 0.5 ml; repeated revaccinations - every 5-10 years: AC - 0.5 ml intramuscularly.

With this immunization system, intense tetanus immunity is maintained throughout life.

2.2. Passive immunization

2.2.1. Antitetanus serum (PSS - horse) 3000 AE forms passive immunity for 2-3 weeks.

PSS is administered subcutaneously, but the body's sensitivity to the foreign protein found in the serum is first examined. To do this, 0.1-0.2 PSS, diluted 100 times, is injected intradermally. If the test is negative (control after 30-40 minutes), 0.1 ml of undiluted serum is injected subcutaneously and after 30-40 minutes, in the absence of a general allergic reaction, the rest of the amount of PSS containing 3000 AE (the contents of one ampoule) is injected.

If the intradermal test is positive, the body is desensitized with the same PSS diluted 100 times. 0.5, 2.0 and 5.0 ml of diluted PSS are injected subcutaneously at intervals of 30-40 minutes. After administering the last dose of diluted serum, 0.1 ml of undiluted PSS is injected subcutaneously 30 minutes later; after 40-60 minutes, in the absence of signs of an allergic reaction, the remaining amount of undiluted serum containing 3000 AE is injected subcutaneously.

2.2.2. ICHPS (human tetanus immunoglobulin) in a dose of 250-1000 IU, administered subcutaneously, creates passive immunity for 30 days. In this case, allergic reactions are possible, which are usually stopped by the administration of antihistamines and corticosteroids.

2.3. Active-passive immunization

When admitting patients with open injuries, it is necessary to accurately determine the timing of their vaccination and revaccination and determine the level of antitoxin in the blood serum.

2.3.1. Vaccinated adults (timely vaccinated and revaccinated) and all children with open lesions are administered 0.5 ml of AS subcutaneously.

2.3.2. Unvaccinated adults and vaccinated, but if after:

More than 2 years have passed since vaccination;

More than 5 years have passed since revaccination;

More than 10 years have passed since repeated revaccination;

it is necessary to inject subcutaneously 1.0 ml of AC and another syringe into another part of the body subcutaneously ICHPS 250-1000 IU or 3000 PSS.

After 30 days, unvaccinated people must be injected subcutaneously with 0.5 ml of AS.

For repeated open injuries up to 20 days after immunization, no immune drugs are administered. For open injuries that occurred from 20 days to 2 years after the previous immunization, only 0.5 ml of AS is administered subcutaneously to patients.

2.4. The choice of a means of specific prevention of tetanus depending on the level of tetanus antitoxin in the patient’s blood at the moment.

When a wounded person is admitted to the hospital, one of the methods for quantitative determination of tetanus antitoxin is to examine its level in the blood serum (IU in 1 ml of serum).

2.4.1. When the antitoxin concentration is equal to or greater than 0.1 IU/ml, the victim is not administered specific tetanus prophylaxis (category A patients).

2.4.2. If the antitoxin titer is in the range of 0.01 to 0.1 IU/ml, the patient is advised to administer only a booster dose of AC - 0.5 ml (patients of category B).

2.4.3. If the antitoxin titer is less than 0.01 IU/ml (patients of category B), then it is necessary to carry out active-passive prophylaxis: AC - 1.0 ml (20 EU) subcutaneously; and then with another syringe into another part of the body - human tetanus immunoglobulin (HTI) - 250-1000 IU or PSS - 3000 IU (according to the method outlined above).

On the 4th day after vaccination, all patients in category B undergo a control determination of the titer of tetanus antitoxin in the blood serum. In cases where the level of antitoxin is below 0.01 IU/ml, patients are immediately administered 250-1000 IU ICHPS or 3000 IU PSS.

INDICATIONS FOR EMERGENCY IMMUNIZATION
1. Open mechanical damage

2. Bite wounds

3. Burns, frostbite (II-IV degrees)

4. Criminal abortion

5. Bedsores, necrosis, gangrene, trophic ulcers

6. Operations related to opening the lumen of the large intestine

7. Extensive hematomas subject to puncture or opening.

Immunization of patients with this pathology is carried out in accordance with the stated principles of active-passive immunization.